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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
" g% l% O0 h; z- H0 aBoy Induced by Indirect Topical
1 u3 [0 _3 Q# M4 z  sExposure to Testosterone. b* k# M- b1 c+ D
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
. w) @! r# a' a3 z: A/ ~and Kenneth R. Rettig, MD1+ ~. @6 Z1 l4 A
Clinical Pediatrics
+ b' b, V$ n% `$ O+ q' ~+ K9 ?Volume 46 Number 60 m7 X% [, _; J$ E
July 2007 540-5434 s. o- B/ _# K' T& W$ G& v) D
© 2007 Sage Publications
# n$ P& d* S8 N. p9 v# A/ N10.1177/0009922806296651
' z! @) s) U; Z$ D0 Y: f+ o- C* Thttp://clp.sagepub.com  z! C" @) _8 o" ]/ X
hosted at
* J. `" E& R5 u, Z5 x) Bhttp://online.sagepub.com8 G! t8 N3 O! v# g  @
Precocious puberty in boys, central or peripheral,
' z1 C: p: N! ~7 Lis a significant concern for physicians. Central
3 @& O/ I0 m$ z2 N5 W, I0 t6 Qprecocious puberty (CPP), which is mediated
5 Y. h* F( \$ e2 mthrough the hypothalamic pituitary gonadal axis, has: v- i3 J- L1 `0 }; v/ I% e9 o' d
a higher incidence of organic central nervous system7 s" \, _" e0 I, K
lesions in boys.1,2 Virilization in boys, as manifested0 I+ w7 X8 D6 o% @* p
by enlargement of the penis, development of pubic: q4 p  c/ k- W; R. K: ^
hair, and facial acne without enlargement of testi-
! D1 w% C$ Y9 ^cles, suggests peripheral or pseudopuberty.1-3 We
) o9 J5 t( [8 }% lreport a 16-month-old boy who presented with the3 K* p. `0 ^& @7 d% Z0 R+ R% I
enlargement of the phallus and pubic hair develop-' K% |' ?) n1 L& q. b3 w3 |
ment without testicular enlargement, which was due# _' ~  p6 O; C4 ^( x  {
to the unintentional exposure to androgen gel used by
& ~: {8 \8 ?! i: l6 Othe father. The family initially concealed this infor-
* g! D1 }3 f5 p, j4 v7 j) @6 x/ hmation, resulting in an extensive work-up for this
( b0 w' \- \, d7 E' f# t6 M  wchild. Given the widespread and easy availability of2 w) d, u6 w! i
testosterone gel and cream, we believe this is proba-3 h8 h. g! \% P: I, v/ Q# o
bly more common than the rare case report in the0 |$ m9 y' E  U8 h' S8 ]
literature.4
6 T" v& h0 z$ IPatient Report) F9 e2 \- J9 Q3 x1 p5 \
A 16-month-old white child was referred to the; k  K6 [5 r8 @* g$ A
endocrine clinic by his pediatrician with the concern
( R5 j! d( W1 F; b9 Sof early sexual development. His mother noticed) _) j; o2 x" V
light colored pubic hair development when he was( G! M4 A! o* I9 f5 \( K  c7 F1 C
From the 1Division of Pediatric Endocrinology, 2University of; k, ]; w0 ]5 f
South Alabama Medical Center, Mobile, Alabama.% f6 O, f3 g# }0 E; {5 Q
Address correspondence to: Samar K. Bhowmick, MD, FACE,8 K; q6 B' t0 u0 [( n/ K
Professor of Pediatrics, University of South Alabama, College of. m5 H. L4 Z: V3 Y8 {
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
3 z- H% q! @! @5 b. |e-mail: [email protected].
/ s$ e' Q! ^0 d# l6 E+ babout 6 to 7 months old, which progressively became
) o: @" K. h, ^4 K& Qdarker. She was also concerned about the enlarge-/ @4 L) B4 I& v: f. J: f
ment of his penis and frequent erections. The child# x, D. p( G0 D. p0 ~. ~& o8 l
was the product of a full-term normal delivery, with
* o* I) C! o( N; ^# Xa birth weight of 7 lb 14 oz, and birth length of
6 a; Q; q" `2 G! y20 inches. He was breast-fed throughout the first year
0 |% @' {; x; ]; Z" U# C$ q5 uof life and was still receiving breast milk along with
# T; S2 g/ @) y1 V) b  \solid food. He had no hospitalizations or surgery,
$ g. B' Y& d" @( Eand his psychosocial and psychomotor development
" r) p' e2 ?( e8 r& g0 owas age appropriate.
/ p- d+ ^* X* w! O0 D7 M+ uThe family history was remarkable for the father,$ b& P* }% i' o
who was diagnosed with hypothyroidism at age 16,
* R5 ?" K  M% U! Bwhich was treated with thyroxine. The father’s
0 o5 p1 O9 ~2 y- H( N3 A- @height was 6 feet, and he went through a somewhat3 ~, l2 u' m- k  T
early puberty and had stopped growing by age 14.
3 z$ U2 E8 P: X/ x9 ]. ~( IThe father denied taking any other medication. The
) ]2 y8 ], o2 ^child’s mother was in good health. Her menarche7 m( `6 o' x7 x3 Y" ~) T( H/ [
was at 11 years of age, and her height was at 5 feet
) y! ]& c- ?; b) P- ~/ U5 [5 inches. There was no other family history of pre-
: u7 B: i* b% X- h/ Wcocious sexual development in the first-degree rela-
# r. h  s) C& h& Btives. There were no siblings., W- ?8 J( B: G5 `
Physical Examination
  i" \" A7 |& x, fThe physical examination revealed a very active,
% p) m; o8 S) u% u; t* e. wplayful, and healthy boy. The vital signs documented
  [; U  {5 ?; g" wa blood pressure of 85/50 mm Hg, his length was
1 W3 ^1 J% A# X# x" W; I90 cm (>97th percentile), and his weight was 14.4 kg
2 e. V/ C8 j$ d(also >97th percentile). The observed yearly growth; u5 z2 {7 J; n% Q8 I/ T
velocity was 30 cm (12 inches). The examination of! j/ |( K8 i3 t; c
the neck revealed no thyroid enlargement.+ x8 F% S# |, p2 c* M) |/ o
The genitourinary examination was remarkable for
: e3 k: s! O' P% F& i- Nenlargement of the penis, with a stretched length of( c  D8 c, K" Q" V1 I
8 cm and a width of 2 cm. The glans penis was very well4 m" x+ T% j! L' [# x1 V. @! v6 y. c
developed. The pubic hair was Tanner II, mostly around* }; U2 T4 j3 A
540% W0 ^/ |1 G* b% n/ P
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
; i, q( V: ?5 l5 |the base of the phallus and was dark and curled. The
; A8 ?# Z" M  q3 g# z) Btesticular volume was prepubertal at 2 mL each.
, ?! L* D: D# V$ L7 aThe skin was moist and smooth and somewhat. ]2 T1 Q5 `; |0 G# u! m" P
oily. No axillary hair was noted. There were no9 M: c; K3 j; J! J: O
abnormal skin pigmentations or café-au-lait spots.* ]( Z4 Q% Y7 n  x% P% _; n
Neurologic evaluation showed deep tendon reflex 2+4 |9 ~+ P: d. `8 I
bilateral and symmetrical. There was no suggestion
% x5 ?8 W+ I# Mof papilledema.
3 f$ }" a; H5 Y9 n; v% sLaboratory Evaluation
' P6 j7 q$ M, A* |1 [7 f9 a; PThe bone age was consistent with 28 months by
. r( B4 N" }3 `+ V7 _: b! Qusing the standard of Greulich and Pyle at a chrono-
# d' @4 J* z4 c* J: H: ylogic age of 16 months (advanced).5 Chromosomal5 g3 X% T5 U9 @% |2 [7 N5 j# J8 K
karyotype was 46XY. The thyroid function test2 w9 B* m8 M( L9 m5 c/ |
showed a free T4 of 1.69 ng/dL, and thyroid stimu-8 r# i3 j. |3 |9 c
lating hormone level was 1.3 µIU/mL (both normal).
) Y$ f( f4 `" n6 d- K- V. TThe concentrations of serum electrolytes, blood
1 u  j- A/ }3 }% F5 Nurea nitrogen, creatinine, and calcium all were
$ w8 k$ `* b$ s* G* Z4 r" I9 nwithin normal range for his age. The concentration
' e/ ~' W4 j1 K: g) Iof serum 17-hydroxyprogesterone was 16 ng/dL/ D  V7 l" T1 P% k0 q* o" k
(normal, 3 to 90 ng/dL), androstenedione was 20$ N. P  b" g3 P! Q8 ?- P* _
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-. m! {* n; c5 R; {/ N9 V
terone was 38 ng/dL (normal, 50 to 760 ng/dL),0 e0 w& ^( e' Y" e% t, N* r
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
0 f1 ~4 s$ {8 k% E49ng/dL), 11-desoxycortisol (specific compound S)
7 c5 ^; L4 L0 R8 {! Lwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
( F+ k9 T% d5 ^/ \8 Ftisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
( x: F$ ?+ _8 E8 h; T) Vtestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
' ^# Z4 B8 }6 Y1 f9 d0 I# \and β-human chorionic gonadotropin was less than
$ Q% ]2 s) U1 @2 ~5 mIU/mL (normal <5 mIU/mL). Serum follicular5 K$ n- ~2 t' a
stimulating hormone and leuteinizing hormone
- }0 s( B3 H/ }" B$ Bconcentrations were less than 0.05 mIU/mL' i0 R- f2 [1 S! l( U6 v+ N
(prepubertal).6 o8 s8 c( Y0 F- @6 N2 ^3 s1 M
The parents were notified about the laboratory* v- p& U/ B2 K9 J
results and were informed that all of the tests were7 e5 J$ g# Y8 N+ L% ^
normal except the testosterone level was high. The: b$ k* u7 B9 Q9 a' h# }
follow-up visit was arranged within a few weeks to( O! P+ F7 o* I: f% Z7 n* F: @
obtain testicular and abdominal sonograms; how-9 M% i! z' y1 X2 k& g* h
ever, the family did not return for 4 months./ R! N6 x, x+ S6 L0 g& j5 B
Physical examination at this time revealed that the# U1 x7 V; \4 H
child had grown 2.5 cm in 4 months and had gained+ j, k( J+ F: M; \3 Y4 ^
2 kg of weight. Physical examination remained
  s$ [* e0 I( }4 ^$ f0 e0 @unchanged. Surprisingly, the pubic hair almost com-! N' f) U3 C& ^% Y+ [
pletely disappeared except for a few vellous hairs at
$ O- {) Z( Q& M0 m# ?# U3 k, Sthe base of the phallus. Testicular volume was still 2) Q$ T' C- l8 v0 \5 }' q+ _6 T
mL, and the size of the penis remained unchanged.$ Q. {; ~) Q0 D- {" P) k& w
The mother also said that the boy was no longer hav-
) l" `  @9 \9 j( E: ]. Wing frequent erections.( f( s9 f) E: @5 T
Both parents were again questioned about use of
2 \4 Z! W: E/ Z% Many ointment/creams that they may have applied to/ Z0 h( ]4 C4 j
the child’s skin. This time the father admitted the+ O1 f4 n6 F5 k$ R
Topical Testosterone Exposure / Bhowmick et al 541  ^% [4 W) r" y
use of testosterone gel twice daily that he was apply-# Q  ?, ?/ D, [: u: h$ }! N
ing over his own shoulders, chest, and back area for$ [# U9 \& g& E: x1 p4 |" W
a year. The father also revealed he was embarrassed: A3 X) S' ^1 f) m  @8 a
to disclose that he was using a testosterone gel pre-
0 y1 K' p  q. T  Mscribed by his family physician for decreased libido
" J) {0 X% m( ~1 Y+ M: {secondary to depression.
  |' z) }/ ]: e$ P$ cThe child slept in the same bed with parents.
4 x! {8 @8 u' G3 m- {The father would hug the baby and hold him on his
- d- [) A7 @# p3 [8 uchest for a considerable period of time, causing sig-
' e* G) T9 m- Y( q4 Cnificant bare skin contact between baby and father.
% z: c7 F( m2 M3 ~7 ?5 g. a* `5 vThe father also admitted that after the phone call,
5 {" ^% U2 I0 ~7 n/ K) wwhen he learned the testosterone level in the baby4 u( `6 x8 B" v8 b# V) S0 u- V# ?
was high, he then read the product information
& h: _2 J" |5 d+ z0 u+ s6 Ipacket and concluded that it was most likely the rea-5 j6 X. L1 W* ?$ b  y4 i
son for the child’s virilization. At that time, they9 f9 A0 I" j. ^1 P$ s
decided to put the baby in a separate bed, and the4 Q# h0 V& X$ E! m( z
father was not hugging him with bare skin and had2 ?7 T! l: P. b( `% h/ V
been using protective clothing. A repeat testosterone( T" p' P3 Y% e5 ~' o  V$ Y
test was ordered, but the family did not go to the
& d& w7 d8 }) [, w$ W$ Blaboratory to obtain the test.! [( n2 n+ g4 g: I! Z9 E6 f/ R; F
Discussion
! G" C# D& i) c2 }Precocious puberty in boys is defined as secondary
' ?! n1 F% k  ?# R: V9 A1 `4 m& D0 v7 Ysexual development before 9 years of age.1,4
, B' I" q. Z# D( k9 N2 YPrecocious puberty is termed as central (true) when/ u, R- b8 n9 ]8 H7 h8 b, ~
it is caused by the premature activation of hypo-
- {' v. J3 q' S) J' F6 G% Athalamic pituitary gonadal axis. CPP is more com-5 z6 K. @: z1 b0 ~
mon in girls than in boys.1,3 Most boys with CPP
2 C$ j( n4 X; D  y+ _) E. {! x) `may have a central nervous system lesion that is- V3 W# w2 d0 b& @( Z0 G
responsible for the early activation of the hypothal-0 j* z/ S7 d& \& O  I0 g2 R
amic pituitary gonadal axis.1-3 Thus, greater empha-
1 [! n+ h3 I5 N, Psis has been given to neuroradiologic imaging in6 A+ |0 g+ g3 }& a, Z6 g$ }
boys with precocious puberty. In addition to viril-
' n2 u. G1 k: E2 A' w7 n9 V$ Kization, the clinical hallmark of CPP is the symmet-6 }1 ^; e  ]+ M; |2 Q
rical testicular growth secondary to stimulation by# P( p7 X5 n/ P: f
gonadotropins.1,3+ o7 Z, z6 u5 R
Gonadotropin-independent peripheral preco-& I- J3 I3 U5 X# W
cious puberty in boys also results from inappropriate7 J- ]( n5 @) q! P% X3 y" ?
androgenic stimulation from either endogenous or3 X) L5 c6 K" f8 Z: V
exogenous sources, nonpituitary gonadotropin stim-
: s/ d& z3 |5 `4 fulation, and rare activating mutations.3 Virilizing
! ^8 A9 `" U" {* N* o) y4 V/ Xcongenital adrenal hyperplasia producing excessive
; K* G) i( r/ P+ w# X; Xadrenal androgens is a common cause of precocious
) Q8 I" n( B+ E, Mpuberty in boys.3,4
4 i5 f9 x" X' D- n! Q1 E# R4 T# hThe most common form of congenital adrenal3 ]1 y0 j* T  b3 N" l
hyperplasia is the 21-hydroxylase enzyme deficiency.- C) ?1 b: s; D8 A. x
The 11-β hydroxylase deficiency may also result in. r) R' k; ~5 \1 p0 o- \
excessive adrenal androgen production, and rarely,
9 h0 P) [# E/ Q0 `$ ~an adrenal tumor may also cause adrenal androgen6 G. K6 v/ a7 s$ n/ V# s
excess.1,3" F, M& t: E/ z" }
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
2 P: i- Z( }" t0 L- y) {5 D9 z0 c542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
- n! W! Y. k+ I4 b' @0 TA unique entity of male-limited gonadotropin-
) k4 x6 H. W* N7 i3 Q$ O! ]. Pindependent precocious puberty, which is also known
0 n. @) s6 V  s4 o) h; p# a, tas testotoxicosis, may cause precocious puberty at a- g! `$ q1 ]( R( v' D
very young age. The physical findings in these boys8 r& X$ v% _8 F$ N- g% f
with this disorder are full pubertal development,9 D7 F1 c4 V4 j
including bilateral testicular growth, similar to boys
, v: R! n: \/ b! q7 Wwith CPP. The gonadotropin levels in this disorder2 p2 w1 d7 r3 u1 v
are suppressed to prepubertal levels and do not show
& w4 W- ?/ l6 N- A# Gpubertal response of gonadotropin after gonadotropin-
6 O5 o. I! P) B" c2 I9 greleasing hormone stimulation. This is a sex-linked
  q% S) ^; ^- W8 t4 p. lautosomal dominant disorder that affects only( s9 h$ j3 O  q5 ^$ L
males; therefore, other male members of the family3 d; D; [! m0 U% b' T) B
may have similar precocious puberty.3
! c2 y* `- ]- C2 {( ZIn our patient, physical examination was incon-- v- ~$ w) p; Q8 k3 [9 ]
sistent with true precocious puberty since his testi-4 v' s6 V8 k- n4 g& X5 j
cles were prepubertal in size. However, testotoxicosis8 l# D! Z, ^2 k7 }  _
was in the differential diagnosis because his father7 {, r! `, j, r- {/ l
started puberty somewhat early, and occasionally,( M9 N1 G  K4 Z. ?  C7 n* `7 C
testicular enlargement is not that evident in the3 F" Q6 M) G6 j% D" B: [2 f7 E
beginning of this process.1 In the absence of a neg-
7 E& z- G. {& ~& `2 h+ Bative initial history of androgen exposure, our8 l/ ?$ @; i+ Z% i) Y: E
biggest concern was virilizing adrenal hyperplasia,
3 u6 Q, D' ^5 Z0 H" |either 21-hydroxylase deficiency or 11-β hydroxylase
% ?1 j$ r; K! b* ~: Xdeficiency. Those diagnoses were excluded by find-
8 Q( j7 J. z# D, Y. Cing the normal level of adrenal steroids.( H* R* c/ H9 t  D& g
The diagnosis of exogenous androgens was strongly
% `$ B' i5 j- m$ Y9 b6 M- F# M" dsuspected in a follow-up visit after 4 months because
% h3 Z4 I1 j- L, P7 ethe physical examination revealed the complete disap-
5 t+ B1 ]* d( G, l4 g/ r# Upearance of pubic hair, normal growth velocity, and  F5 t$ X- Z* J- R9 S) d# [. y6 g$ h
decreased erections. The father admitted using a testos-
/ n# ]) f! Y, E; }terone gel, which he concealed at first visit. He was  M' a( C/ a5 e* o; {$ a
using it rather frequently, twice a day. The Physicians’
/ b; V- E% l7 g$ A6 N6 k( q, ^Desk Reference, or package insert of this product, gel or
4 ~8 D* i! @! n+ E) X2 D3 ^: kcream, cautions about dermal testosterone transfer to. t, g! S3 T6 G! n4 T0 z' m
unprotected females through direct skin exposure.
0 S/ a9 S. O2 L4 [* C; }) sSerum testosterone level was found to be 2 times the' u- d3 d+ x/ i7 b. ~2 g; U
baseline value in those females who were exposed to% K! _, x( R+ q
even 15 minutes of direct skin contact with their male
' g! }2 ^, ~( W3 z. |* D$ q, E* |partners.6 However, when a shirt covered the applica-
, P/ s6 o( T8 f0 B' i8 y" A: Z; Ption site, this testosterone transfer was prevented.
/ D& N3 d$ g, |' w- ]- jOur patient’s testosterone level was 60 ng/mL,
2 E, D4 N) r. E! A+ N( swhich was clearly high. Some studies suggest that% M2 T3 R1 y6 d; m7 @
dermal conversion of testosterone to dihydrotestos-% N* V( q: G4 `
terone, which is a more potent metabolite, is more
4 `4 j; A  N  t! Cactive in young children exposed to testosterone
, g3 i  Z* b$ u# t- Wexogenously7; however, we did not measure a dihy-# O* O; Z8 M& X4 L2 [7 p7 `
drotestosterone level in our patient. In addition to
: i7 J$ Y5 `: fvirilization, exposure to exogenous testosterone in
$ s* Q9 d! N; {- S( A0 echildren results in an increase in growth velocity and
) c, V/ ~# W  g; D% d  Eadvanced bone age, as seen in our patient.
+ m# R  u8 a! x' R4 sThe long-term effect of androgen exposure during5 o1 K) _1 N% e8 w1 R; a+ f( I
early childhood on pubertal development and final
+ k; Q+ r5 N2 Zadult height are not fully known and always remain
- t' x3 N5 {" X/ m, ua concern. Children treated with short-term testos-
# i5 ~" E8 h* `) `terone injection or topical androgen may exhibit some
0 @% |! H8 X  Oacceleration of the skeletal maturation; however, after
3 D; `8 G' O# Jcessation of treatment, the rate of bone maturation
# M+ }& x' I6 a3 I) sdecelerates and gradually returns to normal.8,96 j2 c; N( O, A2 ~5 v; s& H
There are conflicting reports and controversy
" \' o5 p5 T1 P8 S& T% M$ fover the effect of early androgen exposure on adult8 p, {: l- H# r/ p6 u! n
penile length.10,11 Some reports suggest subnormal
+ d5 j  l& T1 N# P0 r3 E  O' c( Wadult penile length, apparently because of downreg-' g# L( h1 z& g( k5 Y4 Z
ulation of androgen receptor number.10,12 However,' k9 _3 ^, \% j0 u
Sutherland et al13 did not find a correlation between5 @5 J0 E  [; c& R8 R7 E4 O
childhood testosterone exposure and reduced adult' n1 v- i8 o8 T% w& X9 e! I$ G
penile length in clinical studies.
- S( z  A: W% ^. BNonetheless, we do not believe our patient is
7 P  i$ i2 e" l: g( jgoing to experience any of the untoward effects from
! f+ h0 N- W" d1 i9 ?/ _! f6 Btestosterone exposure as mentioned earlier because' K! Y5 h3 w5 a6 x
the exposure was not for a prolonged period of time.; c, Q4 L- C/ a7 b
Although the bone age was advanced at the time of6 b; k& h% O) o7 ?% {
diagnosis, the child had a normal growth velocity at
: f  n- b3 ?, f; dthe follow-up visit. It is hoped that his final adult
3 m4 j0 K' X' f- Nheight will not be affected.
5 }7 @  R, v# J8 i" GAlthough rarely reported, the widespread avail-
9 {- z* ?) O9 s$ |ability of androgen products in our society may
4 P8 e" _# e9 N) l8 ~indeed cause more virilization in male or female
: A+ S/ a1 j& O6 H0 V) xchildren than one would realize. Exposure to andro-8 b/ J/ [3 A% d0 m3 w
gen products must be considered and specific ques-8 e6 l3 z; ~# R6 j0 a: M9 `
tioning about the use of a testosterone product or+ F1 S5 J4 r; O
gel should be asked of the family members during' v+ `0 |! m) z9 N
the evaluation of any children who present with vir-6 I# j+ I+ e# L$ p  Z
ilization or peripheral precocious puberty. The diag-
; T- n  Q8 M1 i/ ?2 z# s, i4 ]nosis can be established by just a few tests and by6 \$ F, }( }6 f- c
appropriate history. The inability to obtain such a
' W/ p, o) L  w6 m' C" F/ s- ]history, or failure to ask the specific questions, may
- ]% ^  m; _, a! V4 Sresult in extensive, unnecessary, and expensive2 Q( E. [# @" ?8 b' F5 }2 @
investigation. The primary care physician should be
- M' ^7 n: z  Laware of this fact, because most of these children0 C! g" U2 p/ M# ~# {. O
may initially present in their practice. The Physicians’
* N: E0 b0 B1 F3 PDesk Reference and package insert should also put a
" O. z2 i5 C9 [9 m6 B8 _) rwarning about the virilizing effect on a male or
! ~. X, E# p) d2 }1 d5 ~5 {female child who might come in contact with some-1 [2 ]2 P& [: L/ j; a& `8 E% [
one using any of these products.! q! p, F. a9 w% J1 _7 l
References
; l- ^: C2 d* ~3 i; }7 D  ?  o1. Styne DM. The testes: disorder of sexual differentiation
7 ~% S/ _: ~3 L+ V: Uand puberty in the male. In: Sperling MA, ed. Pediatric
7 a1 u; x& C/ ^. mEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
/ ?  `8 x3 ~" U" W2002: 565-628.
1 h8 Y" O# H1 j) L: c+ j" |7 M2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious0 |* r' f) |! }
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old2 L0 E& O! D! c& f2 U3 G- g' a
Boy Induced by Indirect Topical2 V4 C8 d$ U6 O0 ]3 x4 L
Exposure to Testosterone6 A* o7 K! l: }) R$ Z
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
7 \8 w, b' f. c% uand Kenneth R. Rettig, MD1) @. x, n# i  J$ @
Clinical Pediatrics
7 J! R& o* I0 I( oVolume 46 Number 6
2 R/ C" c! I* ^* k# O0 R$ NJuly 2007 540-543
. Q* H& y2 V$ L: ^! y' s© 2007 Sage Publications! {: i2 J3 U& X2 j
10.1177/0009922806296651
5 c9 m4 P* Z. g5 Nhttp://clp.sagepub.com8 i$ ^7 s7 j; L; s& c  r
hosted at3 s- x- J5 f) L% i9 ~; c6 j' ]
http://online.sagepub.com( z# _* S% G& m4 `
Precocious puberty in boys, central or peripheral,
; W% f( J% V& f( c8 J0 T7 J" Gis a significant concern for physicians. Central
7 R* U: V- A: l2 S$ r8 W6 z3 iprecocious puberty (CPP), which is mediated
6 @! Z8 L! L8 wthrough the hypothalamic pituitary gonadal axis, has
. U; ]" [, C* C8 v# L' v5 ~+ `8 E  ba higher incidence of organic central nervous system
3 c: U0 V+ L) h% T1 `* D* u* t, Nlesions in boys.1,2 Virilization in boys, as manifested
! y) @" W/ q' ~* @by enlargement of the penis, development of pubic
3 d0 i% {3 v: L7 D  bhair, and facial acne without enlargement of testi-
3 S8 P1 q( G6 _! zcles, suggests peripheral or pseudopuberty.1-3 We
, {: q" l' d+ S, g! x/ g  Preport a 16-month-old boy who presented with the
7 s- j3 y/ |1 {& ?9 T/ g/ ~enlargement of the phallus and pubic hair develop-/ O! V; T8 K! w( J# e2 r3 `' A
ment without testicular enlargement, which was due
! m+ ^  `1 f$ o- a. wto the unintentional exposure to androgen gel used by
& e( D5 ]: J. v8 k/ D/ y7 j' I: Sthe father. The family initially concealed this infor-
! }1 X  Z" ]0 u$ s! Y# s) omation, resulting in an extensive work-up for this7 I4 _3 v. }( r
child. Given the widespread and easy availability of& v5 D  y2 h* h8 U) e) a
testosterone gel and cream, we believe this is proba-
; f# O/ P9 J8 G+ s7 H4 obly more common than the rare case report in the/ k( p  p& [) I! J; U) s
literature.4. S6 t# c3 ~1 F" x
Patient Report
2 r9 y& X: T) v  W! C" RA 16-month-old white child was referred to the
( g' |% Y, }$ C3 r/ jendocrine clinic by his pediatrician with the concern
2 j) L& W6 a  [3 h9 V% K0 L2 Dof early sexual development. His mother noticed
# {7 n  ]1 T/ dlight colored pubic hair development when he was3 F; s( G  i2 x4 u
From the 1Division of Pediatric Endocrinology, 2University of
$ @' O0 a6 G+ n8 L1 JSouth Alabama Medical Center, Mobile, Alabama.
0 T" v" q7 `7 PAddress correspondence to: Samar K. Bhowmick, MD, FACE,
8 s: g0 C/ T# [( u4 W; |! N6 \Professor of Pediatrics, University of South Alabama, College of
5 w0 O1 O* z4 c9 _* v9 }Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
) V7 }9 _0 ?0 \: ?9 E7 ], R; |e-mail: [email protected].
3 H) o+ p4 f: ]. E- Mabout 6 to 7 months old, which progressively became
) o3 r) d! l; a( D3 ?darker. She was also concerned about the enlarge-
6 V) c2 h" y% W6 X- u' _0 w" D! ^ment of his penis and frequent erections. The child; x: f1 u# R  }7 |' b/ y. c  q
was the product of a full-term normal delivery, with
- }) ]# K' K" i& Q, U! f+ Q3 {a birth weight of 7 lb 14 oz, and birth length of
1 {& s% k* y* ]( l20 inches. He was breast-fed throughout the first year* X. [7 C- n( i2 X# Z
of life and was still receiving breast milk along with3 q0 i" g' ~2 R7 {" i9 ~$ l6 S% u
solid food. He had no hospitalizations or surgery,* q. G( d) [4 }4 r( J/ X
and his psychosocial and psychomotor development
. G9 x5 @, O+ ^9 l- g/ E5 j3 Nwas age appropriate.( g' I& }$ h) q* k" G
The family history was remarkable for the father,# O& o" ~# e& @
who was diagnosed with hypothyroidism at age 16,5 i) X# s3 O3 ~' w4 K$ L
which was treated with thyroxine. The father’s
% D7 w* K( {) r9 s6 Q) Vheight was 6 feet, and he went through a somewhat
0 t3 B4 L5 f* y5 G- Q+ Zearly puberty and had stopped growing by age 14.
( W/ E0 U) _- e6 R  _4 w- N4 \The father denied taking any other medication. The9 j. x1 }4 P$ Z
child’s mother was in good health. Her menarche
# _' v2 g9 F8 R5 j! o8 M% uwas at 11 years of age, and her height was at 5 feet$ s4 C2 L7 [/ t  f  [, N
5 inches. There was no other family history of pre-
5 I& I) C! |7 [' E/ M/ W) Kcocious sexual development in the first-degree rela-
6 U1 k6 |1 m! M6 atives. There were no siblings.
1 E. M# e6 w6 r& X% ^( \Physical Examination
  ~/ {5 J+ {5 F  z  ~The physical examination revealed a very active,
+ D6 R" ~* q3 `/ B4 ]& pplayful, and healthy boy. The vital signs documented7 t1 U; f' U3 m) u. M! h
a blood pressure of 85/50 mm Hg, his length was5 |4 r. p1 w  i* D. M) j5 R
90 cm (>97th percentile), and his weight was 14.4 kg$ `7 `2 J5 v( `+ D. N
(also >97th percentile). The observed yearly growth$ U% M2 o0 D! t0 |( x
velocity was 30 cm (12 inches). The examination of
: k% N: S! ]3 W: I' n$ {" ^; Vthe neck revealed no thyroid enlargement.; R8 f3 v; S# ~% b
The genitourinary examination was remarkable for
$ {% g2 n3 D) m$ R6 Q; qenlargement of the penis, with a stretched length of
2 d% b2 d* |: A& H8 cm and a width of 2 cm. The glans penis was very well* f6 z4 y1 s$ z) H" M; `/ G8 v4 r
developed. The pubic hair was Tanner II, mostly around# D( D2 A6 M' w, ~, |- T2 q* h
540
0 X4 N) d: {: [+ I) Gat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
$ }$ v  ]" c' M+ @. A1 S) xthe base of the phallus and was dark and curled. The  T0 J7 V* ?& ]8 T' x; D
testicular volume was prepubertal at 2 mL each.
9 U8 B; j3 {2 Y: kThe skin was moist and smooth and somewhat3 e, j0 K% B; C3 \  a* r1 l
oily. No axillary hair was noted. There were no
, v/ F0 A0 a6 zabnormal skin pigmentations or café-au-lait spots.) a) K" Z1 ?: h/ s& G
Neurologic evaluation showed deep tendon reflex 2+- D& w# {/ Z+ Q: x  d9 C: d1 |3 ?
bilateral and symmetrical. There was no suggestion
# v! [. T' @" _3 o" Z5 X9 Zof papilledema.9 F4 Y* _6 m# h  x) v/ Z, v
Laboratory Evaluation
5 o  m( o: |! i! A* lThe bone age was consistent with 28 months by  s! Y4 d1 V$ G8 w, F+ t1 J
using the standard of Greulich and Pyle at a chrono-& C- Q# l' ?9 Q$ [  w2 q3 `" A
logic age of 16 months (advanced).5 Chromosomal
8 _& ~7 j* |! J% C  ^karyotype was 46XY. The thyroid function test
# N* f" h; F! k4 |- @7 Bshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
( H+ M. \! [0 L5 g7 Zlating hormone level was 1.3 µIU/mL (both normal).
0 C2 g+ K0 b3 [The concentrations of serum electrolytes, blood
; s, J3 o4 T, E" b9 Murea nitrogen, creatinine, and calcium all were0 @: ]+ ~  Q8 G# G
within normal range for his age. The concentration1 `$ a7 j9 g4 D5 _
of serum 17-hydroxyprogesterone was 16 ng/dL
) }! [7 I2 e1 H; A! K  q(normal, 3 to 90 ng/dL), androstenedione was 20
- L+ L9 A; @' t9 `9 p+ P) h" t1 ang/dL (normal, 18 to 80 ng/dL), dehydroepiandros-; R: {& @1 o1 o2 O
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
* T$ I# W) V) F, Idesoxycorticosterone was 4.3 ng/dL (normal, 7 to8 [- n, E: P' f7 E( R5 O' D, F8 d0 r
49ng/dL), 11-desoxycortisol (specific compound S)$ {5 f! f7 u) m3 M
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-! T7 b: D: G( v
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total% e- L$ w, j" }$ ~6 d, K5 x: b
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
3 x* f6 [3 j6 cand β-human chorionic gonadotropin was less than9 q0 X1 u% `1 X- _  G
5 mIU/mL (normal <5 mIU/mL). Serum follicular; S3 h* N* @( i1 z. h
stimulating hormone and leuteinizing hormone
/ Z8 g% O5 h& _3 H4 E2 cconcentrations were less than 0.05 mIU/mL
8 r% F+ H: ^7 }( E& p6 U; z% n(prepubertal).
, _$ [. v2 Q6 I) N5 [; b* {The parents were notified about the laboratory1 ?, C; E0 p6 c6 o+ B
results and were informed that all of the tests were3 L5 L* I% {$ G. k1 w# w7 Z
normal except the testosterone level was high. The
9 l2 j& A! |( ~7 Efollow-up visit was arranged within a few weeks to1 A  {( [6 G' \# \0 m7 ~# L
obtain testicular and abdominal sonograms; how-
0 `* j, u* T( t! R8 Z8 never, the family did not return for 4 months.8 ]) n: e( u! o' |8 u# ?0 o
Physical examination at this time revealed that the/ \' O' e9 D/ C7 G
child had grown 2.5 cm in 4 months and had gained
' _# Z$ ^' W1 \8 ~2 kg of weight. Physical examination remained: \" H3 X! u- D8 [; P3 h
unchanged. Surprisingly, the pubic hair almost com-; E4 o0 F5 K7 Y' p. U# _4 Z
pletely disappeared except for a few vellous hairs at7 ^* w) b3 e- ^' Q: s' F; r" ^
the base of the phallus. Testicular volume was still 2
6 `) \; Y. ~& v1 q- P# u  Q$ YmL, and the size of the penis remained unchanged.$ W( G. O7 R$ S* c' X2 k# o) G
The mother also said that the boy was no longer hav-
( Y/ E4 M' ^# A( iing frequent erections.
' f' R0 F+ d; |Both parents were again questioned about use of. r" q1 Z+ T! w! N+ y
any ointment/creams that they may have applied to* v/ g9 g1 A3 ?
the child’s skin. This time the father admitted the
( h3 ?. r9 Q6 \Topical Testosterone Exposure / Bhowmick et al 541
, g- @- W5 ~# R" e; A6 u% q! g& \5 t. Suse of testosterone gel twice daily that he was apply-
# i8 L- N0 ?+ g# B, ^ing over his own shoulders, chest, and back area for6 x7 G$ r6 e+ O+ V( O
a year. The father also revealed he was embarrassed  e. b. _' ^% |, g3 |6 p% o( D
to disclose that he was using a testosterone gel pre-
: g% H: O0 u6 z6 o6 H9 |% C' hscribed by his family physician for decreased libido
0 `  [* ?( z4 u% l1 }! |secondary to depression.' B, k1 c# j% N5 k+ e: c
The child slept in the same bed with parents.
. ]+ t- D: w: a3 V5 r: M, S2 \The father would hug the baby and hold him on his
6 U+ _/ z- h" T+ h. V) Echest for a considerable period of time, causing sig-
+ F- w! V* y+ ?+ y) |. x8 Cnificant bare skin contact between baby and father.
7 `% G4 _& |: A( x2 x% V8 lThe father also admitted that after the phone call,4 U7 p& _% u  E8 D5 h
when he learned the testosterone level in the baby* S* l$ h/ r0 u3 r: x% k
was high, he then read the product information8 b' j9 K0 B+ V/ E
packet and concluded that it was most likely the rea-% n& O( X: B( a9 r3 [
son for the child’s virilization. At that time, they. f. l3 W( g" i! t) l
decided to put the baby in a separate bed, and the
, a0 {7 i' `* N" M# v6 cfather was not hugging him with bare skin and had8 e0 _, }4 P7 O% i# P" C) t. D3 R
been using protective clothing. A repeat testosterone4 F8 B  d# O' h" T$ J4 j8 a' ]3 z
test was ordered, but the family did not go to the
) B9 h3 R& ]; h! B0 v5 Z& ]laboratory to obtain the test.6 L6 Z7 i3 l' F# t# w6 c$ W$ n
Discussion
& L* ]. C0 g1 DPrecocious puberty in boys is defined as secondary
' O5 c0 {1 H( {4 K9 T  i& }- Y& @+ usexual development before 9 years of age.1,4* r, a& I  ~9 @0 X0 k* b
Precocious puberty is termed as central (true) when
$ e& S- m7 E& e# o5 Yit is caused by the premature activation of hypo-) |2 D! x  q. L6 o0 u+ U% `' d
thalamic pituitary gonadal axis. CPP is more com-* A1 G6 l; C$ \3 {* j4 ?) a
mon in girls than in boys.1,3 Most boys with CPP
  v" F2 n  M1 X/ f7 F2 ymay have a central nervous system lesion that is5 ~: d0 o) X5 G
responsible for the early activation of the hypothal-
/ c; H- g2 f& ]9 M; E/ K- Oamic pituitary gonadal axis.1-3 Thus, greater empha-* E( \# _1 g. c8 z* l
sis has been given to neuroradiologic imaging in
9 [/ Q! O6 \! A! S0 y6 o& e, Sboys with precocious puberty. In addition to viril-! c1 D( L5 D3 E5 y. b
ization, the clinical hallmark of CPP is the symmet-
) U  x# u( `" i& ]2 f9 F+ {5 Trical testicular growth secondary to stimulation by
: p$ H. K# c+ t, Sgonadotropins.1,3" ^! K) B3 N7 U/ G1 P
Gonadotropin-independent peripheral preco-
" a+ E2 r# A( s: p) G7 `5 N: ]cious puberty in boys also results from inappropriate
) r! G* h$ Z5 K& R% xandrogenic stimulation from either endogenous or
2 x! M" l2 G8 n" [0 m8 }exogenous sources, nonpituitary gonadotropin stim-
. u% H$ |# U8 K( N. k0 h6 Sulation, and rare activating mutations.3 Virilizing( l/ p- }4 N0 H, ~2 G' \- y
congenital adrenal hyperplasia producing excessive6 T( d# k" k( I3 u3 V1 L* }
adrenal androgens is a common cause of precocious1 I! ^/ ?$ z  U
puberty in boys.3,46 t* d1 d3 T) n; `( i$ [
The most common form of congenital adrenal
% F! f9 O# B$ E- thyperplasia is the 21-hydroxylase enzyme deficiency.% ^1 k5 T* i" ~4 y. a2 Q& h# K) i
The 11-β hydroxylase deficiency may also result in
$ I! A2 S6 G( E' B: z4 Hexcessive adrenal androgen production, and rarely,: F- K& E6 ^: V1 ~+ u
an adrenal tumor may also cause adrenal androgen! l6 L8 |3 ]) p+ q: e4 r
excess.1,3
$ _2 S+ j7 v- p* f8 rat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
/ D# Q  x/ P% s, y: Z542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
' J1 H' }" O/ Q) d$ BA unique entity of male-limited gonadotropin-$ j. J( v6 g  v4 |
independent precocious puberty, which is also known
4 h9 \: @3 ]* Vas testotoxicosis, may cause precocious puberty at a
/ |, j! z* h' [4 \6 qvery young age. The physical findings in these boys1 q* J  X3 Q; f* l" U/ K
with this disorder are full pubertal development,9 p% X2 R: P/ n
including bilateral testicular growth, similar to boys- m1 u% S  S' b  a- `
with CPP. The gonadotropin levels in this disorder- b* S. d& H/ N! m9 c  k- n* f# Q
are suppressed to prepubertal levels and do not show: q2 H. s7 c8 [7 s" ]9 k% U
pubertal response of gonadotropin after gonadotropin-, N5 o/ i3 s2 Y5 Z4 _# U3 P7 W
releasing hormone stimulation. This is a sex-linked6 U. _, B! y4 t- a
autosomal dominant disorder that affects only0 l3 m& A/ A: ~2 C! d, w/ X4 ]0 H
males; therefore, other male members of the family; z$ L8 N* p  ?
may have similar precocious puberty.3
' O6 V3 I. }( AIn our patient, physical examination was incon-9 z* i' J6 a5 `. G& ?* ^
sistent with true precocious puberty since his testi-
$ v. n' Q1 H+ L* j: n# g* hcles were prepubertal in size. However, testotoxicosis
" {; c* Y( R7 Y- h& f2 y$ lwas in the differential diagnosis because his father
# E6 s- D* Q8 o% \8 M; h" kstarted puberty somewhat early, and occasionally,
; r: O* a! p! G# D. Ztesticular enlargement is not that evident in the3 i( U9 `. R) Y5 q" K( I
beginning of this process.1 In the absence of a neg-
' B% }3 K8 P# u5 \; Gative initial history of androgen exposure, our& A- F9 r0 }7 S4 R
biggest concern was virilizing adrenal hyperplasia,
4 W$ d: Y5 K' i, e9 K# Seither 21-hydroxylase deficiency or 11-β hydroxylase
. e2 l  N7 g# @- b$ M: r- Edeficiency. Those diagnoses were excluded by find-: g( H$ I! f0 D' U! P6 I
ing the normal level of adrenal steroids.
& w) K( x5 v( A6 bThe diagnosis of exogenous androgens was strongly7 {- ~! o/ ^# U8 F$ h0 `
suspected in a follow-up visit after 4 months because
( ^' ?$ V/ \: `* s& rthe physical examination revealed the complete disap-
9 r( X6 ~( A1 P/ A. Vpearance of pubic hair, normal growth velocity, and
! a# R' k% `  y, w9 ?decreased erections. The father admitted using a testos-
# A: J5 Z* ^$ u0 m. G8 J4 ?$ W+ uterone gel, which he concealed at first visit. He was
* @9 m. l: i" l' C5 K6 z. iusing it rather frequently, twice a day. The Physicians’- @5 D! n7 K& A
Desk Reference, or package insert of this product, gel or
% T! B. Y' T- ]7 m7 zcream, cautions about dermal testosterone transfer to! Y5 V2 V: j9 f7 z  L
unprotected females through direct skin exposure.
& ~/ D8 _. b+ GSerum testosterone level was found to be 2 times the$ z0 Z! X) g0 r: S; v
baseline value in those females who were exposed to
5 W$ z& [. }* L2 Y% P7 Seven 15 minutes of direct skin contact with their male4 e, d) Z6 k# e; J8 ?7 z6 V
partners.6 However, when a shirt covered the applica-
& S1 q9 i  V) F# t# m* n7 `9 ition site, this testosterone transfer was prevented.
' t7 z- r0 P- n4 ]* p; P1 Y+ COur patient’s testosterone level was 60 ng/mL,
9 b- s0 i! c% w: \which was clearly high. Some studies suggest that: x$ |0 c7 V- J
dermal conversion of testosterone to dihydrotestos-
! |  x/ I; ^9 G" }terone, which is a more potent metabolite, is more
8 U- [( Q2 n" o. b1 F9 C- ]: h. k7 oactive in young children exposed to testosterone
# J7 m. {) [. V& T  x- e# P- G& Vexogenously7; however, we did not measure a dihy-  y+ Y/ b! j% l: q" a) X9 x1 ^  F2 s
drotestosterone level in our patient. In addition to7 ]! N/ L* B. G/ ]( \8 P6 ?
virilization, exposure to exogenous testosterone in
8 ^# p4 r5 T6 I, ~" Y7 y4 c5 |8 b8 {children results in an increase in growth velocity and
6 |- o* G% [0 m+ K9 tadvanced bone age, as seen in our patient.4 f8 @/ J7 u# i# K9 t- d
The long-term effect of androgen exposure during
- `! f; d" t  `2 W9 O, bearly childhood on pubertal development and final
( B6 g( D( U% @( g0 Ladult height are not fully known and always remain
7 o" w" o7 \- v$ K5 qa concern. Children treated with short-term testos-
2 G0 h- D3 G' Uterone injection or topical androgen may exhibit some
' Q2 a( H1 f( T! q( W# M1 |acceleration of the skeletal maturation; however, after
$ P9 m' t0 N+ z1 \1 Dcessation of treatment, the rate of bone maturation# d; p- T, F' \
decelerates and gradually returns to normal.8,9, ?0 i5 s9 B4 A- U! z
There are conflicting reports and controversy
" N' Q1 K6 V7 v  p0 C9 ~: H! B0 y9 vover the effect of early androgen exposure on adult* D* |: C$ A+ F* a: G, i
penile length.10,11 Some reports suggest subnormal7 g8 B! X# H1 `( t2 o9 {
adult penile length, apparently because of downreg-
" R' S& z0 [, `, v/ ~2 P1 Y% xulation of androgen receptor number.10,12 However,
1 q# @- l0 n. [, _) o! {3 J' d: A' pSutherland et al13 did not find a correlation between
$ |% H5 d# V/ {7 }; @1 i( y. Rchildhood testosterone exposure and reduced adult. C9 J2 r3 z4 i. @0 K
penile length in clinical studies.
9 H+ q0 E9 w* t! P  U& l& qNonetheless, we do not believe our patient is
% ^# T  {. D4 J9 I% s# [  |: Wgoing to experience any of the untoward effects from
! K  O  g/ S# ^% L' z7 ]2 rtestosterone exposure as mentioned earlier because! @4 F8 ^/ \. G6 F7 A( o
the exposure was not for a prolonged period of time., L2 S' {8 D8 N# T) \  z
Although the bone age was advanced at the time of
' _1 ~2 g6 t* E# c: O4 w  wdiagnosis, the child had a normal growth velocity at
- y/ \! n7 R  Q$ d/ ^1 @0 othe follow-up visit. It is hoped that his final adult
! R! L% k- b% P  ?  X, `6 Cheight will not be affected.
. ?9 B1 R1 j1 s+ y7 mAlthough rarely reported, the widespread avail-0 E# [- |" t7 B8 U0 `4 P, ?1 i; m
ability of androgen products in our society may9 @/ c; p9 U$ |/ W( h  W  o/ q
indeed cause more virilization in male or female
* O: G( t+ h6 e, g' ], ~- [children than one would realize. Exposure to andro-
7 I* Q& v8 \+ |+ o3 [4 p- Xgen products must be considered and specific ques-& `+ _2 v% f5 O4 L; ^
tioning about the use of a testosterone product or
! s! R0 |) V# T( J2 p5 k- w% G8 ugel should be asked of the family members during
9 n/ J, x7 r* O- M" uthe evaluation of any children who present with vir-
2 q9 Y( K5 O9 T9 Y, F1 l& r( |ilization or peripheral precocious puberty. The diag-
3 W$ e; I/ U1 K* @nosis can be established by just a few tests and by
6 x# X% z/ Q3 {2 n6 rappropriate history. The inability to obtain such a( E! k  x' K- B& V2 _
history, or failure to ask the specific questions, may
, R  S" ^: O7 @& }/ @  presult in extensive, unnecessary, and expensive- c0 `: O2 V6 p5 O  l6 v& E
investigation. The primary care physician should be- S- Q. z2 o9 D2 ]5 R; `
aware of this fact, because most of these children0 \( F7 s+ @# E' f; r! g1 P: z
may initially present in their practice. The Physicians’
$ [9 C" Q' l3 w5 P: T! ADesk Reference and package insert should also put a
+ s6 h4 M- T* c5 [6 Uwarning about the virilizing effect on a male or
/ @4 M; g4 P" S& n  f( l! o0 Xfemale child who might come in contact with some-
; L: \3 p. w9 g& x% U! r2 wone using any of these products.: s* s& d  B8 ~& A/ G5 |. f
References1 b" \, ?' w. h: ~
1. Styne DM. The testes: disorder of sexual differentiation
6 m, D  c/ p0 {" ]and puberty in the male. In: Sperling MA, ed. Pediatric2 E% a/ \( A8 M3 g" X9 B
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;4 j: T6 g+ ?3 {  M/ b/ N0 p
2002: 565-628.
7 o, K; v0 d- r3 M0 W2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
4 K  _- Y/ A$ O5 @puberty in children with tumours of the suprasellar pineal
發表於 2025-1-7 21:59:43 | 顯示全部樓層
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
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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
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

# j( _: r; z% R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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