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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
8 r2 Y3 b/ G" f8 `/ K' }Boy Induced by Indirect Topical$ ?, w; N3 r& O2 g
Exposure to Testosterone
/ k, D9 n  i$ \" ESamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
; V- E; [6 {; i9 `: Hand Kenneth R. Rettig, MD1+ v7 h, X: L3 D. t, _
Clinical Pediatrics
2 E4 R5 E, I5 i) r9 `Volume 46 Number 6
& L, r* F) T6 o. ]( S$ _; MJuly 2007 540-5435 p; I/ \3 j* N: O' ?* `: R0 ?
© 2007 Sage Publications
& f8 c& Y: j5 i10.1177/0009922806296651- O7 Q2 I  u: t9 A
http://clp.sagepub.com
9 t) }8 m# S+ n7 B. [hosted at
- d+ J7 ~# j' L! H5 p( Ghttp://online.sagepub.com% P* F6 b% b$ p$ f4 P: \- g. n5 B
Precocious puberty in boys, central or peripheral,
; F( \: A0 J" p/ _is a significant concern for physicians. Central
& {  g  p  g# q5 H7 tprecocious puberty (CPP), which is mediated% |$ r( ]1 p2 A% P6 [, l
through the hypothalamic pituitary gonadal axis, has
' ]" R: E  u& i! T8 V7 n( Y1 R# N+ sa higher incidence of organic central nervous system6 M. }( m/ B0 o
lesions in boys.1,2 Virilization in boys, as manifested
" e0 h) f# H' C4 a+ Z6 k4 iby enlargement of the penis, development of pubic9 B! }. ~1 M, ]- r+ ?$ K
hair, and facial acne without enlargement of testi-% ^* R( |3 S; Q( _
cles, suggests peripheral or pseudopuberty.1-3 We$ P4 t1 k4 W* r2 a: k
report a 16-month-old boy who presented with the
" i: a, ]2 D+ `. n5 Tenlargement of the phallus and pubic hair develop-
" ~# e$ l+ ]# b. Cment without testicular enlargement, which was due
$ h/ ]7 E& M9 C. u3 ito the unintentional exposure to androgen gel used by
1 l: J# H# a: `" l# q) jthe father. The family initially concealed this infor-
6 q: ^; ^+ g' Ymation, resulting in an extensive work-up for this
( w1 m- Y9 D* L+ u0 v! Lchild. Given the widespread and easy availability of* k7 X, h" ^0 I& r
testosterone gel and cream, we believe this is proba-/ k& s8 S  ^) j! b( I
bly more common than the rare case report in the
; m# U3 y) ?; ?9 _! Yliterature.4
8 `; @' ]- B6 jPatient Report+ [% l( ]5 y7 M. t$ d
A 16-month-old white child was referred to the. X- s: w9 X; K, o% ?
endocrine clinic by his pediatrician with the concern
6 ~' j6 d6 H3 B4 F5 A# ^6 wof early sexual development. His mother noticed
' Z7 }: p% ~' @* s3 _light colored pubic hair development when he was; M0 v7 j! A/ d5 R$ s) y( q7 j
From the 1Division of Pediatric Endocrinology, 2University of( e+ E& N. T+ D6 m
South Alabama Medical Center, Mobile, Alabama.; M  K) p: x- ]$ q" ?
Address correspondence to: Samar K. Bhowmick, MD, FACE,
  l0 l2 }& K7 G: R+ K9 P$ |Professor of Pediatrics, University of South Alabama, College of
! s" G5 O$ |, m/ oMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;" Y& ~- w7 h- u( i2 Q* b1 K
e-mail: [email protected].
, J- b, z. q. w3 }* Nabout 6 to 7 months old, which progressively became7 V) R/ q  f. g: @6 T& F2 I  q8 p
darker. She was also concerned about the enlarge-
( r$ p! P' Z- p6 F, K' B  Kment of his penis and frequent erections. The child
  `( i5 E" l$ O5 ~- ewas the product of a full-term normal delivery, with  K: p, k9 w& o: F2 a
a birth weight of 7 lb 14 oz, and birth length of5 e# w& n- H6 H8 l! h
20 inches. He was breast-fed throughout the first year
6 N6 {  Y3 o* \, Z) ~1 J# Gof life and was still receiving breast milk along with
$ Q( N" }. _3 i, `5 o$ h5 Rsolid food. He had no hospitalizations or surgery,3 B8 W0 ]5 C' e$ `& \
and his psychosocial and psychomotor development2 p: Z, s# y  i
was age appropriate.
4 B2 Q9 E3 _: Q1 F# H( y( ^, o+ \The family history was remarkable for the father,
$ |; O% {( V  V3 B6 m' T0 _who was diagnosed with hypothyroidism at age 16,3 X  i# y) ~+ ]  R0 n- q5 b
which was treated with thyroxine. The father’s( E$ Y/ c: P# }  f
height was 6 feet, and he went through a somewhat8 N1 q7 y3 Z* I" C2 {" |
early puberty and had stopped growing by age 14.
5 q7 i4 W: h, {5 iThe father denied taking any other medication. The9 l) c% D1 R0 q  |7 K
child’s mother was in good health. Her menarche
  q; Y) N& F* i; d! ~was at 11 years of age, and her height was at 5 feet
3 S# K" M; [5 N3 q$ M; Y  F5 inches. There was no other family history of pre-; q* V  p' j% a' j# c$ }7 t/ n
cocious sexual development in the first-degree rela-
8 s8 f, N$ E5 z4 T# otives. There were no siblings.
0 x) s1 u9 \# E3 k0 F% Z5 M% sPhysical Examination
5 j5 b. |1 F' r+ [4 F3 pThe physical examination revealed a very active,
/ d& |& N# P$ hplayful, and healthy boy. The vital signs documented
. x6 n, P) V- A4 N+ F0 ~a blood pressure of 85/50 mm Hg, his length was
: j& O, \- N0 c- P4 k4 r90 cm (>97th percentile), and his weight was 14.4 kg$ Y9 f6 r$ D7 [2 L* G
(also >97th percentile). The observed yearly growth% u6 H3 g+ J+ s( q. L' `( H* G
velocity was 30 cm (12 inches). The examination of
/ A1 ]( x% d% Y. U7 {% G: F, hthe neck revealed no thyroid enlargement.$ m8 M5 |" f: Z: Y! X& Z+ x; D
The genitourinary examination was remarkable for
# J3 O3 S2 K) e, a) Fenlargement of the penis, with a stretched length of& u4 [- O0 W& T; Z
8 cm and a width of 2 cm. The glans penis was very well
% B% P! R0 d: c+ Z6 j( u! Mdeveloped. The pubic hair was Tanner II, mostly around9 P( j4 ^* R! c- b! l! p
540& ]) p/ }1 t- p7 n
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from# \; X$ N) U. g$ |5 G
the base of the phallus and was dark and curled. The
, [; B& _. a1 I* y6 n8 htesticular volume was prepubertal at 2 mL each.5 T$ ^' X+ m: ~2 A  u. |4 b
The skin was moist and smooth and somewhat
  @* D& J/ C, Y" uoily. No axillary hair was noted. There were no
; x. k9 Z4 [* @/ O9 B; }9 m+ Babnormal skin pigmentations or café-au-lait spots.
; D0 Q% j. \- Q/ y+ E& p  ]Neurologic evaluation showed deep tendon reflex 2+) o( |8 v# K4 s9 k/ E
bilateral and symmetrical. There was no suggestion
5 T0 }: N/ b' d* wof papilledema.( {: d" ~9 F' @# T& J) G
Laboratory Evaluation
# ~* t7 O0 F9 `The bone age was consistent with 28 months by
8 Q9 `) K3 c. X9 ~using the standard of Greulich and Pyle at a chrono-2 F0 [. Y' M$ m
logic age of 16 months (advanced).5 Chromosomal
, Z, z7 I" Z: p: Q  A& j$ U" D& c6 vkaryotype was 46XY. The thyroid function test* O! r( w& T  u! E* S" i. N
showed a free T4 of 1.69 ng/dL, and thyroid stimu-2 n" C  x5 e* @
lating hormone level was 1.3 µIU/mL (both normal).
( K; K) ^5 \; [5 c0 jThe concentrations of serum electrolytes, blood* D; E1 M6 B& g4 \+ v3 h8 H* B
urea nitrogen, creatinine, and calcium all were
) A. D2 w! [  g3 uwithin normal range for his age. The concentration- i) z5 l* I) F
of serum 17-hydroxyprogesterone was 16 ng/dL5 K3 u( a- k5 j$ k4 n5 W9 L! Z
(normal, 3 to 90 ng/dL), androstenedione was 20" m* O0 j/ f9 N: r+ u
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-$ Z3 a, K. h; ^' R( h/ j( ~
terone was 38 ng/dL (normal, 50 to 760 ng/dL),: F* N, O6 n& q/ l' \9 }/ K
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
1 f+ o" o$ d/ J0 [  m: B) E. b49ng/dL), 11-desoxycortisol (specific compound S)
9 t% H( L) X- Gwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-7 U! {. I1 `- \' r1 `- H/ N
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
9 |, |" l% e8 W+ }4 \* j2 ttestosterone was 60 ng/dL (normal <3 to 10 ng/dL),  p* L; ^: K" u& ?* H2 x5 r! T
and β-human chorionic gonadotropin was less than
: L9 U7 @; N3 i5 mIU/mL (normal <5 mIU/mL). Serum follicular' r5 h2 F! }& U. j! a  V
stimulating hormone and leuteinizing hormone
) c# O& U5 V! jconcentrations were less than 0.05 mIU/mL4 L/ y( F  f* L6 D& p
(prepubertal).* f# K# K8 ?  q! C9 {+ Z
The parents were notified about the laboratory
& f/ x: K' P: qresults and were informed that all of the tests were, U0 F' K8 Q1 z6 Z; p
normal except the testosterone level was high. The
0 @' t! ?1 O$ qfollow-up visit was arranged within a few weeks to
/ N/ p+ ]5 J$ L5 jobtain testicular and abdominal sonograms; how-
) y( y3 ^5 e! L) A( ]9 y# _; g- G0 zever, the family did not return for 4 months.
) R9 A2 S0 [+ r& O: xPhysical examination at this time revealed that the  ~+ I! }/ v5 m2 q' z
child had grown 2.5 cm in 4 months and had gained2 J6 s' h7 f) r, ~
2 kg of weight. Physical examination remained
2 p7 g  z2 g( e. I/ C8 j6 ?. Hunchanged. Surprisingly, the pubic hair almost com-3 y/ Q; Z% e3 B  _- @, Y
pletely disappeared except for a few vellous hairs at
' y2 j$ ~: P: x8 d  q1 |+ [1 L: A$ Hthe base of the phallus. Testicular volume was still 2* S" H( L! ~: e( \1 D% ^
mL, and the size of the penis remained unchanged.
/ _! d7 `2 q% N. J, |' W) _4 ]The mother also said that the boy was no longer hav-. N/ P& ]+ N0 v7 a& g
ing frequent erections.- u, o- `2 f, {( @6 n6 K  ]+ c; |
Both parents were again questioned about use of2 \# _0 U4 M8 ?" d2 s$ f& ?. u
any ointment/creams that they may have applied to
+ S1 j" y' o# y, L7 y6 j8 @2 ?; }1 Cthe child’s skin. This time the father admitted the0 K2 c. f- C% w1 u
Topical Testosterone Exposure / Bhowmick et al 541* R& V" m. [+ {# n
use of testosterone gel twice daily that he was apply-% h! A- z0 Y2 G" H) J/ N* v6 }
ing over his own shoulders, chest, and back area for
! s8 Z  S$ y! N! u# Ma year. The father also revealed he was embarrassed9 @) W" @) Y2 G1 ?
to disclose that he was using a testosterone gel pre-
% O7 F& o2 ^+ _9 I% d  S6 ]' x1 u9 P1 Sscribed by his family physician for decreased libido
; g. L* Z3 V& h# n8 d" b& ssecondary to depression.% A1 o- Y) c9 z3 r
The child slept in the same bed with parents.* G" ^3 D, _* M. {& A8 J
The father would hug the baby and hold him on his
0 Q6 Y% e7 G! d( m: g1 e6 zchest for a considerable period of time, causing sig-5 d( D+ W0 ?6 g
nificant bare skin contact between baby and father.- @# ~+ V$ {: N1 y1 z4 s# T# }$ S/ e
The father also admitted that after the phone call,
+ a+ ?1 ~$ g* |when he learned the testosterone level in the baby3 N# M! ]( `" T
was high, he then read the product information3 z& }. \# E$ T( W
packet and concluded that it was most likely the rea-
! S% G+ L. L- T, L5 Y% hson for the child’s virilization. At that time, they  D6 s1 W" l/ l; W
decided to put the baby in a separate bed, and the
) j4 C6 Z; q4 hfather was not hugging him with bare skin and had) u' C7 G, \0 i8 [
been using protective clothing. A repeat testosterone7 f2 @/ _  h7 |. S
test was ordered, but the family did not go to the! s% C, P  D$ o, e& c0 a& x' D
laboratory to obtain the test.
( ^, _) m& i) [* ]# h+ s; r! S6 [Discussion. f( I/ ]: n% m1 u7 F
Precocious puberty in boys is defined as secondary$ u7 j0 T$ N  ^/ [2 u( O. z
sexual development before 9 years of age.1,4; H/ m9 l' V* E  _
Precocious puberty is termed as central (true) when
0 G8 s1 }. y( j- @it is caused by the premature activation of hypo-
7 c+ U: ^3 {6 X& Tthalamic pituitary gonadal axis. CPP is more com-; T2 q3 o% E/ _& f9 M$ L- I( K
mon in girls than in boys.1,3 Most boys with CPP
2 r; {, ]/ C2 H1 _: \may have a central nervous system lesion that is
! A3 O' b- ^  y* R) ^responsible for the early activation of the hypothal-! c. F( J% P* r2 ~! _/ f  e
amic pituitary gonadal axis.1-3 Thus, greater empha-
/ ^1 r. q. R+ J5 Nsis has been given to neuroradiologic imaging in
2 B5 B4 h. K2 f( `& kboys with precocious puberty. In addition to viril-* [6 }, Q0 l3 E  L. |  J( K  K
ization, the clinical hallmark of CPP is the symmet-1 }/ b; ]/ }6 w# D& Z& d
rical testicular growth secondary to stimulation by% m0 m7 S' _+ R7 H. s
gonadotropins.1,3/ h3 _3 j6 m4 U) L  Z! ]( L4 |
Gonadotropin-independent peripheral preco-1 B- R9 h0 f7 B) l; N* X
cious puberty in boys also results from inappropriate0 e9 r8 }8 U0 }: p
androgenic stimulation from either endogenous or
, z0 x; }( n2 b0 [+ Q; Uexogenous sources, nonpituitary gonadotropin stim-  _) L1 J8 ~6 l& n' a: G5 m' \$ s
ulation, and rare activating mutations.3 Virilizing* }: P( l/ C* p5 X
congenital adrenal hyperplasia producing excessive* k7 C" \5 K! ^2 @
adrenal androgens is a common cause of precocious
0 g$ R5 f, X9 `  Z! W! gpuberty in boys.3,4/ C( y9 }9 y3 z' m0 I* P
The most common form of congenital adrenal
# {$ |7 g' i: H! E+ _hyperplasia is the 21-hydroxylase enzyme deficiency.
$ Z5 u% r6 {/ y1 b- HThe 11-β hydroxylase deficiency may also result in
6 e! H5 M- M, N) {, z; [excessive adrenal androgen production, and rarely,
' l% m( K4 I: |/ s' w8 E$ \an adrenal tumor may also cause adrenal androgen
) S6 [1 L9 ]* t  qexcess.1,3
4 a, G) g- m) d. J" z! C& Oat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
. e6 w' B3 j0 R6 H; n542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
; \5 K" ]$ }# K. W; XA unique entity of male-limited gonadotropin-% o4 j% n3 z/ \. l; Y4 }
independent precocious puberty, which is also known
0 f% X7 g+ F' @2 ^8 K0 o* Has testotoxicosis, may cause precocious puberty at a
. Q( [) b. r" Y4 q8 E* W$ m- g  k- \very young age. The physical findings in these boys
  E2 |: O; i; Mwith this disorder are full pubertal development,
! t9 a. L' D* K9 y' U# fincluding bilateral testicular growth, similar to boys
) E4 y9 {- K0 P5 m: h( `. R( ~with CPP. The gonadotropin levels in this disorder4 \, o2 |  V; I' `# I+ ^( t9 h5 \
are suppressed to prepubertal levels and do not show
7 S9 _! W5 H/ E" I( c8 J( L8 Bpubertal response of gonadotropin after gonadotropin-/ U$ {9 f0 l1 O! ^9 z. V) G
releasing hormone stimulation. This is a sex-linked
) D# R" e$ _$ D$ ~6 |% kautosomal dominant disorder that affects only8 o+ N, M$ e. s0 Y" Z) Q
males; therefore, other male members of the family
$ m9 I8 @% P0 tmay have similar precocious puberty.3
( \) B7 X! a; k9 D* `+ }In our patient, physical examination was incon-
" o% C4 ~& R+ ]9 t8 Rsistent with true precocious puberty since his testi-
7 l4 N8 W# {& T1 xcles were prepubertal in size. However, testotoxicosis2 F: u4 f( V) n! I. P
was in the differential diagnosis because his father% Y& @/ |0 h& O' P
started puberty somewhat early, and occasionally,
4 C4 H9 m$ L/ {7 W- s. c2 E* Mtesticular enlargement is not that evident in the" X: u2 {. I0 Q/ \$ M( d' X. H; a
beginning of this process.1 In the absence of a neg-0 a9 U$ j$ ~, l7 n. a
ative initial history of androgen exposure, our/ i; t' |" V0 ~3 w
biggest concern was virilizing adrenal hyperplasia,
# d$ ?( g/ t! E* Jeither 21-hydroxylase deficiency or 11-β hydroxylase
' p( v6 {4 r: j! C6 U5 ldeficiency. Those diagnoses were excluded by find-; Q& Q- g3 ?9 `8 T
ing the normal level of adrenal steroids.
) Y4 T6 w' I/ `The diagnosis of exogenous androgens was strongly  W% F* Y# G. G7 T" z
suspected in a follow-up visit after 4 months because
( {$ |* h9 a9 l+ Wthe physical examination revealed the complete disap-
9 j5 J' Z9 l8 ~pearance of pubic hair, normal growth velocity, and
4 I7 x: O4 R; G! W+ ]( M) hdecreased erections. The father admitted using a testos-
3 \% o" A2 g0 l9 q. B0 h7 Lterone gel, which he concealed at first visit. He was
: J5 N% H! V# b: l: u4 husing it rather frequently, twice a day. The Physicians’" u4 f9 g, x7 j$ k5 w+ \
Desk Reference, or package insert of this product, gel or
: d! ^1 Z( U9 Wcream, cautions about dermal testosterone transfer to1 n' M. C1 W* \/ C* \5 ~2 L; \7 n
unprotected females through direct skin exposure.
% U" C1 r7 v- dSerum testosterone level was found to be 2 times the
- r3 i4 y' t) d$ I6 S4 |0 Pbaseline value in those females who were exposed to
$ x1 }% p  X" X0 M- }  Zeven 15 minutes of direct skin contact with their male
- V# z3 |6 ]* y6 F, U4 wpartners.6 However, when a shirt covered the applica-
( @- R! u. I* B, ction site, this testosterone transfer was prevented.( f7 M3 ]# s5 V7 i
Our patient’s testosterone level was 60 ng/mL,
/ k' O" f4 R: X; h3 g& uwhich was clearly high. Some studies suggest that
+ s. l0 t( Z) u* k9 K8 Idermal conversion of testosterone to dihydrotestos-; M+ Z* z. @( }& I3 U: o. q3 z- b/ u
terone, which is a more potent metabolite, is more: E. a( D' P  Z
active in young children exposed to testosterone
5 q' S' s$ z$ K' ~) Fexogenously7; however, we did not measure a dihy-
- y9 d- @2 ?9 C( `$ M" u6 Ldrotestosterone level in our patient. In addition to
: v4 S+ O6 Y% _- t: _3 ]virilization, exposure to exogenous testosterone in
' f4 @* E# o2 e7 }+ tchildren results in an increase in growth velocity and
3 N0 A4 p7 y4 ?5 V9 d2 Badvanced bone age, as seen in our patient.
& r% v1 p3 R- H" ]The long-term effect of androgen exposure during
4 u6 ?) y7 q! C0 bearly childhood on pubertal development and final
0 w' j+ w5 w5 h0 eadult height are not fully known and always remain9 L5 I  w7 M5 K) S; G& ?( ]$ j
a concern. Children treated with short-term testos-
8 f9 `: ^7 ~' t8 [terone injection or topical androgen may exhibit some
! U2 L: I, A* m$ L0 bacceleration of the skeletal maturation; however, after# ~' s: @( _/ ~6 W9 z! Z" k
cessation of treatment, the rate of bone maturation1 w$ K& [. k* f5 M) o! H
decelerates and gradually returns to normal.8,98 w7 Z8 |3 @) q- g% k2 d; N
There are conflicting reports and controversy
$ `5 ]% c6 X( ^. L" D8 {+ Gover the effect of early androgen exposure on adult
3 q" f0 K7 f8 Fpenile length.10,11 Some reports suggest subnormal) f: ]  y) E$ {3 E$ j4 j
adult penile length, apparently because of downreg-
+ q8 z: o# \: I6 Y' o$ P# {: @' xulation of androgen receptor number.10,12 However,; [7 M# N/ U* ]# {4 N; R. B' Z
Sutherland et al13 did not find a correlation between* i5 O5 ~+ x5 b, z, a! h8 [
childhood testosterone exposure and reduced adult9 {7 U; }. E# x/ b1 q4 t, u
penile length in clinical studies.! C/ r2 S  g$ ?; M8 u
Nonetheless, we do not believe our patient is
3 k$ E& i( x+ U  T4 Agoing to experience any of the untoward effects from
5 d, C; V* E( F) S! @7 Q* Q+ Ntestosterone exposure as mentioned earlier because) M' x; G, G, T7 d* v  F- Y
the exposure was not for a prolonged period of time.
5 m$ K) J& V; KAlthough the bone age was advanced at the time of" k8 K* h, Q1 z: |# {+ @7 B
diagnosis, the child had a normal growth velocity at, }3 A7 L# i5 ]5 R0 s) @8 A
the follow-up visit. It is hoped that his final adult7 M9 e$ s# d, t5 r# v
height will not be affected.
; O# B' Y' a0 N! @: }Although rarely reported, the widespread avail-
5 R$ t4 [" k$ @2 f" m, Zability of androgen products in our society may
& I- T# ~. y4 w( d6 y+ ]5 Y) \indeed cause more virilization in male or female
) h. H! r' y( N# _8 I; @0 Lchildren than one would realize. Exposure to andro-4 s" ]  r7 d/ G+ A7 }# X
gen products must be considered and specific ques-9 a( B- p1 Q* r8 \7 P( j
tioning about the use of a testosterone product or
8 x( Z- [& d$ s  ?, o! Zgel should be asked of the family members during
/ h. A( n# L( a+ Kthe evaluation of any children who present with vir-' o: k& T5 i6 [/ M# F: u( A2 L: p
ilization or peripheral precocious puberty. The diag-
- f* d1 `+ }% _- X: rnosis can be established by just a few tests and by
$ A; R. w' L# ~! \/ ~6 fappropriate history. The inability to obtain such a
2 G2 C# N8 b8 I2 vhistory, or failure to ask the specific questions, may
) X3 [0 @- V( y- {& U0 H, aresult in extensive, unnecessary, and expensive
4 R" b7 A" G$ f1 ainvestigation. The primary care physician should be
9 ~4 R& j* E6 ^$ M5 U& Jaware of this fact, because most of these children
1 K  l8 b9 L: b" Smay initially present in their practice. The Physicians’/ l8 z) _3 D  {) }1 }
Desk Reference and package insert should also put a9 {, [5 Y2 T: n% ?
warning about the virilizing effect on a male or
( p# w$ Y( I4 S; T* Efemale child who might come in contact with some-$ ?0 J+ d4 r1 ^
one using any of these products.6 g9 K- @% b  U  T% ^
References
% f, `7 W" L8 j3 v" J% m) @: l1. Styne DM. The testes: disorder of sexual differentiation
( p0 R' b% r' x, ^and puberty in the male. In: Sperling MA, ed. Pediatric- y' B! b7 b5 S' `) m9 C
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
, a% b" Y+ _" l: V. n  V, X9 G2002: 565-628.
8 F3 \5 I7 d2 V; m3 ?0 ]; B/ i2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious: U5 h" V! p8 b0 B
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
: Y4 z" A0 m8 }/ Y* q: oBoy Induced by Indirect Topical) c: S/ K& }, u9 R; ~) X
Exposure to Testosterone
) a6 O; J; z$ N( {* qSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2. }- ], k1 Y" i! o) E0 d5 @* ]8 I
and Kenneth R. Rettig, MD1+ o( z; {0 @$ v6 }
Clinical Pediatrics3 F6 L1 d. D, i/ v% ^/ O3 T0 s8 }
Volume 46 Number 6
/ O$ F! c, }/ e) U$ lJuly 2007 540-5432 S) W# P. @3 g9 |0 `
© 2007 Sage Publications4 c& U/ x+ k! t- x
10.1177/0009922806296651
5 w( t7 ?: [9 j5 I" vhttp://clp.sagepub.com3 U0 o6 [) i* Q1 Y# ]
hosted at
3 U7 {. S( y, nhttp://online.sagepub.com
# T& S. A! ]$ ^! I$ wPrecocious puberty in boys, central or peripheral,
! S: X- H: f+ U2 L& |0 E+ Tis a significant concern for physicians. Central3 v# U1 t" U. {6 L! h3 b
precocious puberty (CPP), which is mediated
& `' X6 q7 \  G( Xthrough the hypothalamic pituitary gonadal axis, has. R1 {. \/ c8 Z- \2 n: X7 _
a higher incidence of organic central nervous system- W% ?8 X$ j4 i6 ~& [& R2 G% X
lesions in boys.1,2 Virilization in boys, as manifested
8 Z/ d. q+ Y: N- d$ Oby enlargement of the penis, development of pubic: V: M- v# e+ ?& E- e5 I+ u* |. O
hair, and facial acne without enlargement of testi-
5 I7 x7 W0 M7 W* ~5 i2 H3 a8 d7 |cles, suggests peripheral or pseudopuberty.1-3 We& F1 B1 T6 h. h; k# ?/ X
report a 16-month-old boy who presented with the2 r* H# @) a/ ]% @
enlargement of the phallus and pubic hair develop-
# {8 C& T- C1 A1 g1 d) L$ qment without testicular enlargement, which was due# Q  A7 l5 p& N( u9 ~+ Y
to the unintentional exposure to androgen gel used by
% o. Y- m  o8 I& i0 H! L+ \: Uthe father. The family initially concealed this infor-; G9 G, v" M0 C
mation, resulting in an extensive work-up for this
" Y( F" k0 i/ F  S/ V; Bchild. Given the widespread and easy availability of
! D8 m" S1 N9 F) W/ G# ltestosterone gel and cream, we believe this is proba-6 [( e' w# E' \) m8 n; S
bly more common than the rare case report in the/ n9 }9 E; @+ d2 |, L9 Z& t
literature.45 R3 U- k* C4 F
Patient Report) v& i/ X3 Y0 t6 I* h
A 16-month-old white child was referred to the
) E  u3 \/ B" b" oendocrine clinic by his pediatrician with the concern
/ i* H* y  c) V. N  Fof early sexual development. His mother noticed
& j$ \1 H( ~( t" olight colored pubic hair development when he was, r# {3 L0 o3 T2 I( y. C
From the 1Division of Pediatric Endocrinology, 2University of) R- F1 X/ t, n7 E2 o7 I  q
South Alabama Medical Center, Mobile, Alabama.
3 j' n3 m. N2 _% O' H& lAddress correspondence to: Samar K. Bhowmick, MD, FACE,
; |$ @: \, F" I$ h0 i  i8 G' a8 L$ KProfessor of Pediatrics, University of South Alabama, College of
- [. O1 z6 T4 e8 B( G% bMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;7 D/ y( U9 u  `6 V: d8 k6 V
e-mail: [email protected].
! D% X! V/ S$ x) w* l- f6 D- T! ]about 6 to 7 months old, which progressively became
, j, y' ]6 B2 I) m5 Ndarker. She was also concerned about the enlarge-
8 [" ]% X6 G) n2 W  zment of his penis and frequent erections. The child4 K: v" o& e6 Y8 T
was the product of a full-term normal delivery, with
) q: M0 G0 q( I  X4 ?: l: q; @- [a birth weight of 7 lb 14 oz, and birth length of
7 c% b5 R* s6 R- {; ], E9 T* }2 P20 inches. He was breast-fed throughout the first year
- `3 `! w: K, W) @, R# w# C+ p- s5 oof life and was still receiving breast milk along with
# _% h1 Y5 i) f! A, v  H' A) Vsolid food. He had no hospitalizations or surgery,
; c* K) \6 h# b8 A" j. r: j8 rand his psychosocial and psychomotor development2 q* H3 _" a. t3 I8 _5 P0 @: a
was age appropriate.
2 y3 s& g  _' U( G3 d: [The family history was remarkable for the father,5 t( p/ b' S! t  u( T2 R3 @1 E
who was diagnosed with hypothyroidism at age 16,9 r# q: P; w7 k- C1 ?; g  F' a
which was treated with thyroxine. The father’s/ M/ j# N$ G3 @4 H: m  U
height was 6 feet, and he went through a somewhat
, m1 b: {3 _. w! T+ Fearly puberty and had stopped growing by age 14.# R- m" i2 [' U
The father denied taking any other medication. The
# w1 r8 |2 C  q$ Y5 ichild’s mother was in good health. Her menarche
5 }$ E  M% ]2 x  K- z" r& T0 K2 hwas at 11 years of age, and her height was at 5 feet9 \. D% p+ B9 Z  q  _
5 inches. There was no other family history of pre-
# u3 n: h! I) B3 u: l6 s  x2 H# vcocious sexual development in the first-degree rela-( I6 \5 d% ~# Y4 K2 F8 [& r/ ?3 W
tives. There were no siblings.% D. s# w& x" F+ m% F( _4 {) G
Physical Examination$ A  ^( w- B" ^" |  A4 r0 {+ ^& @
The physical examination revealed a very active,1 U: c+ t. k8 t6 D9 ^5 _2 Z+ d
playful, and healthy boy. The vital signs documented
- W& o$ A/ Y  B( W- Ka blood pressure of 85/50 mm Hg, his length was$ M0 [$ J! i" ^
90 cm (>97th percentile), and his weight was 14.4 kg
: ?4 u: Z8 _6 v6 }" |(also >97th percentile). The observed yearly growth. T# K2 A, c( u" |# r, v
velocity was 30 cm (12 inches). The examination of& }" B& R9 B' l
the neck revealed no thyroid enlargement.
7 ^, P; _+ d5 r+ [( j0 YThe genitourinary examination was remarkable for, @8 k0 L7 V+ ~" o6 @
enlargement of the penis, with a stretched length of
+ Q7 |$ w  I* M% H6 X$ }3 ~- u8 cm and a width of 2 cm. The glans penis was very well
/ A1 z+ y/ e7 C0 C/ z4 D9 Wdeveloped. The pubic hair was Tanner II, mostly around" `4 a& ~, e( T- B8 t3 ?
540
8 r# r7 V& v  f$ A' a9 Yat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
" e  d' \& n9 a5 o0 ?the base of the phallus and was dark and curled. The
9 A6 h+ X* v5 K) o" w8 }' Stesticular volume was prepubertal at 2 mL each.& s2 |* u% j3 v. C* l3 a. \" Z( `
The skin was moist and smooth and somewhat
* c+ U9 W, ?, ^! T. u: Yoily. No axillary hair was noted. There were no, M) B2 C: Z; q* \  c
abnormal skin pigmentations or café-au-lait spots.' ?" W. [# ?3 y+ |. k! Z
Neurologic evaluation showed deep tendon reflex 2+* F! S6 E0 X6 O" l9 ]
bilateral and symmetrical. There was no suggestion
5 B$ g! @, `8 K: p) h5 jof papilledema.# _# u# a$ I0 t5 n1 O2 E8 y
Laboratory Evaluation8 D/ k. E1 f" F/ A$ T3 {
The bone age was consistent with 28 months by4 f$ r+ l# `5 J- x* \2 V
using the standard of Greulich and Pyle at a chrono-9 L! `* u: x1 E2 ]$ x0 e" u6 B5 X
logic age of 16 months (advanced).5 Chromosomal
' U* Y$ f# C1 S! F0 ]1 i, Ckaryotype was 46XY. The thyroid function test
+ B6 ^. K7 c8 T$ G# f+ k( Jshowed a free T4 of 1.69 ng/dL, and thyroid stimu-' y. f+ ~2 w. x5 N, F2 v9 K9 P  f
lating hormone level was 1.3 µIU/mL (both normal).' y9 {, `9 l+ k
The concentrations of serum electrolytes, blood
/ ~/ ]. e* @8 }7 |/ durea nitrogen, creatinine, and calcium all were' l2 @; y3 f/ J
within normal range for his age. The concentration5 ]+ j/ M4 U7 ?# W* o( N0 {
of serum 17-hydroxyprogesterone was 16 ng/dL
. z' Q3 m; u) ?! e& I(normal, 3 to 90 ng/dL), androstenedione was 20
# z7 _, e4 O2 q% L5 ung/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
0 T- D. J$ m8 G! Gterone was 38 ng/dL (normal, 50 to 760 ng/dL),
% j, u  |- [) @& T1 ^desoxycorticosterone was 4.3 ng/dL (normal, 7 to
" O' S# v$ V  R$ P! V% U9 `& I49ng/dL), 11-desoxycortisol (specific compound S)) a, P, F1 J9 ~- c$ }/ k* ?
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
4 t) b- R& u7 y+ Qtisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
: q+ t& ^. v7 N  M) {$ vtestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
  w' G+ S: I' gand β-human chorionic gonadotropin was less than( {+ E  T: B& [
5 mIU/mL (normal <5 mIU/mL). Serum follicular
% d1 ]1 d2 x8 S4 k; bstimulating hormone and leuteinizing hormone
5 Z# r. ^: \: tconcentrations were less than 0.05 mIU/mL. D3 ]3 X& @! @, J; d1 ^9 `
(prepubertal).6 H) f$ ^4 S9 h* `; ~! K6 V1 a
The parents were notified about the laboratory
) G. D: |9 m9 ^- B1 eresults and were informed that all of the tests were; h( i7 E4 h3 s( X! G# [
normal except the testosterone level was high. The
: b5 z. {7 E* D" ifollow-up visit was arranged within a few weeks to
# q* q  k, x3 S5 @6 M, Qobtain testicular and abdominal sonograms; how-4 n6 z. i6 g8 \9 Q: o, n1 a
ever, the family did not return for 4 months.+ p8 t2 q( @, e: J- i; O
Physical examination at this time revealed that the
  c8 d1 ~5 K: y2 a  J9 A1 Jchild had grown 2.5 cm in 4 months and had gained
3 S+ m# V4 [& M/ ?7 e2 kg of weight. Physical examination remained  c; L# k- ]. A8 N: J* I
unchanged. Surprisingly, the pubic hair almost com-
. u. b; U7 v$ H2 bpletely disappeared except for a few vellous hairs at% D8 R( x$ p) L) X
the base of the phallus. Testicular volume was still 2
) [( o- f* g1 e5 T9 R3 |9 ~mL, and the size of the penis remained unchanged.! Z$ V. n. Q+ q( Q! }, ^* @
The mother also said that the boy was no longer hav-
- k8 Y& |" ]' r5 M- w+ oing frequent erections.6 l- H0 `: ?4 L/ B
Both parents were again questioned about use of, A" m; _/ P( f: f
any ointment/creams that they may have applied to6 g3 d" o* X) v4 O
the child’s skin. This time the father admitted the- E/ d6 l$ @2 y4 \: ~+ s  H) F6 w
Topical Testosterone Exposure / Bhowmick et al 541
) h# J1 `3 r5 i2 _3 F* Kuse of testosterone gel twice daily that he was apply-/ |8 a' n! F) a# N* Z* p' d" W( C
ing over his own shoulders, chest, and back area for
% O' M5 s  q/ L8 _2 W0 ^7 Wa year. The father also revealed he was embarrassed
3 M( X" r) \3 [8 @2 ~1 n0 Tto disclose that he was using a testosterone gel pre-
+ ?" j3 {/ G1 i  bscribed by his family physician for decreased libido8 p) }3 |6 c2 Y! `; w0 t$ B  w9 b
secondary to depression.
6 v0 A+ X. J$ O/ O. HThe child slept in the same bed with parents.
& Q0 n, K/ x" u& a! R/ u1 ]& t8 kThe father would hug the baby and hold him on his
# j! R% Z; r( y6 }chest for a considerable period of time, causing sig-
1 Y# X0 O( B. d, A1 F! D/ Hnificant bare skin contact between baby and father.' J, h: ^7 I2 h3 b7 n
The father also admitted that after the phone call,
* Y- [# I1 N, V, d4 p3 f% ]5 \/ gwhen he learned the testosterone level in the baby
. Z* O( M2 }  |* Z2 wwas high, he then read the product information! k' Q7 |# b$ i9 y+ [9 Z
packet and concluded that it was most likely the rea-" S: O! _6 F8 X- G
son for the child’s virilization. At that time, they; o" g1 M( j7 J& K+ H
decided to put the baby in a separate bed, and the# h( D3 [+ A4 a# o
father was not hugging him with bare skin and had
: G2 Z. b: t( i3 ?) hbeen using protective clothing. A repeat testosterone
4 x* c7 Z8 o) a; b% s2 ]test was ordered, but the family did not go to the" X4 s% G. }% i0 U2 r& n* e1 ^
laboratory to obtain the test.2 t- H8 m' I+ r' X
Discussion
8 L: r$ \- \  q$ ^/ J7 yPrecocious puberty in boys is defined as secondary
& M, r% E; @+ Q) X! f+ H3 x* Xsexual development before 9 years of age.1,40 C- A* R. E* B* }# Q* _* {& g
Precocious puberty is termed as central (true) when
1 L" o7 |: n" }. V) w0 }4 Wit is caused by the premature activation of hypo-& V, ?7 r( E8 i$ E% z( j
thalamic pituitary gonadal axis. CPP is more com-. b$ o% p! i5 n. ]. m6 q
mon in girls than in boys.1,3 Most boys with CPP
" r# i2 K8 ^5 i6 ]may have a central nervous system lesion that is
! u  ?( S' U0 ~8 z' F0 Y/ F% oresponsible for the early activation of the hypothal-
2 `0 f# c! V/ `- @0 y  m# |amic pituitary gonadal axis.1-3 Thus, greater empha-, \( ]& ~, f  ]: b( D& ]& e
sis has been given to neuroradiologic imaging in
) r; K7 U+ w1 f) pboys with precocious puberty. In addition to viril-
0 g0 Q- w3 r- s( kization, the clinical hallmark of CPP is the symmet-
% f( V$ Y- B& crical testicular growth secondary to stimulation by
4 @$ B6 \0 W1 m: }$ M+ p, Kgonadotropins.1,3) t" i& q* U; S  [4 t
Gonadotropin-independent peripheral preco-
7 M/ G4 s% ^4 g! N* b5 t. Q: J, hcious puberty in boys also results from inappropriate
; o' y. t! o& V! Y5 q9 ?androgenic stimulation from either endogenous or' i+ Q  ]4 ?/ S7 K/ C- K9 d
exogenous sources, nonpituitary gonadotropin stim-, ]; O8 y9 Y7 o) Q
ulation, and rare activating mutations.3 Virilizing
3 W' M1 n: g: h3 @; y: K  xcongenital adrenal hyperplasia producing excessive
3 v4 `9 U( }. d7 {; s& j' Oadrenal androgens is a common cause of precocious
5 C9 y. X! J5 q: O- n( l! i0 mpuberty in boys.3,49 Q$ E% z) K* r7 Q1 ?: B0 o0 h
The most common form of congenital adrenal
0 _- L; R% m! X+ rhyperplasia is the 21-hydroxylase enzyme deficiency.
% _" ?$ ?, u% u, ~8 n& CThe 11-β hydroxylase deficiency may also result in! t  [' i2 L7 g0 C: ~# Q
excessive adrenal androgen production, and rarely,
1 E- w1 e0 h4 l/ jan adrenal tumor may also cause adrenal androgen
7 ^8 ^! h0 L: n# D" [# L7 C( m& Yexcess.1,31 Q( T+ w# W# v: `( n$ e3 v) Q
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from) y! L* T: t( R" a; i9 U+ f
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
% d! \% `3 k/ _' s4 sA unique entity of male-limited gonadotropin-9 S' B5 ^6 n  M
independent precocious puberty, which is also known/ |: ]# ^9 c: v  u4 |1 e/ e
as testotoxicosis, may cause precocious puberty at a' P& \0 V6 I+ W. ]# y% C9 f
very young age. The physical findings in these boys
5 d$ S0 p# ^4 Q$ cwith this disorder are full pubertal development,. Q9 K( }' D. u# V) u9 P, x
including bilateral testicular growth, similar to boys
0 r9 g: ]+ G) ?/ pwith CPP. The gonadotropin levels in this disorder
2 r  l- y& K2 X0 S, s1 y, V6 X5 Fare suppressed to prepubertal levels and do not show" G3 i( ]1 [2 x: B. l+ w  }
pubertal response of gonadotropin after gonadotropin-" d7 w* Q+ C3 p9 s, l
releasing hormone stimulation. This is a sex-linked( v2 ?5 P$ }0 n: {
autosomal dominant disorder that affects only7 n) o4 a' P. T- l' n; ]  E! `
males; therefore, other male members of the family
$ O3 l9 o$ C8 \/ @! lmay have similar precocious puberty.3
/ D# Y8 M' B/ w# ^In our patient, physical examination was incon-) J8 G" _3 w) F2 v
sistent with true precocious puberty since his testi-# x4 C1 G2 o1 C
cles were prepubertal in size. However, testotoxicosis
' {. \. M! M0 B9 bwas in the differential diagnosis because his father
/ M7 D, R& U" o# Y3 kstarted puberty somewhat early, and occasionally,% G4 I$ _. Y: d5 @
testicular enlargement is not that evident in the) b  U' r5 [6 D$ C2 \/ D
beginning of this process.1 In the absence of a neg-; ?2 D4 ?0 {2 {1 M( Q9 x3 \4 _
ative initial history of androgen exposure, our0 Z9 Z6 Y9 }3 Z4 I" X1 a" ^* e
biggest concern was virilizing adrenal hyperplasia,5 W, ~4 A" n, s
either 21-hydroxylase deficiency or 11-β hydroxylase
+ R- A' A+ H' ]2 _- G" ]" }deficiency. Those diagnoses were excluded by find-# V& u7 r* q2 |! ^" J1 F
ing the normal level of adrenal steroids.
6 O. ~6 c1 g1 x8 j' l+ LThe diagnosis of exogenous androgens was strongly
3 g. r( T3 J/ @( [suspected in a follow-up visit after 4 months because) t7 N' {% J( Y0 ~; i8 N
the physical examination revealed the complete disap-  p$ r' B/ W2 M  y( M/ [/ p9 s6 r
pearance of pubic hair, normal growth velocity, and. y, U+ D, k5 t0 K$ c
decreased erections. The father admitted using a testos-& K6 T) [! _) Y/ G7 S
terone gel, which he concealed at first visit. He was% r) \' e; Q3 J3 H9 a; U' D! N
using it rather frequently, twice a day. The Physicians’
+ T. U; x7 M# s9 _  ]" K% @Desk Reference, or package insert of this product, gel or
+ Y8 t& \# X" F% G) ?cream, cautions about dermal testosterone transfer to' o9 H$ F2 q2 b' @1 f9 {0 z
unprotected females through direct skin exposure.
6 v% C5 x  ]; m8 J  xSerum testosterone level was found to be 2 times the
# r, q4 ^; \% j( y! Rbaseline value in those females who were exposed to' N4 V3 D5 j1 r7 Y* ?# T+ D
even 15 minutes of direct skin contact with their male
( f2 B/ F& h7 Opartners.6 However, when a shirt covered the applica-" I* R2 m% O% M! Y/ |' x5 {! p
tion site, this testosterone transfer was prevented.
# d5 _# W* }- C9 FOur patient’s testosterone level was 60 ng/mL,
) W& S5 t8 Q8 n1 l: Q& J% Vwhich was clearly high. Some studies suggest that
1 N5 N. m0 h: W, x) g& Zdermal conversion of testosterone to dihydrotestos-
. T7 n: v. \- R- {' W) C# Hterone, which is a more potent metabolite, is more
/ G* M8 O% o6 H5 b. \active in young children exposed to testosterone
6 p4 t( y3 {5 |exogenously7; however, we did not measure a dihy-
) ^! i2 F5 Y) O: g# Ydrotestosterone level in our patient. In addition to
; q1 \7 @/ w/ k( x" X( h, z3 ]6 }virilization, exposure to exogenous testosterone in8 A5 z/ o- ?6 S, {
children results in an increase in growth velocity and
' N, p+ y8 [! c4 v2 Q# u8 G+ |* ^: Dadvanced bone age, as seen in our patient.& L. S; p8 ]5 \6 E+ ?+ P1 |9 L
The long-term effect of androgen exposure during0 J+ d6 \% T4 V& |
early childhood on pubertal development and final  e- ?* x3 e+ z) g# ]% d
adult height are not fully known and always remain
. D; _3 b5 P# @2 W8 aa concern. Children treated with short-term testos-  D# V& Y% [4 f& K
terone injection or topical androgen may exhibit some9 A; k1 L; C) M
acceleration of the skeletal maturation; however, after) L4 B4 `0 w/ U. t& {9 y5 d7 |# C9 z
cessation of treatment, the rate of bone maturation
- I2 A+ S/ X% G5 H. J( Jdecelerates and gradually returns to normal.8,9
7 |8 L- u. s8 p4 _) P# WThere are conflicting reports and controversy
- M. T  N1 W2 |% t" U" C0 ?; yover the effect of early androgen exposure on adult- \; e# c* j  U4 \# e* g$ w$ a
penile length.10,11 Some reports suggest subnormal0 X" G, ~2 d' w- u6 U+ L$ t
adult penile length, apparently because of downreg-
1 g7 i* j8 h/ r  b6 \ulation of androgen receptor number.10,12 However,3 t/ \# I3 C- Z- v% ]
Sutherland et al13 did not find a correlation between
' h4 x: V5 j9 h( ]/ Ychildhood testosterone exposure and reduced adult' K9 O# d9 A5 j1 N
penile length in clinical studies.2 I3 e9 x- |# f+ v7 ?+ F
Nonetheless, we do not believe our patient is' Q$ q1 ^$ Y2 f
going to experience any of the untoward effects from3 i/ K: s7 q8 t3 Y; ^
testosterone exposure as mentioned earlier because
3 J+ T9 z; S5 Q* s, sthe exposure was not for a prolonged period of time.
9 I0 [: p, z5 H8 W# AAlthough the bone age was advanced at the time of3 }1 D6 s7 N" W4 |
diagnosis, the child had a normal growth velocity at& |" h: G* b2 [9 a8 k
the follow-up visit. It is hoped that his final adult
8 _' z/ o7 j/ `2 C  E+ d1 t" ^height will not be affected.
( m; Q' p4 ~; I; u8 i  HAlthough rarely reported, the widespread avail-, V; [8 y$ @) D+ H; A' j+ z
ability of androgen products in our society may
( V7 R. f1 S6 k9 T, Z7 y3 U9 Eindeed cause more virilization in male or female9 T# E" L9 D5 h3 x( }+ I/ ^
children than one would realize. Exposure to andro-
, {& I8 R$ H2 J6 Vgen products must be considered and specific ques-, p4 E$ ~! L: r. S% G
tioning about the use of a testosterone product or
& Z' ]& m9 h7 [gel should be asked of the family members during
1 C/ s( w& O% m, J* O0 Tthe evaluation of any children who present with vir-8 i5 X1 `0 k- f/ Q) z9 N
ilization or peripheral precocious puberty. The diag-
7 w! _$ O6 `( |) Qnosis can be established by just a few tests and by
1 G: y6 V: u( D: W' tappropriate history. The inability to obtain such a( w- Z4 g+ R9 w( q$ Y, K; Z
history, or failure to ask the specific questions, may
+ O7 w. R; ^2 |% o% J4 h9 U- j9 R; Xresult in extensive, unnecessary, and expensive# D4 K) G( w6 C+ d
investigation. The primary care physician should be, _1 o; M' ~5 s! {# [. m/ ]5 f
aware of this fact, because most of these children" f0 B) H$ p( U6 y
may initially present in their practice. The Physicians’% w2 G* f0 A7 O2 \9 M4 E
Desk Reference and package insert should also put a
4 J  l7 t( \/ e6 j+ h+ k2 Bwarning about the virilizing effect on a male or) x' a0 h  h6 p9 z0 K3 y1 N
female child who might come in contact with some-; z2 ?" M6 x. W' Y
one using any of these products.
! N  d0 Y0 @0 Y3 Y( kReferences
2 I0 v  F. `6 Y  p6 g5 M3 {; S7 B) N1. Styne DM. The testes: disorder of sexual differentiation
' Y' W7 F, o0 s  L" |& p) ^; U+ M( b& zand puberty in the male. In: Sperling MA, ed. Pediatric! U8 A: _% G2 b# ?: `
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;) ]; @: a2 S" L" s5 ?5 v, N
2002: 565-628.
! N+ x- Y  a$ D2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious0 s/ A4 N* `6 Z( L0 O
puberty in children with tumours of the suprasellar pineal
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這個我收藏了!謝謝分享!WK的資源越來越豐富,這少不了大大的辛勞!
發表於 2025-1-10 10:43:39 | 顯示全部樓層
VIP精品區,資源無限好賺金任務區,輕松賺金幣
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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
0 @# f) x5 k* ?; c8 Y& G" u5 q
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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