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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-Old1 e7 [# e: x6 u. U( a
Boy Induced by Indirect Topical
* L% P9 R1 M6 Q- K& OExposure to Testosterone
3 q2 F/ C* q5 q9 O3 L- @8 ZSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2% a0 Y5 {" z# l5 k
and Kenneth R. Rettig, MD19 U" R/ D: f* N. m3 T( a
Clinical Pediatrics) f: }" i+ A# A" W( U- y
Volume 46 Number 6
, |) [8 Y0 u1 m3 ?1 _% E8 UJuly 2007 540-543
5 S9 E0 R+ k  p% V2 B- W© 2007 Sage Publications
8 ~( ]' d$ J7 d# x: n0 P10.1177/0009922806296651
5 u7 j9 _; z; @+ i- ~http://clp.sagepub.com
4 o" N2 x5 m6 r( a5 P  u: R4 Hhosted at. G% q0 |( a+ [# |
http://online.sagepub.com1 y! Y& i- y+ n# u) R/ ?" T; Q4 {
Precocious puberty in boys, central or peripheral,# h* u* ^; w! C% ~
is a significant concern for physicians. Central9 _! I) ?' s- X/ I  C
precocious puberty (CPP), which is mediated" r) t' K: q: U
through the hypothalamic pituitary gonadal axis, has
* b$ i0 s% _; H8 B& pa higher incidence of organic central nervous system% r  K0 W$ Y' S1 ^' D7 P0 b& u
lesions in boys.1,2 Virilization in boys, as manifested
  {1 O, j6 r% l; i5 k7 pby enlargement of the penis, development of pubic( Z) U8 v6 p  ^9 s2 ~( K! U9 P
hair, and facial acne without enlargement of testi-
  ~# S8 O0 x( N0 D0 {4 W0 ucles, suggests peripheral or pseudopuberty.1-3 We% P1 \4 m) }( l7 T2 I8 T
report a 16-month-old boy who presented with the! X7 {2 ]9 c% D9 f+ j& C
enlargement of the phallus and pubic hair develop-+ q$ \; i$ {4 j* o( |, }6 U
ment without testicular enlargement, which was due1 m: u/ `- U2 V+ f+ d5 C1 F1 v4 N
to the unintentional exposure to androgen gel used by
; t6 |: Q$ Q5 |the father. The family initially concealed this infor-2 J+ K/ V8 _5 h+ d* j
mation, resulting in an extensive work-up for this
# u6 Y$ K4 M; S  s0 |7 E3 `" @child. Given the widespread and easy availability of6 m' j* M* {3 Z; z- G/ M! F
testosterone gel and cream, we believe this is proba-5 W8 ]% @2 b: \& D7 r
bly more common than the rare case report in the2 ^: e* A7 K: k- Y
literature.4: }) x+ l0 H- B5 x" Y9 E
Patient Report/ n8 c$ U6 a2 b
A 16-month-old white child was referred to the' H1 ?  v/ ?/ G& F4 b- d5 F
endocrine clinic by his pediatrician with the concern% Y7 z1 V+ S+ Q5 W  r7 c2 n- q
of early sexual development. His mother noticed2 j6 S. J" e/ P
light colored pubic hair development when he was
/ d0 f. [) w1 [$ Q) rFrom the 1Division of Pediatric Endocrinology, 2University of
6 \4 L  y& r! I% n, C9 eSouth Alabama Medical Center, Mobile, Alabama.1 u7 B3 \4 Z9 n/ Z$ Y
Address correspondence to: Samar K. Bhowmick, MD, FACE,
/ ~- O+ u% \4 s9 G& [Professor of Pediatrics, University of South Alabama, College of
3 g0 V$ G/ c2 }( oMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;; J5 S5 a2 D) Z+ p% c% Y
e-mail: [email protected].9 Z5 j' N0 p& ?  M# w
about 6 to 7 months old, which progressively became
6 v5 S7 [- t6 i6 Z6 I6 U1 Q+ idarker. She was also concerned about the enlarge-
7 Q  f5 ~4 ^; J. o  s/ Zment of his penis and frequent erections. The child
& \# c) t+ W& mwas the product of a full-term normal delivery, with
! w9 k4 h/ W( y" ya birth weight of 7 lb 14 oz, and birth length of
4 ^3 |% P: j% @( K20 inches. He was breast-fed throughout the first year
& Y5 A: ~# ?  r4 @" Oof life and was still receiving breast milk along with
. H& Z& z& t  A' A; i+ C7 qsolid food. He had no hospitalizations or surgery,9 |. p. |, e* T6 p7 V) V( y( o) m
and his psychosocial and psychomotor development
' S6 ?7 V9 X/ z" u+ o: v- o; \was age appropriate.
" W/ P; L) G0 V& V1 e3 Y1 LThe family history was remarkable for the father,
6 i; @3 ?" d% G5 e* v' _( pwho was diagnosed with hypothyroidism at age 16,6 E- \1 s% R' W+ V7 |
which was treated with thyroxine. The father’s
6 J9 ~" ^7 s1 A; a3 ~height was 6 feet, and he went through a somewhat" J* W" G4 i4 a8 h' X/ q! q9 z+ ]
early puberty and had stopped growing by age 14.5 `7 V) {0 u: R
The father denied taking any other medication. The# U7 q; h: r* [% e1 U
child’s mother was in good health. Her menarche5 o0 y2 s$ x: P0 ^2 E/ m: }4 c
was at 11 years of age, and her height was at 5 feet
' A# N9 R8 Q) p* [8 I8 q5 inches. There was no other family history of pre-% s0 g5 I' s) K, M3 S
cocious sexual development in the first-degree rela-8 |9 l" j5 z. u+ [
tives. There were no siblings.
4 q6 o, e1 y1 U4 j0 W0 X3 qPhysical Examination/ G& b7 L6 _( O7 h
The physical examination revealed a very active,
/ P; d, i7 y! I7 d* Hplayful, and healthy boy. The vital signs documented
0 X: k5 u" }: pa blood pressure of 85/50 mm Hg, his length was
0 R$ b1 m( I9 ]( f" w( w' a) d90 cm (>97th percentile), and his weight was 14.4 kg' y; [. y7 p' l1 e& @
(also >97th percentile). The observed yearly growth
; a( C: {1 ?1 o6 Hvelocity was 30 cm (12 inches). The examination of
% ~+ \+ y2 k: D8 H. Pthe neck revealed no thyroid enlargement.
! [1 B5 `6 H/ z! f0 K2 rThe genitourinary examination was remarkable for8 |2 _( Z# r5 u2 K+ `8 s
enlargement of the penis, with a stretched length of7 D  j+ Q& J4 l2 M/ r
8 cm and a width of 2 cm. The glans penis was very well
' E6 c% K6 @& X$ ~( Mdeveloped. The pubic hair was Tanner II, mostly around( ~# ?* V1 L0 D
540; M  K5 e8 K7 X* b7 H7 I! L
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from4 T% N& Y& Z7 r
the base of the phallus and was dark and curled. The' X( n2 m: A$ M& y* S1 J# A3 D
testicular volume was prepubertal at 2 mL each.. U6 O) k6 `0 h8 m+ T  l! @
The skin was moist and smooth and somewhat
  n$ B  B* A5 A( {3 K5 X; toily. No axillary hair was noted. There were no% J$ c0 t" T9 m3 T+ P
abnormal skin pigmentations or café-au-lait spots.
* H* @- D, F1 v5 ?Neurologic evaluation showed deep tendon reflex 2+1 v3 ?+ w/ M  K
bilateral and symmetrical. There was no suggestion: ~/ J2 s% A, x6 ~
of papilledema.
$ S& Z) \$ e" c! CLaboratory Evaluation" _$ \2 E& \6 G. ~6 t; G  I
The bone age was consistent with 28 months by' P1 O' \. N6 F" D
using the standard of Greulich and Pyle at a chrono-9 X4 P* Z3 V, R+ z/ X
logic age of 16 months (advanced).5 Chromosomal' t, A; c2 z( j, z3 p
karyotype was 46XY. The thyroid function test. u7 G5 j1 K5 Y) x1 e  ]. `" [
showed a free T4 of 1.69 ng/dL, and thyroid stimu-/ z3 U% ]  i# Z& t6 k$ s
lating hormone level was 1.3 µIU/mL (both normal).- B  o( x* t1 }2 y6 D2 r
The concentrations of serum electrolytes, blood
& P3 d# r+ N$ U& T" j5 J% V3 ^urea nitrogen, creatinine, and calcium all were
1 `# O# r% K  L, s( _; D# Ewithin normal range for his age. The concentration
9 c, D4 C( x6 @/ Vof serum 17-hydroxyprogesterone was 16 ng/dL, e5 Q; O( Y" D5 ?
(normal, 3 to 90 ng/dL), androstenedione was 209 F  M2 d( Y  {2 l- D
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-  _# i9 z3 _% ~3 K# f
terone was 38 ng/dL (normal, 50 to 760 ng/dL),/ [1 f' W6 m9 I  T8 B8 y/ T* I
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
) c+ R, E/ h* c2 K49ng/dL), 11-desoxycortisol (specific compound S)* E) H' A6 O) u% x( \/ R
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
8 g! K" n6 L2 L8 _/ O4 mtisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total6 P' n  Q# Z- u
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
4 D* A. ^# X1 x5 c" H( Xand β-human chorionic gonadotropin was less than
, ]" V; Y- Z% g: |6 C. @$ `5 mIU/mL (normal <5 mIU/mL). Serum follicular  n8 Q+ q, C- }& c; [7 X7 h
stimulating hormone and leuteinizing hormone2 I% I8 [6 x! E
concentrations were less than 0.05 mIU/mL
* }; R: f, r* `' h. J(prepubertal).
  F5 c6 [, C) e( S7 BThe parents were notified about the laboratory  e5 ?2 y+ Y* S% g0 c+ q0 e8 F2 v
results and were informed that all of the tests were7 I' n  d) I+ A/ K
normal except the testosterone level was high. The
; l4 _+ s, R8 C4 s& `, n" Bfollow-up visit was arranged within a few weeks to
" B: {* z' f5 Nobtain testicular and abdominal sonograms; how-
2 \5 d# \" _9 G$ w, L8 }- Kever, the family did not return for 4 months.
' P; {5 k3 z4 e9 k4 i- h. D" G& QPhysical examination at this time revealed that the  R7 ?& D# b( w
child had grown 2.5 cm in 4 months and had gained
1 a0 r' s$ n- J4 Y: X1 X8 q' O2 kg of weight. Physical examination remained  ^8 V1 S3 E4 X8 J/ ~" G
unchanged. Surprisingly, the pubic hair almost com-
1 t$ j8 z1 y! ^+ ipletely disappeared except for a few vellous hairs at
/ P) a0 D8 S  s& q0 E/ jthe base of the phallus. Testicular volume was still 2
1 X3 v) [* Q6 l" x* QmL, and the size of the penis remained unchanged.
9 l8 Y+ f/ |8 C. cThe mother also said that the boy was no longer hav-
+ q% s/ v" C' b& N! wing frequent erections., [# m' Z$ }, ~
Both parents were again questioned about use of0 y# ~! Z4 ]" M  {
any ointment/creams that they may have applied to
! u6 @# }0 w8 W6 r# P' ~the child’s skin. This time the father admitted the
2 o+ F4 `3 L, K# e/ E4 JTopical Testosterone Exposure / Bhowmick et al 541
9 g, ?4 z) d+ N# t" I! p  Fuse of testosterone gel twice daily that he was apply-
3 F: Z) i0 y/ V8 Iing over his own shoulders, chest, and back area for
8 I5 ~  R: R: t& _5 D" r" w. @a year. The father also revealed he was embarrassed& G# y7 K  @4 p+ b/ [
to disclose that he was using a testosterone gel pre-
1 L* G. L4 ?( h$ W1 v/ ?scribed by his family physician for decreased libido! \+ ^2 S# o( k, [
secondary to depression.
' b3 h5 v4 h( g3 h, T0 r& _# y' SThe child slept in the same bed with parents.
1 H7 G$ s8 U( Q0 @* V  l8 zThe father would hug the baby and hold him on his
" W0 ]" @. x' A4 T: schest for a considerable period of time, causing sig-
3 |3 {' ?: Z& c& Z# Cnificant bare skin contact between baby and father.2 s. U" K$ K7 ?! J' a+ j( A' |1 i
The father also admitted that after the phone call,
) Y/ u, j$ V1 z4 d3 U% ?* dwhen he learned the testosterone level in the baby
7 ~% ~! T* |0 F7 Kwas high, he then read the product information) J3 {; ]- K/ b; y# x. R
packet and concluded that it was most likely the rea-
7 _3 m( w% @  S8 N2 sson for the child’s virilization. At that time, they
$ @2 H6 P# }7 x2 R+ {decided to put the baby in a separate bed, and the# f2 Q2 r) O$ Q* b4 U
father was not hugging him with bare skin and had
3 b  e6 h9 j$ ?6 m4 _% W8 r0 gbeen using protective clothing. A repeat testosterone% S$ ^; Y3 \/ w. R: m
test was ordered, but the family did not go to the
" O: e* ?. ~8 I; ?9 o$ k+ Qlaboratory to obtain the test.
9 B: j' q$ P& y6 N  _8 eDiscussion
( p# s  R+ `5 R. M( FPrecocious puberty in boys is defined as secondary7 O/ H7 A, I. ~
sexual development before 9 years of age.1,4( A0 N' a4 k5 {
Precocious puberty is termed as central (true) when
" p' j9 D( W( g( l9 jit is caused by the premature activation of hypo-
  U2 K4 I5 f9 U* l2 Gthalamic pituitary gonadal axis. CPP is more com-
) Z- D( `/ _; p  \2 `2 imon in girls than in boys.1,3 Most boys with CPP
" T) ~: H% L8 F$ pmay have a central nervous system lesion that is. [- Q" L/ Q7 K. s! {0 o
responsible for the early activation of the hypothal-7 F3 j3 ]9 V7 X- g6 d# H& p* k
amic pituitary gonadal axis.1-3 Thus, greater empha-5 M: V$ T. u: v. q, n4 W5 j
sis has been given to neuroradiologic imaging in
8 T: k9 Y9 z$ E9 ~boys with precocious puberty. In addition to viril-/ c5 i0 h1 j" O+ }
ization, the clinical hallmark of CPP is the symmet-
# F) Y' \6 o/ S  Z% t% krical testicular growth secondary to stimulation by) V( ~$ \9 K7 k. v8 R
gonadotropins.1,3
1 T7 z1 \' I9 \Gonadotropin-independent peripheral preco-* C% n6 I0 m7 Q6 m0 ~# [6 _1 C
cious puberty in boys also results from inappropriate
( s2 W3 u- `$ d$ n* vandrogenic stimulation from either endogenous or3 y5 P  _; A- i; b* T4 r
exogenous sources, nonpituitary gonadotropin stim-; P- q4 i3 {8 x. Z# \
ulation, and rare activating mutations.3 Virilizing
3 Q3 Q7 }* r: {congenital adrenal hyperplasia producing excessive6 ?# W$ `3 k; N/ L1 v! J3 J6 O
adrenal androgens is a common cause of precocious; l: P& O) ]) }. g
puberty in boys.3,4+ y" v  J% M2 |+ @/ t
The most common form of congenital adrenal$ i* Q6 }( ], h( X# b0 O
hyperplasia is the 21-hydroxylase enzyme deficiency.9 I. O) f% q  ^5 l6 Q
The 11-β hydroxylase deficiency may also result in& Y  c: ]+ s. n0 u" U3 i
excessive adrenal androgen production, and rarely,7 r1 \4 B  i5 E! w$ x% l$ b6 w
an adrenal tumor may also cause adrenal androgen
! @+ D) D( v4 U5 h; l* Iexcess.1,3
' u$ S# @% y+ c; u" c, |9 [at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
( U+ Z( c! V0 o4 c542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
  u' y3 |, F3 l- l0 KA unique entity of male-limited gonadotropin-
. F- n) Y) E: I. oindependent precocious puberty, which is also known% B$ }1 w  a7 d; [8 O* E; S) S' m- g
as testotoxicosis, may cause precocious puberty at a$ ^* e2 g2 N+ _2 _2 f/ l
very young age. The physical findings in these boys
3 Y* T8 J. ]4 j$ w! b- h7 t; |! n' Fwith this disorder are full pubertal development,/ T! D5 K# }- z
including bilateral testicular growth, similar to boys0 n% ]1 a. J# o6 }: L
with CPP. The gonadotropin levels in this disorder+ J$ b5 S- ?" `4 L) o
are suppressed to prepubertal levels and do not show) Y. ~: W- Q8 H! K
pubertal response of gonadotropin after gonadotropin-
4 {0 x9 D3 \- N3 _$ {. U8 e# h/ Lreleasing hormone stimulation. This is a sex-linked) J6 l& |1 V1 G& ]- u
autosomal dominant disorder that affects only9 }" z4 W3 e, k6 C& f0 V; x
males; therefore, other male members of the family) P( P* I6 h7 @/ M" n3 X8 e' R# M
may have similar precocious puberty.3
" [- n* I1 c" h( `1 ~4 PIn our patient, physical examination was incon-8 M" S+ T- n9 ^2 p0 }& F
sistent with true precocious puberty since his testi-
3 r( S( g2 E; T- q: l% lcles were prepubertal in size. However, testotoxicosis
* }1 U0 b/ A& L& K) Uwas in the differential diagnosis because his father4 T- H3 a, j2 q9 @9 U, D% ^7 U
started puberty somewhat early, and occasionally,/ C, M; O  I3 J" q% N4 f
testicular enlargement is not that evident in the
/ z! C/ r7 W+ }, t5 J. sbeginning of this process.1 In the absence of a neg-" t& f7 c3 x; m: k3 o
ative initial history of androgen exposure, our
% S  K& P' [; r: [biggest concern was virilizing adrenal hyperplasia,
% R; C$ \+ C" u( xeither 21-hydroxylase deficiency or 11-β hydroxylase
+ d7 m6 k$ {8 @6 ~+ `  t( odeficiency. Those diagnoses were excluded by find-0 V, z- `) C# y. W2 V2 I
ing the normal level of adrenal steroids.! w5 m1 F) M+ ~+ x, D$ m4 j
The diagnosis of exogenous androgens was strongly
. r9 p/ S/ M( Y3 n( fsuspected in a follow-up visit after 4 months because! w% P, v7 T% U, `
the physical examination revealed the complete disap-
, v$ f0 ]" D9 n( J+ u+ L% m2 jpearance of pubic hair, normal growth velocity, and
& S" K* s" u+ w2 t& S  H9 u  wdecreased erections. The father admitted using a testos-
( U0 H( Y( J) Iterone gel, which he concealed at first visit. He was
1 `5 m2 Z) A4 f, Z- K, vusing it rather frequently, twice a day. The Physicians’
: ^; p+ h% p2 oDesk Reference, or package insert of this product, gel or5 T9 J& [' ?. w1 A# }
cream, cautions about dermal testosterone transfer to
) R  Z4 q0 e& F+ Lunprotected females through direct skin exposure.
: A7 O  e) A3 k: USerum testosterone level was found to be 2 times the- l* {. H8 W# w. ?% V; J
baseline value in those females who were exposed to- G0 @. E: {+ f- K9 v* T
even 15 minutes of direct skin contact with their male
& a1 f7 X& z7 Ypartners.6 However, when a shirt covered the applica-
6 l; _5 P: j" F0 ~" |tion site, this testosterone transfer was prevented.& ]2 o$ ]( S2 d2 I
Our patient’s testosterone level was 60 ng/mL,) E2 v/ C2 j0 u" L0 C3 I1 U. X
which was clearly high. Some studies suggest that. a7 L& L! i& {/ s# W% t: b
dermal conversion of testosterone to dihydrotestos-& R: x" Y0 M7 |$ \2 a/ V
terone, which is a more potent metabolite, is more
) ~9 x% ^( }5 K* X* N9 factive in young children exposed to testosterone( u8 _5 r* `0 |; y, L
exogenously7; however, we did not measure a dihy-
' R; u, f1 K  ^2 X0 Hdrotestosterone level in our patient. In addition to* B  S3 p! r' `" k' b
virilization, exposure to exogenous testosterone in
- C9 q8 T0 W) E3 V  A' B& [children results in an increase in growth velocity and
; T; m5 A8 P8 L* |advanced bone age, as seen in our patient.8 M5 i9 z6 F7 j
The long-term effect of androgen exposure during
' K9 ^, W  e( s6 Y) E) A, u# \6 uearly childhood on pubertal development and final
4 e1 k5 A7 Q# S" y# g: cadult height are not fully known and always remain
6 q. s/ Q5 @2 ^7 r+ w) Ha concern. Children treated with short-term testos-* y6 P" u+ {$ C2 ]/ A. N2 f3 u7 P+ F
terone injection or topical androgen may exhibit some& k' Y, g! o5 H
acceleration of the skeletal maturation; however, after1 {- F3 p* _/ D2 ~) ^
cessation of treatment, the rate of bone maturation
6 q) A7 p/ P2 A# _( u% adecelerates and gradually returns to normal.8,9
: v' w. {  X5 _  H6 W$ vThere are conflicting reports and controversy6 T7 @9 Q. ?8 Y% N- Y5 N
over the effect of early androgen exposure on adult! x- k1 D6 H0 T$ g( T
penile length.10,11 Some reports suggest subnormal) V' T0 t: J% x
adult penile length, apparently because of downreg-) e; o3 A5 W! G, x8 z
ulation of androgen receptor number.10,12 However,; Z9 x2 p6 P  M) {& u$ a
Sutherland et al13 did not find a correlation between
1 p9 @4 }0 n0 @" |childhood testosterone exposure and reduced adult+ n% i3 r4 `, O- f
penile length in clinical studies.
, c* |$ X9 V( N+ N2 ~/ X/ {Nonetheless, we do not believe our patient is
/ z2 W. O6 K; `  D% ^# \; v' xgoing to experience any of the untoward effects from. M/ a# \- \& C6 _) o& {% B
testosterone exposure as mentioned earlier because
# F  \+ Y/ k+ }9 J% X7 P2 R% kthe exposure was not for a prolonged period of time./ J/ S1 z2 |% o0 ^
Although the bone age was advanced at the time of
* s4 I  z# T5 ]' v' C9 kdiagnosis, the child had a normal growth velocity at# j; y1 I  x" p/ N' W- q, l
the follow-up visit. It is hoped that his final adult+ M3 o2 r  t$ x5 O) m6 J
height will not be affected.0 r9 a' f5 N1 R
Although rarely reported, the widespread avail-
# G+ [# K4 a( X" k0 k6 sability of androgen products in our society may* U; h4 q& R( d; L( l" y
indeed cause more virilization in male or female! K5 [- F/ ?% D
children than one would realize. Exposure to andro-& l7 ?* g) m$ x. t1 I* B7 `% C' z% ~
gen products must be considered and specific ques-
* y& }1 A/ Y. J! S; O4 V2 Btioning about the use of a testosterone product or: S. f8 v8 O% g1 n$ c3 Z  I
gel should be asked of the family members during
! Y$ [2 S9 S3 [  |  l- ?the evaluation of any children who present with vir-& ^& r9 m3 n) D4 u- M7 O
ilization or peripheral precocious puberty. The diag-% c0 V9 I5 d0 E% |' [5 r
nosis can be established by just a few tests and by( K1 \  A& B4 a2 k0 N2 D( Z
appropriate history. The inability to obtain such a2 q, V# {( |  V3 U1 W
history, or failure to ask the specific questions, may/ `0 _' R- r. Z; Q! c2 h- J- q. ^$ P
result in extensive, unnecessary, and expensive5 ^3 i! R, Q% f  f
investigation. The primary care physician should be+ G8 Z6 a  _2 Y- h; c# S2 p; P
aware of this fact, because most of these children
' J% Y% g6 ?5 |2 `! n3 u3 Z5 Vmay initially present in their practice. The Physicians’( ~) \% m% L4 `; V
Desk Reference and package insert should also put a
! o& H$ ~# i- u) E2 u* R5 ?, Ewarning about the virilizing effect on a male or7 i: J* \/ b0 s+ L$ R  r7 o% |
female child who might come in contact with some-1 Q) I& l5 \& }0 E, @
one using any of these products." c- U* X5 p$ R; x' `* T* Y" s
References
2 [8 Y& J3 T. V: _2 u0 {/ W1. Styne DM. The testes: disorder of sexual differentiation! I7 E' v2 X& J0 \
and puberty in the male. In: Sperling MA, ed. Pediatric
3 ~/ c' d, t% _- ^* }* _0 aEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
9 O+ U+ B9 _0 N4 u2 i% ^2 A2002: 565-628.
& e; Q, {8 G+ H, O2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
; O1 b1 q# a  v, W. @7 G: Gpuberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old2 E7 @* M& C7 n' ~
Boy Induced by Indirect Topical* A, m. C. @5 ^! d
Exposure to Testosterone* T. m/ O. C2 Q9 r8 J) e
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
  x; y' \" b9 E' V4 V! f* L1 Vand Kenneth R. Rettig, MD1
. ?+ Z& U* ]5 {# xClinical Pediatrics
9 V$ h# ^  s: iVolume 46 Number 6
  f& ~2 X; z7 U8 x" D  u" X) m( O) }July 2007 540-543
; S( J6 Y# e# [6 m5 u, l; p© 2007 Sage Publications( D7 V) T" Z& y1 o5 y6 {; U
10.1177/00099228062966512 R7 k7 T& y7 B/ U
http://clp.sagepub.com5 ~+ [7 W4 `! [9 C% t
hosted at2 f" w9 S7 I$ U" R7 k- {" z7 G7 x5 f# C  F
http://online.sagepub.com
. ^. X5 O( E, P1 P4 }& U7 [Precocious puberty in boys, central or peripheral,
4 j* @# }" b, m( ?6 W9 Iis a significant concern for physicians. Central3 k6 W  K9 I2 h
precocious puberty (CPP), which is mediated
# m' ?! _. r& n8 V* \# `1 lthrough the hypothalamic pituitary gonadal axis, has
8 }/ }+ n5 M( u! `% |* Na higher incidence of organic central nervous system
/ m8 @  Q+ }: @5 ~lesions in boys.1,2 Virilization in boys, as manifested
- x; l& P! A" n. K7 X6 N9 `by enlargement of the penis, development of pubic
) W; `' ?2 h' Y6 @; Rhair, and facial acne without enlargement of testi-
  G5 w$ f" l; M! O) ?cles, suggests peripheral or pseudopuberty.1-3 We& C0 c( P9 n' Z7 O, O
report a 16-month-old boy who presented with the
$ O" @+ R4 c! o* ~enlargement of the phallus and pubic hair develop-
: B/ y+ }. `6 ~" E$ Ument without testicular enlargement, which was due
$ {" O9 i7 }4 z& X0 ~. ~7 Wto the unintentional exposure to androgen gel used by
' Y3 v, ?' p3 c( }9 f1 }the father. The family initially concealed this infor-
! _# d3 @3 Z0 N8 F/ hmation, resulting in an extensive work-up for this  R8 o& P1 ^( X: W  f( l) i. P
child. Given the widespread and easy availability of
- b4 ~4 s& I" ktestosterone gel and cream, we believe this is proba-. E0 |# w2 w% {) ]* U+ Q6 j
bly more common than the rare case report in the9 ~% P# s" l3 F* |$ v! P' ^
literature.49 x) `( ]* B& g8 {* s+ o  y# }
Patient Report! ~  l4 `1 p" |1 i
A 16-month-old white child was referred to the2 d1 n; C6 m! ]8 p( y
endocrine clinic by his pediatrician with the concern
5 B4 \" r& O' r: Y' Z' gof early sexual development. His mother noticed
8 y) M8 C$ y' @3 q( {  v6 hlight colored pubic hair development when he was! i, y8 G8 G8 Y. z
From the 1Division of Pediatric Endocrinology, 2University of- V7 {; H5 w: V7 s3 M
South Alabama Medical Center, Mobile, Alabama.
1 n& P/ C- G, M" M/ _- QAddress correspondence to: Samar K. Bhowmick, MD, FACE,
# h2 x9 U, Y% H3 D8 Z: d) ]! Z( A# ]Professor of Pediatrics, University of South Alabama, College of
5 N! L& n" O' _7 \" E2 w, lMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
! _* N' X- w" v9 m5 s+ G. Le-mail: [email protected].
( u" S8 O5 I; U, }4 S) ^about 6 to 7 months old, which progressively became. Y6 S& P4 J! B) w" t
darker. She was also concerned about the enlarge-8 v" o1 Q, f8 Y0 q5 H6 w+ c2 D
ment of his penis and frequent erections. The child
1 n9 A: b5 o$ \- y7 Uwas the product of a full-term normal delivery, with
1 S8 w1 }) o% D8 u7 H) C6 z  ja birth weight of 7 lb 14 oz, and birth length of8 A. t% H1 b+ }
20 inches. He was breast-fed throughout the first year: M7 H( I' k5 {" N; Y5 a$ d. I" X  h, a1 J
of life and was still receiving breast milk along with0 P* z. T+ W9 Z
solid food. He had no hospitalizations or surgery,
  A' ]) ]3 v/ A7 G, Y# r1 [and his psychosocial and psychomotor development
( d& }$ q/ `0 E) ^# u2 G+ W7 Lwas age appropriate.. ~# Q  k/ N! h" j& @
The family history was remarkable for the father,5 k) V! n# P7 _# Q' |
who was diagnosed with hypothyroidism at age 16,: z* T( M/ L3 u& g3 y0 R# G! H5 o
which was treated with thyroxine. The father’s+ T1 o0 I! v; R9 B: C5 o
height was 6 feet, and he went through a somewhat
' D" S  U' b( E% z) t2 [+ u& aearly puberty and had stopped growing by age 14.; o. Q/ D, P6 _8 C' z" L' A
The father denied taking any other medication. The8 p% T5 g" n# Q3 }, R: k
child’s mother was in good health. Her menarche; K9 w7 q  r  m: h; Q/ L" q
was at 11 years of age, and her height was at 5 feet2 v; A( o, P4 S7 C9 e% X
5 inches. There was no other family history of pre-
" C( u- [3 i# M: F+ dcocious sexual development in the first-degree rela-  \# i1 S$ ~3 ~+ S' N
tives. There were no siblings.
$ d: {% h4 W1 @% c: a$ {) r+ q8 EPhysical Examination9 |+ T$ ~- q- o. z
The physical examination revealed a very active,
: \0 |. A1 O4 v/ V% z( q, wplayful, and healthy boy. The vital signs documented
9 Y8 p( L: [: g9 M2 S5 ta blood pressure of 85/50 mm Hg, his length was
8 D5 h7 S0 e& c- }9 Q( [, N90 cm (>97th percentile), and his weight was 14.4 kg2 W. `+ Y: _  l# D! W' g5 s
(also >97th percentile). The observed yearly growth8 u* Y' U2 O' B( A1 N. T7 I
velocity was 30 cm (12 inches). The examination of
2 p- G- q6 ^1 c8 {5 t) l6 i5 H: P  Rthe neck revealed no thyroid enlargement.
; U' f& o& P4 o& oThe genitourinary examination was remarkable for9 M- O" P0 T6 K/ y  b
enlargement of the penis, with a stretched length of
3 t# f& N! B  d0 `! V8 cm and a width of 2 cm. The glans penis was very well
, U% C* S- V- C( m+ ?+ Pdeveloped. The pubic hair was Tanner II, mostly around1 _' t% W, B2 f* j! w" p5 z) g
540
& y) L5 s, p, J3 t7 Uat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from5 {2 R* C0 M! E  y" B* g! }
the base of the phallus and was dark and curled. The
% h8 F# o# @+ I; Utesticular volume was prepubertal at 2 mL each.1 C& V. ^+ c8 u
The skin was moist and smooth and somewhat' h* P8 X  K$ y! d/ a# m* B
oily. No axillary hair was noted. There were no
: j! R; I/ W- Q# J. Tabnormal skin pigmentations or café-au-lait spots.' O) d7 E  u( V
Neurologic evaluation showed deep tendon reflex 2+
( D& o# q1 _$ [7 L: i& M' \) L  gbilateral and symmetrical. There was no suggestion
% `, a8 X: f) ?of papilledema.
3 |% u5 s0 B* _- @Laboratory Evaluation( O7 ~, k( W) f1 g
The bone age was consistent with 28 months by
. [$ a% o: x8 u3 Busing the standard of Greulich and Pyle at a chrono-
5 ^+ f% R' X6 V: P1 N; Flogic age of 16 months (advanced).5 Chromosomal
! Q7 n% m2 {, @* D2 `/ \karyotype was 46XY. The thyroid function test
6 @! V0 s; O  _% M3 eshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
4 h1 ^" U' @+ Alating hormone level was 1.3 µIU/mL (both normal).4 D/ N% r5 H5 r& f9 R" I
The concentrations of serum electrolytes, blood
/ l& |$ u3 n1 |3 xurea nitrogen, creatinine, and calcium all were
9 g) `9 _& N: G4 h9 h1 Swithin normal range for his age. The concentration/ b! w7 Z; ?) @" ]# y7 ?0 m
of serum 17-hydroxyprogesterone was 16 ng/dL8 b2 ~# a% J" D, m2 v6 l
(normal, 3 to 90 ng/dL), androstenedione was 20
% C% H$ _$ x" Hng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
% o- r8 Q9 e* k; z2 N/ Kterone was 38 ng/dL (normal, 50 to 760 ng/dL),
; g8 n7 o, w8 J- T) f! Xdesoxycorticosterone was 4.3 ng/dL (normal, 7 to+ u2 ]! {' W, |  `0 }% L0 p
49ng/dL), 11-desoxycortisol (specific compound S)
; [- h( E" U5 }1 P4 s' G* Zwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
& D# |# N8 z+ j+ M* Y8 ltisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total& _2 |/ w/ j3 X
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),$ m7 R3 _8 I+ |; M% i# o
and β-human chorionic gonadotropin was less than
/ F9 k$ G4 @3 @! i7 G) ?, }, I. i% M5 mIU/mL (normal <5 mIU/mL). Serum follicular( e+ Z4 T* H/ s$ z: o6 l
stimulating hormone and leuteinizing hormone" j8 R, [, B1 U6 E$ ]' f& `
concentrations were less than 0.05 mIU/mL
% N" f3 o, L7 p2 u' L  L(prepubertal).' G1 s4 S0 p* @. E, V  V# k9 J
The parents were notified about the laboratory, }; r/ f7 w3 c3 s! L: y3 H' t+ c
results and were informed that all of the tests were$ k! W9 Z8 j* l! c: x( \
normal except the testosterone level was high. The( e; L: d; [" `) ~8 ^/ U, L
follow-up visit was arranged within a few weeks to
) K2 n" T% @0 I2 wobtain testicular and abdominal sonograms; how-
3 V" V1 A$ [7 N" Rever, the family did not return for 4 months.: G+ r8 ]7 G7 N/ W/ l2 w
Physical examination at this time revealed that the) G- t. {. ?# n# S
child had grown 2.5 cm in 4 months and had gained0 Q3 L* a# k/ s! g
2 kg of weight. Physical examination remained
8 n8 L5 J, L2 f4 E3 H; u" Punchanged. Surprisingly, the pubic hair almost com-
9 r' p- Y( ~7 f5 _, Y* [pletely disappeared except for a few vellous hairs at5 \" A" f( }( C+ L
the base of the phallus. Testicular volume was still 2. h- @" V5 n" a0 X* [7 p8 D
mL, and the size of the penis remained unchanged.
+ ^5 g& P5 ~. b/ x1 {# @+ n# CThe mother also said that the boy was no longer hav-# E* c( V" o+ E
ing frequent erections.
5 y+ S& f  C* b$ ?" _! r/ vBoth parents were again questioned about use of
$ j. e! v. T% e8 B6 B& F5 L: \" Many ointment/creams that they may have applied to5 ?; r) y2 B/ P7 G& \4 p% x. Q
the child’s skin. This time the father admitted the
* i  M: Z3 C' b$ ETopical Testosterone Exposure / Bhowmick et al 541
  r$ h( f$ v1 U; T2 D" Ouse of testosterone gel twice daily that he was apply-( z( k' _/ N, u2 ^  o5 c% W8 Y
ing over his own shoulders, chest, and back area for, G- ]" o: u: u- k4 r3 V! b, H2 y
a year. The father also revealed he was embarrassed1 Z2 d. }/ \9 c# b& Q$ _
to disclose that he was using a testosterone gel pre-# _& {/ l' G! O
scribed by his family physician for decreased libido
) x0 S0 s2 l, xsecondary to depression.; f1 Z( T- k8 m3 y; V& f. r/ T& r
The child slept in the same bed with parents.
7 g5 ]8 I$ t# c* o. q6 _The father would hug the baby and hold him on his, t2 j0 [' F. p  h+ N% k7 M! c
chest for a considerable period of time, causing sig-! E% }% H' ~4 Z3 _: g% S3 @9 h
nificant bare skin contact between baby and father.
- Z$ l  Z9 A' \8 {: f. G  I/ dThe father also admitted that after the phone call,
2 w. S. B$ \. x$ Y! Twhen he learned the testosterone level in the baby( N* E6 c6 S) i2 K
was high, he then read the product information/ n# E% G3 X8 \& t' z
packet and concluded that it was most likely the rea-
9 o8 p4 D0 K& o6 nson for the child’s virilization. At that time, they1 h) j; m7 S% C& \+ w9 H( ?
decided to put the baby in a separate bed, and the; [8 N7 C! c  x2 R
father was not hugging him with bare skin and had8 i9 A1 Q# d2 j1 x; ~
been using protective clothing. A repeat testosterone; G9 B5 U' q( p( i/ v7 j9 {2 W
test was ordered, but the family did not go to the  C4 s% C% R6 D) w+ \
laboratory to obtain the test.
) o, \0 k# T! v3 nDiscussion
$ q( |' T6 ]( OPrecocious puberty in boys is defined as secondary9 l- F7 k) o' U9 ?0 M" g+ U
sexual development before 9 years of age.1,4) F# F. w9 V0 C& @& t) l8 [
Precocious puberty is termed as central (true) when% {$ [: \2 v" U2 I0 @- o; G. m
it is caused by the premature activation of hypo-% r7 Q' T: m0 G/ U5 t
thalamic pituitary gonadal axis. CPP is more com-
+ R7 X; d% J" ]5 M: d' l4 ^mon in girls than in boys.1,3 Most boys with CPP( H2 r+ ?$ ^3 M% v& R- N
may have a central nervous system lesion that is  F! s, t# r5 |  l  W# w! q
responsible for the early activation of the hypothal-; P- P& ]; @3 w! g
amic pituitary gonadal axis.1-3 Thus, greater empha-
3 p" z% O, \6 t% k/ H5 w) wsis has been given to neuroradiologic imaging in
( C5 n9 h* Z( v8 p2 f; Qboys with precocious puberty. In addition to viril-. g/ q1 C2 [1 t$ [6 {3 e) _
ization, the clinical hallmark of CPP is the symmet-
$ u  N8 p5 ^. Y: x" Q! D3 ]; v( orical testicular growth secondary to stimulation by  l. [/ J8 t8 A; X/ R
gonadotropins.1,3
0 j- |7 A. N* ]2 C/ H' Y- gGonadotropin-independent peripheral preco-* V0 `7 j8 \- o2 s& V) r% ?
cious puberty in boys also results from inappropriate
* n2 k( i. e) d  t  d2 ^5 Qandrogenic stimulation from either endogenous or# h7 k/ K9 S: m* f
exogenous sources, nonpituitary gonadotropin stim-
1 Y2 ?% P0 x# r; u. m: Aulation, and rare activating mutations.3 Virilizing" q* @* C  J$ i4 q
congenital adrenal hyperplasia producing excessive
! d& K' h% S: ?6 J# Uadrenal androgens is a common cause of precocious
; ~" B7 u$ E( N: `, }puberty in boys.3,40 i6 p) k  M, {/ {$ A$ e
The most common form of congenital adrenal& w9 K3 x! @' P( ~# w: J9 n0 v) B% O
hyperplasia is the 21-hydroxylase enzyme deficiency.0 {" x" T% b% q3 x4 c
The 11-β hydroxylase deficiency may also result in
& v( l& R+ a4 z4 Gexcessive adrenal androgen production, and rarely,
" B/ N! n1 F* o5 Zan adrenal tumor may also cause adrenal androgen
. f  l9 r3 M/ u. V7 Lexcess.1,3
* o% U0 k: t4 cat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from7 R# n7 u  J4 j* D
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
5 h+ |) F" Q9 e. |- V- ~A unique entity of male-limited gonadotropin-& S  B1 p! Q, `. ^( J  u, Z- `' G
independent precocious puberty, which is also known  q* O; L' q/ f! R9 ^
as testotoxicosis, may cause precocious puberty at a
- H" Y; Y& z! s" J9 [+ I* Svery young age. The physical findings in these boys
! X( F, z- T8 v7 B) k$ ^* J" F3 Y4 Iwith this disorder are full pubertal development,
  D8 Q  _  N4 L4 J' ~including bilateral testicular growth, similar to boys
+ k! {7 t4 g  D/ p0 O0 ~with CPP. The gonadotropin levels in this disorder
( ]9 q* E/ ]# u- h# c* `are suppressed to prepubertal levels and do not show
) C8 y) R( a3 a7 G2 _0 |: Vpubertal response of gonadotropin after gonadotropin-
1 s- j8 _3 Y; a% T1 f1 {5 n; R* ^releasing hormone stimulation. This is a sex-linked
/ D* i# A: s, J  uautosomal dominant disorder that affects only
5 }2 M9 }/ ]* g, f% p4 V( ?males; therefore, other male members of the family
& }% H  V2 H  T" |# g! c1 emay have similar precocious puberty.3
( p* H$ S% n7 T! y. L; J# ~In our patient, physical examination was incon-- \/ R4 Z8 e- C) J, }7 N
sistent with true precocious puberty since his testi-
/ F- f3 t8 D0 a7 |  l: V5 xcles were prepubertal in size. However, testotoxicosis6 U! j: ~/ W4 Y' R0 d% W0 Z; o
was in the differential diagnosis because his father
* s$ Q+ ^. }# q. g4 R: E& f. ?started puberty somewhat early, and occasionally,( s0 f2 T% ~6 d# e% ]9 _( V6 I% Z6 b
testicular enlargement is not that evident in the
8 o% K; k3 ~8 B4 b5 ?# ybeginning of this process.1 In the absence of a neg-
* s$ Z/ N/ P; m* a; r0 u8 oative initial history of androgen exposure, our
& H0 g4 I( E# ?2 _! m! a2 c7 Z" I# Qbiggest concern was virilizing adrenal hyperplasia,
5 Z0 w1 B  W5 S3 Qeither 21-hydroxylase deficiency or 11-β hydroxylase
' b& x8 ]; t: v' t) S- Mdeficiency. Those diagnoses were excluded by find-
: o+ |9 K2 I( R5 S$ `ing the normal level of adrenal steroids.9 Q) N" `* x+ @. N3 Z
The diagnosis of exogenous androgens was strongly8 @" Y! ~" O2 v! [* \1 o
suspected in a follow-up visit after 4 months because1 \# B" |- J0 K. e1 x" E  b
the physical examination revealed the complete disap-
% ]6 f( I3 R# f; j$ T# E2 Jpearance of pubic hair, normal growth velocity, and5 O* U) X5 y, b
decreased erections. The father admitted using a testos-- Z/ v. m, N- x. Q
terone gel, which he concealed at first visit. He was* H, b' a( [% M$ Q$ }. z$ s# D
using it rather frequently, twice a day. The Physicians’
- g* K- ^6 I, F/ f  o( x9 JDesk Reference, or package insert of this product, gel or( m) t' o/ l! x6 F8 ^* N* `+ d% E
cream, cautions about dermal testosterone transfer to
9 m9 o. q, H' |' wunprotected females through direct skin exposure.
, B: L6 g! k* `0 p5 WSerum testosterone level was found to be 2 times the
4 L/ @- B1 T) I1 T6 T9 K" S( B1 ibaseline value in those females who were exposed to
$ y+ y' i& l: }! t+ M/ Veven 15 minutes of direct skin contact with their male- D8 X" H8 V5 `7 |6 \5 u  n
partners.6 However, when a shirt covered the applica-
. {+ ]' i* i* c9 X5 Y9 Ltion site, this testosterone transfer was prevented.
+ Q7 R4 G/ V+ ?  q5 \& ]  o' XOur patient’s testosterone level was 60 ng/mL,
* y8 t$ D+ k& E( Zwhich was clearly high. Some studies suggest that
9 A- t5 M4 R" n9 J- S3 P* i( Sdermal conversion of testosterone to dihydrotestos-3 J# ^6 C+ w# b# ]: x
terone, which is a more potent metabolite, is more/ D8 R$ K' t. ~  t2 g/ t8 M: V
active in young children exposed to testosterone# N) X) N$ K* Y4 g& ~# T& N8 H
exogenously7; however, we did not measure a dihy-
5 H$ `; Q3 o# e2 }. \  V+ sdrotestosterone level in our patient. In addition to
% ^- h7 q1 I3 r* B4 ~0 Gvirilization, exposure to exogenous testosterone in
2 _) e. y8 d: K- @1 e+ \7 mchildren results in an increase in growth velocity and
; W+ Y0 l( d1 t1 R5 |1 Qadvanced bone age, as seen in our patient.
4 T! [# |; U9 o3 ]2 Q* L+ I: JThe long-term effect of androgen exposure during4 d: a1 g* {) l8 ^" c
early childhood on pubertal development and final& l6 D8 [* b9 J# B
adult height are not fully known and always remain+ K9 z& |' T* M. w! @+ l3 [
a concern. Children treated with short-term testos-4 e0 S" a, i9 R# m' i
terone injection or topical androgen may exhibit some
4 ~# G$ A; B$ |, x$ P! yacceleration of the skeletal maturation; however, after$ b* o4 f9 |, \5 x- E2 p
cessation of treatment, the rate of bone maturation
8 y: {$ B) w) s/ `: C- Pdecelerates and gradually returns to normal.8,9
- f, Q: |+ N1 {7 eThere are conflicting reports and controversy
8 i# D; w0 U% C' e+ q2 k; \2 nover the effect of early androgen exposure on adult7 Z7 C# I2 g; N3 l
penile length.10,11 Some reports suggest subnormal" B1 t' @1 P" q- j+ [! g4 l
adult penile length, apparently because of downreg-
' `, m: L% }6 G7 X7 j4 k- _ulation of androgen receptor number.10,12 However,6 G( ^' s4 x! X' @' I* u, H1 r
Sutherland et al13 did not find a correlation between$ U6 L# r: U+ K- U2 E& q
childhood testosterone exposure and reduced adult) M# O0 e/ p/ Q1 U3 |+ ~+ D3 f
penile length in clinical studies.
1 j; P' g' `7 |Nonetheless, we do not believe our patient is
- E) n% F. D# b, Zgoing to experience any of the untoward effects from" k6 ?9 t: R3 L8 W0 [+ s3 Y
testosterone exposure as mentioned earlier because
5 j9 z2 w6 T( n. h/ Fthe exposure was not for a prolonged period of time.; F6 i0 P+ K- n$ g, _
Although the bone age was advanced at the time of
" e# E3 O) V: _diagnosis, the child had a normal growth velocity at  p7 W3 M7 {% \% b; \, g# _
the follow-up visit. It is hoped that his final adult" i4 @% Q, F9 P7 h4 X
height will not be affected.
$ K2 ^& V! p- `Although rarely reported, the widespread avail-
8 A' y1 T3 G4 N5 R$ b' v1 H2 Aability of androgen products in our society may
2 Y$ }* `. `" sindeed cause more virilization in male or female
) W' b6 l' `) H. |' P$ F4 N4 _5 Kchildren than one would realize. Exposure to andro-
$ A! |" B* X: S9 y. u8 G# fgen products must be considered and specific ques-
5 v8 X% S; M& d3 I- }  n1 j4 B4 J. stioning about the use of a testosterone product or
5 C1 t; J, t2 B" ]4 b& j. agel should be asked of the family members during1 }# W4 e+ K: g/ P* a0 ]
the evaluation of any children who present with vir-
) W0 r% O7 y& r( oilization or peripheral precocious puberty. The diag-, \: B- ^1 V( u. v0 A* W
nosis can be established by just a few tests and by, X6 w+ h7 r9 x
appropriate history. The inability to obtain such a
% i0 y: M% b8 h3 u( x9 Y- lhistory, or failure to ask the specific questions, may
" B5 k! z1 w0 d9 u1 N6 lresult in extensive, unnecessary, and expensive" t1 O4 l6 E- }5 W. C
investigation. The primary care physician should be
2 M) K) X0 A4 F4 y& }aware of this fact, because most of these children6 z5 @, H) c( ~+ M$ x# @: Q0 Y
may initially present in their practice. The Physicians’
- J: h$ w+ z# d  r/ BDesk Reference and package insert should also put a
8 H) n1 m9 l/ A8 I9 j$ Y. a/ Gwarning about the virilizing effect on a male or
) h  y. O( _8 k( ^. Vfemale child who might come in contact with some-
; K; T( y4 V3 |+ a) Q, sone using any of these products.
) J& b7 m0 u+ R8 x2 uReferences! o1 s0 b$ b% @4 l0 S; x
1. Styne DM. The testes: disorder of sexual differentiation" G% u# F( u0 ]
and puberty in the male. In: Sperling MA, ed. Pediatric
0 Y- x* s- Y6 V/ eEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
% O* ~: F* ~7 x9 I2002: 565-628., l8 e3 a2 B7 a6 l
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
/ `: X- \- r2 S" U9 \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
2 n: G% k; ^% P9 }% q6 x- p. ?
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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