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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
5 L$ `/ I; ~9 @/ b( _Boy Induced by Indirect Topical: X- v  L" M7 \: G) \8 V# J0 I( B: n) G
Exposure to Testosterone
+ E5 W3 d9 h- j; z8 x& j; t/ JSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2% G3 ~" V) p. B. n
and Kenneth R. Rettig, MD1
+ A! L& [# m1 G- NClinical Pediatrics6 p; q9 V+ s/ E6 b! I+ r
Volume 46 Number 6
/ o. c% E( e$ MJuly 2007 540-543
# X4 @5 l, }: X& s: E1 S© 2007 Sage Publications
. f7 f3 l5 q* c) ^& _10.1177/0009922806296651
+ y) R: {" e# h' B6 Fhttp://clp.sagepub.com
. _6 d' w) ?/ h6 B- W) U- @hosted at( w+ k7 d9 u* M9 u, r, T4 K
http://online.sagepub.com
6 s. E& T) u: Y: QPrecocious puberty in boys, central or peripheral,
& b" S6 S0 Z2 j. ?4 Kis a significant concern for physicians. Central2 v! {2 c) k+ U9 o, w+ w
precocious puberty (CPP), which is mediated: f+ _5 \; M, }4 _7 J/ C
through the hypothalamic pituitary gonadal axis, has: C2 m7 C( E* c
a higher incidence of organic central nervous system! r- y8 n1 E' ]
lesions in boys.1,2 Virilization in boys, as manifested+ v1 S7 q/ D; z
by enlargement of the penis, development of pubic( [* F8 E7 w* Z4 Z
hair, and facial acne without enlargement of testi-
8 {# ~, I' m& E* \- e) \cles, suggests peripheral or pseudopuberty.1-3 We2 L5 w( e' ?0 |1 P0 P
report a 16-month-old boy who presented with the
# d4 Q" f) l8 H0 ^enlargement of the phallus and pubic hair develop-4 a* ^/ d# H' g3 \* r
ment without testicular enlargement, which was due" W( V) O+ B2 L  C1 c  U, B% L- J
to the unintentional exposure to androgen gel used by
+ I" o( l/ K& |# I, s. S. Nthe father. The family initially concealed this infor-
4 z7 j6 u/ R/ N3 W: E5 c' B( mmation, resulting in an extensive work-up for this! O  B4 s3 F# I& M
child. Given the widespread and easy availability of2 B4 ]  L/ H- _# ^$ X6 b
testosterone gel and cream, we believe this is proba-* m' Y; r% `# P, g9 j& N# `7 h
bly more common than the rare case report in the' B! f7 j) o) W. m* F
literature.47 D# B. ?" H9 p
Patient Report
6 u$ m" g) l' D$ d, x3 ]A 16-month-old white child was referred to the0 V3 T) _' \, u, s8 v9 g5 {) L( g
endocrine clinic by his pediatrician with the concern
+ w+ u+ n) n) G( Y" {of early sexual development. His mother noticed  X* ]' |# h) _; T% C3 J+ w* }) `# r
light colored pubic hair development when he was
- ~, y# I* m) N8 O9 BFrom the 1Division of Pediatric Endocrinology, 2University of
4 U4 I6 g) J: ~2 Q) ZSouth Alabama Medical Center, Mobile, Alabama.
( H0 ?! \( Z& D, t1 [- N. NAddress correspondence to: Samar K. Bhowmick, MD, FACE,
! I( d7 F  w$ u1 I6 JProfessor of Pediatrics, University of South Alabama, College of) K- e' b: i' _+ G3 t
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;4 o3 W1 x* r+ c7 s$ H  ?7 U
e-mail: [email protected].
3 }/ Z3 b/ C. e8 }" Pabout 6 to 7 months old, which progressively became
/ ~6 }. u- O0 ?darker. She was also concerned about the enlarge-5 C+ }+ F# w+ B: K
ment of his penis and frequent erections. The child* X( g& @; S/ N8 Y/ y: f( O- |
was the product of a full-term normal delivery, with
% p0 J/ ~5 \5 v3 y8 H+ U, Fa birth weight of 7 lb 14 oz, and birth length of& Z8 b" I% a5 L& `' y. p8 e
20 inches. He was breast-fed throughout the first year
# B  q, _7 j7 d+ Nof life and was still receiving breast milk along with9 B9 z! q6 z8 h& X
solid food. He had no hospitalizations or surgery,8 l/ s' ]! U8 b5 p6 W
and his psychosocial and psychomotor development
9 @4 R" O. p) d1 Cwas age appropriate.  O. R" Z0 A- X' l3 A/ J* s
The family history was remarkable for the father,5 s: A' U9 m6 Q2 A: q
who was diagnosed with hypothyroidism at age 16,
6 `% D2 J2 y, r. x$ C7 X" x( Z8 _7 G7 W& ywhich was treated with thyroxine. The father’s
1 Y3 n' `" j6 I- Qheight was 6 feet, and he went through a somewhat4 C. m( O: J. w* U6 Q2 p! A
early puberty and had stopped growing by age 14.
, c/ w: v' ], R& d( P1 w5 O+ YThe father denied taking any other medication. The$ i9 j0 w! ]( Y6 N8 \! r0 C
child’s mother was in good health. Her menarche$ h7 J, d% d% }  n
was at 11 years of age, and her height was at 5 feet
. _: j, |7 J/ b" v% \% Q- A5 inches. There was no other family history of pre-# ^/ g4 M, N; W- f$ e$ s7 n$ ?1 k9 k
cocious sexual development in the first-degree rela-4 u! s( |' \$ j
tives. There were no siblings.
4 J: r8 m* c) l/ s6 |4 ]Physical Examination" R3 d! }7 T: [0 m. c1 H0 z$ Q
The physical examination revealed a very active,6 r" O- {& F% g4 O( q
playful, and healthy boy. The vital signs documented5 O2 B1 b3 W4 \
a blood pressure of 85/50 mm Hg, his length was
: x9 [2 Z- O, e9 ~) d# ^# D# F90 cm (>97th percentile), and his weight was 14.4 kg
( [5 ?3 g9 G# C0 F(also >97th percentile). The observed yearly growth
  U; c" \& A2 J+ M6 Q, ?velocity was 30 cm (12 inches). The examination of
8 z1 E, ]  L+ ~3 D) Lthe neck revealed no thyroid enlargement.
4 ?: h9 U. z4 \$ `The genitourinary examination was remarkable for' g( g4 G6 T9 E" i+ X& ]2 m  s0 U" E
enlargement of the penis, with a stretched length of
9 A* ]. ]) o3 D6 U, c! T7 Y8 cm and a width of 2 cm. The glans penis was very well- a& M/ p) u; M: \$ b1 L. j
developed. The pubic hair was Tanner II, mostly around
* a" P8 Z% T! I0 H. j# L* o7 G540
: L5 l. L" S$ E+ v' D; j# S2 [" dat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
* \) w& Q) _9 @  Lthe base of the phallus and was dark and curled. The
& J; n( L6 k% z' Etesticular volume was prepubertal at 2 mL each.+ _+ i3 u' d( p! K* m% a
The skin was moist and smooth and somewhat& R8 u8 b$ e4 G6 e  e6 c5 G
oily. No axillary hair was noted. There were no
/ T* c4 L4 D8 q# l3 cabnormal skin pigmentations or café-au-lait spots.
; I* m/ w  g& t; T) Y) ]Neurologic evaluation showed deep tendon reflex 2+
) L  O+ l6 T, S9 @- s* x  Kbilateral and symmetrical. There was no suggestion% D( K( ^3 f. z& q/ r. r) d
of papilledema.
# L% o+ t/ K' Z1 I0 C0 e+ L9 _5 k8 B  \Laboratory Evaluation! j3 Q. ?' F' n
The bone age was consistent with 28 months by7 Z) z' j! I$ |9 D0 s
using the standard of Greulich and Pyle at a chrono-
$ a- \2 ~1 v3 e7 k  v. z/ Klogic age of 16 months (advanced).5 Chromosomal
6 G& B0 @2 X' h5 skaryotype was 46XY. The thyroid function test
, m; ~1 S2 w" V% y" Cshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
7 k4 s- ]1 t% u+ d  \: P1 ^" }lating hormone level was 1.3 µIU/mL (both normal).
3 X, y5 K" K3 Z7 p3 {The concentrations of serum electrolytes, blood
; {5 V" a( x# J+ [urea nitrogen, creatinine, and calcium all were
7 a! E: {, i% q. j. w! i9 Fwithin normal range for his age. The concentration5 g7 U: E, ]7 h* l: B9 m- e0 a
of serum 17-hydroxyprogesterone was 16 ng/dL' ?  ]: x+ A: t
(normal, 3 to 90 ng/dL), androstenedione was 203 {7 J2 d2 C; `1 n! H7 n
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
8 W& H9 W* l; i! yterone was 38 ng/dL (normal, 50 to 760 ng/dL),0 i' W3 K- [1 S! ^) J" Y7 a# y
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
( z4 _. ~! M( |49ng/dL), 11-desoxycortisol (specific compound S)
9 [7 A' h6 J5 b3 \* k: nwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-% z0 G* h9 g/ \4 }8 q4 l
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
0 u) f# [% s* J& j- d0 @testosterone was 60 ng/dL (normal <3 to 10 ng/dL),/ x7 d. G6 M0 ~: H0 A1 }3 C6 k
and β-human chorionic gonadotropin was less than
5 Q7 }* H2 I. H9 W0 ?8 k! U5 mIU/mL (normal <5 mIU/mL). Serum follicular
6 o' W, E% F4 b; x8 w2 W) }stimulating hormone and leuteinizing hormone' z! U5 N/ w* t4 @
concentrations were less than 0.05 mIU/mL  S' J$ i, b& G7 w
(prepubertal).
( R3 m" w% g2 m# \- [8 }$ [: G! @The parents were notified about the laboratory
& o' A6 ~6 |% o. xresults and were informed that all of the tests were; U; Z$ f* w/ }
normal except the testosterone level was high. The
+ r! c3 e4 q4 D5 v5 B7 {* Q; Jfollow-up visit was arranged within a few weeks to
' y4 |* N4 B2 Y8 ?* Z7 s. yobtain testicular and abdominal sonograms; how-* H" d8 S! G/ i) ?) s
ever, the family did not return for 4 months.
; |7 {" B7 `; Z+ J5 dPhysical examination at this time revealed that the7 n( L, G' Q+ G' B6 r" o+ T
child had grown 2.5 cm in 4 months and had gained. _* P  d$ o; _" ~, @# [/ ~
2 kg of weight. Physical examination remained) N* j. V9 `+ X/ m! w+ B
unchanged. Surprisingly, the pubic hair almost com-4 e; y. Y3 f) p  ~+ {: ?' o: Y
pletely disappeared except for a few vellous hairs at3 d8 y& p; Z) P! e1 R
the base of the phallus. Testicular volume was still 2  U: ~% n" v1 B& b
mL, and the size of the penis remained unchanged.
* B5 p6 m  M2 X9 W8 I' AThe mother also said that the boy was no longer hav-7 v/ n/ @5 P) w: S) O
ing frequent erections.
( S( D% }: ]" \) |7 O- jBoth parents were again questioned about use of
' k( |, {, M( Dany ointment/creams that they may have applied to
( Q6 L! J" V% J# d* V) Jthe child’s skin. This time the father admitted the
4 Y: a7 _# w! b- k% `1 {. k/ BTopical Testosterone Exposure / Bhowmick et al 541/ H% ]" r4 ?9 q1 u
use of testosterone gel twice daily that he was apply-
# N2 a. W( W, o( t8 xing over his own shoulders, chest, and back area for
6 _. v) T& O5 y$ _0 L8 Ba year. The father also revealed he was embarrassed
' h7 b9 M! L; F, j/ a5 ^. Sto disclose that he was using a testosterone gel pre-! N5 T/ {5 v( k
scribed by his family physician for decreased libido
+ E3 C' b4 A) Nsecondary to depression.8 w) [) |8 P& P5 P
The child slept in the same bed with parents.9 J, V! P  S! ?3 Q. |" w2 U- b
The father would hug the baby and hold him on his) b% @+ f% |# k+ d/ Z0 r
chest for a considerable period of time, causing sig-
* C7 j! O0 j2 x8 O3 D- H8 }nificant bare skin contact between baby and father.' E0 @1 g9 T5 y( L- r: B
The father also admitted that after the phone call,/ S! u8 G, k$ S# x: y, U1 ]' O4 A
when he learned the testosterone level in the baby  B- g% P$ E3 b+ s7 Z
was high, he then read the product information
9 J# b) R( ]- O  o  r6 xpacket and concluded that it was most likely the rea-
/ W: R0 a2 m2 z1 n7 Hson for the child’s virilization. At that time, they, c0 `6 q8 _+ F( [7 b
decided to put the baby in a separate bed, and the
( U) A/ [& B+ k9 O+ o& q( nfather was not hugging him with bare skin and had6 {/ e6 Q7 G/ H- R+ {! D( i! p6 b- h
been using protective clothing. A repeat testosterone
) j$ o/ h& q" ntest was ordered, but the family did not go to the
- B% S0 ]$ d3 J. Y8 [# |, Ylaboratory to obtain the test.
! G8 q1 g- _$ wDiscussion; R" Q+ r5 B  Z& ?5 E& B3 b2 |
Precocious puberty in boys is defined as secondary
; q! b0 a4 L! y5 Hsexual development before 9 years of age.1,4: h2 \+ I$ g+ N9 z
Precocious puberty is termed as central (true) when
% Z* a5 a! q4 |2 A% p/ hit is caused by the premature activation of hypo-0 `7 p& \6 g, J
thalamic pituitary gonadal axis. CPP is more com-
9 Q3 Z5 L: k% _! E+ Q: Mmon in girls than in boys.1,3 Most boys with CPP) y/ i- ]3 E5 S# s% I
may have a central nervous system lesion that is6 U& I# T+ T/ \3 Q$ ]4 m
responsible for the early activation of the hypothal-' U0 U- P$ |/ P- R6 y5 c' b# m7 m2 c
amic pituitary gonadal axis.1-3 Thus, greater empha-0 {' ~! \8 j" ~8 ~# G- ?4 C+ \4 z
sis has been given to neuroradiologic imaging in
2 y' x/ Q6 G& t( aboys with precocious puberty. In addition to viril-4 x' L: x1 N3 s
ization, the clinical hallmark of CPP is the symmet-
, W8 ?% f$ W  E7 V* A' y& W  Urical testicular growth secondary to stimulation by. g5 Q1 |7 J( R2 }; \& ?5 O6 i, r
gonadotropins.1,33 o9 C# L8 e6 g/ L, G
Gonadotropin-independent peripheral preco-
6 U* e* L6 ?% [cious puberty in boys also results from inappropriate6 s5 \$ i; g1 G( S
androgenic stimulation from either endogenous or
9 g! E5 v* _# a# d( Rexogenous sources, nonpituitary gonadotropin stim-
% i$ w& W0 G+ d  @ulation, and rare activating mutations.3 Virilizing# n8 K( y- j) g" d/ N9 o
congenital adrenal hyperplasia producing excessive: P' N' `, Y' m; ^; `
adrenal androgens is a common cause of precocious2 m" V6 a3 l% O0 v: J
puberty in boys.3,4
1 H, S/ @: G; Y& p# F  S7 K# c' XThe most common form of congenital adrenal
3 K) N3 r; W- C2 ^9 W+ D' @# Qhyperplasia is the 21-hydroxylase enzyme deficiency.& b3 _5 ~# k. S9 Y
The 11-β hydroxylase deficiency may also result in
* q- B! f/ }- ~2 I( {  Mexcessive adrenal androgen production, and rarely,7 y6 Y9 a  ~! |: e2 J, h8 P
an adrenal tumor may also cause adrenal androgen
% i6 |3 @4 a$ ]excess.1,39 y; ^: S& h* c
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
) j! d0 j5 x# T# Z3 r1 i! F542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
5 U" \+ ~# |. U* L2 zA unique entity of male-limited gonadotropin-( a( @' n5 }) @$ C' J
independent precocious puberty, which is also known; r: G, E$ {* J+ O' D' @$ S
as testotoxicosis, may cause precocious puberty at a$ N: B2 I2 V& z4 y: w5 [8 n/ m
very young age. The physical findings in these boys8 V. ^5 f0 h$ c0 W
with this disorder are full pubertal development,
) g* L! z( F+ lincluding bilateral testicular growth, similar to boys
. b+ ^/ @4 r2 q& b' V9 Kwith CPP. The gonadotropin levels in this disorder
* H# ]2 [+ E! _9 }2 @( Hare suppressed to prepubertal levels and do not show' L2 M7 E. V% ~3 d
pubertal response of gonadotropin after gonadotropin-& K6 a" h4 G% D+ R
releasing hormone stimulation. This is a sex-linked1 d% ]; \- T6 a) z4 O9 }
autosomal dominant disorder that affects only5 U0 E, k& d  z5 S3 J
males; therefore, other male members of the family4 N% @4 z0 D6 V: K4 X2 A
may have similar precocious puberty.3' t$ R0 B; g! K' i
In our patient, physical examination was incon-
( @- K' P4 ]& C/ h4 _, ~7 l2 Usistent with true precocious puberty since his testi-
1 w( }4 X: Z, L3 y2 p' c5 Ycles were prepubertal in size. However, testotoxicosis
6 s7 @& V+ `- \/ M# t4 I' S3 Owas in the differential diagnosis because his father! c. B. [. @9 ^
started puberty somewhat early, and occasionally,2 _( B8 y, b4 D
testicular enlargement is not that evident in the! G( n4 c3 P1 \* n1 X' Q
beginning of this process.1 In the absence of a neg-, r, v; k, S* f
ative initial history of androgen exposure, our
8 ^- e, Q  M7 a& r) z$ gbiggest concern was virilizing adrenal hyperplasia,
5 N% M' t) y# ~& feither 21-hydroxylase deficiency or 11-β hydroxylase% M5 L# S( a, ?9 _
deficiency. Those diagnoses were excluded by find-8 m) s* V* V3 D. X0 p& z9 I
ing the normal level of adrenal steroids.
9 ?+ Y( \) S( h% m7 F  }' M4 GThe diagnosis of exogenous androgens was strongly
1 k- ^3 K; x7 T) E1 O  B- A- |2 _+ vsuspected in a follow-up visit after 4 months because
6 U' p; w0 y) K+ Dthe physical examination revealed the complete disap-
. l9 J2 Y+ J  k* i9 Y; E7 ^pearance of pubic hair, normal growth velocity, and1 [4 B7 D& s# ?
decreased erections. The father admitted using a testos-7 ?. b2 D1 C0 e2 Q9 v! i
terone gel, which he concealed at first visit. He was% p- c4 R( M8 z, c8 Q
using it rather frequently, twice a day. The Physicians’* G) B* a9 _# M
Desk Reference, or package insert of this product, gel or# i3 s- X" s# j7 P% N( Y
cream, cautions about dermal testosterone transfer to
; G0 q$ x6 X6 ~5 g. o. w5 d: tunprotected females through direct skin exposure.5 D! n* X+ O$ d, ^3 H* m
Serum testosterone level was found to be 2 times the
# Z# Z* t) Q; Vbaseline value in those females who were exposed to
0 F7 L' t4 N$ V5 weven 15 minutes of direct skin contact with their male1 i% M. u- I8 L; Y; G
partners.6 However, when a shirt covered the applica-
6 G  n! K* `8 T+ q/ Z3 \+ ution site, this testosterone transfer was prevented./ D8 J4 Q, [0 n5 ?) M, N* z) i* Q0 U
Our patient’s testosterone level was 60 ng/mL,
! Q  e( [7 i& [, O" e/ z3 h! e* Kwhich was clearly high. Some studies suggest that
% v& B; b% v, L1 _dermal conversion of testosterone to dihydrotestos-
/ W+ P) r5 e7 v8 P* L4 {/ D$ ?terone, which is a more potent metabolite, is more6 S' W) Y1 R! r" ?
active in young children exposed to testosterone2 z5 w% Y1 y) k) q* ~! ?/ s0 c
exogenously7; however, we did not measure a dihy-
0 X: i/ i3 `' g/ _' F0 `. O6 i, Edrotestosterone level in our patient. In addition to
- e3 Q2 J6 p/ l- u8 ^3 c) pvirilization, exposure to exogenous testosterone in, j" K* L0 d- y- L4 _% d
children results in an increase in growth velocity and
! n. c& I% ~! i% a5 \advanced bone age, as seen in our patient., r8 s. v- h5 W2 z0 }0 j( ]( x
The long-term effect of androgen exposure during
& F# {0 l1 D  N2 |) p% `0 D# Jearly childhood on pubertal development and final, z9 k" e' M3 Z8 {9 F/ f" k
adult height are not fully known and always remain& s& p# T, v$ S3 X$ ?5 _, Y* l
a concern. Children treated with short-term testos-
2 Z, A- z, o- {# ^3 Aterone injection or topical androgen may exhibit some
, }& ]- A* f% [. o. @acceleration of the skeletal maturation; however, after
1 C" S! x  r; w5 ~( Tcessation of treatment, the rate of bone maturation
7 Z& B4 G6 C: l6 ~decelerates and gradually returns to normal.8,9
' w+ l7 v0 t$ X9 E+ tThere are conflicting reports and controversy
' c1 q8 B' G# F) sover the effect of early androgen exposure on adult
- j6 u" d1 Y* t  G% u5 jpenile length.10,11 Some reports suggest subnormal
7 B! U1 N9 \3 i) X7 @adult penile length, apparently because of downreg-; L! V9 ]8 ^1 `
ulation of androgen receptor number.10,12 However,
* @2 c' a8 n! m) a3 |* eSutherland et al13 did not find a correlation between
% F" }" G1 _" w8 k& O; ]( _childhood testosterone exposure and reduced adult8 F" k: B$ s  h9 a' b" D* g( V
penile length in clinical studies.
9 f. `* T2 Z$ G0 _- `( ~: H0 P$ WNonetheless, we do not believe our patient is
2 H- l1 M1 R. l# t6 Y( wgoing to experience any of the untoward effects from* I5 L" Q! D! G& _8 v" I
testosterone exposure as mentioned earlier because
6 G2 v( j- R7 v# C$ lthe exposure was not for a prolonged period of time.& d: P9 @: B  k$ }2 g: }+ I- t3 F- A* h
Although the bone age was advanced at the time of
- `. e( D% E4 i, R/ Ndiagnosis, the child had a normal growth velocity at
7 }6 N" n% d, p/ Nthe follow-up visit. It is hoped that his final adult0 I' X, v9 A1 e" [+ p
height will not be affected.) V/ t& T! W" H7 ^) m
Although rarely reported, the widespread avail-
. F- {: _% ]( R9 M/ Lability of androgen products in our society may
( U8 {/ t+ J5 g' k$ [indeed cause more virilization in male or female
; G* Z: I+ B% z2 }children than one would realize. Exposure to andro-
# ]( ]5 c) Z# g" k- g& Q3 igen products must be considered and specific ques-  i1 i0 P5 f" x, P( @8 w- v! ?
tioning about the use of a testosterone product or
& H' w4 n3 g* ggel should be asked of the family members during5 j+ g0 ]% V5 l
the evaluation of any children who present with vir-' b( c; o1 \4 U/ y/ o7 l! N
ilization or peripheral precocious puberty. The diag-
' C0 G7 j4 z6 h) I) ]8 G( onosis can be established by just a few tests and by
, L$ ?. T$ F! l  `, z- Zappropriate history. The inability to obtain such a
# ~) H* }! ~. q; W- Ihistory, or failure to ask the specific questions, may
6 T' m( x: i6 d6 vresult in extensive, unnecessary, and expensive: x# U: S, n( T0 b" ^9 b& _
investigation. The primary care physician should be% u  i# b5 P. }" X: y( W% Y
aware of this fact, because most of these children1 l6 G1 b" N2 d' e1 o! v7 i$ R
may initially present in their practice. The Physicians’
) c; C% D" D  ]Desk Reference and package insert should also put a
1 M7 U- D5 K! z% x' swarning about the virilizing effect on a male or. A! C! _% ^# n8 U( X6 V+ t
female child who might come in contact with some-
$ h6 c# l& Y1 F2 Y8 C( R9 Cone using any of these products.
) Z) y5 x$ k& Q, N& F+ p# HReferences( T# o0 V& `3 c7 }6 R7 K! z6 z, D8 Q
1. Styne DM. The testes: disorder of sexual differentiation+ r* t# i: h: [$ s7 i
and puberty in the male. In: Sperling MA, ed. Pediatric
& l) R; _" a% S3 u( F- SEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
1 i  v8 A8 |, C( Q: d: {2002: 565-628.
' p5 M. S7 D* D/ V$ F1 w2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious- E7 R: f9 x* @/ w
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
: u, s3 b1 X& c# Y! n& F( YBoy Induced by Indirect Topical
+ ~) @7 ]1 L* M: E# B8 z. S$ MExposure to Testosterone7 C, j( ?$ K1 a; R
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,21 ?! D7 n! ^8 f# {9 @& P
and Kenneth R. Rettig, MD17 V* C; C3 _. n# ]. ~: _. Z" k3 @
Clinical Pediatrics7 g* ?9 S$ W) @, W; n
Volume 46 Number 6. ^; d. |% _; q6 h& J
July 2007 540-543
- [6 @. y" O" u* h, i© 2007 Sage Publications. l( `* D8 X' F" ^+ t
10.1177/0009922806296651! r* f: u- }5 S9 G/ j0 d& H8 a
http://clp.sagepub.com  d6 ^6 Y* P' g" m/ Q$ w! [
hosted at  [- S) {$ {9 T! F; D' Y' t; h
http://online.sagepub.com! B" T/ I# O& X$ X* O
Precocious puberty in boys, central or peripheral,
; h9 z, _+ @6 l; g8 uis a significant concern for physicians. Central2 d; ?! ?) y/ v$ A: ]
precocious puberty (CPP), which is mediated1 P9 O7 Y6 S! @
through the hypothalamic pituitary gonadal axis, has
2 V5 }/ N" m- da higher incidence of organic central nervous system( q7 @. _7 c+ t& d
lesions in boys.1,2 Virilization in boys, as manifested
6 G  z8 W# E+ U8 {# X$ Tby enlargement of the penis, development of pubic, {. e' E, A* i
hair, and facial acne without enlargement of testi-3 d; k( a7 @8 q3 @5 G
cles, suggests peripheral or pseudopuberty.1-3 We
6 Q2 B6 ~9 Z/ A' x% Qreport a 16-month-old boy who presented with the
- i2 G' O1 M6 P# n) b+ ~% n4 Genlargement of the phallus and pubic hair develop-) s# j8 s% q: Q% O5 G6 x( r% a( g: t
ment without testicular enlargement, which was due! ^- g9 M5 O- ?; v% p0 a
to the unintentional exposure to androgen gel used by' z) |$ t: s1 W( l
the father. The family initially concealed this infor-: ^  H2 J8 g3 \$ H, p" |' y- G
mation, resulting in an extensive work-up for this
0 C" `- f# E9 o/ Q# m8 ?; [child. Given the widespread and easy availability of
4 Q$ `0 l5 A) I6 p, R  x# Ctestosterone gel and cream, we believe this is proba-
# P( v! I7 w3 V& @5 Obly more common than the rare case report in the
5 {* y4 @" V3 u* O4 Hliterature.4
7 _+ u1 y1 ~7 f; v+ z8 E4 z/ uPatient Report
/ N$ A9 V$ E" e# c3 w! R: T' jA 16-month-old white child was referred to the
& v: A9 D4 y3 I% ~- `& Nendocrine clinic by his pediatrician with the concern
  x+ u; V$ i! m/ k) ~0 [of early sexual development. His mother noticed
  k. S: ]8 u' a0 Y) g8 Y  H2 P3 {$ plight colored pubic hair development when he was: U7 E6 U* y4 h4 n/ K5 G2 t
From the 1Division of Pediatric Endocrinology, 2University of
3 z6 v7 c6 O) D( m3 X- Q. M6 YSouth Alabama Medical Center, Mobile, Alabama.
2 c* _) B/ W9 O- ~8 [+ T: DAddress correspondence to: Samar K. Bhowmick, MD, FACE,
1 J8 }) [1 h' g+ ~; a; eProfessor of Pediatrics, University of South Alabama, College of0 r; |1 s. _- B( E; ]! I6 c! J
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;2 P" a0 U2 h* Z& y0 W2 F4 h
e-mail: [email protected].8 h* C5 k4 ^! j0 c5 x, L0 T$ `
about 6 to 7 months old, which progressively became
* h4 [4 Q7 L/ F/ R! V+ mdarker. She was also concerned about the enlarge-7 z4 B# Q. z; D
ment of his penis and frequent erections. The child
9 x' U- l2 R7 u0 P# T( R- p3 Xwas the product of a full-term normal delivery, with
4 w: M% }! B# w7 x% Oa birth weight of 7 lb 14 oz, and birth length of
1 B7 m4 J( q5 B3 F6 N1 }1 d. R20 inches. He was breast-fed throughout the first year! \4 C3 v% G+ l$ Q3 }
of life and was still receiving breast milk along with, |0 K; Q) D, _( c9 G; n
solid food. He had no hospitalizations or surgery,2 t. z4 v4 H6 r" j, W9 V
and his psychosocial and psychomotor development& [, U3 `: p- ~: ?5 D
was age appropriate.$ p& ]' O3 Y: H$ U
The family history was remarkable for the father,
& U- d$ m  h6 c% h$ ^$ m- y" M: ]who was diagnosed with hypothyroidism at age 16,
: G9 |0 n  `7 nwhich was treated with thyroxine. The father’s: l7 Q5 J- X% V; m3 a
height was 6 feet, and he went through a somewhat6 e9 k6 U7 Z$ t( j5 W
early puberty and had stopped growing by age 14.0 c$ @. K+ Z8 e5 a
The father denied taking any other medication. The! j. o+ o5 H1 R+ r4 l3 [
child’s mother was in good health. Her menarche. `, @- @( l. `$ b2 S& `
was at 11 years of age, and her height was at 5 feet
3 k' ?# P: Z: G: l5 inches. There was no other family history of pre-$ [6 n! [1 P: Z
cocious sexual development in the first-degree rela-2 J5 F5 H6 {4 P6 |
tives. There were no siblings.
# z. q1 f6 k1 d3 B9 U2 D, iPhysical Examination! c8 S1 e6 n& R0 Z/ F+ J) }
The physical examination revealed a very active,
+ ?! o+ w9 m8 [5 tplayful, and healthy boy. The vital signs documented
- [3 Z7 I5 M8 q$ S; Y; w5 A5 pa blood pressure of 85/50 mm Hg, his length was
0 \- S" S) @6 {& b$ A90 cm (>97th percentile), and his weight was 14.4 kg
- U4 f2 O$ j! H(also >97th percentile). The observed yearly growth, ]( ^7 w3 _+ i+ V0 s  q- v- _
velocity was 30 cm (12 inches). The examination of9 G- k! u& M+ Y) f) |8 B' W! E
the neck revealed no thyroid enlargement.- ]: X1 E' P7 G3 o
The genitourinary examination was remarkable for) }, B: ]4 y: c; ?
enlargement of the penis, with a stretched length of
$ d- l/ ^8 W, V8 cm and a width of 2 cm. The glans penis was very well( N/ M- t2 Q# r9 l
developed. The pubic hair was Tanner II, mostly around3 t$ t" u$ g2 s2 K3 Y$ g" q+ f
540% [) ~  y& h# S- ~! G0 u! v+ T! a
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
) g' {% D& Q3 R9 J2 ?1 Ythe base of the phallus and was dark and curled. The
$ E1 w3 G/ H0 k3 b" C4 atesticular volume was prepubertal at 2 mL each.( N9 H( m% y. ]" Y6 |
The skin was moist and smooth and somewhat
. `# ^$ p2 h7 t* v7 {oily. No axillary hair was noted. There were no4 X2 d6 ]  f8 ]
abnormal skin pigmentations or café-au-lait spots.
( ~3 r1 Y8 j5 P4 DNeurologic evaluation showed deep tendon reflex 2+
9 O$ Z9 `. n5 X7 c! O. [bilateral and symmetrical. There was no suggestion
+ t$ \  X, B+ G% U& c+ L( pof papilledema.( r# u3 \* E3 _% W* e& B9 _$ X
Laboratory Evaluation# B! Y: V" d! H4 [' ^! D! g
The bone age was consistent with 28 months by
" _0 L0 k4 q! t, xusing the standard of Greulich and Pyle at a chrono-6 i. V% G8 m9 W  l3 N( m& Z
logic age of 16 months (advanced).5 Chromosomal. R3 e3 ?& w: P3 c- I, h
karyotype was 46XY. The thyroid function test* B7 O/ P! I  P( f0 `0 z# I* Y
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
- M8 ]: R' s( u) Alating hormone level was 1.3 µIU/mL (both normal).$ Y  z+ ~# F' T, h4 {4 B  x
The concentrations of serum electrolytes, blood) t4 K/ f4 ?$ z4 _  L4 ?
urea nitrogen, creatinine, and calcium all were
4 r4 Q* Z& |, ~; ]( i) cwithin normal range for his age. The concentration
/ j6 X% y5 h$ @4 j1 X* kof serum 17-hydroxyprogesterone was 16 ng/dL
7 j4 l4 |* l  i$ N6 t! x(normal, 3 to 90 ng/dL), androstenedione was 20
  o" W! u0 S4 l  l: E' y. x+ Cng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-+ G& Z% J. _" w8 W. @" j& e$ C( H
terone was 38 ng/dL (normal, 50 to 760 ng/dL),% U# k4 P0 K. |. A' P9 Y
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
- [, R6 L* u) u# B& s  }( M49ng/dL), 11-desoxycortisol (specific compound S)
* H; N) m5 G2 a0 Xwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
: Z9 C" K5 {+ _7 o/ |- Ttisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total+ S' E2 G, A' o2 v/ K, s# I
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),0 {' K& ]" o( {! Q+ y
and β-human chorionic gonadotropin was less than
; m5 O3 O. p* B( L' n$ B: D1 f( N5 mIU/mL (normal <5 mIU/mL). Serum follicular
! P5 F7 U8 q/ K( J. Xstimulating hormone and leuteinizing hormone
4 u- k2 J( L4 N1 ]" W' v4 bconcentrations were less than 0.05 mIU/mL
) i8 Q* ~! ^  g8 m$ d1 A: C(prepubertal).
  n" `, m# F' z" q$ d; gThe parents were notified about the laboratory+ Q4 s* k) K9 g3 K1 M6 u
results and were informed that all of the tests were
# n* i$ _2 H+ @  onormal except the testosterone level was high. The
& t# E: z& D' Ifollow-up visit was arranged within a few weeks to
5 I7 b# `7 K( ?4 X" \) hobtain testicular and abdominal sonograms; how-* i. a" M3 d1 F/ C" U
ever, the family did not return for 4 months.
! j( s4 ^5 ?5 tPhysical examination at this time revealed that the
- ~6 T7 }( @" }% r  ]5 D; gchild had grown 2.5 cm in 4 months and had gained* y. P4 ~  o7 Z  C% N  E  P
2 kg of weight. Physical examination remained
$ D- c( t6 w3 W2 N5 @4 A3 U0 g3 Qunchanged. Surprisingly, the pubic hair almost com-4 P; A* f0 K3 \* {3 P- g* K; `
pletely disappeared except for a few vellous hairs at
7 X% [$ g6 m, S* k7 Ethe base of the phallus. Testicular volume was still 2
2 o, |. h0 b  g7 Q# `3 pmL, and the size of the penis remained unchanged.9 g. ~# g9 i) Y; Y
The mother also said that the boy was no longer hav-& M# J* U# [& M8 b: X+ c! z
ing frequent erections.
/ @% h; \( {0 U) l7 IBoth parents were again questioned about use of, Q! X5 ]. _8 D; o; l- X2 L
any ointment/creams that they may have applied to+ B  E( w" c6 ^9 |
the child’s skin. This time the father admitted the
. i5 y# S+ t5 |Topical Testosterone Exposure / Bhowmick et al 5411 @  ~, R% n: k, ^+ e, `
use of testosterone gel twice daily that he was apply-
4 q; p# D/ }/ Y7 o7 aing over his own shoulders, chest, and back area for4 R) d/ \3 g0 ^3 k( u
a year. The father also revealed he was embarrassed3 p3 z* R! Y" Q
to disclose that he was using a testosterone gel pre-
1 U) K: e" }+ X; v: T' C5 hscribed by his family physician for decreased libido1 h2 ]& {' q8 K% {& Y* x6 q
secondary to depression.
! E" ~6 j2 V1 V4 z, g+ ?5 h0 {% Y9 vThe child slept in the same bed with parents.
( e' f6 |6 }! z" F# N/ q; iThe father would hug the baby and hold him on his
0 v, @3 a' t# G, \chest for a considerable period of time, causing sig-
+ `: y  {0 n  o, G( `# l( Inificant bare skin contact between baby and father.; Q: s4 W1 o0 E8 G9 v0 r. o
The father also admitted that after the phone call,/ Y" }! h, }  k/ ^3 R
when he learned the testosterone level in the baby) K! {. n# [: q0 x4 i
was high, he then read the product information
# x  l$ }  W5 fpacket and concluded that it was most likely the rea-: g2 n5 t& F/ @" X
son for the child’s virilization. At that time, they
* l# f* H+ r2 g' \decided to put the baby in a separate bed, and the3 R! u' p( o7 w' l* D$ Q
father was not hugging him with bare skin and had
  y1 C! L' C# T6 Fbeen using protective clothing. A repeat testosterone! v- n$ Q( E+ L; K, I+ G- a
test was ordered, but the family did not go to the: D- H9 K6 E% z9 @$ ]4 B
laboratory to obtain the test." V  W% r3 Y9 H" z: b3 p
Discussion
: i' q1 o! w5 ~# y, KPrecocious puberty in boys is defined as secondary
* e4 q* d' t4 k& t8 J( K* vsexual development before 9 years of age.1,4
" d1 V4 S; }% C9 UPrecocious puberty is termed as central (true) when$ V: {- m7 x5 l# [6 N
it is caused by the premature activation of hypo-* Y" _3 c/ D1 i! e
thalamic pituitary gonadal axis. CPP is more com-
  ^, ]2 G" ~7 O: Y6 F$ m6 ^mon in girls than in boys.1,3 Most boys with CPP* q% k/ U3 R: s
may have a central nervous system lesion that is) K7 u! L  A  i! u& }0 J
responsible for the early activation of the hypothal-
, I+ Y8 D/ e* K8 L" ~. M. a5 G; }+ Lamic pituitary gonadal axis.1-3 Thus, greater empha-8 I2 Q2 L% F* S+ Q6 ]* \% Z( H
sis has been given to neuroradiologic imaging in+ E# {& F) n3 |' O3 C9 m. j- O
boys with precocious puberty. In addition to viril-' u; v  ~) c! Q/ W
ization, the clinical hallmark of CPP is the symmet-) m8 n- z+ l% i+ x" p2 v
rical testicular growth secondary to stimulation by0 D+ q3 Z0 @1 ^( @
gonadotropins.1,3. B. W; {# t$ J
Gonadotropin-independent peripheral preco-4 T1 y6 x, b8 V
cious puberty in boys also results from inappropriate/ W- a! u( G3 M3 y: n# b! d
androgenic stimulation from either endogenous or' n8 b0 S- i8 _( E
exogenous sources, nonpituitary gonadotropin stim-
0 d" K; v8 R3 A5 Zulation, and rare activating mutations.3 Virilizing$ p* K( P* W/ t
congenital adrenal hyperplasia producing excessive
  }) b1 N0 N/ z* aadrenal androgens is a common cause of precocious
/ m6 F9 T5 y) u7 J' ^puberty in boys.3,4
- O2 {! r6 Q0 K+ M. zThe most common form of congenital adrenal
" F  W( T9 o/ w$ H) A6 i" n# p4 s# r4 Qhyperplasia is the 21-hydroxylase enzyme deficiency.
6 [6 x; H  ^) u3 x9 \3 }; ~/ `/ mThe 11-β hydroxylase deficiency may also result in  f5 W; B+ {# F/ _7 j
excessive adrenal androgen production, and rarely,$ E4 f3 e$ ?+ F- Q, r
an adrenal tumor may also cause adrenal androgen' [* e! y* _- W2 y
excess.1,33 f0 s9 e! i/ ?- D8 @) t
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
" Q9 b  H* j* T9 y+ F  M. u542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
: E4 b% p% ], D. o. B* X% o% YA unique entity of male-limited gonadotropin-% D" K5 A6 @$ p
independent precocious puberty, which is also known: D$ c' ]: q! [* f+ l) `- n3 [
as testotoxicosis, may cause precocious puberty at a
$ m! K' }: _4 |# r$ C# O0 y9 V" Pvery young age. The physical findings in these boys3 y3 p. g" r  n/ {4 F7 H6 p% h1 ]
with this disorder are full pubertal development,: H" a! d3 J4 p0 s# m( \
including bilateral testicular growth, similar to boys' _2 h( W' @0 j& C2 J2 N  G
with CPP. The gonadotropin levels in this disorder1 u$ C& j* s( E, X+ h! l. Y6 n9 i
are suppressed to prepubertal levels and do not show5 o* N, `/ W" e. E' V
pubertal response of gonadotropin after gonadotropin-
9 D% j$ O' [4 V+ I, d8 s+ f5 }, wreleasing hormone stimulation. This is a sex-linked
! |1 C- U' ]* W3 Dautosomal dominant disorder that affects only3 v8 l+ ^9 J9 l
males; therefore, other male members of the family
, n7 U- z* O, m, b& N3 E( N5 Vmay have similar precocious puberty.3
& K# T6 r+ N; R2 R+ f2 |In our patient, physical examination was incon-
( U, X3 n# Z" U, hsistent with true precocious puberty since his testi-
4 u- u) d/ W4 D: Z0 o, O3 \cles were prepubertal in size. However, testotoxicosis
$ Z8 }& N! v" D! Wwas in the differential diagnosis because his father
: y! k1 G& _; ~# cstarted puberty somewhat early, and occasionally,
' T& V. B# }6 r; Ftesticular enlargement is not that evident in the
/ U( S* U# @! q" \beginning of this process.1 In the absence of a neg-
5 N+ j( X  `) Y; |1 N% Q: @ative initial history of androgen exposure, our
& Y# i) M; F$ A7 g" ]( Xbiggest concern was virilizing adrenal hyperplasia,# y/ ]6 Y7 j; z9 B1 W2 r
either 21-hydroxylase deficiency or 11-β hydroxylase1 U' @9 L4 |2 I4 m8 ^6 t1 J& \
deficiency. Those diagnoses were excluded by find-
" h7 a7 N' O/ t1 `& d) U; @! t7 [. sing the normal level of adrenal steroids.1 ]" t! r5 {+ `# J; K+ O- c
The diagnosis of exogenous androgens was strongly
1 X& t# m$ |* csuspected in a follow-up visit after 4 months because
8 y7 [% K) r: U% k+ y7 Pthe physical examination revealed the complete disap-9 P+ ~8 o1 i! I
pearance of pubic hair, normal growth velocity, and
; `+ N/ ^* E9 g! T' S& d+ l8 Z4 f, Gdecreased erections. The father admitted using a testos-2 z" Z/ F3 U5 `. q, V$ m7 Z
terone gel, which he concealed at first visit. He was1 n% E9 R+ ]; p
using it rather frequently, twice a day. The Physicians’
  X- U; x- h" }9 dDesk Reference, or package insert of this product, gel or! W- W2 Z! |6 r
cream, cautions about dermal testosterone transfer to; ^+ [  A; M& }- a/ h
unprotected females through direct skin exposure.
0 M, V  l& Q7 H. z3 R6 T  ]Serum testosterone level was found to be 2 times the3 V7 c# u0 Z% c) i
baseline value in those females who were exposed to
5 ^+ f) f; _& xeven 15 minutes of direct skin contact with their male% D. {7 ^, N4 {" A, h2 E9 b/ M
partners.6 However, when a shirt covered the applica-8 \' ?' e( o2 Z; L& Z7 n
tion site, this testosterone transfer was prevented.. F" n; K* o9 X, J$ W
Our patient’s testosterone level was 60 ng/mL,
" _3 Y% o" [+ g5 h2 r) m* U# hwhich was clearly high. Some studies suggest that, v% m, t9 K( e% _) T/ c
dermal conversion of testosterone to dihydrotestos-3 ?0 p5 I9 W- H* @
terone, which is a more potent metabolite, is more
) W5 C( M7 u. M' Iactive in young children exposed to testosterone- ^: o' r, x- G; J1 Y
exogenously7; however, we did not measure a dihy-3 S& Q; ~! S9 p  ^: y
drotestosterone level in our patient. In addition to
2 p2 w- H# s% A5 [* T  p. Hvirilization, exposure to exogenous testosterone in: ^+ N* {. q1 X3 h- y1 D0 x5 c. k: Y
children results in an increase in growth velocity and
: t- k  [: q: s# u& Iadvanced bone age, as seen in our patient.1 P2 x7 Y3 u+ h! M. y1 r7 Q: ^
The long-term effect of androgen exposure during
, d8 ^; |) L6 V- P% C4 ?early childhood on pubertal development and final
+ O& D6 X0 Q, H: Fadult height are not fully known and always remain
5 d# w6 ^4 J# R7 W2 m- Ga concern. Children treated with short-term testos-
4 D; j. M3 n( b* M" iterone injection or topical androgen may exhibit some1 f1 b- d, |& J" v2 Y4 n- T! ]
acceleration of the skeletal maturation; however, after
4 _) K$ m+ G/ }% S; mcessation of treatment, the rate of bone maturation  m; G; S) [0 d+ j  I" R" u
decelerates and gradually returns to normal.8,9. b$ u4 Q8 D1 w' Q$ J& N
There are conflicting reports and controversy/ i( C* U# }1 g8 W
over the effect of early androgen exposure on adult
6 i' Y8 j: {" Z) M- cpenile length.10,11 Some reports suggest subnormal
# }, N& Y' E4 _2 |1 r& ]1 _6 uadult penile length, apparently because of downreg-% Q5 ]; T  o1 M$ g
ulation of androgen receptor number.10,12 However,
$ ]1 M0 y' e( \8 `! H- s7 Z/ ^Sutherland et al13 did not find a correlation between0 ]1 v: U# f( w  Z$ r3 z' A, _
childhood testosterone exposure and reduced adult
6 B# n, z; y' }/ K4 Y9 b* G: ?penile length in clinical studies.
5 t. Q4 x7 m. k, h" \& f$ tNonetheless, we do not believe our patient is
% d2 j# Z  a8 P* [* M5 zgoing to experience any of the untoward effects from, S9 O+ \. B, I% {  ~
testosterone exposure as mentioned earlier because( A+ ]6 `3 X) h/ u, C! o! U: h
the exposure was not for a prolonged period of time.4 Y2 c% M4 C4 [$ L4 {( D
Although the bone age was advanced at the time of
% C! q- _0 l4 Bdiagnosis, the child had a normal growth velocity at. P% \4 H8 A+ T+ F6 M
the follow-up visit. It is hoped that his final adult" H# B: W1 N- \/ }# v
height will not be affected.
- L1 F$ S1 c' }" ]; w. n2 @Although rarely reported, the widespread avail-
7 l* F& P4 H: q6 m' H/ ?" kability of androgen products in our society may
, D7 h3 Z7 N. I! }indeed cause more virilization in male or female+ S0 A, I* c2 \# t' B* r- N
children than one would realize. Exposure to andro-
" f  O1 l7 C  M4 L& p# ^7 M: egen products must be considered and specific ques-" j  m  k& G6 Y
tioning about the use of a testosterone product or
( h1 v8 f& K6 \/ K' J5 fgel should be asked of the family members during
4 Z: h. ~( l8 o$ H0 E$ }! Zthe evaluation of any children who present with vir-1 S. _/ F: j' W
ilization or peripheral precocious puberty. The diag-
% {- l! e( V; m0 Z  `$ H& X/ }nosis can be established by just a few tests and by8 ]+ k, U: O' o: @! O
appropriate history. The inability to obtain such a
: c+ y% G& T9 X" [# M# chistory, or failure to ask the specific questions, may1 f/ _# x4 M( ^/ o/ {+ J
result in extensive, unnecessary, and expensive
) \% s! f( w# ^' r: g+ D2 Vinvestigation. The primary care physician should be
3 T& E& m' B; y: Q4 maware of this fact, because most of these children0 Q) `7 W' C4 K, H4 @) W
may initially present in their practice. The Physicians’
5 e3 ?' a6 V+ q- b5 X( N0 Q' p) `Desk Reference and package insert should also put a
- p( U5 o  n' zwarning about the virilizing effect on a male or: D# f- n- l' M3 Q
female child who might come in contact with some-' D6 U) X( P0 y$ Q% N
one using any of these products.# X+ d8 t% a( S" j- f, ]
References
* B, u7 l0 P% l" c  D1 J# F/ X1. Styne DM. The testes: disorder of sexual differentiation
, _& O5 z* ?' z$ u" @/ J3 Qand puberty in the male. In: Sperling MA, ed. Pediatric
3 J6 E; B& A8 pEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;, m$ g/ E7 U  M9 @; [# Z; i
2002: 565-628.$ e: o' ~! P4 \! W" k
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious( ?, j+ X- t* w2 W0 r$ V2 O
puberty in children with tumours of the suprasellar pineal
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感謝大大的辛勞分享!我會繼續在WK關注大大的文章!
發表於 2025-1-11 22:18:01 | 顯示全部樓層
女厕偷拍辅导班主任尿尿老师的逼很嫩还有一点
發表於 2025-1-17 16:31:39 | 顯示全部樓層
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
" k6 T% N$ I: U$ S! }
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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