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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-Old0 \7 }# C: |" s. h
Boy Induced by Indirect Topical( K" @% D. ~6 B0 w9 M3 D; Q
Exposure to Testosterone
2 p3 B5 f8 |- ~, |, r5 [Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
( n( X5 [9 \( m! O0 g; Band Kenneth R. Rettig, MD1+ r! U  M/ f3 N, t% Y$ a3 {
Clinical Pediatrics
# J. y: n- z2 }" k& q7 s3 O6 F  yVolume 46 Number 6  d1 [. r4 ?8 G3 b
July 2007 540-543" k6 W: z( r# I; Z! p2 s5 a
© 2007 Sage Publications5 a+ A4 S- @  u9 {! W* h
10.1177/0009922806296651
6 O- }; P$ J5 n$ y: \2 ahttp://clp.sagepub.com
: o5 |9 s7 L$ _" ?  |: dhosted at
! |3 D* V+ |2 F, b8 chttp://online.sagepub.com% D. \5 s. a6 }# a. d
Precocious puberty in boys, central or peripheral,' `: m  r$ C1 ?- j
is a significant concern for physicians. Central
& b+ K3 h/ ]6 A# B& Wprecocious puberty (CPP), which is mediated% q8 A) U/ b# f$ g' ?
through the hypothalamic pituitary gonadal axis, has
# d2 o  v- B3 S5 x4 qa higher incidence of organic central nervous system
* Q9 n1 J. W6 Zlesions in boys.1,2 Virilization in boys, as manifested  C+ s# s' d6 c* Q$ @4 t& R
by enlargement of the penis, development of pubic! ]9 A7 g; ?+ u3 |; s) L! ~. B
hair, and facial acne without enlargement of testi-
3 c6 H+ S' Y0 c- s  u9 ^2 Ycles, suggests peripheral or pseudopuberty.1-3 We
/ J: M7 ]8 @% k4 a9 greport a 16-month-old boy who presented with the
4 ]* B8 |0 Z4 kenlargement of the phallus and pubic hair develop-, D! A+ `" N# c
ment without testicular enlargement, which was due
4 J9 q3 J9 \5 pto the unintentional exposure to androgen gel used by: J" T, |' p( w9 w" L3 I# U
the father. The family initially concealed this infor-
( `8 o9 e7 G* ymation, resulting in an extensive work-up for this
, k$ ~9 [3 D3 G8 ichild. Given the widespread and easy availability of4 I: M6 R4 v, j  @+ o! z; B
testosterone gel and cream, we believe this is proba-6 T& z- ]1 ~$ G0 J
bly more common than the rare case report in the( V" l9 R, }& c8 a  c! P
literature.4& e# t: Y5 i9 N/ j8 Q
Patient Report8 |+ a& V2 U4 }6 m  D
A 16-month-old white child was referred to the8 ~: f. b2 W/ g$ S
endocrine clinic by his pediatrician with the concern
' z1 c6 n; A: O2 m" M+ ]of early sexual development. His mother noticed
: Z$ m9 i% |4 M& m% ylight colored pubic hair development when he was/ h2 I' {$ v7 X
From the 1Division of Pediatric Endocrinology, 2University of9 R* V5 X' G% o9 [2 x
South Alabama Medical Center, Mobile, Alabama.. F/ _9 G8 H7 t# q5 B1 O
Address correspondence to: Samar K. Bhowmick, MD, FACE,
7 I4 t5 c' O& }$ s' g1 L# |) eProfessor of Pediatrics, University of South Alabama, College of
" G4 h" O% O5 y& G- O3 S# `0 jMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
, H; o1 X1 G/ ?: Ae-mail: [email protected]., E9 x* S  K' A( p
about 6 to 7 months old, which progressively became
3 V* F( L& d! w0 Fdarker. She was also concerned about the enlarge-
9 s7 Y4 a- o1 ?6 H; k. o; K, Jment of his penis and frequent erections. The child
3 o+ c  |( z4 [* g) `was the product of a full-term normal delivery, with6 c4 O' w6 T: H, v+ {* w* s/ Q
a birth weight of 7 lb 14 oz, and birth length of, \3 V) N: t- k
20 inches. He was breast-fed throughout the first year
" {* x- b  Q( V1 k; Wof life and was still receiving breast milk along with
$ ^' L7 H; c+ P' p+ d; e$ csolid food. He had no hospitalizations or surgery,
$ A' z& N# J7 [& G/ J6 R8 qand his psychosocial and psychomotor development6 c+ u8 k4 i' q
was age appropriate.0 E& ~& U. ^# D5 L8 k. K$ H
The family history was remarkable for the father,- i$ o6 w) S. I
who was diagnosed with hypothyroidism at age 16,
) o* Y% d: P* H0 y8 L$ D0 D: hwhich was treated with thyroxine. The father’s9 M9 S5 i5 p" _4 C2 D8 W% n4 y
height was 6 feet, and he went through a somewhat; D# J' C1 |+ x1 q2 t
early puberty and had stopped growing by age 14.
) v- l) P4 u4 e) l0 A3 j- SThe father denied taking any other medication. The
" O. |% p- J( n/ ?" f6 |. schild’s mother was in good health. Her menarche0 Q3 h8 K1 ^$ y( a! X- p( o- B
was at 11 years of age, and her height was at 5 feet
" H* P) p3 p- w' G, C+ u8 i# V5 inches. There was no other family history of pre-
' r/ T/ @* E4 k7 Y5 p( p0 q5 G- kcocious sexual development in the first-degree rela-+ w( m  g8 p9 r6 w; a( O- X. c
tives. There were no siblings.& O9 Z! Z3 z4 i
Physical Examination" U( K" ^* M+ E- a0 n
The physical examination revealed a very active,; ?- t$ e* I! k
playful, and healthy boy. The vital signs documented
, n6 I* g& [: ?5 [8 P; c6 \a blood pressure of 85/50 mm Hg, his length was9 H4 x$ u* d, U
90 cm (>97th percentile), and his weight was 14.4 kg
* t7 d; Y0 N* C- t(also >97th percentile). The observed yearly growth
. ]4 q2 U( Q; V" w9 ~- q" hvelocity was 30 cm (12 inches). The examination of7 M. p4 Y7 J. B# q
the neck revealed no thyroid enlargement.
& j7 D/ N  W; `1 J5 C5 H- b5 f3 NThe genitourinary examination was remarkable for9 e: `4 O" S, I  P9 Y" B
enlargement of the penis, with a stretched length of/ V) z, a; \+ V, y
8 cm and a width of 2 cm. The glans penis was very well
7 q0 U& k# N6 A$ u1 K+ J5 |" l3 {developed. The pubic hair was Tanner II, mostly around
1 K1 N6 i, b) |9 U540
& Z% g5 \  b9 G. r7 Qat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from' n% L( s& R5 c4 n$ y( ^1 b3 s
the base of the phallus and was dark and curled. The; f' Z1 r  W2 \) P
testicular volume was prepubertal at 2 mL each./ w& _, O5 ~. X) I; M0 [5 S
The skin was moist and smooth and somewhat
% o' _4 X& w( |( l. toily. No axillary hair was noted. There were no
! {- k( Z( w3 {3 k3 n- E3 Zabnormal skin pigmentations or café-au-lait spots.9 D, [  ?) g& Z  w$ Y* [
Neurologic evaluation showed deep tendon reflex 2+: }) `( F. X, I0 k, U6 T/ E- r0 K
bilateral and symmetrical. There was no suggestion
' }& V7 M! q" z1 n5 d" A  c4 kof papilledema.4 I+ m# x0 {1 b( ~
Laboratory Evaluation
0 q9 k& m( d) a; i, gThe bone age was consistent with 28 months by' x' F* D3 q7 W1 b
using the standard of Greulich and Pyle at a chrono-
! ?8 ?7 K  J0 ?6 O" N9 Y% llogic age of 16 months (advanced).5 Chromosomal8 R, U+ }& c8 [1 t" e
karyotype was 46XY. The thyroid function test
! M7 q$ {! b0 sshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
8 S. ^: \. f2 e& p" Rlating hormone level was 1.3 µIU/mL (both normal).
: X3 c, A% L( j- k1 r+ A/ {+ aThe concentrations of serum electrolytes, blood
9 Z! @& [1 k( B1 f, a" g/ T! X4 curea nitrogen, creatinine, and calcium all were' F  U' o! w3 G  ~
within normal range for his age. The concentration( s/ B# A3 h/ s
of serum 17-hydroxyprogesterone was 16 ng/dL
7 B1 z0 G2 ?  z3 M(normal, 3 to 90 ng/dL), androstenedione was 20
6 R5 Y: e8 |& I" Q/ i$ N! _% H4 J7 sng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
2 E# p2 l2 I: {; c( Uterone was 38 ng/dL (normal, 50 to 760 ng/dL),
# E' r/ q* F  L* P) odesoxycorticosterone was 4.3 ng/dL (normal, 7 to
7 Q" ^) X7 h3 e49ng/dL), 11-desoxycortisol (specific compound S)
- a4 C4 g% l: kwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-- {0 [  v+ @; ]) L" V9 J1 ^( A
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total5 [/ Y* q# x" K; k( v* a
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),+ j$ U7 Y$ k+ ]' Z, E. }
and β-human chorionic gonadotropin was less than7 h( G) j+ s- O" N0 n
5 mIU/mL (normal <5 mIU/mL). Serum follicular0 Q) ^* j7 i# c5 B2 B
stimulating hormone and leuteinizing hormone* ~/ C, V, u; b5 G) x  u9 C
concentrations were less than 0.05 mIU/mL
6 ?5 i: ]( o% I; R(prepubertal)./ f% c- k7 Q4 n+ \9 H4 `
The parents were notified about the laboratory. Y; j7 _8 L7 f. e3 [9 Q
results and were informed that all of the tests were. g( g/ i8 B9 c: Y4 W
normal except the testosterone level was high. The( G! Y6 H0 |8 J" r, N  s
follow-up visit was arranged within a few weeks to1 c' ]2 _6 x' n2 O
obtain testicular and abdominal sonograms; how-
6 h8 I0 k+ X( {1 h& x! v3 Bever, the family did not return for 4 months.
! @0 W( K3 b2 T3 WPhysical examination at this time revealed that the
) N/ F1 R' O) D  R* ^child had grown 2.5 cm in 4 months and had gained- K' O$ s2 u( t; w, i
2 kg of weight. Physical examination remained5 Z- ?, I) s3 a
unchanged. Surprisingly, the pubic hair almost com-
. o" L( m7 ?7 U/ f$ zpletely disappeared except for a few vellous hairs at
; R! @! d4 i$ n! S( K$ @! q! ithe base of the phallus. Testicular volume was still 2
7 J4 r" F. R3 l; x+ [mL, and the size of the penis remained unchanged.8 ]8 s* H6 n/ v( z1 I* ]# k
The mother also said that the boy was no longer hav-  h4 w% L- k3 _8 D6 t: Q
ing frequent erections.
! g" N# w8 \( e: `  M; i: }9 f1 VBoth parents were again questioned about use of
- }7 s% B0 v; S) b5 dany ointment/creams that they may have applied to
" u3 ~" y. q: f: h7 _the child’s skin. This time the father admitted the/ W5 ]9 t# X  ?1 ]5 y& \/ y
Topical Testosterone Exposure / Bhowmick et al 541
- u* t. i, B/ @" W7 A! B) \use of testosterone gel twice daily that he was apply-
; k5 G" M# i$ d7 N! _4 U: ving over his own shoulders, chest, and back area for
2 K8 I# I4 ]1 ?' o# l. b. Ha year. The father also revealed he was embarrassed7 Z1 M7 Y% K8 }8 q: |6 F
to disclose that he was using a testosterone gel pre-
  h% J" j5 j, c. w" sscribed by his family physician for decreased libido
" M$ G2 i8 V7 wsecondary to depression.4 J$ y: n% l- X) b( k. _! `
The child slept in the same bed with parents.9 I! J; o7 w- n6 C
The father would hug the baby and hold him on his
: |6 @  z9 }9 Dchest for a considerable period of time, causing sig-
9 E$ e" Q( {& {2 E  ]- T5 d! Vnificant bare skin contact between baby and father.' c0 j; j  r* E0 l' d
The father also admitted that after the phone call,! V; \% G# Z+ o( i; b1 E+ b
when he learned the testosterone level in the baby
8 ^9 A% W% V1 [1 wwas high, he then read the product information
. ~( _# M1 n: D# ]% Tpacket and concluded that it was most likely the rea-# j; i- G% @" Y# L6 U% X9 o! f* q. _
son for the child’s virilization. At that time, they4 n2 l5 d% f* w: y5 w- H
decided to put the baby in a separate bed, and the1 ?" R$ C7 m# `. Z9 s* H
father was not hugging him with bare skin and had
3 f! B+ `. D( J, F! ]been using protective clothing. A repeat testosterone
# k8 f# n3 O( @: R* u# ~test was ordered, but the family did not go to the
% k2 m$ b6 y" Q) X# b, Elaboratory to obtain the test.$ E2 z7 v" x8 h& A0 M
Discussion
# w. q/ a1 ~0 d  G0 P; {0 q& _6 aPrecocious puberty in boys is defined as secondary
/ k- }: J8 l% r% _sexual development before 9 years of age.1,4
3 W' E7 s$ Y8 P- \: S; y7 X- vPrecocious puberty is termed as central (true) when
$ n& t$ u5 ]- Vit is caused by the premature activation of hypo-
6 y" h3 N" |' H. A# ithalamic pituitary gonadal axis. CPP is more com-8 I) W: |( t+ y7 Q/ g
mon in girls than in boys.1,3 Most boys with CPP
7 M; t, d; O3 Y* S8 Rmay have a central nervous system lesion that is6 u* W6 K/ t4 _: A+ m  K; S
responsible for the early activation of the hypothal-9 Y5 }; Z; P& C. e4 B9 m8 V
amic pituitary gonadal axis.1-3 Thus, greater empha-- C6 F) u0 E- f! f+ m8 @, C
sis has been given to neuroradiologic imaging in
1 V+ v9 T  K9 m: Y# fboys with precocious puberty. In addition to viril-
. R$ L& r7 R8 H8 Nization, the clinical hallmark of CPP is the symmet-8 L, q9 b3 L# q, r& m4 J
rical testicular growth secondary to stimulation by7 B# h; ?/ j' J  {6 l, i
gonadotropins.1,3( t5 N% q3 W3 y/ B/ B6 c
Gonadotropin-independent peripheral preco-
, L- k2 D9 T9 L. M; pcious puberty in boys also results from inappropriate
& g; H+ A# y2 i0 ^6 l5 l, Candrogenic stimulation from either endogenous or6 W9 F2 D. P# K' _' L
exogenous sources, nonpituitary gonadotropin stim-
+ p6 Q" H/ }: g- Mulation, and rare activating mutations.3 Virilizing
, I0 T; k8 C0 |# d) \7 v( bcongenital adrenal hyperplasia producing excessive& m/ f1 x) |" j6 {) n9 f' b; ?; P
adrenal androgens is a common cause of precocious$ }/ I6 |( U+ P+ d5 ?
puberty in boys.3,44 F* H: B/ _6 v# d& F
The most common form of congenital adrenal
. s  T' n9 ^9 i  |; rhyperplasia is the 21-hydroxylase enzyme deficiency.
' G# |" |" m  ]9 q# hThe 11-β hydroxylase deficiency may also result in3 ]1 v) e2 W+ E6 N6 C
excessive adrenal androgen production, and rarely,
$ Y" z; V" l4 N# K; oan adrenal tumor may also cause adrenal androgen* t4 {, G; T3 `' k$ M4 |
excess.1,3
3 {6 r6 V& Z* @1 D4 ?+ Nat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
6 \$ i9 c: M( s/ x. C- r542 Clinical Pediatrics / Vol. 46, No. 6, July 2007& v$ T; P$ X( k0 r- b
A unique entity of male-limited gonadotropin-
5 ^& J6 q" x9 R# e' M2 windependent precocious puberty, which is also known
; P* h0 N% e3 Zas testotoxicosis, may cause precocious puberty at a$ {7 m& j) q( f! E! i  p4 R
very young age. The physical findings in these boys$ w* _3 ^/ E3 p' u- y- I
with this disorder are full pubertal development,5 B1 A) ]' }+ r  h
including bilateral testicular growth, similar to boys9 _% s6 \  Q  u+ |, p
with CPP. The gonadotropin levels in this disorder5 Y$ a5 m# @' |. t! i. C
are suppressed to prepubertal levels and do not show! m' y, M, E! F8 I; G. `
pubertal response of gonadotropin after gonadotropin-8 \; k- X' L. F) Y& A( Z3 b( N
releasing hormone stimulation. This is a sex-linked
) H3 ~- ^! s- P' V* U/ Jautosomal dominant disorder that affects only
0 b* m# e5 P  N+ c! F4 emales; therefore, other male members of the family3 B' F! b) ]1 g4 D
may have similar precocious puberty.3, f& g4 ~3 \3 I& I2 }( m* e
In our patient, physical examination was incon-7 ^4 x9 g: O/ d! ^  s
sistent with true precocious puberty since his testi-
  {' i" a& D. }) M0 b. Ucles were prepubertal in size. However, testotoxicosis
! ~* z/ i% z0 m% U8 ]  t3 ewas in the differential diagnosis because his father
% F1 F  q* V8 A3 Z, `started puberty somewhat early, and occasionally,
% X1 K3 N/ e4 A: o, K7 itesticular enlargement is not that evident in the/ h( `. n: g1 _( a5 `% o
beginning of this process.1 In the absence of a neg-- c# U' `9 W7 x' G/ j: X
ative initial history of androgen exposure, our
" o; N& g7 _4 M, G/ kbiggest concern was virilizing adrenal hyperplasia,
, ]& q, _3 o7 D/ {9 h- K3 Oeither 21-hydroxylase deficiency or 11-β hydroxylase% \4 m: A+ J; u  n9 Q
deficiency. Those diagnoses were excluded by find-, ?6 z7 h4 n3 u/ N
ing the normal level of adrenal steroids.
* g  }. Q( X$ n  [3 UThe diagnosis of exogenous androgens was strongly
" J) b! p. h* x& d! N2 Lsuspected in a follow-up visit after 4 months because5 C* R1 W* v  ]. x: m/ Y( P% N
the physical examination revealed the complete disap-
2 e, K! q( s. o8 U/ i' [! {pearance of pubic hair, normal growth velocity, and
7 w* |# b: ?' J0 B* D+ Sdecreased erections. The father admitted using a testos-
% j! v( S9 S! R7 x0 Zterone gel, which he concealed at first visit. He was, V3 ]; y+ @$ t5 m& q4 A. V& Q
using it rather frequently, twice a day. The Physicians’8 J$ Y9 g8 x* z4 |, I3 X+ N
Desk Reference, or package insert of this product, gel or
- x7 u5 T/ l/ q3 u" }cream, cautions about dermal testosterone transfer to1 R9 K! L# n. w2 v
unprotected females through direct skin exposure.
- L9 y, i) C, J2 P2 e5 LSerum testosterone level was found to be 2 times the5 c+ P# O) f$ J! d. c
baseline value in those females who were exposed to
' U( Z# D2 y8 q- N3 m- f. `even 15 minutes of direct skin contact with their male
+ g+ u0 v" Q6 L5 ^+ G8 j; ypartners.6 However, when a shirt covered the applica-( ^0 K9 x$ g8 `$ d6 y
tion site, this testosterone transfer was prevented.
$ H! g! [, i, W4 f4 x! b6 xOur patient’s testosterone level was 60 ng/mL,
0 D6 y5 O/ O/ B' {which was clearly high. Some studies suggest that
+ }+ w* I. i6 R: x9 Z( l7 T7 Ndermal conversion of testosterone to dihydrotestos-6 g/ L* l$ a5 c- A' `) D
terone, which is a more potent metabolite, is more2 f1 b' E( R* S  t; I) d/ X! |
active in young children exposed to testosterone
# g. {* A5 J: u0 H/ x. _exogenously7; however, we did not measure a dihy-* G/ c* m* w2 v: r) H
drotestosterone level in our patient. In addition to
1 K- h5 P) \7 {+ Nvirilization, exposure to exogenous testosterone in
/ \. g) N5 u1 D5 J8 {: Kchildren results in an increase in growth velocity and! _; [$ C6 H& A- I# V3 N
advanced bone age, as seen in our patient.! W5 \) `2 J3 U
The long-term effect of androgen exposure during8 `2 D0 O1 a: f% [
early childhood on pubertal development and final. w7 a" r  i4 c. D7 i
adult height are not fully known and always remain
7 ^8 @: X+ S0 T, z6 s  [! ^a concern. Children treated with short-term testos-
" ]; L" |7 x0 o3 {terone injection or topical androgen may exhibit some
& c9 R2 k& C/ c+ s! Bacceleration of the skeletal maturation; however, after
' ~+ D9 b8 n% x. @- q0 Pcessation of treatment, the rate of bone maturation
% b6 j5 J/ v& C; w$ L9 Adecelerates and gradually returns to normal.8,9
+ G5 `3 W. f! K& C) Y7 nThere are conflicting reports and controversy2 b) ]+ t" H, P' \2 P# y1 S6 M* I: U
over the effect of early androgen exposure on adult
" d, B: S- j& G; tpenile length.10,11 Some reports suggest subnormal4 Z; w3 C9 a' ~4 g5 C
adult penile length, apparently because of downreg-; v5 v0 F- Y+ q/ Q7 b8 _
ulation of androgen receptor number.10,12 However,! ^5 w6 x. U+ F. g# _* m9 B, ]
Sutherland et al13 did not find a correlation between% f* l( l  S( y2 [! |! e
childhood testosterone exposure and reduced adult% ?' b) A& c5 H! Y% i1 ^* x
penile length in clinical studies.& R* ^. f. Y8 W2 e" `  |4 u5 T
Nonetheless, we do not believe our patient is
+ x! H, A( G" k. [( _" xgoing to experience any of the untoward effects from3 H$ n& {) s" j9 _$ z" m, }
testosterone exposure as mentioned earlier because& Q% \: f9 W1 g$ K
the exposure was not for a prolonged period of time.4 Y  E; [! ]2 P: ]9 S. u
Although the bone age was advanced at the time of
2 V4 P2 b/ `( c" ?2 Y3 L# Xdiagnosis, the child had a normal growth velocity at) S& `5 r$ K+ d; V2 e7 V" a: w4 J- C, n
the follow-up visit. It is hoped that his final adult* s, i4 p, j( s6 v3 q; r
height will not be affected.! n% L; [# M: o4 e% j% g4 P) b: i
Although rarely reported, the widespread avail-1 _2 g: ^7 _- ], K" }
ability of androgen products in our society may
0 r% l6 [# V" K5 F# a" r$ R: a8 Windeed cause more virilization in male or female0 {: `1 l% e- `
children than one would realize. Exposure to andro-5 v' I7 t( _' @/ w" U: A4 L
gen products must be considered and specific ques-7 b: v6 W) b$ ^# f
tioning about the use of a testosterone product or
. \6 r) y" Y7 q2 i7 E8 Ggel should be asked of the family members during
' v+ r* B" y4 }6 \: n+ Tthe evaluation of any children who present with vir-
1 I4 J4 a) v+ T# R* s& |ilization or peripheral precocious puberty. The diag-
- |" A: {- I+ ?6 D& F; I" Unosis can be established by just a few tests and by; e: c: W0 c0 K, F4 b
appropriate history. The inability to obtain such a
* s0 k6 z; ]6 d3 q" O' p4 Khistory, or failure to ask the specific questions, may1 E4 C, G# M: }, P
result in extensive, unnecessary, and expensive! D; Y9 k; _: V* p
investigation. The primary care physician should be1 L; V- r% O& }1 }, I
aware of this fact, because most of these children$ s5 x! ]' {4 U9 C! N
may initially present in their practice. The Physicians’
1 r. U) X/ n3 G/ F" NDesk Reference and package insert should also put a! x0 g5 P; Y, o/ a( }7 r
warning about the virilizing effect on a male or3 X; c- |9 E0 N5 g8 x
female child who might come in contact with some-
; b/ A3 X8 w- R; ?% D7 Eone using any of these products.' a1 ]/ ]6 O/ j1 C4 z
References7 O; a3 }  T, {9 W& O. s0 P
1. Styne DM. The testes: disorder of sexual differentiation: q6 Q( [& E* d% p6 l: o
and puberty in the male. In: Sperling MA, ed. Pediatric
( h% m; {" V2 y+ _# `: a8 h" a4 ]Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
. u3 |) g" `+ r, s/ H0 y7 q2002: 565-628.: ~# o9 K. s+ y6 o: g
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
6 i9 H8 L8 ^6 A" D( [- d! Cpuberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
* y; Y" ]2 b+ m6 ]Boy Induced by Indirect Topical
0 c. z$ w! V4 [( f5 s2 m% `8 b+ H  n# ~Exposure to Testosterone1 u4 v2 o7 |9 H; k
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
- h. x1 `+ a4 Z5 d- ?% G$ wand Kenneth R. Rettig, MD1
3 q- z/ p! s# ~# y% eClinical Pediatrics* h+ ~2 E3 o6 b* N: D( W8 `$ n
Volume 46 Number 6
* O6 A% t" C1 ZJuly 2007 540-543
- T# r* y4 G# c/ s, w© 2007 Sage Publications
) ?) S* j* r6 x3 o10.1177/0009922806296651
# [7 r0 L3 _% L4 A/ w. Whttp://clp.sagepub.com
5 B* i4 e; |$ Q( shosted at
+ F* o4 i3 `& b# shttp://online.sagepub.com- x1 v, i+ O: T4 z- S
Precocious puberty in boys, central or peripheral,1 l; Z; i, J2 @3 C" |: ?4 u0 K
is a significant concern for physicians. Central
  t4 a& r+ o/ \precocious puberty (CPP), which is mediated
0 @# V  O( j8 v3 G- Ithrough the hypothalamic pituitary gonadal axis, has, }5 g3 b5 f' p) @6 L3 P
a higher incidence of organic central nervous system9 I$ a- h6 R! z$ ?/ G" s
lesions in boys.1,2 Virilization in boys, as manifested
% F0 n1 J; `  d* aby enlargement of the penis, development of pubic: g: Q) S0 U* F$ p% G0 j% n% `* ^7 Y
hair, and facial acne without enlargement of testi-
0 K. o% F( @' h# w2 o3 Vcles, suggests peripheral or pseudopuberty.1-3 We
. l$ I7 [# p8 r. R0 sreport a 16-month-old boy who presented with the
7 m0 S' R! h6 R/ a5 Venlargement of the phallus and pubic hair develop-. {% C, `* t5 s7 U+ e7 Q1 I1 T5 Y
ment without testicular enlargement, which was due
+ s, a- K5 J. b! Rto the unintentional exposure to androgen gel used by
% Z8 ?& m9 s, l7 Cthe father. The family initially concealed this infor-4 w0 b5 z4 Y* q
mation, resulting in an extensive work-up for this2 M8 v& @2 L$ j: ?
child. Given the widespread and easy availability of' B& ?+ \/ w# l; a4 B9 m) m4 \
testosterone gel and cream, we believe this is proba-5 \# _* V# J/ A2 r$ h" g) S7 p$ @
bly more common than the rare case report in the! l; |8 e6 C- }; ?/ U, k% \1 D
literature.4, g) m$ C$ l& r: V/ Z, A
Patient Report, I% B. p6 P5 d; W" n" G
A 16-month-old white child was referred to the* ?( V8 s1 d; \3 Z6 n' d; |  ?! m
endocrine clinic by his pediatrician with the concern$ G5 o& b0 [8 z6 M- z5 P! G
of early sexual development. His mother noticed1 X# g5 `5 c5 Q9 y# s5 V0 n
light colored pubic hair development when he was9 c  m: X; K. v8 A9 P+ R' o- ~& D
From the 1Division of Pediatric Endocrinology, 2University of* ]( a1 J, y: t, P2 J
South Alabama Medical Center, Mobile, Alabama.
# r' ]& m' {* B9 |; J9 H( wAddress correspondence to: Samar K. Bhowmick, MD, FACE,! H3 q+ }, B  Y2 I# }- m% O2 K
Professor of Pediatrics, University of South Alabama, College of
# J8 C3 Y9 m) f; |Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
- y* u8 ^" t+ P) Q/ Ne-mail: [email protected]./ l9 N4 p2 A3 q3 X  `, ?7 |! L
about 6 to 7 months old, which progressively became& K1 H$ U! ~# ]( Y: U, p. ^, D
darker. She was also concerned about the enlarge-
" ^  w, C1 |$ ~  rment of his penis and frequent erections. The child
+ l1 i- w! j' K  @( `( Fwas the product of a full-term normal delivery, with4 Z! u. v, p; m4 l; {# I6 j7 O. Q
a birth weight of 7 lb 14 oz, and birth length of" [! B( J$ S2 E- F- _. |$ t# P
20 inches. He was breast-fed throughout the first year) W! Z$ q; I6 X+ @+ r5 y
of life and was still receiving breast milk along with
' `; R$ n5 y; ?' V- W- {/ Y) ysolid food. He had no hospitalizations or surgery,7 h% A5 L% N0 H& t
and his psychosocial and psychomotor development% ~7 ?# U8 K! B8 w5 ]. B
was age appropriate.9 l. }" `2 G# w" }1 V
The family history was remarkable for the father,
# W7 P. t* j" Y. L. S1 Twho was diagnosed with hypothyroidism at age 16,. K. ~- [" o, V/ K  @
which was treated with thyroxine. The father’s4 L& i9 B1 E; X& A; @
height was 6 feet, and he went through a somewhat* p% Z* ~+ O8 B+ Z: P
early puberty and had stopped growing by age 14.
  T  \6 D, C! b2 M; M9 L9 WThe father denied taking any other medication. The
# S! N( |! h% l) m# f9 j& e! O: o$ gchild’s mother was in good health. Her menarche
/ S9 l- G( ~  l/ o) J  n% ?6 awas at 11 years of age, and her height was at 5 feet
" J. `# l  o( g6 ~) y/ `( J9 x; s. _5 inches. There was no other family history of pre-
( J3 a( `8 |3 Jcocious sexual development in the first-degree rela-
2 n# V) D1 U: Ttives. There were no siblings.
$ u$ E: C, I: r; g3 s! F  rPhysical Examination
' o9 w) x  r7 xThe physical examination revealed a very active,
; H; ?, x: b0 h; p; o* }  Jplayful, and healthy boy. The vital signs documented
+ q, Q8 `7 L& k% }: va blood pressure of 85/50 mm Hg, his length was
+ O$ Y: g7 m+ A. {/ U5 K" `" i# {90 cm (>97th percentile), and his weight was 14.4 kg; m2 l: k$ _' i9 [1 |! O
(also >97th percentile). The observed yearly growth5 B+ \! y4 P) w* Z4 \$ w9 M8 Y
velocity was 30 cm (12 inches). The examination of
2 t) f. ]/ s; `2 M2 m7 n* ethe neck revealed no thyroid enlargement.( z  t2 e7 F5 t3 Y
The genitourinary examination was remarkable for
+ B2 s* l2 w% t6 I- A$ S: Henlargement of the penis, with a stretched length of7 G) K* c7 G# o( ~4 k
8 cm and a width of 2 cm. The glans penis was very well9 o% Y& n" \/ L; F! v' u
developed. The pubic hair was Tanner II, mostly around6 s" d! S4 U, L/ ~) P
5403 Y' j% Z7 d/ K
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
! r; m. h3 i2 O5 o) kthe base of the phallus and was dark and curled. The8 D  P$ o0 s: l, r
testicular volume was prepubertal at 2 mL each.
( R, O  ?' n; E+ u; k  xThe skin was moist and smooth and somewhat
0 q$ ^3 r' K7 v1 woily. No axillary hair was noted. There were no! t5 J3 D$ o7 b1 d. [- e
abnormal skin pigmentations or café-au-lait spots.
* A! ~5 p  t' I: f1 CNeurologic evaluation showed deep tendon reflex 2+3 V( i/ v9 P+ K4 f2 m) b1 v- {
bilateral and symmetrical. There was no suggestion3 g. j: b* N" Z4 F- e' _
of papilledema.
/ |7 x, `. @* F7 ~9 R7 [Laboratory Evaluation
( K; c5 |; X; S& u$ x3 \The bone age was consistent with 28 months by4 r( m9 F0 J: y; H; D
using the standard of Greulich and Pyle at a chrono-: Q+ Q7 c* `6 F
logic age of 16 months (advanced).5 Chromosomal
4 V  i8 I6 w5 a: M6 V  rkaryotype was 46XY. The thyroid function test+ [% B* _" |: f$ [: D
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
& r, m7 e) o$ Q2 t% qlating hormone level was 1.3 µIU/mL (both normal).# I! o9 x4 d, Y
The concentrations of serum electrolytes, blood8 |) v. D) ?6 A2 r+ Q
urea nitrogen, creatinine, and calcium all were, h3 d8 J. d. y% t
within normal range for his age. The concentration
3 E; o/ M* t( x' ~! t: Cof serum 17-hydroxyprogesterone was 16 ng/dL
1 p1 N/ k# b  z$ X' ?(normal, 3 to 90 ng/dL), androstenedione was 20
, _$ Z, H& [6 T. r+ ung/dL (normal, 18 to 80 ng/dL), dehydroepiandros-* ^6 z) V- n# F
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
/ q5 F6 v  y  R8 p  F: g, q6 }desoxycorticosterone was 4.3 ng/dL (normal, 7 to* {8 R, O6 B/ l2 l! X
49ng/dL), 11-desoxycortisol (specific compound S)$ U4 j& o9 J$ R/ S
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
0 S8 w1 k6 g3 w* ~7 `tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total+ |' p% E: X. A2 {2 G$ x7 Z& f
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),6 x4 {% S1 R- b+ O; k9 _) y- ^; `
and β-human chorionic gonadotropin was less than0 @2 b: G2 ^7 h) H# f
5 mIU/mL (normal <5 mIU/mL). Serum follicular" \% P6 |2 X6 L' `3 l
stimulating hormone and leuteinizing hormone8 ]0 ?# {$ `) b; z1 i7 o! r
concentrations were less than 0.05 mIU/mL( z3 u% i+ T0 N5 o3 z
(prepubertal).
6 ?, R. k) ]. _! X( t7 ?% MThe parents were notified about the laboratory
- ^* Z' r# Q1 _/ x' U* I: j/ n" [results and were informed that all of the tests were
8 l4 A8 o6 J' X( ]normal except the testosterone level was high. The) I4 c7 D3 y- j) R
follow-up visit was arranged within a few weeks to
# H' |0 Q3 Z+ T  H* W/ H; _obtain testicular and abdominal sonograms; how-
# }( F- m. P# ]4 t: G7 |0 Jever, the family did not return for 4 months.! e7 m7 ?% p5 @7 A3 b& s. g9 p6 W
Physical examination at this time revealed that the0 E6 y2 d6 d3 r
child had grown 2.5 cm in 4 months and had gained$ E" G3 l2 Y$ y  l
2 kg of weight. Physical examination remained
$ C7 ?7 e/ P" ?' Nunchanged. Surprisingly, the pubic hair almost com-
. s) a; x4 f% `. i( S0 Ypletely disappeared except for a few vellous hairs at* ]: V! y3 f! Y& o; i5 s
the base of the phallus. Testicular volume was still 2
- I" V$ ?' p/ `  K# P) w* ]4 Y" kmL, and the size of the penis remained unchanged.
4 y8 v8 F' z* |$ n1 K8 n2 GThe mother also said that the boy was no longer hav-
: A" I% Q9 h) J6 B" ]ing frequent erections.8 @9 L8 g% {9 v6 c' c5 o
Both parents were again questioned about use of
: q" S8 F4 R" c+ x0 `4 k9 j4 gany ointment/creams that they may have applied to1 O0 j: O2 X6 w
the child’s skin. This time the father admitted the
/ G, k+ k6 x3 R9 VTopical Testosterone Exposure / Bhowmick et al 541# g8 T2 h6 y( c
use of testosterone gel twice daily that he was apply-3 p( I; X8 e8 O, V
ing over his own shoulders, chest, and back area for
3 F8 K, ]  Q* ka year. The father also revealed he was embarrassed1 o) m6 W+ a" F
to disclose that he was using a testosterone gel pre-" T! P1 P( x# V/ \! f
scribed by his family physician for decreased libido
# _( l6 C6 @; Y2 }: m: Asecondary to depression.
' Z. p' h+ m# dThe child slept in the same bed with parents.0 U* R9 a3 ]* O2 t9 o! r( F
The father would hug the baby and hold him on his  Q& I3 d& \# V: J
chest for a considerable period of time, causing sig-
" O0 D% s8 }2 \4 hnificant bare skin contact between baby and father.
# E) t: b- r5 _7 T5 AThe father also admitted that after the phone call,
9 R/ h, C0 v5 ~6 W- uwhen he learned the testosterone level in the baby
" j  Q! s# h. B# `( x7 H' ~7 [* Qwas high, he then read the product information0 e# @* ]5 P- g
packet and concluded that it was most likely the rea-# S2 |3 k5 p+ o' n0 u. `; d1 m
son for the child’s virilization. At that time, they) {5 J2 L$ |* y. k  T3 m
decided to put the baby in a separate bed, and the
5 x: ~: l+ O  c7 mfather was not hugging him with bare skin and had( H4 [' Q) i- X7 E! K9 ]
been using protective clothing. A repeat testosterone
2 l) X$ n: E9 Jtest was ordered, but the family did not go to the  S. [0 ?  L8 s& Q$ B/ O/ T
laboratory to obtain the test.
, m; N+ M- ]5 G/ q* N$ PDiscussion
; T+ R, j# N# S) q& |, l3 LPrecocious puberty in boys is defined as secondary
* h/ Y  i1 v% l# f' ?! Y6 c8 zsexual development before 9 years of age.1,4
; L6 C, h( r" M. q8 a" e0 x4 l) UPrecocious puberty is termed as central (true) when
* f3 R& s! V2 _6 O/ Git is caused by the premature activation of hypo-
  @) K% a7 M. y7 M" Ythalamic pituitary gonadal axis. CPP is more com-
) C8 g0 g4 w0 K3 M, imon in girls than in boys.1,3 Most boys with CPP
* ]7 v; b! f5 V  gmay have a central nervous system lesion that is
  M& J3 b9 B& ~1 ?5 `* i) O" Oresponsible for the early activation of the hypothal-
+ I: l9 Z' a  R% ^2 R, E: J  Famic pituitary gonadal axis.1-3 Thus, greater empha-7 t1 G$ F  a3 \7 R' B: s+ i5 F1 b
sis has been given to neuroradiologic imaging in
/ {# p- o, g+ Z& C5 h& q6 C7 A- eboys with precocious puberty. In addition to viril-' O( T6 [/ W! _5 n  X
ization, the clinical hallmark of CPP is the symmet-/ c5 r. @  D; O& d0 x6 N
rical testicular growth secondary to stimulation by8 q3 k  |+ P& E0 ]; L
gonadotropins.1,3, Y+ B9 b$ o$ T
Gonadotropin-independent peripheral preco-+ ~5 m9 d% t+ O0 g; K( K) r
cious puberty in boys also results from inappropriate
& @1 s( n" _; candrogenic stimulation from either endogenous or# R  f# z# w1 W* s( A9 x
exogenous sources, nonpituitary gonadotropin stim-) t# }& O9 Y% s; K
ulation, and rare activating mutations.3 Virilizing
  Y5 X& ?) i# [( rcongenital adrenal hyperplasia producing excessive
* R3 }2 T5 T5 Nadrenal androgens is a common cause of precocious" @! H) N# \- R8 U" v% V2 l
puberty in boys.3,4: ]% [+ g: D' c& a5 c* L# N
The most common form of congenital adrenal0 j* X" o$ h  p  I) r0 |" O
hyperplasia is the 21-hydroxylase enzyme deficiency.5 T' v3 L/ |+ g  _( r/ H
The 11-β hydroxylase deficiency may also result in
  C$ @1 K# X! Q' g$ Y/ n0 P  i1 B  Dexcessive adrenal androgen production, and rarely,* l7 o. Y* @" R2 q1 G2 Z& L/ ?
an adrenal tumor may also cause adrenal androgen& _; r0 N* ^% C5 T& y9 m3 M
excess.1,3
" J2 T4 c4 A3 u; d4 ?/ ?at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
# d. B+ O& A7 q& E8 ]- n+ A. T542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
" }5 D. ?8 ]  t2 t1 bA unique entity of male-limited gonadotropin-
. t3 g1 y9 N; b, j& Z- w1 ^independent precocious puberty, which is also known
, @: ?- ]% @+ A6 i4 T; H4 ]as testotoxicosis, may cause precocious puberty at a$ l- l" \/ u! g- c$ ^1 [! d7 W
very young age. The physical findings in these boys. D  u' e* M7 t1 z5 D) c
with this disorder are full pubertal development,
3 f. ~0 x) `' Z0 y8 U" o/ Y2 fincluding bilateral testicular growth, similar to boys; g7 {8 X  X; [* E+ Q. C, G: }
with CPP. The gonadotropin levels in this disorder
/ Z! u! v( ]1 H! u+ B$ y$ ~! uare suppressed to prepubertal levels and do not show
7 v  q# W# R& R4 @! Cpubertal response of gonadotropin after gonadotropin-
, A9 \0 \5 ?' [$ m1 j: breleasing hormone stimulation. This is a sex-linked4 |( [4 `! z1 V2 |( j
autosomal dominant disorder that affects only
: Q7 a: j! K4 V! Omales; therefore, other male members of the family- ~+ w7 T# _) U
may have similar precocious puberty.3( I' _9 I3 ]% q9 I% J$ @! q
In our patient, physical examination was incon-6 G: i7 Y. b: p  a7 d4 @% \4 c1 ]2 @
sistent with true precocious puberty since his testi-
" m, S$ c; a# E1 D* u8 j' ncles were prepubertal in size. However, testotoxicosis5 ^1 o) e5 }5 c
was in the differential diagnosis because his father3 ?& ]$ X6 I6 f6 P& s
started puberty somewhat early, and occasionally,; v- U5 s" m8 w. K$ a
testicular enlargement is not that evident in the
. S# c& V! e  p; e' Cbeginning of this process.1 In the absence of a neg-: X, }1 V, l$ {! r. t* p' K
ative initial history of androgen exposure, our& R: w6 A: v- W
biggest concern was virilizing adrenal hyperplasia," X2 L# i- I$ E/ w1 K! e
either 21-hydroxylase deficiency or 11-β hydroxylase: Y* }0 F5 l* F" ]8 c
deficiency. Those diagnoses were excluded by find-
8 n0 b, I3 ~3 O. [% Ling the normal level of adrenal steroids." ]6 W( W) o7 c" B# j9 `
The diagnosis of exogenous androgens was strongly6 E3 R7 V2 Q8 ~* k
suspected in a follow-up visit after 4 months because2 U+ H8 [) T! f1 u: Y3 E
the physical examination revealed the complete disap-' B" C* u" T. m8 b1 A+ _* Z
pearance of pubic hair, normal growth velocity, and
5 i7 u! w$ e6 e  c* n4 m/ I/ ?decreased erections. The father admitted using a testos-
$ i: P) n& L2 }- v/ Dterone gel, which he concealed at first visit. He was
- w' o7 C) c4 N0 pusing it rather frequently, twice a day. The Physicians’1 S- r. R3 M6 Y5 H& S. g
Desk Reference, or package insert of this product, gel or
4 A+ }1 |2 x" W3 U% G6 ?cream, cautions about dermal testosterone transfer to; X3 h" G0 Z0 O+ k, Y
unprotected females through direct skin exposure.
9 x7 I3 E! K% }8 qSerum testosterone level was found to be 2 times the9 F8 N6 Z# {' e% j- W- E: m( D- D
baseline value in those females who were exposed to
) O: h4 V% O$ A2 k* Aeven 15 minutes of direct skin contact with their male
2 t- u9 S0 X6 ~% Gpartners.6 However, when a shirt covered the applica-: u* D: s% x) @
tion site, this testosterone transfer was prevented.1 D8 ]. e/ t1 ^) Q! D; ]0 N1 P
Our patient’s testosterone level was 60 ng/mL,' P0 H$ w& z1 a6 b- d( ?( J
which was clearly high. Some studies suggest that
- E; Q" a0 U' j4 Udermal conversion of testosterone to dihydrotestos-
6 n5 W3 g, e+ D) C' y6 \0 uterone, which is a more potent metabolite, is more- n& y* b- G" C# ^
active in young children exposed to testosterone
( W4 A6 ]& O5 c  i$ G5 B8 W( v% A+ wexogenously7; however, we did not measure a dihy-
/ B* F! q! @6 \$ bdrotestosterone level in our patient. In addition to
8 w; ?# h# D3 E' e: Q" ~- K1 S' M0 ivirilization, exposure to exogenous testosterone in7 L+ H5 p4 u" U- ?  n
children results in an increase in growth velocity and$ _8 {8 p) N- q( O4 c+ M9 g' B7 y
advanced bone age, as seen in our patient.
. h9 t; O. J$ X# X4 AThe long-term effect of androgen exposure during
/ {3 u' _0 C2 A- E1 Kearly childhood on pubertal development and final/ p% a0 e+ e% B  _4 J
adult height are not fully known and always remain
0 u3 `! l! o1 |$ p* [: k2 ca concern. Children treated with short-term testos-
% d5 D) \; u# _4 y% }0 mterone injection or topical androgen may exhibit some% C8 ~# q' {2 |
acceleration of the skeletal maturation; however, after
* C/ }7 j  ?4 O" P) |, Acessation of treatment, the rate of bone maturation
0 Y9 t' c% l& }$ C9 v' |; Q1 `decelerates and gradually returns to normal.8,9
: @) z* p3 N: ?2 L! H, \2 \There are conflicting reports and controversy
/ l" B4 }! l8 Z/ L" Oover the effect of early androgen exposure on adult
8 [' H, T4 d  V5 k8 Apenile length.10,11 Some reports suggest subnormal
( F) j( V& E' M" p" ?adult penile length, apparently because of downreg-! X5 c; y. @5 ~) Q
ulation of androgen receptor number.10,12 However,' h4 v; O- l' \) P0 f3 A
Sutherland et al13 did not find a correlation between
. d" t7 t2 C- |4 Q4 ]childhood testosterone exposure and reduced adult0 K+ @+ ^- p% I; z5 |3 w
penile length in clinical studies.
) E8 g# s% N5 L/ L) KNonetheless, we do not believe our patient is
4 D2 E. Q5 D  ?& d! @6 q  Z4 \, Zgoing to experience any of the untoward effects from: `& G: i; H- e2 U7 H
testosterone exposure as mentioned earlier because
) g5 ]) G1 P: G! I; N+ ythe exposure was not for a prolonged period of time.) h3 r& i0 c  L6 F0 G+ x# L
Although the bone age was advanced at the time of
8 @6 L8 w+ ?  R, {* H8 k/ D  t( ldiagnosis, the child had a normal growth velocity at
- @0 b( Q( A5 x; Othe follow-up visit. It is hoped that his final adult
7 e6 p, z* R, G& Q5 |6 O3 theight will not be affected.
: m* ?- d/ ~! Q! v4 GAlthough rarely reported, the widespread avail-
1 C' t* F0 N& Y! K% |# \( iability of androgen products in our society may  ~8 }3 o, J( J5 {# B# y$ g0 I+ o5 n  h
indeed cause more virilization in male or female
2 P1 K- t. o5 Rchildren than one would realize. Exposure to andro-
1 k0 s. u0 Z/ ugen products must be considered and specific ques-
. [  K& c5 h. j7 F- p# ctioning about the use of a testosterone product or5 K6 w! R: R; _4 h: Q5 P! u" Z
gel should be asked of the family members during
$ d& K8 j1 ^% ?, |8 c' lthe evaluation of any children who present with vir-
6 X8 w) L; w5 n& a6 m' |) Kilization or peripheral precocious puberty. The diag-
3 n; B% j5 M0 onosis can be established by just a few tests and by6 F- N0 ~0 |) c8 d7 p
appropriate history. The inability to obtain such a
8 R( H2 P+ G& u# }history, or failure to ask the specific questions, may
) _3 a1 d! Q' ]9 x0 e' q) P7 Wresult in extensive, unnecessary, and expensive
! E  k$ [; Q9 f0 Finvestigation. The primary care physician should be
5 M3 \& ]; o2 R6 K. Gaware of this fact, because most of these children3 v$ {1 [% s* c" S0 g+ Z
may initially present in their practice. The Physicians’
% r* s* R; m) `& V5 A( P  YDesk Reference and package insert should also put a
# v1 L! }$ ]6 X1 hwarning about the virilizing effect on a male or
0 c& U( }. y! M) p/ |female child who might come in contact with some-3 l+ b1 L' N, ?3 W
one using any of these products.
8 }/ b' A4 b; |References: W: [# _3 e6 L, ]7 _" T0 A" z8 M
1. Styne DM. The testes: disorder of sexual differentiation0 m7 [8 F7 D1 d$ R2 y5 t
and puberty in the male. In: Sperling MA, ed. Pediatric
7 k9 ^8 ?% Q" d2 ^) z8 FEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;" c) a  e- }) R$ U9 e$ g9 {
2002: 565-628.' ]& Y* f; O$ O) z- z4 }
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious& y, ~: b# w* R9 W# b4 M
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

, T" e2 H9 K, Q- J0 r; C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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