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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 \' U) m4 h) o, i# d4 l1 p8 {/ F1 f" eBoy Induced by Indirect Topical5 ~7 w! F& f7 z; A3 `
Exposure to Testosterone, U3 |/ v- h( d7 L- w& @
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
, J. `6 [) G) ]" [; H- @( e$ Gand Kenneth R. Rettig, MD1
1 Y# |) N  {: h4 b& I! U+ `Clinical Pediatrics. g$ e: u6 m0 n0 n
Volume 46 Number 6
' v% W1 B: e9 Q. i8 bJuly 2007 540-543: m2 S, |$ I9 D) Z4 [! Q
© 2007 Sage Publications
  o: C0 ]7 B. v/ `10.1177/0009922806296651
4 |4 u2 J0 r3 D& _% ^! P6 bhttp://clp.sagepub.com: j  n; k; u1 z; u1 M
hosted at; K0 O  n/ r' k$ f
http://online.sagepub.com' y  k" C* z* p0 ^; U& A
Precocious puberty in boys, central or peripheral,
) O1 C* K- `) z5 j  @is a significant concern for physicians. Central
( @- b7 d: h/ l$ F. cprecocious puberty (CPP), which is mediated+ [- C: y% w( f, `
through the hypothalamic pituitary gonadal axis, has/ j+ i' b" h( N5 ~
a higher incidence of organic central nervous system  l& t9 V( L* e2 U0 W
lesions in boys.1,2 Virilization in boys, as manifested
! k$ D) d& ]* Z7 xby enlargement of the penis, development of pubic3 g' P6 S0 R4 n" W3 H. Y+ U
hair, and facial acne without enlargement of testi-9 e- m7 O; t" Z. n! F$ ?7 M
cles, suggests peripheral or pseudopuberty.1-3 We
6 m; Q# ]2 Q* `  y$ @8 F( s2 ireport a 16-month-old boy who presented with the
  I5 w# Q, N" i, F1 L; Fenlargement of the phallus and pubic hair develop-! c& h( e3 r2 G
ment without testicular enlargement, which was due# b! X( e- `, I
to the unintentional exposure to androgen gel used by
$ o5 Q4 Y$ j' g6 Gthe father. The family initially concealed this infor-0 R! D1 c; b/ p3 c1 M* ~+ j
mation, resulting in an extensive work-up for this
. u+ Y4 w% L( R3 {6 v0 Lchild. Given the widespread and easy availability of  a- Z# }. Y! T+ M
testosterone gel and cream, we believe this is proba-! g6 o$ i& ~. f' w
bly more common than the rare case report in the
1 Z% A$ x! O; q1 ~' y, V  [literature.4
' U* H+ J/ M( RPatient Report1 A) `& N( q8 s* N3 A. k$ g, W
A 16-month-old white child was referred to the% O! d6 x( }2 |- j
endocrine clinic by his pediatrician with the concern
# N% `8 n. J1 I2 x% U$ |! Z8 cof early sexual development. His mother noticed5 j0 R# W! P2 D. q+ M  q) l
light colored pubic hair development when he was
0 \' d. B+ M; zFrom the 1Division of Pediatric Endocrinology, 2University of
4 A6 h' S% o  E) l5 MSouth Alabama Medical Center, Mobile, Alabama.5 E, J" v9 M" N2 v( {  X
Address correspondence to: Samar K. Bhowmick, MD, FACE,/ c' U7 v8 p3 Y" x
Professor of Pediatrics, University of South Alabama, College of1 x/ H% A/ n$ s0 e! \0 ^7 d
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;  ?0 p1 @+ [  a# L' x
e-mail: [email protected].
# m( Q  Z% j" {7 a6 f! I& F& }about 6 to 7 months old, which progressively became; {$ f0 ]& Y5 L& Q/ j5 |, L+ `
darker. She was also concerned about the enlarge-1 o- V3 ~1 t5 w
ment of his penis and frequent erections. The child
, ?( w. C- o: _/ cwas the product of a full-term normal delivery, with  o* V. F) r9 E- D2 A% X/ P# o
a birth weight of 7 lb 14 oz, and birth length of
1 @# U6 c, o$ q/ J0 w( k; p20 inches. He was breast-fed throughout the first year+ Q  H4 q% T6 s" Y
of life and was still receiving breast milk along with
$ B6 z. S8 z6 h6 qsolid food. He had no hospitalizations or surgery,7 v! r6 m6 V5 c' ~
and his psychosocial and psychomotor development
1 K# {" X6 |# A7 Z+ {was age appropriate.* K5 j0 t! y$ E$ ?
The family history was remarkable for the father,
" i+ ]3 a2 h% Rwho was diagnosed with hypothyroidism at age 16,
0 ?* c, ?9 X1 ^* E% u2 |2 O/ U1 vwhich was treated with thyroxine. The father’s% W$ [1 E+ }; f& q
height was 6 feet, and he went through a somewhat
8 D0 v  J2 i9 f, q5 r/ y& Mearly puberty and had stopped growing by age 14.' M- I( i1 @- P0 H1 t
The father denied taking any other medication. The5 R. y+ l6 m1 J8 A- p
child’s mother was in good health. Her menarche
) d9 s5 m1 S- L8 E. Qwas at 11 years of age, and her height was at 5 feet# F) n! X7 ?0 |5 b6 U
5 inches. There was no other family history of pre-$ w9 a% L: c% ]. c
cocious sexual development in the first-degree rela-3 P' z& H6 Z0 k" a
tives. There were no siblings.' z& ^1 R5 h0 n6 C, v7 |
Physical Examination
+ j& S+ T' s: |The physical examination revealed a very active,
6 @5 m  Y8 z- P* X3 x9 Bplayful, and healthy boy. The vital signs documented( Z; a" o2 k- i# g, ]
a blood pressure of 85/50 mm Hg, his length was
0 D0 ^; ]6 B5 n90 cm (>97th percentile), and his weight was 14.4 kg# n( q0 M6 |% p9 B1 [  }' h6 Q
(also >97th percentile). The observed yearly growth5 d0 C8 o, l% L5 m5 S
velocity was 30 cm (12 inches). The examination of2 ~' p4 z, g0 F- ~+ |; J. y& G
the neck revealed no thyroid enlargement.
# A* f, A( v/ B. K+ |7 i* I1 mThe genitourinary examination was remarkable for/ l" |) ^- p( t+ ~
enlargement of the penis, with a stretched length of
# m/ {+ x" Z  P7 @6 O8 cm and a width of 2 cm. The glans penis was very well
! K( Y9 u: N% t- g: R" f! s; \$ bdeveloped. The pubic hair was Tanner II, mostly around
: V8 D- l1 I6 J540
) E* x4 ]2 r! o, m8 |3 Z1 vat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from# X( ~+ o" u' v" X9 A1 |
the base of the phallus and was dark and curled. The
0 j  ?7 ^+ b0 ^0 q% l7 H9 j' r1 @" r6 Itesticular volume was prepubertal at 2 mL each.
5 F' R! H. L0 A  A: m* q3 q+ lThe skin was moist and smooth and somewhat
* G2 Y* T# y" f0 s) s  U9 boily. No axillary hair was noted. There were no
" ]# U. _1 C' k) ~0 I$ xabnormal skin pigmentations or café-au-lait spots.
. i6 w9 ~; K/ j0 N, P2 \Neurologic evaluation showed deep tendon reflex 2+) w) J' B! A. p' \5 Y
bilateral and symmetrical. There was no suggestion
0 ?. B, j: b! }& ]: i3 W. gof papilledema.
* f+ ?* y) u# q, ?Laboratory Evaluation
$ y. }+ d0 ~# e) eThe bone age was consistent with 28 months by, a8 U1 M; s; N. X/ C3 n
using the standard of Greulich and Pyle at a chrono-
: Y# e. b& e* C$ B/ g" Flogic age of 16 months (advanced).5 Chromosomal
2 ]6 W4 @6 J' P# rkaryotype was 46XY. The thyroid function test4 g+ V% C1 }# U& t& p0 E6 h/ d
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
5 I* J) Y; k4 t! D( }8 glating hormone level was 1.3 µIU/mL (both normal).$ r+ S% L' p1 h6 Q
The concentrations of serum electrolytes, blood
3 m/ d: R7 n. v( x+ h6 ^1 b8 aurea nitrogen, creatinine, and calcium all were! [. D4 z- O2 V' J7 E# `  f
within normal range for his age. The concentration; X: J: G/ X! E1 W* j# |4 B
of serum 17-hydroxyprogesterone was 16 ng/dL$ Z! u5 A, ~% E; s% J
(normal, 3 to 90 ng/dL), androstenedione was 20
, _% R) D# M5 \9 Y: O+ Kng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
! w! S+ F' v$ W$ S7 k" Mterone was 38 ng/dL (normal, 50 to 760 ng/dL),$ F) d& f9 ~5 s
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
  G& F( T, O/ ~7 @4 r; K49ng/dL), 11-desoxycortisol (specific compound S)
. z$ k' J2 t/ H  m5 @( ewas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-; d, |0 J2 v1 z; I
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total6 R) h& p9 T& ^# ^( J* q9 p
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
1 Y* j) B+ u/ B' h' x7 `and β-human chorionic gonadotropin was less than3 r  H# Y0 n- ~3 f: N
5 mIU/mL (normal <5 mIU/mL). Serum follicular
; B- H" i/ Q" Gstimulating hormone and leuteinizing hormone8 U" q# s; ]$ o+ G/ H
concentrations were less than 0.05 mIU/mL) m3 V# w1 E: E, I5 K( Z( L
(prepubertal).8 ~1 Y) A5 L0 C& [7 _$ c
The parents were notified about the laboratory  f9 S! \  L+ U0 c1 K
results and were informed that all of the tests were
+ @' ~1 o' L9 g$ R9 j9 Knormal except the testosterone level was high. The
/ ^* e, Q, I2 F/ _" b4 T/ hfollow-up visit was arranged within a few weeks to
: n, |- E( i2 e0 x* m+ [' r: Hobtain testicular and abdominal sonograms; how-
) ]4 A' I; b  S2 V* u0 Kever, the family did not return for 4 months.
/ a7 ~2 }3 n- Q1 K8 ^Physical examination at this time revealed that the- V1 }- H: E) G" w9 M; ^. f
child had grown 2.5 cm in 4 months and had gained
" B" ]" K' G/ _+ e8 F. p2 kg of weight. Physical examination remained
/ |$ e8 u: |5 ]' C8 Vunchanged. Surprisingly, the pubic hair almost com-5 o+ g" z5 N( n8 y9 P- y+ {9 T! t
pletely disappeared except for a few vellous hairs at. z3 C. e1 n& b& ~
the base of the phallus. Testicular volume was still 2* Q3 h" U# J  e" a" J5 h
mL, and the size of the penis remained unchanged.
( K  F! m2 Q! v2 B0 mThe mother also said that the boy was no longer hav-
( \1 h- z+ }3 p& B, {ing frequent erections.
# W+ K. |8 `. |: n- g) S6 `: T: _, PBoth parents were again questioned about use of" o$ i9 w+ |" r# `# o) o
any ointment/creams that they may have applied to
; _) k, _6 m/ [( d$ q/ bthe child’s skin. This time the father admitted the+ {" Q6 `( B0 g5 G5 P
Topical Testosterone Exposure / Bhowmick et al 541" K$ I1 I4 N% L5 j# D
use of testosterone gel twice daily that he was apply-
4 A! W7 k5 K: A9 O2 t5 oing over his own shoulders, chest, and back area for
. {* d. r+ ?7 w4 G! ya year. The father also revealed he was embarrassed8 W3 q+ }) J0 T; J. c/ f0 V$ d
to disclose that he was using a testosterone gel pre-
7 R2 N$ ~1 [5 X% A0 X7 ~) }scribed by his family physician for decreased libido
- {. x. X* D3 Z! Wsecondary to depression.
# j" s, n) `' i5 UThe child slept in the same bed with parents.
  e# b6 s6 W7 T' i  i* WThe father would hug the baby and hold him on his7 I' w) F9 U7 M9 _- D! Z
chest for a considerable period of time, causing sig-
& o4 N. S8 _8 B. m/ _2 Pnificant bare skin contact between baby and father.# c/ j! U, e7 a% R1 p
The father also admitted that after the phone call,7 S& u1 g  f- s+ o9 O( K: [
when he learned the testosterone level in the baby7 ~) `9 T( v. i) |0 @( t  N+ E" o
was high, he then read the product information
; D$ H" Y1 I/ k" u9 Epacket and concluded that it was most likely the rea-
1 g9 j* _, `/ |* z) Bson for the child’s virilization. At that time, they1 N- ?3 W* F& C# c6 E) p6 P' m8 Y  }
decided to put the baby in a separate bed, and the
0 c9 X" e/ R4 X, Jfather was not hugging him with bare skin and had
% Y4 _. h1 f; cbeen using protective clothing. A repeat testosterone" o6 A7 ^8 R+ q
test was ordered, but the family did not go to the
- h, F: S6 s  Y  Ulaboratory to obtain the test.$ U+ p9 h! }6 _5 S6 w
Discussion
/ r" I3 o% u( D! M9 Q0 N$ pPrecocious puberty in boys is defined as secondary
- A$ t5 G$ X6 |4 B# \: Fsexual development before 9 years of age.1,4
8 }! r: ]8 F0 a0 j, \Precocious puberty is termed as central (true) when. ]/ A$ v5 P( f9 V, ]
it is caused by the premature activation of hypo-4 i3 _0 M7 l5 `: j2 ]! [
thalamic pituitary gonadal axis. CPP is more com-
. a7 m* _% x: T" Y! a- X3 bmon in girls than in boys.1,3 Most boys with CPP
5 e  b9 R, ~2 @  D7 Hmay have a central nervous system lesion that is3 m* ~$ d2 x  @) r
responsible for the early activation of the hypothal-
  B3 C6 z: K: u2 J* R: P6 damic pituitary gonadal axis.1-3 Thus, greater empha-
9 o8 T! N( @% J8 Qsis has been given to neuroradiologic imaging in
7 D% j/ h6 l, V+ \6 a5 U9 i& B' `boys with precocious puberty. In addition to viril-2 g1 D3 ]6 S+ q7 c8 Z. q. s4 y
ization, the clinical hallmark of CPP is the symmet-8 b9 {- t& `1 T9 U3 [
rical testicular growth secondary to stimulation by
( {! l: `" L- w9 r* l( bgonadotropins.1,3
8 M; }0 W9 W, |1 o$ ?% F/ t$ _' hGonadotropin-independent peripheral preco-
2 H1 U9 v- l7 o' S0 S" U  Ycious puberty in boys also results from inappropriate5 Y( |- V5 ~0 N0 Y
androgenic stimulation from either endogenous or- W, g! `; i# {  L0 A; H
exogenous sources, nonpituitary gonadotropin stim-
# v3 A/ J5 S2 O( Xulation, and rare activating mutations.3 Virilizing
; g- ~1 h! R: W- o3 c$ z3 B6 [congenital adrenal hyperplasia producing excessive  @4 C; b; q( C& L, K9 r
adrenal androgens is a common cause of precocious
5 b; B- g" V# Y3 m0 Qpuberty in boys.3,4' ]5 h8 w2 }8 m$ v2 c8 f, G
The most common form of congenital adrenal# u+ V$ r' x) k) w9 [3 t
hyperplasia is the 21-hydroxylase enzyme deficiency.
; w5 y/ t6 x& ^& p! SThe 11-β hydroxylase deficiency may also result in2 l% w8 f/ U  |: [2 A( J" x
excessive adrenal androgen production, and rarely,
6 J  y) U) o) }an adrenal tumor may also cause adrenal androgen
# m6 \' `- }- k7 e# @) b% W9 Jexcess.1,3  ~: U6 ]! G) r
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
" k. e! I2 |( T) ~3 B4 I# P$ z! v542 Clinical Pediatrics / Vol. 46, No. 6, July 2007) Z( D+ w  }, q8 {4 Q- ]; y) [; |
A unique entity of male-limited gonadotropin-* y$ @- n( P6 w! y
independent precocious puberty, which is also known
$ u3 G. i; e2 l6 }as testotoxicosis, may cause precocious puberty at a. A! `* c  |& ~% g/ e
very young age. The physical findings in these boys9 H! }. v- k( c! B
with this disorder are full pubertal development,
, b8 _$ g& L7 m) k' sincluding bilateral testicular growth, similar to boys) e5 e9 y# k: |% @6 |0 R5 V. T+ o
with CPP. The gonadotropin levels in this disorder
' L" a1 q9 \, K" W1 {are suppressed to prepubertal levels and do not show6 w# o/ v# l& q* h" |1 F( D+ N
pubertal response of gonadotropin after gonadotropin-! Q1 e2 ~: u' E5 r: }+ w
releasing hormone stimulation. This is a sex-linked
* x" B8 M& w, b% z* T/ V( gautosomal dominant disorder that affects only
. n  F& F7 d. ^males; therefore, other male members of the family
8 f; q# j' K0 _" {% K8 S3 Wmay have similar precocious puberty.3
- {% j' z5 R, i+ G2 Y" n! \5 T8 |In our patient, physical examination was incon-  Q( }( }7 x1 B5 D# V5 B5 Z0 ^! u3 e
sistent with true precocious puberty since his testi-
; ~4 A6 C+ F! b8 x/ jcles were prepubertal in size. However, testotoxicosis# l" o/ @" t$ H
was in the differential diagnosis because his father/ {1 o2 M- z( d4 _
started puberty somewhat early, and occasionally,* u$ w; O4 I# B2 I* U) o) a4 V
testicular enlargement is not that evident in the
( @' z# ^/ v1 N% n  gbeginning of this process.1 In the absence of a neg-
& V( b; x$ h0 w3 t3 Rative initial history of androgen exposure, our9 _' R4 Y: I! L  I/ D4 l
biggest concern was virilizing adrenal hyperplasia,; @/ }+ A/ h+ `' B9 q1 X! p
either 21-hydroxylase deficiency or 11-β hydroxylase
+ P/ y, V5 W* ]# }deficiency. Those diagnoses were excluded by find-
9 u1 [: Y/ ^4 ^" U, king the normal level of adrenal steroids.7 U+ x8 R' H9 q7 r, p: `( s
The diagnosis of exogenous androgens was strongly' n' L" w. x7 w4 l; O) b* k
suspected in a follow-up visit after 4 months because; x" m& i2 z8 d, ?6 T1 o5 f
the physical examination revealed the complete disap-
  F4 l$ {9 V9 U5 Z9 q6 Z- c  Y$ spearance of pubic hair, normal growth velocity, and
% R; e5 N! h. p/ S4 Rdecreased erections. The father admitted using a testos-
$ f, U; U! q. {- a) z$ Pterone gel, which he concealed at first visit. He was' g9 a4 @" ~# E# V
using it rather frequently, twice a day. The Physicians’
2 m8 Z* _, ^2 \# ~6 ?Desk Reference, or package insert of this product, gel or4 p: I. ?: G% n0 [( B
cream, cautions about dermal testosterone transfer to
5 ]* ^, K0 R0 e$ [0 ^: ~unprotected females through direct skin exposure.4 T9 X9 u+ l" m, I2 j: x
Serum testosterone level was found to be 2 times the4 p! f$ v* i7 Z" h* k9 Y
baseline value in those females who were exposed to
7 A+ g. P- }/ i$ ?( k, ieven 15 minutes of direct skin contact with their male8 A% Q+ c  M+ S1 \: f7 ~* M
partners.6 However, when a shirt covered the applica-8 M9 J8 ]- w! V' |1 t
tion site, this testosterone transfer was prevented.  ~! ~$ t) h2 A7 H& l! e% L* a) K2 X. R
Our patient’s testosterone level was 60 ng/mL,
$ M3 V8 X$ [" k6 _; t1 n- Wwhich was clearly high. Some studies suggest that; v9 p8 S, F% O  [6 @
dermal conversion of testosterone to dihydrotestos-
0 d5 q% V, R# L$ p5 g6 Fterone, which is a more potent metabolite, is more
! Q" \, m* j) a" g+ Pactive in young children exposed to testosterone
. O! M- D4 r3 q1 ~8 E0 |5 z+ ^" N  M8 I/ |exogenously7; however, we did not measure a dihy-
! @1 j6 `# W2 l0 i  _! Vdrotestosterone level in our patient. In addition to8 B. a( Z* k. g! E/ n2 K
virilization, exposure to exogenous testosterone in
* e. E; `6 ^2 @$ r. ychildren results in an increase in growth velocity and5 j5 N) N0 n5 G4 `) H
advanced bone age, as seen in our patient.+ `% \# b* c" _
The long-term effect of androgen exposure during
+ h$ I1 i) J& q* x0 S5 `early childhood on pubertal development and final7 Z# j! R  p* P- P7 Y
adult height are not fully known and always remain' _/ ]8 H) W. m' r& \9 R& E
a concern. Children treated with short-term testos-5 S/ K, t7 j2 W
terone injection or topical androgen may exhibit some: C7 @* [4 }* E' D% g; V# Y
acceleration of the skeletal maturation; however, after) [5 {# w) w4 n% v( r- d
cessation of treatment, the rate of bone maturation
$ o0 F8 J1 |2 i, |' e, Cdecelerates and gradually returns to normal.8,9. G$ E9 N0 d  i, p0 y5 {: q
There are conflicting reports and controversy
: M9 D2 R. ^. @1 m. w2 fover the effect of early androgen exposure on adult- y7 H* R( W3 ~$ Y3 }: M
penile length.10,11 Some reports suggest subnormal: B6 D, |, w) X6 d- e; G
adult penile length, apparently because of downreg-
9 U# s9 Q: T. L! C* q: Dulation of androgen receptor number.10,12 However,
/ N9 i6 M' r: S7 g: f# e$ kSutherland et al13 did not find a correlation between! u9 b& q: P. u- l$ p
childhood testosterone exposure and reduced adult
. r& T+ I1 {1 K4 Kpenile length in clinical studies.$ T/ I+ h9 U: J1 B0 w  ~
Nonetheless, we do not believe our patient is
. E( f  {0 v8 P3 `: u4 u0 C* t  Ngoing to experience any of the untoward effects from$ ^4 _/ i3 ^9 L4 L) [
testosterone exposure as mentioned earlier because
# D; b: l9 @2 U5 J7 f, _the exposure was not for a prolonged period of time.8 @9 z6 ^+ _/ N1 l  x: A4 F
Although the bone age was advanced at the time of
3 r. ^  B8 _& i: @. z! }- Jdiagnosis, the child had a normal growth velocity at
+ W8 }* t8 b5 {9 b0 hthe follow-up visit. It is hoped that his final adult
/ l* f3 ~  |9 u- mheight will not be affected.
* v7 K' x0 Q  y  F: l: O8 QAlthough rarely reported, the widespread avail-2 ?# s7 G9 N$ U+ Y  @
ability of androgen products in our society may4 V' i0 n3 b% _% ^& d8 y, I1 l
indeed cause more virilization in male or female
( Y3 V+ T5 C- Y# ^children than one would realize. Exposure to andro-
; C* c, n5 N3 p/ tgen products must be considered and specific ques-9 u2 c( ?7 A9 X8 f; w- k% J/ A3 K
tioning about the use of a testosterone product or
# E$ `8 a+ v- i7 l3 Hgel should be asked of the family members during
& J! n6 ^/ Z- N1 F  d. Hthe evaluation of any children who present with vir-
' V- P$ {( K( V) `ilization or peripheral precocious puberty. The diag-" R& `1 M4 _* c1 N! `
nosis can be established by just a few tests and by6 P- |. X( X2 Y; [+ S- l
appropriate history. The inability to obtain such a
- @9 A& x! i6 y' h6 H: Qhistory, or failure to ask the specific questions, may9 S/ Z& @& O8 T8 J7 c6 F8 E/ g
result in extensive, unnecessary, and expensive0 E* S; ~# R$ U" L5 x% e5 o
investigation. The primary care physician should be
( l% l. z1 P4 Jaware of this fact, because most of these children" M* B/ [% H) U3 V6 Y
may initially present in their practice. The Physicians’. h4 Y2 V* E6 Q8 }2 \. t; ]
Desk Reference and package insert should also put a) w2 Y) q1 ^0 w  |- [: O. q1 Z
warning about the virilizing effect on a male or
# F2 W- F7 C* ^) \/ \female child who might come in contact with some-
( [5 D7 q6 h' `: o* k- Sone using any of these products.
# y. G5 P! W  M7 g' j6 PReferences; _, p) f7 L( D( ^" Y. R( ^* W( x
1. Styne DM. The testes: disorder of sexual differentiation
9 l2 a7 E: x$ w2 Zand puberty in the male. In: Sperling MA, ed. Pediatric
; o; u, `, ?( y+ sEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;& X( ~# F% J1 C! U" k/ d
2002: 565-628., C3 l; R' n; @
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
, C; Q9 l, r2 H9 ^. I: \puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old; h2 b# i& ~3 i3 w# J2 @
Boy Induced by Indirect Topical
* R1 Q# y: d" T! f7 GExposure to Testosterone
; ]" C- |; R8 E% n( |: l8 A* X8 I/ v5 KSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
4 Z! N( Y3 h/ S9 z7 M; n' S% Aand Kenneth R. Rettig, MD1& q. O* u; j% R
Clinical Pediatrics! \' G; K; M2 P; H' x& I! e  N* y
Volume 46 Number 6
2 n8 e) T: U1 F2 f+ V9 g( YJuly 2007 540-543
: F, g+ P7 y, w1 {  a2 j$ K© 2007 Sage Publications" F% S6 w& o% V2 p
10.1177/0009922806296651
# G- @2 o! j3 g' g: r" lhttp://clp.sagepub.com
) b6 P5 _8 i: t2 E: f* y( khosted at
+ f: ^" e6 v% ?$ b1 |http://online.sagepub.com
5 f, ?- O- u  Z6 b# a' VPrecocious puberty in boys, central or peripheral,/ u  x; w8 m' M( \& H8 m, h! V
is a significant concern for physicians. Central; m# H; g* ^2 J' ~0 _* y
precocious puberty (CPP), which is mediated* q& p# u0 {: W! q4 [$ J
through the hypothalamic pituitary gonadal axis, has
" w, T0 b4 I" Z/ Z( na higher incidence of organic central nervous system
3 z) q5 A; N1 ?* K: Slesions in boys.1,2 Virilization in boys, as manifested
0 \: C3 a! D! n( y  X' Oby enlargement of the penis, development of pubic
4 {; ^5 a" I; k7 Vhair, and facial acne without enlargement of testi-& ]) L9 m- ^3 s1 P
cles, suggests peripheral or pseudopuberty.1-3 We
$ c( m, }( ^+ t" `) p! n5 X8 Z! vreport a 16-month-old boy who presented with the
0 p: `  H; L7 o6 w% H) xenlargement of the phallus and pubic hair develop-
. ^2 C$ C( T5 [6 C+ `$ qment without testicular enlargement, which was due: t. J) |1 @6 G  w
to the unintentional exposure to androgen gel used by0 S" ], ^+ F! \; k0 X
the father. The family initially concealed this infor-
5 H' r' N5 d* `. `% Kmation, resulting in an extensive work-up for this
) A& ]% V. \7 `+ u3 Jchild. Given the widespread and easy availability of
8 D& Z# G. w3 P  |2 P' J1 E, z' z3 v0 z. Ztestosterone gel and cream, we believe this is proba-
1 \# K. @" g/ Z" G- ?6 F1 O' l- nbly more common than the rare case report in the
- v: V6 E; [' U0 N# l  ^# Fliterature.4; Y* M, W+ W9 y
Patient Report- i0 d! R& {$ i9 s; y
A 16-month-old white child was referred to the
. e! W- y( J: \6 Mendocrine clinic by his pediatrician with the concern2 y7 G2 l0 i. F+ g4 B- R' N
of early sexual development. His mother noticed# u4 @' q6 S! |% g& K
light colored pubic hair development when he was
0 r, y. U7 u9 l1 P% x. K* IFrom the 1Division of Pediatric Endocrinology, 2University of
. D; f& T/ Y- WSouth Alabama Medical Center, Mobile, Alabama.
  H3 B; x1 \: e: W7 Q3 z: bAddress correspondence to: Samar K. Bhowmick, MD, FACE,$ ?" \; N' w' R5 e% C2 W
Professor of Pediatrics, University of South Alabama, College of
( w* b4 \: \! j6 j. c: NMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;4 i/ Z$ N4 L3 ^$ O
e-mail: [email protected].
' _2 n+ J3 V) y, T9 b% s% E& m, Pabout 6 to 7 months old, which progressively became
  N( N7 f3 b! h6 |0 M+ ^darker. She was also concerned about the enlarge-( V" P, W: Z0 z. G- y
ment of his penis and frequent erections. The child
( j1 F+ {- w0 N, ^3 bwas the product of a full-term normal delivery, with4 Y$ y. W; u6 Q, ~7 X+ n9 T! v
a birth weight of 7 lb 14 oz, and birth length of
1 a( Z- |, k; S5 `) M20 inches. He was breast-fed throughout the first year' o/ o: A' m0 H1 _
of life and was still receiving breast milk along with1 F( \# [! r  J+ V
solid food. He had no hospitalizations or surgery,. R* E7 c# f# h9 O
and his psychosocial and psychomotor development. j# M2 q) z4 Z& Y
was age appropriate.! d* x( i( I$ _" P
The family history was remarkable for the father,$ G/ \$ ?$ J' U2 ]
who was diagnosed with hypothyroidism at age 16,+ U0 F) L3 h0 @- }; ?. I# P/ f  m
which was treated with thyroxine. The father’s8 Z0 u" R) Y! j/ l, e5 J( B1 t
height was 6 feet, and he went through a somewhat- s+ k* E% @/ R4 `# Y0 R& `% ^& ~
early puberty and had stopped growing by age 14.
  F4 Q" X9 R7 q3 O' [2 NThe father denied taking any other medication. The
. y% A# M" O" C* A+ \. v. y" S  qchild’s mother was in good health. Her menarche
! h, l3 {- {! V. Y$ D: e1 ^2 O  Uwas at 11 years of age, and her height was at 5 feet" X' T/ K- M5 p" c4 G$ P2 H
5 inches. There was no other family history of pre-
  X& S7 J$ C/ j/ k! gcocious sexual development in the first-degree rela-
9 {" y2 |' Q: \- P% Ztives. There were no siblings., x: |: s+ y' n) \! t2 j: _
Physical Examination) Q+ l# I) X- ?, {
The physical examination revealed a very active,2 i0 g7 V6 {$ Q0 n+ ^
playful, and healthy boy. The vital signs documented
2 z- M7 \# \) r3 d1 s( m+ h* n/ j0 e4 Ya blood pressure of 85/50 mm Hg, his length was
" [2 Y; _$ v* l5 Q+ P5 _% g90 cm (>97th percentile), and his weight was 14.4 kg
+ {  T- q% S; l(also >97th percentile). The observed yearly growth
8 o6 b; `6 K& X! F. A2 h+ cvelocity was 30 cm (12 inches). The examination of
( \. k, v' D, N) l7 g0 D: jthe neck revealed no thyroid enlargement.
# J2 E0 s) b/ @/ TThe genitourinary examination was remarkable for5 g1 x% f+ w5 i; y& m% R
enlargement of the penis, with a stretched length of$ {+ }4 H+ q+ J7 L- |8 j
8 cm and a width of 2 cm. The glans penis was very well9 Y9 z7 @5 k1 N4 k$ J) M
developed. The pubic hair was Tanner II, mostly around
7 a1 ?* Y! T9 e9 Y2 a+ e540
9 j& r: {( S9 J% n% a: Zat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
& I, q4 r6 R& Wthe base of the phallus and was dark and curled. The. N- c" e4 Q( y7 J8 K6 K" b
testicular volume was prepubertal at 2 mL each.; z& G* d7 E8 ^
The skin was moist and smooth and somewhat/ V2 X8 J5 S, M$ {- S( B) d
oily. No axillary hair was noted. There were no4 @9 ?9 l" ^0 S1 p/ C
abnormal skin pigmentations or café-au-lait spots.
  P4 c: K) _# p7 T# G. P: w( ]Neurologic evaluation showed deep tendon reflex 2+9 `# C" S# [+ c6 J* x
bilateral and symmetrical. There was no suggestion
- C% y% e4 N6 p+ _5 D9 [of papilledema.1 m5 ~+ Q6 S/ O8 Y# ]# c
Laboratory Evaluation
; B/ C6 O' X; G( }The bone age was consistent with 28 months by
+ _- q/ g) `/ e# pusing the standard of Greulich and Pyle at a chrono-0 }; e  T* V6 Y' K
logic age of 16 months (advanced).5 Chromosomal, J( o9 M# u# O
karyotype was 46XY. The thyroid function test
- }6 |  {' o* T" dshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
! |9 T1 v6 i! k# V" ?* J3 N# Mlating hormone level was 1.3 µIU/mL (both normal).
( A* b* _, I( k7 F  ^* {The concentrations of serum electrolytes, blood. g& X- t! K; ?
urea nitrogen, creatinine, and calcium all were
: v0 k! E. k4 |/ Y( U- Pwithin normal range for his age. The concentration2 F( c3 @9 F0 b1 G+ _6 }& Q* Q' L
of serum 17-hydroxyprogesterone was 16 ng/dL
6 ^& t) u0 m) `. @  R6 {  O(normal, 3 to 90 ng/dL), androstenedione was 20- F+ Z4 x) r/ K/ @$ H' p
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-, Y  }' I8 j' j( e; K* j
terone was 38 ng/dL (normal, 50 to 760 ng/dL),; v! Y% b5 F9 J9 A+ M' v% X9 q2 J  M& I! A
desoxycorticosterone was 4.3 ng/dL (normal, 7 to! G( \( p- E6 ?( X: [1 m& _
49ng/dL), 11-desoxycortisol (specific compound S)
0 {. w, Q( I1 J5 h$ `was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
4 w5 C, t; N  |! X3 E: Itisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
: k  D- I$ f! c! |- V& Vtestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
  H5 j7 B% Q6 X7 H6 l3 ^6 ?: O# iand β-human chorionic gonadotropin was less than9 v- g6 c- Z9 v
5 mIU/mL (normal <5 mIU/mL). Serum follicular
) y- `6 [; y1 ]# S1 |3 bstimulating hormone and leuteinizing hormone) B) M$ l2 N6 u6 S/ {
concentrations were less than 0.05 mIU/mL; }) R) [7 W6 E. U2 n, R% N6 \5 G$ }  D
(prepubertal).
8 z8 l) E$ S& @' s8 TThe parents were notified about the laboratory
1 j" R. N' |2 s; V7 V1 m5 r$ Hresults and were informed that all of the tests were0 N8 O: V( L9 c2 @
normal except the testosterone level was high. The
: ?% z6 g. o1 W5 g5 ufollow-up visit was arranged within a few weeks to
2 e; }+ Y  D! c- uobtain testicular and abdominal sonograms; how-
* n9 Z. z: R: xever, the family did not return for 4 months.6 {8 ~: w# P: \3 g1 k
Physical examination at this time revealed that the( `2 n6 C7 H7 j" U- o+ x8 _! W
child had grown 2.5 cm in 4 months and had gained, ~- D# e, A. B8 `% Z
2 kg of weight. Physical examination remained
' ]& F( ~, E1 X+ F5 i7 w( l: bunchanged. Surprisingly, the pubic hair almost com-
& O6 @& ^- _6 C8 l* vpletely disappeared except for a few vellous hairs at1 {# R$ P8 Q1 v1 s4 X% q
the base of the phallus. Testicular volume was still 2
" N3 X' x% u9 N8 p! x  rmL, and the size of the penis remained unchanged.
/ L3 }  g2 R8 E- r+ R' m, N/ {, IThe mother also said that the boy was no longer hav-/ ]: C& A* N+ j7 V2 t. D2 v, E
ing frequent erections.
* J4 M3 T' o+ u0 rBoth parents were again questioned about use of
# c' s9 K1 ~: A$ c7 gany ointment/creams that they may have applied to6 y* i9 v! g7 R: }9 ]
the child’s skin. This time the father admitted the
- P0 I4 ^# d. b) x' K, t( WTopical Testosterone Exposure / Bhowmick et al 541( W- O1 p1 r* p8 B) r2 L5 i7 b
use of testosterone gel twice daily that he was apply-7 h* Y/ m. V- x
ing over his own shoulders, chest, and back area for
6 Z/ Y+ g4 O# ?. R2 xa year. The father also revealed he was embarrassed6 z/ v  \0 X3 l8 ^: a. l
to disclose that he was using a testosterone gel pre-
/ L+ T4 b9 n0 T& f2 k' }, Vscribed by his family physician for decreased libido
5 S$ e1 C, x# N: bsecondary to depression.& `1 s& t9 K% D) L
The child slept in the same bed with parents.1 k8 \- b% F& W1 [
The father would hug the baby and hold him on his
$ @7 Y0 b- O) [; }: rchest for a considerable period of time, causing sig-
% \0 @. N- U. h% |nificant bare skin contact between baby and father.
: i1 q8 y" i* fThe father also admitted that after the phone call,+ o6 w' d/ ^3 c0 M. d$ k8 b+ n
when he learned the testosterone level in the baby
, \$ x/ ?1 R0 C! i8 _was high, he then read the product information
( ~3 ]$ T1 \# u8 y3 Y8 ^+ Lpacket and concluded that it was most likely the rea-( T1 r8 p' W( d) v
son for the child’s virilization. At that time, they
/ A: [6 T" D) m' \/ r# O* N+ |9 e8 Ndecided to put the baby in a separate bed, and the
5 U% h% m; Q5 {7 S' m. s# bfather was not hugging him with bare skin and had
% f0 l/ P& U  A* h( Abeen using protective clothing. A repeat testosterone; U% Z$ \* j. F! Q1 E
test was ordered, but the family did not go to the# K5 `6 L7 G! x! m; w$ Q
laboratory to obtain the test.  n$ Q: b; T8 r, Y1 D+ z
Discussion, w3 [- h0 F) t4 w  @) ~7 }
Precocious puberty in boys is defined as secondary' E! m0 C7 s/ N3 M+ t2 ?
sexual development before 9 years of age.1,4
! U$ D: t9 a3 u2 H8 U2 o5 YPrecocious puberty is termed as central (true) when
: P4 A, V5 q: |+ U( Vit is caused by the premature activation of hypo-
5 j# ~- f6 T! L, h! ithalamic pituitary gonadal axis. CPP is more com-
( Z3 |& q& Q5 z' Pmon in girls than in boys.1,3 Most boys with CPP) i/ [3 I- N3 S2 ?2 ^& S
may have a central nervous system lesion that is, Z, n/ a$ h9 J. }
responsible for the early activation of the hypothal-4 ]5 ?) n3 A4 e. ?4 L; p2 o. a
amic pituitary gonadal axis.1-3 Thus, greater empha-7 v" v: h7 K$ b6 D- l$ b# ]- v1 O
sis has been given to neuroradiologic imaging in
+ |8 w8 B4 ^. \; z* m0 {3 xboys with precocious puberty. In addition to viril-
$ l8 p- v% K& `1 lization, the clinical hallmark of CPP is the symmet-9 f. j- n0 h% u2 o
rical testicular growth secondary to stimulation by
' [" `/ D6 V2 m& N2 T- F/ I& ygonadotropins.1,3
3 [+ ]# _" H3 o5 l7 wGonadotropin-independent peripheral preco-
* p- m9 s8 J8 x8 X( Kcious puberty in boys also results from inappropriate
- O; r% i0 p8 d9 h+ mandrogenic stimulation from either endogenous or# u3 \4 J1 f( S" s! `3 s
exogenous sources, nonpituitary gonadotropin stim-
- j9 P3 P' m7 P! i. q, ?. ~9 |. Pulation, and rare activating mutations.3 Virilizing
  {2 Y: y8 c& Jcongenital adrenal hyperplasia producing excessive
2 p! A' d9 d. G; r4 u: |) z( \1 Eadrenal androgens is a common cause of precocious
) [7 v6 v1 U/ e/ q( j$ u9 N% gpuberty in boys.3,4
" a, t9 W2 B& w# x- \0 oThe most common form of congenital adrenal
+ T6 W: Q' J: T' H* S  X; A3 c7 [7 Dhyperplasia is the 21-hydroxylase enzyme deficiency." c' x% E6 P9 y* N5 [2 R
The 11-β hydroxylase deficiency may also result in
" ^$ F$ h# n$ Lexcessive adrenal androgen production, and rarely,3 a! e- l4 x* v4 N% x) I) z# G0 J
an adrenal tumor may also cause adrenal androgen) t0 [$ c1 g9 e- {, G
excess.1,3
3 J( u" T$ @/ I3 K- K  |at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
  }" r7 e# k" D& f542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
% h& ]/ ~$ e! v3 [  p; R  J4 GA unique entity of male-limited gonadotropin-
8 F1 l  q  H( P2 q% w! x( ^, J0 k0 Kindependent precocious puberty, which is also known: Z9 J3 U" K" @6 e1 f
as testotoxicosis, may cause precocious puberty at a
- `9 Z8 Q, ]. avery young age. The physical findings in these boys+ t( G  M- d, R6 A
with this disorder are full pubertal development,0 q# ~3 n* D3 @5 O. E, \5 t5 r- S$ U
including bilateral testicular growth, similar to boys
# }/ U4 h+ o3 R+ k. L; Kwith CPP. The gonadotropin levels in this disorder
2 L! n; i6 K/ a0 T5 zare suppressed to prepubertal levels and do not show; A! _# C+ [- c  X! S  t3 T
pubertal response of gonadotropin after gonadotropin-# m1 n0 ~: f" x4 q3 z; p
releasing hormone stimulation. This is a sex-linked
2 F; S7 W& Y9 J3 G+ }6 c7 xautosomal dominant disorder that affects only
5 m! |. C# v# }2 x9 v4 gmales; therefore, other male members of the family; F1 x- T- q+ O' q9 L! z: [
may have similar precocious puberty.3; @5 C  M, j8 W0 s9 o8 d, E5 B* g7 Z
In our patient, physical examination was incon-
# z6 r: C$ D% @. Jsistent with true precocious puberty since his testi-. G  L- l" x# S) Q: Q) A' v$ U
cles were prepubertal in size. However, testotoxicosis
1 p0 [+ [- W$ I/ z/ E% j' vwas in the differential diagnosis because his father7 B/ S& U* W5 }" m3 J, v
started puberty somewhat early, and occasionally,
5 r+ c, Q# H5 p- m! g6 Ftesticular enlargement is not that evident in the$ f; J" y* A7 H* b  N" R
beginning of this process.1 In the absence of a neg-* K! u7 Z" ]/ j. C) e4 Z& `
ative initial history of androgen exposure, our
" Z! t! j# }2 \. hbiggest concern was virilizing adrenal hyperplasia,6 s, M3 g: A; R, m8 Y4 @4 n
either 21-hydroxylase deficiency or 11-β hydroxylase6 K0 G$ c5 l& M: G
deficiency. Those diagnoses were excluded by find-
7 U) K* [+ G' D6 Wing the normal level of adrenal steroids." t, Q' Q. y" F) g  R0 \1 p
The diagnosis of exogenous androgens was strongly2 C8 e" U) W' `: [" b9 s
suspected in a follow-up visit after 4 months because
  I1 t, w2 k$ h& ithe physical examination revealed the complete disap-
4 S, p. Z- `% K: G3 t: F  G3 H+ hpearance of pubic hair, normal growth velocity, and: {* ^- l" [- ^% m; }8 x, E. y, t
decreased erections. The father admitted using a testos-7 d3 y% C- B0 {3 j# E, B9 k8 G( R
terone gel, which he concealed at first visit. He was1 o8 U; k6 {6 o5 s) M0 _9 h: }6 |3 f
using it rather frequently, twice a day. The Physicians’
) A* ]# T# s& x3 z! r% KDesk Reference, or package insert of this product, gel or
3 f1 W& U0 `. T  G% r) r( rcream, cautions about dermal testosterone transfer to% k3 w. l3 n- [: `! z& B
unprotected females through direct skin exposure.( `0 q* w1 T6 E+ a
Serum testosterone level was found to be 2 times the
! z4 E0 D) m; p1 W! Jbaseline value in those females who were exposed to
) j1 C) ?: a9 F- h6 t7 O# `4 @5 g: eeven 15 minutes of direct skin contact with their male+ x) Q8 F5 f+ A- r6 p; K) L
partners.6 However, when a shirt covered the applica-/ f: J/ V& U7 E9 _4 S3 W
tion site, this testosterone transfer was prevented./ k. |- W8 s9 ?+ m
Our patient’s testosterone level was 60 ng/mL,
9 I% C0 U. @4 U; E( Swhich was clearly high. Some studies suggest that
( ?: X# ]: E$ Q3 Xdermal conversion of testosterone to dihydrotestos-8 I6 O: y+ l- s* s  Y
terone, which is a more potent metabolite, is more
+ m. Q+ H6 l! y! K- |) {active in young children exposed to testosterone
# @2 p4 C$ N) lexogenously7; however, we did not measure a dihy-+ l& p; K, S6 M5 M! G. C
drotestosterone level in our patient. In addition to  Q/ y6 H/ @# Y  i8 Z
virilization, exposure to exogenous testosterone in
1 j9 r; A4 c# m5 lchildren results in an increase in growth velocity and# N0 H/ o. P" C* u" j
advanced bone age, as seen in our patient.
5 F  M1 E$ u# D& t9 N0 w7 GThe long-term effect of androgen exposure during0 z/ ]/ g# G7 o8 a
early childhood on pubertal development and final
8 |+ p) D% z/ `adult height are not fully known and always remain
" ^8 A$ W% O$ X: k( t) U9 R0 Za concern. Children treated with short-term testos-
  v7 k( x. s9 q: N5 wterone injection or topical androgen may exhibit some
; x% K2 I- g% g3 B1 K, xacceleration of the skeletal maturation; however, after/ W3 [6 S% c" i' f/ z- J1 d5 k
cessation of treatment, the rate of bone maturation
) R- x' C1 Q) `2 Z2 g0 vdecelerates and gradually returns to normal.8,9
/ e0 K+ d; H) ]$ x. K1 p( [' [  g9 wThere are conflicting reports and controversy
  X# I% K! Z, S1 L) q: fover the effect of early androgen exposure on adult6 l+ u4 N: c; g4 N2 e$ @- |9 A
penile length.10,11 Some reports suggest subnormal$ J) F# a' {1 x
adult penile length, apparently because of downreg-3 d5 @1 p1 z9 U+ U1 F) P- W
ulation of androgen receptor number.10,12 However,# U1 L& |% U: m( H% F
Sutherland et al13 did not find a correlation between- F2 h3 D- c' B- D
childhood testosterone exposure and reduced adult, I' {1 D7 A) F, K' d% o$ P
penile length in clinical studies.6 A- d. g, H! p/ U% L# G! s
Nonetheless, we do not believe our patient is) ~& @: z8 l* [1 w
going to experience any of the untoward effects from" ?7 M) L) ?, `' w  Q- i3 I9 R
testosterone exposure as mentioned earlier because* f# V) q$ b. \7 z) w
the exposure was not for a prolonged period of time.5 B  O+ t' y/ i8 C
Although the bone age was advanced at the time of
. w* Q* Y, ]; a0 Rdiagnosis, the child had a normal growth velocity at
& D$ S/ F: `  b: Gthe follow-up visit. It is hoped that his final adult1 Y/ l7 `- H9 t( @) d0 {
height will not be affected.& P) }; p9 l8 W5 B
Although rarely reported, the widespread avail-/ R9 F: r/ n6 C  R, w* v. G8 l
ability of androgen products in our society may
% |# |5 m' E; n: t, q3 T2 pindeed cause more virilization in male or female* e) I0 Q; ^  k0 N" \
children than one would realize. Exposure to andro-
' x! z  p; E5 Z; W  k% hgen products must be considered and specific ques-
, X7 Z8 ?/ u+ \+ e8 ^, x% |tioning about the use of a testosterone product or* {/ s8 N$ g6 s+ `6 O1 l& N, q
gel should be asked of the family members during2 ^7 V) R* C' U2 Y& z
the evaluation of any children who present with vir-
& j: u7 g  }  @) M5 G3 m; E! ]ilization or peripheral precocious puberty. The diag-' n0 m! l& z2 R; M1 U7 g& J
nosis can be established by just a few tests and by
( Y3 O) S4 G! c* m7 y0 A' vappropriate history. The inability to obtain such a! K: K) j" o  t3 L
history, or failure to ask the specific questions, may
, y* ?( l7 u  u* @6 Zresult in extensive, unnecessary, and expensive( K+ W6 d9 y% R
investigation. The primary care physician should be
1 b# t, a6 m0 Q- y7 _. Q; Oaware of this fact, because most of these children5 b) A, C. Y8 l- j
may initially present in their practice. The Physicians’
5 Q! x5 F% W) v9 v/ ~Desk Reference and package insert should also put a1 ~' i" J  ~7 F
warning about the virilizing effect on a male or
; o- k3 `$ L" ]- ?: t) [female child who might come in contact with some-5 Y' e3 u. |( O; H' W7 g( M( N" x
one using any of these products.- e( ]8 ~2 z) e0 @6 X4 I
References
6 [4 r% W' R' [' I3 n0 D3 c1. Styne DM. The testes: disorder of sexual differentiation
2 y9 v) ?: W3 J: W- x$ T0 F0 band puberty in the male. In: Sperling MA, ed. Pediatric+ u( d& f- J+ w+ w5 Q" X
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;# h7 _5 l0 S) y* U# a
2002: 565-628.
/ Y, `3 P6 T" u* K+ }2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
" b. [) i3 W) k4 S8 \1 G  B, W1 Xpuberty in children with tumours of the suprasellar pineal
發表於 2025-1-7 21:59:43 | 顯示全部樓層
這個我收藏了!謝謝分享!WK的資源越來越豐富,這少不了大大的辛勞!
發表於 2025-1-10 10:43:39 | 顯示全部樓層
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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
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4个什么样的?
發表於 2025-1-19 02:41:05 | 顯示全部樓層

0 D: H, C8 v  y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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