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鄉下的妹子太便宜,一次四個都要了[12P]

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Sexual Precocity in a 16-Month-Old1 x$ }. b, M* z+ S
Boy Induced by Indirect Topical
0 [: q7 [! }8 T6 C  Q0 `, K; G- QExposure to Testosterone
2 x' j8 a/ T8 k# E: h8 eSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,27 R4 l; v( I% Z* }
and Kenneth R. Rettig, MD1
) K. X8 K: y( P% j. e1 @Clinical Pediatrics+ y! b$ @' v1 C  q9 F
Volume 46 Number 6/ s! N$ o6 u! B4 ]: u1 U
July 2007 540-543) x# Q; J7 c5 {3 J) G
© 2007 Sage Publications9 d( A* ]0 b! _% x1 N9 @
10.1177/0009922806296651. ?1 e+ }# ~) ]" d
http://clp.sagepub.com' X- ^# [; M( I  f7 J3 f
hosted at
: v) E. T- |9 T+ T! hhttp://online.sagepub.com
& P3 |3 o* U. R8 p% D, i0 s7 m; P( _. qPrecocious puberty in boys, central or peripheral,
. w  Y  _( F1 Y% p$ A+ c4 ]" uis a significant concern for physicians. Central3 _. D7 q- j) _) f9 w
precocious puberty (CPP), which is mediated
1 K: ]2 n# W' k; m( j) E# zthrough the hypothalamic pituitary gonadal axis, has+ V$ |7 u/ g1 s6 e1 f+ H5 Y) U. p6 m
a higher incidence of organic central nervous system4 v- g. x( V: S' m& r
lesions in boys.1,2 Virilization in boys, as manifested, L' d' z' J6 d2 F% v9 a9 a
by enlargement of the penis, development of pubic
5 ^" z) K7 s) Y9 C. Q) _hair, and facial acne without enlargement of testi-
4 p& b) q) @0 I- B" U6 u. S  |! Qcles, suggests peripheral or pseudopuberty.1-3 We
; w- L0 M3 k! G5 n5 i4 D( s+ ~report a 16-month-old boy who presented with the
) p; b3 F% p: q! m6 f% A! p2 D) Benlargement of the phallus and pubic hair develop-
9 w8 t6 K- [/ \  `/ {; I) wment without testicular enlargement, which was due
  e1 a$ I9 a) u" c6 i4 r( Ato the unintentional exposure to androgen gel used by" C* R+ j4 a; `3 D( c3 ~
the father. The family initially concealed this infor-& G* ]  O5 P* \. F
mation, resulting in an extensive work-up for this4 a7 q' n: p9 Q4 S- \/ p
child. Given the widespread and easy availability of- _) K5 u2 A/ O( L% X+ [
testosterone gel and cream, we believe this is proba-
  B1 V8 e! R# b6 V( ~bly more common than the rare case report in the
7 D& P6 O0 W0 B3 }3 j: p2 ^literature.4
6 l9 t, `/ [) K3 b. J0 tPatient Report  ^7 H) |% _+ I: c$ E
A 16-month-old white child was referred to the
* p$ {$ k4 v/ cendocrine clinic by his pediatrician with the concern
, R1 k1 |, k4 y% lof early sexual development. His mother noticed
" m* r6 W5 g8 f$ F0 Hlight colored pubic hair development when he was
, s( E1 }* B' h( r9 m0 A- HFrom the 1Division of Pediatric Endocrinology, 2University of8 A  a' O) C/ h" J# O
South Alabama Medical Center, Mobile, Alabama.
7 r$ C* F: b; s" k; X$ u( \/ s& fAddress correspondence to: Samar K. Bhowmick, MD, FACE,
$ \$ J% `. z0 v, @# rProfessor of Pediatrics, University of South Alabama, College of
( r' [2 Q4 p. B$ E+ [( g$ cMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
- C, A& b4 Z6 q4 u# A0 Y/ D/ Ae-mail: [email protected].
0 g% g; U" a. Mabout 6 to 7 months old, which progressively became
& s  o  j/ w: Z6 O! Y! ~darker. She was also concerned about the enlarge-
' W9 a$ _6 f9 V. _& |ment of his penis and frequent erections. The child
  a0 x; K3 U! ?2 C  Z$ t9 _was the product of a full-term normal delivery, with4 L; H; F7 Y$ x. V2 v
a birth weight of 7 lb 14 oz, and birth length of
/ M  b% Y  s( h20 inches. He was breast-fed throughout the first year* q" `0 E. z* f
of life and was still receiving breast milk along with8 E: X% h. k) b  @/ C6 E
solid food. He had no hospitalizations or surgery,
' X3 _+ u/ u3 u; fand his psychosocial and psychomotor development' n1 x. F7 U/ T5 V4 H) z0 W6 k
was age appropriate.: X" {0 x4 M8 Y! J. L6 ^/ e
The family history was remarkable for the father,
6 Y& j! {+ ~' b& t& R# xwho was diagnosed with hypothyroidism at age 16,8 z+ u, u$ R8 T3 J
which was treated with thyroxine. The father’s
5 Y( c/ r0 a5 G; ~- Kheight was 6 feet, and he went through a somewhat
6 q: J+ B% _8 `" C& xearly puberty and had stopped growing by age 14.% v2 l* ~5 y: J2 b* I5 J
The father denied taking any other medication. The$ `* S$ I& s3 w, c
child’s mother was in good health. Her menarche. {" \4 x& a/ s% H& @
was at 11 years of age, and her height was at 5 feet
% d% ^( U- r4 a) w5 _  z" i5 inches. There was no other family history of pre-
' n, {2 l' k# ~5 t  ~' Q) xcocious sexual development in the first-degree rela-" S% R7 d5 R+ c$ ]! d) O; Q( v
tives. There were no siblings.
) N6 Y# o& i- \8 ]+ |) PPhysical Examination
; ~! X3 }3 o# a. f5 rThe physical examination revealed a very active,1 v" t. R3 F7 S0 C+ e) T
playful, and healthy boy. The vital signs documented
) P- y4 l% f0 e( L' r. H* k# wa blood pressure of 85/50 mm Hg, his length was
2 r( X6 N7 q0 j; s90 cm (>97th percentile), and his weight was 14.4 kg; Y* W: @6 |; a
(also >97th percentile). The observed yearly growth3 ?  p6 a. T2 @7 J
velocity was 30 cm (12 inches). The examination of
4 l2 r8 @4 c& u3 H: P7 x+ hthe neck revealed no thyroid enlargement.% n3 Q. {: z4 ~5 G& g; d4 n; ?) O5 g% ~
The genitourinary examination was remarkable for$ ^5 u' _( G  h  `9 T0 B
enlargement of the penis, with a stretched length of3 v% e& Y6 @" k9 D7 g
8 cm and a width of 2 cm. The glans penis was very well, _1 s& ?0 S/ {& I
developed. The pubic hair was Tanner II, mostly around
( A# m5 J! P+ E- O5406 i, M0 q5 [, V* |' U
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from* J$ R* ?" k4 D6 H8 _
the base of the phallus and was dark and curled. The
3 c! H( H* ?+ Htesticular volume was prepubertal at 2 mL each.
6 H0 [4 u/ b* QThe skin was moist and smooth and somewhat2 h2 g. L. b. b6 X2 ?1 ~
oily. No axillary hair was noted. There were no1 V5 d* a$ d- W# u1 s/ `
abnormal skin pigmentations or café-au-lait spots.9 b/ F% k7 s; ^  T2 W8 Q( a- I1 h
Neurologic evaluation showed deep tendon reflex 2+
9 l" W2 a( _$ C4 X% r! u/ wbilateral and symmetrical. There was no suggestion
' B6 e7 L6 v3 d* S' O, ?/ i! S4 ^of papilledema.
7 L+ G7 T) ?4 g$ [Laboratory Evaluation
% Y% ?- o5 i, r1 mThe bone age was consistent with 28 months by
6 v! {/ u$ a; Husing the standard of Greulich and Pyle at a chrono-- v+ j$ L4 e! k2 a
logic age of 16 months (advanced).5 Chromosomal( V' J6 V) S0 @# b  G
karyotype was 46XY. The thyroid function test
5 f3 Y: T4 y+ a8 n; C+ t/ G8 Ishowed a free T4 of 1.69 ng/dL, and thyroid stimu-5 m3 j- ?' o% _! L+ K9 g  g/ ?
lating hormone level was 1.3 µIU/mL (both normal).
5 D- r: s* W- eThe concentrations of serum electrolytes, blood
: f6 p% r% g; p9 p3 Q$ m" r% Surea nitrogen, creatinine, and calcium all were
9 u7 i  B9 L3 Q- {within normal range for his age. The concentration6 |' g- T# F2 t5 j# V- w% _) m
of serum 17-hydroxyprogesterone was 16 ng/dL
; e2 K* W9 d9 c* K9 W& v4 s% [' a(normal, 3 to 90 ng/dL), androstenedione was 20  s; s( H% _- t; W7 X9 s
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
7 M* n2 _/ T% W7 Jterone was 38 ng/dL (normal, 50 to 760 ng/dL),
8 f9 h* A- i. s& gdesoxycorticosterone was 4.3 ng/dL (normal, 7 to
- E; S) B# D5 L6 j49ng/dL), 11-desoxycortisol (specific compound S)
; V) N6 x) i# p* q$ c: lwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
* i" Y, [0 {* t- ?tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
' A' v: Q- f. v: t; Htestosterone was 60 ng/dL (normal <3 to 10 ng/dL),: r! W4 z8 P8 J0 J2 d2 p! u& e: V% f
and β-human chorionic gonadotropin was less than# h& S- k6 A" D+ r6 D
5 mIU/mL (normal <5 mIU/mL). Serum follicular
4 w- L+ o# ?: C" i1 W+ {stimulating hormone and leuteinizing hormone
, B$ Q* E0 H% R3 Sconcentrations were less than 0.05 mIU/mL
' I4 ?+ C# Z8 _, _6 ^$ f(prepubertal)., R% d" Q! E4 q
The parents were notified about the laboratory
! ~# N* }3 W: jresults and were informed that all of the tests were
, b* P$ h9 k0 jnormal except the testosterone level was high. The
. h; I- H- i0 J4 Ufollow-up visit was arranged within a few weeks to, C7 o! m9 a( M; A$ R$ r
obtain testicular and abdominal sonograms; how-6 n9 |1 \& G; E& d  O. j3 o% ]
ever, the family did not return for 4 months.1 i8 C9 i7 P2 M6 h$ Q
Physical examination at this time revealed that the- P1 z% d+ _/ a- O$ }6 Y7 A; g
child had grown 2.5 cm in 4 months and had gained+ |* H: J6 i; A% E
2 kg of weight. Physical examination remained0 L$ W) n9 i8 V0 m4 q$ c
unchanged. Surprisingly, the pubic hair almost com-& n% k3 |5 q  _5 A. H% f
pletely disappeared except for a few vellous hairs at* l! c' F- k& x$ L$ Q: M
the base of the phallus. Testicular volume was still 2
5 B- |# U5 `7 _: mmL, and the size of the penis remained unchanged.& C- U: E7 h& o+ R2 T* j4 k
The mother also said that the boy was no longer hav-
1 q. D& z' ]* L$ Hing frequent erections.
. c8 g# d7 K; c0 n. |& e& }- sBoth parents were again questioned about use of* t$ }2 t& d* z
any ointment/creams that they may have applied to4 w9 k6 q% @8 Y
the child’s skin. This time the father admitted the
( @$ f7 }4 G# H. u* ITopical Testosterone Exposure / Bhowmick et al 541( {9 G% i+ f+ j- {: Q7 x
use of testosterone gel twice daily that he was apply-
) L2 O+ o- M, ^9 V3 ving over his own shoulders, chest, and back area for
/ H5 S5 V; i" c. La year. The father also revealed he was embarrassed
7 R+ k8 u) G* K3 {to disclose that he was using a testosterone gel pre-) [, ?8 c7 ]( {+ N+ ?: L
scribed by his family physician for decreased libido
7 P3 o% n7 }/ u1 Y& ysecondary to depression.
0 \* m+ s8 r4 c7 ?% yThe child slept in the same bed with parents.
" }+ J$ r/ r& ~) GThe father would hug the baby and hold him on his
0 y: F* w2 S/ q) f- [# cchest for a considerable period of time, causing sig-5 E0 b6 e; B; P
nificant bare skin contact between baby and father.+ S' h8 ^. j$ S% Z$ N
The father also admitted that after the phone call,
$ Y+ G0 B5 k! D$ N* S, x' U2 Lwhen he learned the testosterone level in the baby7 [5 M, U7 m2 g; N+ p2 \* r
was high, he then read the product information+ x4 ?  d0 _# G4 F
packet and concluded that it was most likely the rea-* r- m/ d+ o! d
son for the child’s virilization. At that time, they
7 q- v% K- W4 ]) \decided to put the baby in a separate bed, and the
, F% B0 q8 A0 E3 G: M& Afather was not hugging him with bare skin and had
/ O8 i3 R% Y; C; ]9 v$ l9 U+ dbeen using protective clothing. A repeat testosterone
* b% z+ T# F: P/ rtest was ordered, but the family did not go to the& Q& h7 \" `7 r# N6 A
laboratory to obtain the test.
$ c5 w$ P( R, x) F- O- y& GDiscussion2 A4 t+ t1 i# E6 a
Precocious puberty in boys is defined as secondary' S7 a; |2 c* z  \1 l8 _4 i
sexual development before 9 years of age.1,4
7 T" J7 H' m/ o, \Precocious puberty is termed as central (true) when
. r7 Q: d6 l, mit is caused by the premature activation of hypo-1 z3 d; z5 d8 U3 A8 z8 h  ]
thalamic pituitary gonadal axis. CPP is more com-$ l- U5 b; W8 S  y4 S
mon in girls than in boys.1,3 Most boys with CPP
: r0 S1 n% v5 |$ ?& i( U# v# imay have a central nervous system lesion that is( [4 J% _+ ~% y8 a  ?6 Z" O& Y; }
responsible for the early activation of the hypothal-
3 @* Y( V( ]8 V" ]% Jamic pituitary gonadal axis.1-3 Thus, greater empha-% [! V# H& U' R
sis has been given to neuroradiologic imaging in
7 M# n9 ^) t' x, o9 O4 j% o# @+ u% S5 aboys with precocious puberty. In addition to viril-
6 O+ }0 c7 i% ^, f( f: z0 kization, the clinical hallmark of CPP is the symmet-
, K7 t; p+ E( q. S! \' hrical testicular growth secondary to stimulation by( L& g  @1 H+ O' J* A
gonadotropins.1,35 |( V2 w; u) I. c2 q+ d
Gonadotropin-independent peripheral preco-
9 j. H7 m* m# H* x% x& S! B" Ycious puberty in boys also results from inappropriate9 k0 n1 Z* K7 `$ I0 s( _" L( L
androgenic stimulation from either endogenous or7 T2 q4 n( c8 q
exogenous sources, nonpituitary gonadotropin stim-
6 J/ ~4 ~7 N" N' |. _! dulation, and rare activating mutations.3 Virilizing. C8 a1 |, f. ~: g* t1 j/ T
congenital adrenal hyperplasia producing excessive
; O8 a' ~/ k8 ]2 [# jadrenal androgens is a common cause of precocious4 T" m3 c3 Z+ H0 ?
puberty in boys.3,46 P, o6 J, M1 ^/ O4 c0 m
The most common form of congenital adrenal
. C& Z* g# O8 O4 _- h/ Q  k2 ]hyperplasia is the 21-hydroxylase enzyme deficiency.9 h* k% K; Q' u7 v9 t
The 11-β hydroxylase deficiency may also result in
" V( y5 z. u1 A1 Aexcessive adrenal androgen production, and rarely,* A8 n/ _& B5 W1 B" S
an adrenal tumor may also cause adrenal androgen9 Q& [$ W6 [6 q# a$ E8 u
excess.1,30 d% s  T8 U; Y8 i3 C9 Z0 _* T
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from' K3 s8 k- W) j' A
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007# ?! F3 T8 J9 `
A unique entity of male-limited gonadotropin-
0 V8 ~* \% d7 h; k4 ]independent precocious puberty, which is also known
$ W$ n5 {9 e+ R1 k1 j4 w& Bas testotoxicosis, may cause precocious puberty at a
& Y* M" H9 R/ O. ~+ p& R) jvery young age. The physical findings in these boys
) s* V+ Q9 R* @with this disorder are full pubertal development,. o7 m* k6 f' O0 {& G0 \* Q# k
including bilateral testicular growth, similar to boys
: O4 Z  b9 B: S, d9 iwith CPP. The gonadotropin levels in this disorder+ q9 f1 G% ^$ B2 ^# `( `
are suppressed to prepubertal levels and do not show
2 i& ]! K3 @! L; @9 c& I! {" ~pubertal response of gonadotropin after gonadotropin-
( {& B9 p1 E$ x/ ~  H7 r& sreleasing hormone stimulation. This is a sex-linked
* j; k5 q9 h  X# ^& g3 g% Wautosomal dominant disorder that affects only4 ]! l( A" g! J& d8 A! T& J+ G
males; therefore, other male members of the family5 S" V* @) V) ]* o! q
may have similar precocious puberty.3- C- Y$ ~! p& H7 K: e0 H2 q5 E
In our patient, physical examination was incon-: S; q3 `& i6 v: c" {8 h- b0 `
sistent with true precocious puberty since his testi-/ B1 K4 ]* ]2 \5 {2 Z
cles were prepubertal in size. However, testotoxicosis/ v. v5 A! m& f) A
was in the differential diagnosis because his father7 V1 m! N- V" b7 q! ]; W# l0 d
started puberty somewhat early, and occasionally,+ V9 G. O- U2 S" m$ k
testicular enlargement is not that evident in the
( Y" f6 {$ R" k2 w# {; K( gbeginning of this process.1 In the absence of a neg-
! Q  \. P! [9 v$ n! b8 V$ Y6 Pative initial history of androgen exposure, our
# F' m4 ?. o1 Y( bbiggest concern was virilizing adrenal hyperplasia,
1 _( P0 g$ c; t3 ^( ?. y+ [/ Aeither 21-hydroxylase deficiency or 11-β hydroxylase
9 j! y9 A. R1 o5 k2 l8 fdeficiency. Those diagnoses were excluded by find-
2 T- J$ Q- a0 \5 V4 k: H" c4 l% ting the normal level of adrenal steroids.: |/ ^! w) s* o  w( O& R  m& G
The diagnosis of exogenous androgens was strongly
; ^" H" s. N+ R9 f& i; p5 k% osuspected in a follow-up visit after 4 months because2 G: d$ S% x6 u  H6 y
the physical examination revealed the complete disap-
3 Y( W' N5 D4 Q; [0 o6 z9 hpearance of pubic hair, normal growth velocity, and* k  @4 r8 ]) N
decreased erections. The father admitted using a testos-
/ B- U$ M) J3 ^; I% G3 Yterone gel, which he concealed at first visit. He was
% ~. B# M$ p" V* w' d% e1 `using it rather frequently, twice a day. The Physicians’, P  C) d3 {/ V' `0 u4 {
Desk Reference, or package insert of this product, gel or
$ U3 Z* g! X6 i# x" ~cream, cautions about dermal testosterone transfer to! E4 L5 }/ `+ T% A& F3 p: V
unprotected females through direct skin exposure.
( n" d0 w% C6 p5 fSerum testosterone level was found to be 2 times the, X4 n! u: Z6 ]/ F
baseline value in those females who were exposed to
, g0 n. A2 [$ t! q' g3 t( X/ ^0 beven 15 minutes of direct skin contact with their male
& r+ V+ z* ~  ~" Bpartners.6 However, when a shirt covered the applica-
* j2 T1 h& Z+ p7 S5 H( b5 ition site, this testosterone transfer was prevented.
  W( B: |- ]( w* ~1 e& xOur patient’s testosterone level was 60 ng/mL,) ~; w) c" b9 v
which was clearly high. Some studies suggest that" K1 g) H, q+ x% n2 L
dermal conversion of testosterone to dihydrotestos-% _% r0 M/ |7 c/ G  w
terone, which is a more potent metabolite, is more
! X. {& I2 Y7 k. \4 oactive in young children exposed to testosterone9 ^; r4 U2 b9 B! p
exogenously7; however, we did not measure a dihy-
1 M# J6 U( a4 n3 p0 adrotestosterone level in our patient. In addition to5 Q* U% a! e8 A
virilization, exposure to exogenous testosterone in
" i+ N; n& w9 D; U* cchildren results in an increase in growth velocity and3 b5 ]- m" D3 i3 A; Q+ j
advanced bone age, as seen in our patient.% ^5 Q$ e5 f; Q# ]
The long-term effect of androgen exposure during
8 ~; n9 f1 }6 l3 fearly childhood on pubertal development and final$ W- `2 O  @1 Y
adult height are not fully known and always remain6 y. ?+ f7 a8 A
a concern. Children treated with short-term testos-
- v0 m1 D# L2 |: Y- jterone injection or topical androgen may exhibit some
8 h* i( C- m# y5 S% \acceleration of the skeletal maturation; however, after
5 u. M4 w' \" j( r" c! m3 q* r; P' d9 icessation of treatment, the rate of bone maturation6 K# K5 B( c1 U% C+ p, }
decelerates and gradually returns to normal.8,9: j( f- C" i8 X6 e/ R( X
There are conflicting reports and controversy
- p/ R: C, o0 R. h2 s, [over the effect of early androgen exposure on adult
2 x+ K9 `  h8 wpenile length.10,11 Some reports suggest subnormal8 z1 T1 Y# v) C" I; l
adult penile length, apparently because of downreg-! e# s: I8 c5 V* ~& D
ulation of androgen receptor number.10,12 However,
6 z1 o9 ~/ i2 J7 `; \# y" HSutherland et al13 did not find a correlation between* ~. _; E( z' A& b
childhood testosterone exposure and reduced adult
6 ?: o, @/ f- n3 }# tpenile length in clinical studies.6 ~. Z$ e  C7 r9 c
Nonetheless, we do not believe our patient is/ W- A! L% B) P7 w, v+ W
going to experience any of the untoward effects from
5 ^& c+ ]! {$ C$ O- Ctestosterone exposure as mentioned earlier because7 r# S4 N0 N9 d+ B% m4 Z, ?
the exposure was not for a prolonged period of time.+ g* E' H: X; [( k
Although the bone age was advanced at the time of, G: Q5 ?: n9 d1 f
diagnosis, the child had a normal growth velocity at
/ e9 ~# b6 t  r9 }8 @) _% bthe follow-up visit. It is hoped that his final adult
2 J: c8 ~; {+ f5 x2 |, ~$ Lheight will not be affected.
* k, k6 f# ^* U" r+ C6 P" c1 e5 SAlthough rarely reported, the widespread avail-
* }% h& l, I1 i- n( N' t+ [3 B& B% ^ability of androgen products in our society may
2 `6 r5 U$ ]  }- B0 [- Lindeed cause more virilization in male or female8 _7 x7 V% K; s" v8 p; H
children than one would realize. Exposure to andro-
: h" L. T( {9 {! O. s- F; Ngen products must be considered and specific ques-* P0 n7 g! o0 H3 a
tioning about the use of a testosterone product or* E0 u+ y: H' |
gel should be asked of the family members during/ ~+ W; J* `2 k+ [/ g
the evaluation of any children who present with vir-, E" z$ O* @4 T& X% Y5 i
ilization or peripheral precocious puberty. The diag-
# G: E; m1 G( @5 snosis can be established by just a few tests and by
' @' n5 b" ^/ |& P; w9 m) x6 D/ `% bappropriate history. The inability to obtain such a* q* U6 J6 f* A
history, or failure to ask the specific questions, may9 g4 X2 x3 G, m8 i" N% M
result in extensive, unnecessary, and expensive
/ q6 T& n( b7 b. O* c: q0 C  Y' uinvestigation. The primary care physician should be
, I, r  S" t0 @' h, [0 z! F( haware of this fact, because most of these children. T6 H) ]9 T1 w' j" q4 y4 x8 @0 n* n
may initially present in their practice. The Physicians’
" i! c" C3 l+ b: aDesk Reference and package insert should also put a
% Y, W5 K, }4 vwarning about the virilizing effect on a male or
# ~! w# {0 [1 h3 x6 k. g- R8 vfemale child who might come in contact with some-* B2 g/ B0 T2 {1 H6 q
one using any of these products.
- F0 }0 r2 X5 d" n5 c1 F' x  L' QReferences8 X* ?3 b/ h1 M0 s" n1 \3 z
1. Styne DM. The testes: disorder of sexual differentiation8 Z$ ]; y. s; W
and puberty in the male. In: Sperling MA, ed. Pediatric/ P) j+ T9 Q! k% w) f- W
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
& t# j: i( [9 {/ \0 G2002: 565-628.5 {& i/ g+ K( Y! F0 S& d' v7 g
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
9 ]& B7 ^) u5 e6 f( H' B/ Spuberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
% a% B6 `/ z1 c0 X. eBoy Induced by Indirect Topical
0 n% y5 Y- p# P* F$ @- iExposure to Testosterone# [0 f5 z9 {3 h, N5 k6 g1 \. Z- @
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2  ]6 n9 H% ]! p9 p9 F
and Kenneth R. Rettig, MD14 t; i% Z' c/ r1 w6 c9 c# d
Clinical Pediatrics2 g7 i* c3 C8 x8 W7 V4 _
Volume 46 Number 6
+ Q: i0 y$ T  u1 X  c9 y4 ~July 2007 540-543
, b& z3 Y( Y+ s! w8 g0 {© 2007 Sage Publications
8 K& i% b% l: C10.1177/0009922806296651
- Y1 q. j! q; zhttp://clp.sagepub.com
, U" _& \% h0 \" d6 ]  F, [hosted at" v$ M0 M, Y( Y! i+ P" f
http://online.sagepub.com5 M  {8 |0 j) i0 z" p* @# a( J! m. w
Precocious puberty in boys, central or peripheral,
4 S8 f, {, f$ M* G9 }# _is a significant concern for physicians. Central$ |* `+ s: S! ]" |; K9 Z; |
precocious puberty (CPP), which is mediated6 y8 `0 G( A" Q
through the hypothalamic pituitary gonadal axis, has
  _+ u5 k0 W2 Ha higher incidence of organic central nervous system" }* ~& I2 c6 {1 J) L& \- {( F* i
lesions in boys.1,2 Virilization in boys, as manifested  R3 r3 `: l, W
by enlargement of the penis, development of pubic2 ~: Y1 v- K' ?
hair, and facial acne without enlargement of testi-
6 s" b4 F5 ~: D. q) F, z$ b( t" S/ Mcles, suggests peripheral or pseudopuberty.1-3 We$ E+ A) C4 U) W0 b& h" I
report a 16-month-old boy who presented with the. X! X8 L& y" a1 g, T/ K
enlargement of the phallus and pubic hair develop-
: b' ?' ?' o; {: M: Qment without testicular enlargement, which was due% v+ d% N  l" n. E0 g7 ]- B
to the unintentional exposure to androgen gel used by
% n' a/ }. j8 E6 O, P9 O* tthe father. The family initially concealed this infor-0 D9 ?9 `5 \  j1 e: }( `
mation, resulting in an extensive work-up for this+ f- B: x0 C+ V1 n2 G+ R  s$ \
child. Given the widespread and easy availability of
# F/ P- ?  U5 n1 [  utestosterone gel and cream, we believe this is proba-
! k6 m3 m& |/ l$ s# m% ^4 Dbly more common than the rare case report in the
5 q8 ^7 @. T( k. r: g/ {4 Yliterature.4  X) r, O8 W1 P
Patient Report4 q. g8 n4 o: y+ I) `# h
A 16-month-old white child was referred to the
0 I  ?! b" M" j2 V2 Nendocrine clinic by his pediatrician with the concern
& P$ F, K/ n3 J5 w' O: X) s, b2 Fof early sexual development. His mother noticed
/ d4 Y/ r% g5 N4 R! {light colored pubic hair development when he was' j$ {* l, D+ f+ }' }% ?+ w
From the 1Division of Pediatric Endocrinology, 2University of
( }1 x- V2 W% z7 ~' ?* L, w; SSouth Alabama Medical Center, Mobile, Alabama.
7 N+ A6 ^0 Z$ ]& l5 e  o6 u4 P! h$ fAddress correspondence to: Samar K. Bhowmick, MD, FACE,
1 x3 V3 X/ Z% A# EProfessor of Pediatrics, University of South Alabama, College of* G4 m5 t) Z, W7 r6 v
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;7 n' V4 [0 O' Y/ P9 Q8 d
e-mail: [email protected].* O. S& N' }; Q% N; a- W
about 6 to 7 months old, which progressively became$ H1 ]$ l5 d; }  i" r
darker. She was also concerned about the enlarge-
2 ^: F* s$ X, y6 N0 D2 o7 i+ n; D* fment of his penis and frequent erections. The child9 I0 s4 b$ v+ [, T6 J/ {7 ?
was the product of a full-term normal delivery, with& ?5 s. G3 _9 }) M+ S! i
a birth weight of 7 lb 14 oz, and birth length of) t6 A: X0 l' U& F/ V: n
20 inches. He was breast-fed throughout the first year
/ |9 s+ ~1 _( L$ _7 w* Oof life and was still receiving breast milk along with; ~, ~* ^1 n) O3 F# k# d, @. O
solid food. He had no hospitalizations or surgery,& v& ^6 t6 Q/ n' E! Z
and his psychosocial and psychomotor development2 h0 }7 R, q* e& I/ t
was age appropriate.& V" n0 M8 w3 W  l
The family history was remarkable for the father,
; C' p; i! J* o: `0 s0 Z% W  H4 Pwho was diagnosed with hypothyroidism at age 16,
5 r2 z& a1 s' m& P% p) _5 Cwhich was treated with thyroxine. The father’s
" y+ t# p+ b: ^5 e# g+ X: xheight was 6 feet, and he went through a somewhat
  s# a4 C$ g- P; ]& t6 ^9 bearly puberty and had stopped growing by age 14.
8 U' m& _1 B5 ^2 cThe father denied taking any other medication. The
* f' S2 N, Z: \+ T$ n/ |child’s mother was in good health. Her menarche
, T6 ]3 p; q/ O1 k# j  fwas at 11 years of age, and her height was at 5 feet
6 ^* w5 s8 E3 o6 V) B) M5 inches. There was no other family history of pre-
1 j; e7 ?6 \* W5 U' E) H% Jcocious sexual development in the first-degree rela-6 ^+ }2 U& u! ]( t9 ]8 ?
tives. There were no siblings.( q/ ?/ s% }5 S8 l, `: d% S
Physical Examination5 T) s8 k+ @  n2 k
The physical examination revealed a very active,
+ I+ S- A( f% w/ c) Y! rplayful, and healthy boy. The vital signs documented0 g) D* H  L. K9 p7 n
a blood pressure of 85/50 mm Hg, his length was
, p! f: [; V0 m: m$ R$ J90 cm (>97th percentile), and his weight was 14.4 kg8 I5 l+ g9 i2 T) k% {& q
(also >97th percentile). The observed yearly growth
$ L5 [; S/ t1 bvelocity was 30 cm (12 inches). The examination of
5 L& l! ]& d8 @the neck revealed no thyroid enlargement.
% o' r. `/ D5 N$ \) w% l- |The genitourinary examination was remarkable for- k+ Y# w1 W9 n) Y/ C8 r: B
enlargement of the penis, with a stretched length of
( ]* o/ `; M0 ^+ N8 cm and a width of 2 cm. The glans penis was very well9 h" T; n6 t, K* R8 R5 D: |( O
developed. The pubic hair was Tanner II, mostly around+ j$ Z8 U4 r+ I6 l8 u3 u8 M
540! Z: {  E5 c5 u2 O$ B
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
3 r8 y* q  F! N( w& ]the base of the phallus and was dark and curled. The; B# j$ g# ?" G  |8 e, t1 p* }
testicular volume was prepubertal at 2 mL each.- z5 U/ Q! U5 \0 o
The skin was moist and smooth and somewhat" F8 @7 a3 x/ M8 i9 W5 _5 R
oily. No axillary hair was noted. There were no
' ~3 {  y7 v. a3 R" Rabnormal skin pigmentations or café-au-lait spots.5 T5 X3 X. b+ n: j- |
Neurologic evaluation showed deep tendon reflex 2+; \( I: i1 H2 K% S" W, U3 `: H$ [
bilateral and symmetrical. There was no suggestion
. D; b3 F. \2 Y4 C9 _6 g, B# yof papilledema.# o% U3 C- _, d) G+ [- J" k0 j9 y
Laboratory Evaluation
& |3 C7 F2 Q6 hThe bone age was consistent with 28 months by7 [" B4 |" U# \9 Z# j  f
using the standard of Greulich and Pyle at a chrono-
+ {$ Y) A% w8 K3 elogic age of 16 months (advanced).5 Chromosomal
( K1 k: [5 X+ ukaryotype was 46XY. The thyroid function test- a3 k. e. A$ T, o# r% r4 W! j( F
showed a free T4 of 1.69 ng/dL, and thyroid stimu-+ W$ M8 J+ n* v1 ]. ~$ F/ j
lating hormone level was 1.3 µIU/mL (both normal).% z2 [5 i4 k4 b' ^+ A
The concentrations of serum electrolytes, blood9 W* T) ~1 W1 s3 s; x; g3 O* a
urea nitrogen, creatinine, and calcium all were0 `  p9 g3 [! R, S+ E5 P" T) o
within normal range for his age. The concentration
3 e" T5 ]4 f+ j9 W! Q+ ^3 }" p7 m5 Dof serum 17-hydroxyprogesterone was 16 ng/dL* \$ b- l" K$ I4 t% _
(normal, 3 to 90 ng/dL), androstenedione was 20
+ U4 z) n5 {6 G% jng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
  U5 P7 p" N8 N& u' F" G# d9 Q# ]terone was 38 ng/dL (normal, 50 to 760 ng/dL),$ H: Q( O8 \6 c* j% D
desoxycorticosterone was 4.3 ng/dL (normal, 7 to$ K7 E+ N, ?" C4 Z1 @
49ng/dL), 11-desoxycortisol (specific compound S)
+ P/ z% |+ i  v5 jwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-5 @9 [% D! }2 h- t- J
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total/ k" k/ U+ i) H
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
5 u; u, {; b  W; G* |; Cand β-human chorionic gonadotropin was less than
9 e% z, H* @6 d9 X6 S8 C1 [5 mIU/mL (normal <5 mIU/mL). Serum follicular
3 z2 |0 r: U3 f' b, f! r1 W" Astimulating hormone and leuteinizing hormone
2 h, w6 _! F1 B/ ?% l' g+ vconcentrations were less than 0.05 mIU/mL
0 h" s, G& l0 v+ a(prepubertal).# i1 e8 F, D9 _; w
The parents were notified about the laboratory
. P2 A8 `2 [- H& V7 A+ Gresults and were informed that all of the tests were+ h7 z3 ]4 e: Y4 p8 V
normal except the testosterone level was high. The
# W$ M$ M; K4 [+ ?1 W# u0 Jfollow-up visit was arranged within a few weeks to2 T' P% @8 i5 f4 j9 {
obtain testicular and abdominal sonograms; how-/ r! z) i' e; d7 j6 v. g: p
ever, the family did not return for 4 months.# ~4 k$ \7 S3 _* j
Physical examination at this time revealed that the
6 f8 T9 c+ H0 _! T6 A# ychild had grown 2.5 cm in 4 months and had gained: I7 l0 z& _1 z/ U) V; `0 c; |) M/ }
2 kg of weight. Physical examination remained- `5 T2 T9 s' w! G6 E" s
unchanged. Surprisingly, the pubic hair almost com-
+ D8 z- x6 J& A) @4 Mpletely disappeared except for a few vellous hairs at
8 K( z2 W; _' ]' V! [7 C. qthe base of the phallus. Testicular volume was still 2
* c1 D$ r7 o, a8 I" ^9 amL, and the size of the penis remained unchanged.
+ J, p! q, ]. l0 w% M+ F7 CThe mother also said that the boy was no longer hav-
6 \1 n( w! D9 qing frequent erections.
; Q: d' [: F1 |1 W; ?" D, V/ l0 jBoth parents were again questioned about use of
; m% k" ?2 r( E; xany ointment/creams that they may have applied to1 @3 B) r% U) h# d+ y0 i# J/ F& \7 C
the child’s skin. This time the father admitted the
0 Z* h+ g" a0 s  h! T$ |5 H6 LTopical Testosterone Exposure / Bhowmick et al 541
# B$ ~0 Z, f  ?$ R6 ~! e6 ]use of testosterone gel twice daily that he was apply-3 v4 s# w' Y* W0 B. W9 g$ z7 N
ing over his own shoulders, chest, and back area for
2 r5 w3 ~' F( L( r3 _0 h5 J3 Aa year. The father also revealed he was embarrassed
  A* b; D% k: J* D) i2 i( lto disclose that he was using a testosterone gel pre-
# P& A! o% K0 m5 w+ Escribed by his family physician for decreased libido
8 ]2 [! q* f: ~9 ^0 V- v& ^$ R4 vsecondary to depression.
+ g$ b& }$ u3 mThe child slept in the same bed with parents.
4 \/ w  u  d  G& R. n1 {The father would hug the baby and hold him on his
9 r6 Q( |: R4 a! R( t) xchest for a considerable period of time, causing sig-
5 I$ j' C1 {: r2 S3 Bnificant bare skin contact between baby and father.
* i! v- R2 Q" a7 m0 g3 A) v/ l2 A8 x; ^The father also admitted that after the phone call," W  `1 Y- i6 e, |3 |7 B
when he learned the testosterone level in the baby
: l, p0 v% q% p9 @2 m" C) b8 Pwas high, he then read the product information
( q7 C' J+ w" s7 [' k1 ipacket and concluded that it was most likely the rea-
3 W! U/ q, F7 t; C% e6 G% Ason for the child’s virilization. At that time, they6 }  B& J5 F' ^3 d0 G
decided to put the baby in a separate bed, and the0 r) U7 l3 X/ G: ^  m" d3 m
father was not hugging him with bare skin and had
# F0 r$ c0 s% s/ C1 G: O  Abeen using protective clothing. A repeat testosterone
$ E- x0 I) m- B& L1 Mtest was ordered, but the family did not go to the
/ P! e3 m2 S" z4 J' \1 l* v7 Xlaboratory to obtain the test.# O7 H! [) k6 E1 G) A5 P  i3 f
Discussion
# N7 b+ R! r# T2 B# x. oPrecocious puberty in boys is defined as secondary: p2 R( K" d3 X( k: n0 J) o* }
sexual development before 9 years of age.1,4
2 r7 ]3 I6 V: G3 ^& l. ?Precocious puberty is termed as central (true) when' i. N4 i4 D* P7 F% ^& l( |
it is caused by the premature activation of hypo-; Z! i) E1 ?( a, R+ Y- s: M
thalamic pituitary gonadal axis. CPP is more com-
, |8 A& \; g0 @' k& u/ @! `! w3 }mon in girls than in boys.1,3 Most boys with CPP. l' B! [( d: ^' i1 K* B; B, A+ m+ x
may have a central nervous system lesion that is
5 Y% Z; a. K7 \4 uresponsible for the early activation of the hypothal-/ ~5 Y) U. z: S1 s* L( Q  j* A
amic pituitary gonadal axis.1-3 Thus, greater empha-+ a; k0 Q( ]; z$ ~3 w: U5 _
sis has been given to neuroradiologic imaging in" w' E. }: K/ [; y1 a2 P5 ^+ n' a
boys with precocious puberty. In addition to viril-* i$ X# j1 ~( B) I7 V
ization, the clinical hallmark of CPP is the symmet-
# s" ~. z: u. U) Y( L+ Nrical testicular growth secondary to stimulation by
$ H1 d* H8 s( _! i; ygonadotropins.1,3
& p: e/ y) U! [6 J: m1 CGonadotropin-independent peripheral preco-, f0 @! W0 v# `: X4 P+ g. q0 a
cious puberty in boys also results from inappropriate
- C% C# i  g5 Sandrogenic stimulation from either endogenous or1 _! f7 x1 z4 L" k
exogenous sources, nonpituitary gonadotropin stim-
% A2 i5 R! l$ T8 r' x7 o% m% W/ Uulation, and rare activating mutations.3 Virilizing: c/ F) F, \/ O1 J( A5 y1 A
congenital adrenal hyperplasia producing excessive' h  Y, q) k0 |. ~6 U' J5 y( X
adrenal androgens is a common cause of precocious" k- ]6 ^+ R  k' A  B- M
puberty in boys.3,4
/ {( N' x( }4 y: z9 \$ h; ?2 eThe most common form of congenital adrenal$ s$ n0 _8 `& y0 c3 O
hyperplasia is the 21-hydroxylase enzyme deficiency.4 ?: q3 X5 m; b& y( ]
The 11-β hydroxylase deficiency may also result in
% l& V. Z# {0 o6 H8 kexcessive adrenal androgen production, and rarely,
" \1 b% d9 ?1 tan adrenal tumor may also cause adrenal androgen
* \$ X" ^4 V9 S$ Oexcess.1,3' C$ P" n5 C6 K2 d
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- V" t1 R. D: p- c4 B; [542 Clinical Pediatrics / Vol. 46, No. 6, July 2007/ h4 u7 @9 S; R- ]9 t" K( E& v
A unique entity of male-limited gonadotropin-
* D9 k- Q+ y2 {. r, @7 `0 U0 Windependent precocious puberty, which is also known
6 p; R# F* c2 s" B+ T: U+ H9 e9 g+ das testotoxicosis, may cause precocious puberty at a  F$ E: |/ |# K: Y2 Q3 T) h
very young age. The physical findings in these boys
! C7 S! s7 Z  x: swith this disorder are full pubertal development,6 v: A% p# C8 P4 g" Q, O
including bilateral testicular growth, similar to boys
: V9 i+ }3 C! `( d$ y! K! iwith CPP. The gonadotropin levels in this disorder
1 W3 ~5 y) T0 n2 J- yare suppressed to prepubertal levels and do not show. X. R) Z5 k9 l* A
pubertal response of gonadotropin after gonadotropin-
4 m3 R6 h  X% J! t) ]( j8 d' Sreleasing hormone stimulation. This is a sex-linked! R1 K% Q1 k, l, h- o6 P- T* V
autosomal dominant disorder that affects only
1 |0 g  g$ M: J( E4 c' Ymales; therefore, other male members of the family
; G1 u" O+ I3 w: v" P7 |may have similar precocious puberty.3
- J5 [$ ~2 V/ h3 X- N# C& _9 lIn our patient, physical examination was incon-& Q, e! k6 i% W# x
sistent with true precocious puberty since his testi-
3 |, ]! l, e4 ]* _( Ecles were prepubertal in size. However, testotoxicosis
& i7 \- L6 j! `9 k, \2 Mwas in the differential diagnosis because his father* O) p) f: ^. x
started puberty somewhat early, and occasionally,: R" k" c! `# o, @9 E7 q. C/ W3 c
testicular enlargement is not that evident in the; A$ F: g0 i/ W, N- h
beginning of this process.1 In the absence of a neg-
3 G4 h1 _+ X% k6 q2 D7 `ative initial history of androgen exposure, our' `7 u' A, W5 d1 E0 H4 l
biggest concern was virilizing adrenal hyperplasia," s0 t, t- I, J
either 21-hydroxylase deficiency or 11-β hydroxylase
, d4 R) _/ K5 l" D6 Edeficiency. Those diagnoses were excluded by find-
/ g, a# v7 ?. Q% |+ H+ H, |. ~ing the normal level of adrenal steroids.
; O$ _! H! `: k% S* i" `: fThe diagnosis of exogenous androgens was strongly% u4 Q$ X& `5 l$ q: L8 d0 v# N
suspected in a follow-up visit after 4 months because
! |! j* V: d! P* r2 }% ?; k( p8 tthe physical examination revealed the complete disap-
  |/ P* _! v. V' Bpearance of pubic hair, normal growth velocity, and
4 Z/ m* s; y* b: x1 u3 G. o! edecreased erections. The father admitted using a testos-
8 G3 G; s! ?2 b5 w" w. e% j$ Pterone gel, which he concealed at first visit. He was
9 A& J) l# E& \# a" eusing it rather frequently, twice a day. The Physicians’
# v9 R3 I, S$ IDesk Reference, or package insert of this product, gel or: l7 i6 D/ T" f, J& i3 j
cream, cautions about dermal testosterone transfer to7 g( x: c7 ]" f
unprotected females through direct skin exposure.
9 j. V, E- e3 ?; [! N, |9 V( LSerum testosterone level was found to be 2 times the
2 ?% S! R  R1 bbaseline value in those females who were exposed to
2 {2 j; |; P# u8 a! ceven 15 minutes of direct skin contact with their male1 v! t; f. M9 U- T. n/ O
partners.6 However, when a shirt covered the applica-6 |! ]1 [; s5 I* M% S
tion site, this testosterone transfer was prevented.
1 e  @* ?  G% W. A5 GOur patient’s testosterone level was 60 ng/mL,1 Q8 i3 R  z! u, d2 x
which was clearly high. Some studies suggest that
- k; s# t+ t" l, R; g* Z& _& ]- g: xdermal conversion of testosterone to dihydrotestos-
! i- ~+ _+ F9 w) G8 R  hterone, which is a more potent metabolite, is more
; K$ U. u7 O. U& factive in young children exposed to testosterone
( r4 s( s, k& E1 ^  [; _' y. ]exogenously7; however, we did not measure a dihy-
+ m9 [4 f& o' x5 F5 Idrotestosterone level in our patient. In addition to- S% v9 D" n' K' o$ L& N  v2 R$ K
virilization, exposure to exogenous testosterone in8 J$ g# m& o/ I6 {4 L
children results in an increase in growth velocity and
* w3 n: Z  z1 N$ ?) ]4 b6 h! G) Fadvanced bone age, as seen in our patient.
  [$ j- v+ Y; D5 jThe long-term effect of androgen exposure during
# g6 l, B/ ^- B( O3 oearly childhood on pubertal development and final* k: s( x) g5 ]# S$ u6 B6 I
adult height are not fully known and always remain
! F5 l# q+ x7 N) \+ _  U0 Xa concern. Children treated with short-term testos-
0 M& U  K: g) Qterone injection or topical androgen may exhibit some
) G3 b8 }+ U# b+ t. h- L/ }acceleration of the skeletal maturation; however, after  C7 |$ G; D5 S6 O  c8 C  @
cessation of treatment, the rate of bone maturation' |& I) Q0 O. c( ~7 o+ c/ i$ t% c* K4 \
decelerates and gradually returns to normal.8,9" `$ G, Z5 l6 Q5 ~( r. r( k
There are conflicting reports and controversy( G( u. E7 @" f5 H. E
over the effect of early androgen exposure on adult
+ G" q! ~: L$ Q* Hpenile length.10,11 Some reports suggest subnormal
- O$ [$ L: @$ }' uadult penile length, apparently because of downreg-
4 P0 V3 D, g3 ~. F9 a! nulation of androgen receptor number.10,12 However,7 W9 c1 ], r8 R) c4 A
Sutherland et al13 did not find a correlation between. R" K% f, z4 ]9 _* `7 c7 |6 ]1 a
childhood testosterone exposure and reduced adult
( U" `6 a3 i) I/ D! Z8 m3 h% i6 ppenile length in clinical studies.
: e4 d( n! F3 x7 PNonetheless, we do not believe our patient is3 s4 ]# \, p# j+ O2 C! ?1 \! P
going to experience any of the untoward effects from
! u6 f  `* ~/ g7 r. }: Y' jtestosterone exposure as mentioned earlier because& P& W2 x# N$ }) |
the exposure was not for a prolonged period of time.
! S# N2 I' U3 m+ OAlthough the bone age was advanced at the time of) M% m( f6 c$ `3 V5 g1 [" ?
diagnosis, the child had a normal growth velocity at
7 F9 X; P+ T$ X0 H$ o! @the follow-up visit. It is hoped that his final adult  T! ^6 F: W- q; n" i. U. u
height will not be affected.
6 c/ I7 c0 X5 j; s. q: ^: X' zAlthough rarely reported, the widespread avail-
* b5 o8 Q8 N; a  sability of androgen products in our society may: {* t" r- T' s( W( a" o- z
indeed cause more virilization in male or female
7 C4 @- C) U0 K% H' Hchildren than one would realize. Exposure to andro-
# J+ c7 d. \! \gen products must be considered and specific ques-
. h' K) f0 X% Btioning about the use of a testosterone product or; F5 R; x+ a1 H* S! U/ f
gel should be asked of the family members during
% e( _$ _6 j1 h. [% `the evaluation of any children who present with vir-
* C8 R/ \6 }; k9 G0 oilization or peripheral precocious puberty. The diag-
: D9 w6 g" |- y1 I4 c) Pnosis can be established by just a few tests and by8 o6 o# O+ D1 |, D! j
appropriate history. The inability to obtain such a
9 {! M. _7 N9 h$ k& h* dhistory, or failure to ask the specific questions, may' G# V: b7 b: N, ^: t
result in extensive, unnecessary, and expensive
+ R8 U- M5 L6 T* Hinvestigation. The primary care physician should be
. C# T" Q9 z* i" ^. U' Raware of this fact, because most of these children
- n3 G7 Q7 o7 @2 V( I# Ymay initially present in their practice. The Physicians’; V8 E* W1 _. w* f& ^: F
Desk Reference and package insert should also put a
; H% }# X/ y( p! k) M/ k/ l# Kwarning about the virilizing effect on a male or1 o: y0 [( Y( c! e( Z' l6 R
female child who might come in contact with some-
" |) R3 Z0 n6 d6 k9 f4 jone using any of these products.7 c/ Z# Y: r" m/ g1 s
References
: A) Z1 l* K& w1. Styne DM. The testes: disorder of sexual differentiation7 {  m+ O0 k, G; B( l8 x
and puberty in the male. In: Sperling MA, ed. Pediatric1 p' ~! h- H2 R7 C
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;5 t# C+ o! g* V  y
2002: 565-628.5 ~! q4 @! r# F$ @: {% I. D
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious! }1 j' v3 J- \8 Z9 c
puberty 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
' T# |+ q' {+ C; p5 B+ H: Y- 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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