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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( [8 M$ u' X1 P, G( m
Boy Induced by Indirect Topical/ l" t6 P; \, h7 Z% ?3 B. b
Exposure to Testosterone5 k# v7 W  r5 ?6 V/ b
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
! u% {$ \! L4 O5 g2 ?9 |) ]and Kenneth R. Rettig, MD1# D& t1 o: b  ?; [3 R. b
Clinical Pediatrics  {9 S2 @; U6 A
Volume 46 Number 6+ ?/ ^+ ]. v. l8 C, v3 i
July 2007 540-543
: x, ~0 [" Z* p& L© 2007 Sage Publications( e8 D  ~' P. d8 c
10.1177/00099228062966516 F. f$ j& C* l6 K) f; v. c. Y
http://clp.sagepub.com7 V" Q7 A; X) k8 W/ L' x% x
hosted at$ D6 D3 @0 X* i8 M- k
http://online.sagepub.com
$ U) R7 W, Q7 Z7 j: {8 o5 ^Precocious puberty in boys, central or peripheral,
' U! H1 c  @% C4 c5 ]* c6 Bis a significant concern for physicians. Central
! ^& ]* r$ S. |precocious puberty (CPP), which is mediated% h( E4 I6 x7 {
through the hypothalamic pituitary gonadal axis, has
  ~! P5 j! D- u0 F  k( e" T, |a higher incidence of organic central nervous system
% Q: L6 H8 @7 }* N  z4 _5 W* z9 dlesions in boys.1,2 Virilization in boys, as manifested
' P8 ?; D# J  Q* C3 N* D1 Bby enlargement of the penis, development of pubic$ I- Y+ l% w! g% L. b1 A
hair, and facial acne without enlargement of testi-
' S, |, W& x1 A8 R* K: j% Qcles, suggests peripheral or pseudopuberty.1-3 We
7 H6 f3 U! e% z" f; w8 qreport a 16-month-old boy who presented with the
* P& k- x! J& X. j% o  T! Lenlargement of the phallus and pubic hair develop-' Q" e* y& d  _' L8 Y1 _0 ]! m/ J- F
ment without testicular enlargement, which was due- Q  O% q8 B% A8 J7 `! \
to the unintentional exposure to androgen gel used by
; h7 {; w# R0 Z# o) Xthe father. The family initially concealed this infor-
1 \. D4 r9 F. d0 _5 Hmation, resulting in an extensive work-up for this& c7 u2 W  @- \  |3 t% x
child. Given the widespread and easy availability of1 W  t: {# A/ U& E/ l$ V
testosterone gel and cream, we believe this is proba-
4 s2 d% s0 J4 B( Q+ ?- }bly more common than the rare case report in the/ ]. y: q+ O4 J1 G: l2 @
literature.4
; V- M2 U& ?& J+ T3 BPatient Report0 j# g8 c  Z2 ~
A 16-month-old white child was referred to the, t8 u5 ^5 A3 n% h) Q
endocrine clinic by his pediatrician with the concern
) b/ ?. t# z" O5 Y6 i$ @, Vof early sexual development. His mother noticed
6 Y( _/ w4 F4 S3 b; y- Ylight colored pubic hair development when he was
) L) c+ L  q( G9 g2 mFrom the 1Division of Pediatric Endocrinology, 2University of
; C* [/ {- r. ^South Alabama Medical Center, Mobile, Alabama.# A) g/ |8 _& h1 G
Address correspondence to: Samar K. Bhowmick, MD, FACE,
* L& |7 P: H: L( XProfessor of Pediatrics, University of South Alabama, College of
( H) r2 e# |* h( L9 aMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
: J  i& p7 _: Be-mail: [email protected].% U; v, ]3 Q  ~* J# c0 F9 e
about 6 to 7 months old, which progressively became
6 l- W* }6 P6 f4 |6 Jdarker. She was also concerned about the enlarge-
9 n# v1 c. x/ \' Kment of his penis and frequent erections. The child
" P; g8 F+ @% {. r" h$ k0 ~was the product of a full-term normal delivery, with
% N/ t2 I$ S' q" A9 @5 v1 k3 z: Na birth weight of 7 lb 14 oz, and birth length of
7 `! b, C7 ^1 ~: m20 inches. He was breast-fed throughout the first year2 w$ H4 z+ d5 Z6 Y
of life and was still receiving breast milk along with
' H/ ]; u+ U8 ?# b8 m% nsolid food. He had no hospitalizations or surgery,
9 j! P" i0 V% Mand his psychosocial and psychomotor development
! {! l% m, C; |$ n) P  x- k7 dwas age appropriate., y! V$ a3 ^; T
The family history was remarkable for the father,- o9 _$ h2 ~' a" L- i
who was diagnosed with hypothyroidism at age 16,# V1 K: M( C, D0 q5 b
which was treated with thyroxine. The father’s
* c6 [% B' E% Zheight was 6 feet, and he went through a somewhat4 k& `% i3 |" J- d( D) f
early puberty and had stopped growing by age 14.
$ a; ?. L8 o6 M' ZThe father denied taking any other medication. The
- K3 `2 x' K6 A9 m2 W# hchild’s mother was in good health. Her menarche
2 t0 G1 ~1 C" O0 A" v- l7 y* Ywas at 11 years of age, and her height was at 5 feet% e3 }* E0 \/ A
5 inches. There was no other family history of pre-' D1 N/ B" |" y; w  u
cocious sexual development in the first-degree rela-6 a. ]0 ^7 O9 Y
tives. There were no siblings.- u! X" j9 I7 e. [$ s
Physical Examination: s* u- w$ L9 \' L4 y
The physical examination revealed a very active,) W# E) d1 `, h! @# J
playful, and healthy boy. The vital signs documented% i. b4 ?6 m" p6 |- b$ j! u
a blood pressure of 85/50 mm Hg, his length was/ W5 o8 R2 t" W; v
90 cm (>97th percentile), and his weight was 14.4 kg
0 @& S9 L% ?7 L' q* Z. N6 X(also >97th percentile). The observed yearly growth
, b8 X& u' K" Z7 k& T5 Evelocity was 30 cm (12 inches). The examination of
5 s+ }& K& \9 S: E3 u* F0 G" \0 v7 ithe neck revealed no thyroid enlargement.
5 I; {+ q/ h2 PThe genitourinary examination was remarkable for3 |1 l/ D8 z( K: M* C, U
enlargement of the penis, with a stretched length of" i8 \6 C5 X+ U& G
8 cm and a width of 2 cm. The glans penis was very well
2 y5 S$ z$ C% \& |developed. The pubic hair was Tanner II, mostly around' Y' @" z0 p4 a! j5 I% K2 y1 x
5403 |  g4 l3 W# z6 S9 s& I
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from/ _1 W/ q5 Y! N2 a
the base of the phallus and was dark and curled. The9 K5 m; d. N6 M! E# ^, u) t
testicular volume was prepubertal at 2 mL each.
; j; I3 {0 V% R  G% vThe skin was moist and smooth and somewhat' x; z& s9 T3 x+ i/ d; h
oily. No axillary hair was noted. There were no  r- s8 o( J$ V, v6 T$ c/ P
abnormal skin pigmentations or café-au-lait spots.* {. S/ W& ^4 [/ _
Neurologic evaluation showed deep tendon reflex 2+
& p- @6 A% Q* j$ `bilateral and symmetrical. There was no suggestion
$ ^/ J4 o( k2 E$ [of papilledema.
* V' l3 d- d: ~# F2 m* c2 u* C4 GLaboratory Evaluation; ?. {9 a" ^. [4 e
The bone age was consistent with 28 months by
! d# i- ]; `) {: ]using the standard of Greulich and Pyle at a chrono-" v0 Y, x- q1 [8 K) X( n; \" E
logic age of 16 months (advanced).5 Chromosomal$ t: \/ l, v/ l' G: D
karyotype was 46XY. The thyroid function test
0 _+ |$ [+ X8 R: Eshowed a free T4 of 1.69 ng/dL, and thyroid stimu-+ G" [# K+ I% a' e# T- \
lating hormone level was 1.3 µIU/mL (both normal).
0 x* W- [9 K6 q( E9 D4 y+ j% }The concentrations of serum electrolytes, blood
( {6 ^( @% G: M$ o9 r- turea nitrogen, creatinine, and calcium all were
4 r& L7 d8 r, Jwithin normal range for his age. The concentration
& ~$ {8 s' \  E1 x0 _8 Y; T* A8 G/ ^of serum 17-hydroxyprogesterone was 16 ng/dL% O& W" e) N; M& c
(normal, 3 to 90 ng/dL), androstenedione was 20
: N( T: K# c! h2 Rng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-( H5 j) [+ R/ f2 e# I
terone was 38 ng/dL (normal, 50 to 760 ng/dL),2 T6 F0 a1 E2 \3 U
desoxycorticosterone was 4.3 ng/dL (normal, 7 to( \5 U  ^$ X" x+ {# _) w
49ng/dL), 11-desoxycortisol (specific compound S)2 c- P6 r8 ~  o# p( R' O' v/ g8 E
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
3 k: b5 f! f1 ?* ]  J) gtisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
/ j4 {8 w( s: i7 B  s3 Ftestosterone was 60 ng/dL (normal <3 to 10 ng/dL),( z6 p, g' t) y: m+ r1 F+ t; h1 ~& G
and β-human chorionic gonadotropin was less than: k! s" h7 r) d- M* `
5 mIU/mL (normal <5 mIU/mL). Serum follicular5 R7 y6 C6 U, ]0 O
stimulating hormone and leuteinizing hormone) a5 N& H/ g2 X0 W. f( Q
concentrations were less than 0.05 mIU/mL! {! ~# [, W6 N6 k$ U; F
(prepubertal).2 H' H  I/ j" B+ I$ p5 g
The parents were notified about the laboratory/ n: q: a5 F& w( Y. C- D
results and were informed that all of the tests were$ F6 l. J7 m8 w: F* T
normal except the testosterone level was high. The
4 t6 a% z% @  ifollow-up visit was arranged within a few weeks to, d" y0 X$ m+ k% B! `3 j
obtain testicular and abdominal sonograms; how-# u% p7 C, F; \, f0 F
ever, the family did not return for 4 months.
( [, W1 Q6 t: H* L* JPhysical examination at this time revealed that the
* |, C$ f6 r0 b2 q* [child had grown 2.5 cm in 4 months and had gained
+ X: b3 M) g$ p$ b, Z5 ]; A4 |2 kg of weight. Physical examination remained: ^, H. L( h- {- x& N
unchanged. Surprisingly, the pubic hair almost com-. p. S+ N% v, N' \% r6 _( Z: ^
pletely disappeared except for a few vellous hairs at, r; ]' Z7 C' v7 i
the base of the phallus. Testicular volume was still 2
) w3 Z" q# j" W7 g4 }$ A) h) QmL, and the size of the penis remained unchanged.
# y( z9 {* h6 PThe mother also said that the boy was no longer hav-, E: T( k( i9 d: t( F6 [7 E4 E, j
ing frequent erections.
0 t8 h; I/ f& h' C  H. xBoth parents were again questioned about use of0 H3 o% v8 F7 l
any ointment/creams that they may have applied to+ R8 ?" W/ G0 \7 @4 C) {: g
the child’s skin. This time the father admitted the4 u: R, p6 I* L5 Y
Topical Testosterone Exposure / Bhowmick et al 541$ s: |- ~- F% I2 a
use of testosterone gel twice daily that he was apply-8 B0 \7 ~: }, R& K% |; d% T
ing over his own shoulders, chest, and back area for- E' z# s* e5 k: p
a year. The father also revealed he was embarrassed
4 x2 ]6 {: o( p- Gto disclose that he was using a testosterone gel pre-
' Y  P+ j3 n9 e5 V) c. Q$ ?scribed by his family physician for decreased libido
3 o7 k' _. C( |/ T0 N9 ~4 f" W! hsecondary to depression.; U0 L0 V' W8 s" ]
The child slept in the same bed with parents.; r# Q8 J# s5 k% T$ k: d  ~' o
The father would hug the baby and hold him on his
3 @) l% O1 n9 U* Z( c+ p1 w! bchest for a considerable period of time, causing sig-0 W  Y# R" B2 E/ s
nificant bare skin contact between baby and father.4 U$ J, I: O/ w2 g
The father also admitted that after the phone call,' f/ H% i* ], S& A
when he learned the testosterone level in the baby
1 ^" f# s/ x0 Qwas high, he then read the product information  Y6 [) S7 E, h- X$ [9 ^) |
packet and concluded that it was most likely the rea-
, ^) f2 }, J; x/ j5 \" k. [  d- Kson for the child’s virilization. At that time, they+ v( @, e1 Q1 t
decided to put the baby in a separate bed, and the
; w( E- O  k& a" u& h2 L% rfather was not hugging him with bare skin and had
' s, @, J3 ?4 Hbeen using protective clothing. A repeat testosterone4 w3 l# f- g1 m! C
test was ordered, but the family did not go to the
! B/ x; O3 D) E) G; T5 Ilaboratory to obtain the test.( {# w' t3 m. j, u
Discussion  P2 q, k' B' k$ e. n
Precocious puberty in boys is defined as secondary
8 r# t+ W, l- L3 F! H4 d/ e" Wsexual development before 9 years of age.1,4: h: n6 B  ?% H5 |, A* C( J
Precocious puberty is termed as central (true) when5 F9 U* k8 L% z# N9 O! |
it is caused by the premature activation of hypo-! I$ N2 K: A+ }4 j' k/ r% Z
thalamic pituitary gonadal axis. CPP is more com-$ P4 ]$ ^: a2 i( u- h
mon in girls than in boys.1,3 Most boys with CPP2 Y; Y! Z' j9 D# s% Q6 L: j
may have a central nervous system lesion that is; n1 A* _& T5 D8 l( A
responsible for the early activation of the hypothal-6 T& l! L* k6 B8 C2 d
amic pituitary gonadal axis.1-3 Thus, greater empha-0 n, n) e" c4 l- M
sis has been given to neuroradiologic imaging in
. t0 X; U# d) N+ D8 pboys with precocious puberty. In addition to viril-
+ u, K+ O4 J! x8 w) R2 s- \ization, the clinical hallmark of CPP is the symmet-7 d) ^/ k1 ?) ^4 a8 }
rical testicular growth secondary to stimulation by( z$ W0 y& I2 }2 A! L2 x4 s% e
gonadotropins.1,3
9 B7 N1 Q+ l' ^4 X4 eGonadotropin-independent peripheral preco-
7 d  O8 f. [  q& Lcious puberty in boys also results from inappropriate
  o) I4 g0 w6 _androgenic stimulation from either endogenous or" ^# d* F; ~; N+ p
exogenous sources, nonpituitary gonadotropin stim-
( p. C2 t9 Z6 Vulation, and rare activating mutations.3 Virilizing; v. |$ ]0 Z, b9 B3 D+ k  E* W
congenital adrenal hyperplasia producing excessive
6 b" f" \0 i7 cadrenal androgens is a common cause of precocious
& E, q6 x) |: [- n5 ^  }5 Zpuberty in boys.3,40 {. M' x; n5 T- c5 @/ ~
The most common form of congenital adrenal
5 s- L6 `" J7 }+ `: Ghyperplasia is the 21-hydroxylase enzyme deficiency.
& S( \* W6 Z1 J" n' dThe 11-β hydroxylase deficiency may also result in
. E8 l8 }, c) @; K4 |excessive adrenal androgen production, and rarely,+ r5 g7 b0 [4 v5 J* G4 f% ]+ f
an adrenal tumor may also cause adrenal androgen
- @% X7 P3 c" X: r" F8 dexcess.1,3& A6 {2 V- S# `6 w' E; w4 ]
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
2 R  A) M! ^/ y# b542 Clinical Pediatrics / Vol. 46, No. 6, July 2007( r3 \, Q% P9 X! I0 I3 d8 [, z
A unique entity of male-limited gonadotropin-
' I  s2 _2 D0 A) s9 R7 F6 i, cindependent precocious puberty, which is also known
# x6 d$ Q* @: ?) {; c3 K! Sas testotoxicosis, may cause precocious puberty at a4 n* t- i" l$ @- Q  a) Y0 I1 u% l
very young age. The physical findings in these boys
' ]$ C( E. X, {0 Hwith this disorder are full pubertal development,
0 y9 o" n8 E1 t$ e- z  zincluding bilateral testicular growth, similar to boys% J2 Z# F/ ~7 {) g; [% V( ^
with CPP. The gonadotropin levels in this disorder4 k4 [6 C) f  T0 B4 `' `0 t
are suppressed to prepubertal levels and do not show3 }, h2 p9 E; D
pubertal response of gonadotropin after gonadotropin-  v4 w" b8 X  |3 w5 ?' h
releasing hormone stimulation. This is a sex-linked
! l# [3 ~$ A# \) G3 \, wautosomal dominant disorder that affects only! l" }3 G) V) \+ L& s
males; therefore, other male members of the family* h, Y5 e6 a( a6 V6 b5 K: \+ O
may have similar precocious puberty.3# t% G' g4 X: ^  l/ I" @
In our patient, physical examination was incon-
, ?5 X, o1 S" a, o  e8 ksistent with true precocious puberty since his testi-
7 ]* c  b6 `- Q* O* hcles were prepubertal in size. However, testotoxicosis
8 M, j( k: E7 S- J2 ^' `was in the differential diagnosis because his father% W, e) ~+ A* {
started puberty somewhat early, and occasionally,3 I4 J& N* H: k3 {3 z1 z% B
testicular enlargement is not that evident in the5 d, t1 F3 z8 [6 f
beginning of this process.1 In the absence of a neg-
3 e- ^; p7 d" ^& `9 v. ^- Fative initial history of androgen exposure, our# d  t& _% a( h( D' n; f
biggest concern was virilizing adrenal hyperplasia,
$ e; Z/ N* y' S* ]either 21-hydroxylase deficiency or 11-β hydroxylase% m+ s" N9 {; w8 K. ~. [
deficiency. Those diagnoses were excluded by find-8 p* q0 w8 l( j* ~9 D  n& \' o
ing the normal level of adrenal steroids.
: m6 m" ~! D' |3 J' C; h5 UThe diagnosis of exogenous androgens was strongly6 \% f1 M9 E. Z/ B& f9 s' j/ ^0 `
suspected in a follow-up visit after 4 months because9 \. P; B/ C# P9 b
the physical examination revealed the complete disap-
% M# G6 v2 O# e& W, Y, l3 _5 Y% o9 x7 R" Fpearance of pubic hair, normal growth velocity, and
- G9 A, @. R# o, L- X, u, X% |decreased erections. The father admitted using a testos-: O; P; O8 w% f2 b! \0 N  q* l& g, ^
terone gel, which he concealed at first visit. He was" M: p7 K! [- k$ i8 H( e
using it rather frequently, twice a day. The Physicians’
8 j% a$ F9 U0 c# }2 F0 g" J$ sDesk Reference, or package insert of this product, gel or$ @! m( r- u* e
cream, cautions about dermal testosterone transfer to6 O- V7 R/ b1 p9 c0 G2 c
unprotected females through direct skin exposure.2 O) Z$ y' h( r8 v) G# L! [
Serum testosterone level was found to be 2 times the
7 Y* K3 N3 l0 V7 @3 [  S1 nbaseline value in those females who were exposed to
( m! e' z' Z6 j7 Peven 15 minutes of direct skin contact with their male
( p  c% I1 C) O; B: {6 z$ xpartners.6 However, when a shirt covered the applica-
1 s( k& ~9 x# C% \+ x4 s& y6 ition site, this testosterone transfer was prevented.+ {! ^( \, |4 w, a+ b  i
Our patient’s testosterone level was 60 ng/mL,
* _/ y* _+ k) D3 y' _which was clearly high. Some studies suggest that4 v+ F* E% L- ?& ~7 X$ S! r
dermal conversion of testosterone to dihydrotestos-6 q" Q, v2 ?& A4 v
terone, which is a more potent metabolite, is more9 x& w/ o5 }$ B! V/ @/ S4 f0 v
active in young children exposed to testosterone
2 }9 \, x6 s) f4 c9 S; w( Iexogenously7; however, we did not measure a dihy-
, R' I5 m' r( p- A8 ]drotestosterone level in our patient. In addition to
& P* i2 z1 ?! j& V0 X: @virilization, exposure to exogenous testosterone in
& {  E! k# Y+ g' G- kchildren results in an increase in growth velocity and
# Z+ j7 \+ |  m) _' \advanced bone age, as seen in our patient.# r( Z) s. @6 z. p8 }8 B: E5 c
The long-term effect of androgen exposure during7 \8 P/ G0 X! }- T
early childhood on pubertal development and final7 o* R' J) L$ s, J8 f8 x
adult height are not fully known and always remain
" H4 d" V9 d6 _9 e  ^a concern. Children treated with short-term testos-0 }0 m; x2 |' {5 t# x
terone injection or topical androgen may exhibit some6 k# M& [& x! I7 ?
acceleration of the skeletal maturation; however, after
$ E( U6 I- o* Rcessation of treatment, the rate of bone maturation
  H+ [6 e6 V" S" b7 v' r8 E2 N% _decelerates and gradually returns to normal.8,9
/ I, t9 v. S( fThere are conflicting reports and controversy
) t$ w# p3 V+ N& [' m% i: jover the effect of early androgen exposure on adult! _& Q) Q. |3 S  x6 z7 L
penile length.10,11 Some reports suggest subnormal- w* y9 n6 U% T" Q* D1 h
adult penile length, apparently because of downreg-
5 z/ Z' V! G8 }2 sulation of androgen receptor number.10,12 However,
2 X1 [( i% e2 [! R' e- ySutherland et al13 did not find a correlation between
# J2 z, T3 F: {8 B5 ]# G* Wchildhood testosterone exposure and reduced adult
/ i! F/ I: v% Q, v# K* Zpenile length in clinical studies.
: ^& }% d( K5 z4 o4 m5 G4 Q6 a' CNonetheless, we do not believe our patient is" q: v( r$ q: x) [0 V/ m' O
going to experience any of the untoward effects from
( J( _0 [  X; O) Wtestosterone exposure as mentioned earlier because' M2 I5 `% T0 \
the exposure was not for a prolonged period of time.6 I. y3 V6 R$ ]& [) o3 k
Although the bone age was advanced at the time of( m& ]4 u( P3 E3 i! ^1 K, Q- A
diagnosis, the child had a normal growth velocity at
5 |3 r$ t- f# ?4 cthe follow-up visit. It is hoped that his final adult: G' b/ |1 t' k$ ^; R
height will not be affected.+ x% r0 ~9 J. d. A
Although rarely reported, the widespread avail-
+ U' T( j# |" O7 ^# R) kability of androgen products in our society may
" y8 f" G6 H7 y  {9 ?: hindeed cause more virilization in male or female
/ d$ V. |; v* ?$ ~, g: y+ q/ Y  ^5 Nchildren than one would realize. Exposure to andro-
( ^0 U- W6 J3 Sgen products must be considered and specific ques-
2 R1 h( N; h9 e7 k5 ^5 Vtioning about the use of a testosterone product or
% L, Y8 X* u, R- Pgel should be asked of the family members during& T- A9 p3 Y# T, A  U
the evaluation of any children who present with vir-, ]8 a& C8 Q- n
ilization or peripheral precocious puberty. The diag-
1 {9 {' b+ x6 @) D0 gnosis can be established by just a few tests and by
) q" R" A/ U# [) z. z4 X) A: [appropriate history. The inability to obtain such a1 i1 T6 D6 r" p) r. e/ C1 B
history, or failure to ask the specific questions, may
/ O! f  X. C# F: h7 O2 f5 \2 aresult in extensive, unnecessary, and expensive
7 n+ F9 G, d- Ainvestigation. The primary care physician should be
" q# d1 C" W/ q$ O) B% Maware of this fact, because most of these children0 y( i0 d) M1 i# J& i
may initially present in their practice. The Physicians’
: S8 P) \; P, Q8 ^' uDesk Reference and package insert should also put a
+ U6 e; y+ B' v5 @( Qwarning about the virilizing effect on a male or
* l$ d( U& G3 H$ Z/ ]: U" M% Q, Jfemale child who might come in contact with some-0 F2 I# z: g* B. k6 U
one using any of these products.
2 G3 A" [* w3 e! d2 LReferences/ P( [: f9 K) ]/ G, F
1. Styne DM. The testes: disorder of sexual differentiation
+ u; C; m3 x. W7 T6 ?4 n( vand puberty in the male. In: Sperling MA, ed. Pediatric. y2 }2 U  n6 S$ T! ]
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
4 G0 @/ H7 n) q2 e8 ^1 U2002: 565-628.
- s' r" @, ~% O  V- ~' d2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious) K$ ]: t$ r, v
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old* r5 W4 y  ?. I% [# U1 Q; S
Boy Induced by Indirect Topical) _$ T' \8 u5 o8 g6 J. ]
Exposure to Testosterone
. N' @% t; b4 o' |) |* ySamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2' v6 R8 @1 ~6 S& m! @* T
and Kenneth R. Rettig, MD1
7 L; s6 r2 a; nClinical Pediatrics2 X- q# U* s% [1 ^4 j1 M
Volume 46 Number 6* Q1 Q! L$ R) S. K  U
July 2007 540-543
$ K2 n% i6 i7 Q8 S; s5 p$ _' ^© 2007 Sage Publications+ t. D% @' \: b* n; C  D
10.1177/0009922806296651
! Q4 O5 L6 \, n- n9 G, |" Jhttp://clp.sagepub.com; w% d, u  D$ J0 @8 H
hosted at" L3 x7 O1 V. }) Y( X2 N  j2 b: Y
http://online.sagepub.com( F% U" q3 k0 t$ E; I/ @0 M
Precocious puberty in boys, central or peripheral,1 M/ J5 d8 n. F) r, j- @4 W  A* @1 H" D' ^
is a significant concern for physicians. Central/ w$ O. V, t% ^+ k6 u5 A2 `- C; T' i
precocious puberty (CPP), which is mediated
  M& T$ b& L# g; q7 s+ Y3 Uthrough the hypothalamic pituitary gonadal axis, has  x) L% v/ m* g  }  {5 g
a higher incidence of organic central nervous system
0 |. Z) A1 x* blesions in boys.1,2 Virilization in boys, as manifested( K" a$ R8 Z7 `, T% b. E5 `6 y
by enlargement of the penis, development of pubic
2 @+ a+ Z8 P7 @9 p7 I3 xhair, and facial acne without enlargement of testi-
0 A" b7 q+ ^% ^3 ^5 Y3 M0 Vcles, suggests peripheral or pseudopuberty.1-3 We! h1 P1 V. P2 o' f7 N7 `( S' ^' p
report a 16-month-old boy who presented with the
2 I% W; h* D" K' [  uenlargement of the phallus and pubic hair develop-
/ |8 d5 M+ y. x$ L4 g) P& ^: Kment without testicular enlargement, which was due* ?6 [2 [, P% U$ ?$ Z
to the unintentional exposure to androgen gel used by
; v/ j8 r  o+ c6 L* r+ nthe father. The family initially concealed this infor-; P0 P2 ]# b0 w- ^$ l  a
mation, resulting in an extensive work-up for this# R5 ^& w! w3 ^0 Y# S- U0 L& H
child. Given the widespread and easy availability of
2 F  e% c% ?( X! D" T5 |2 _testosterone gel and cream, we believe this is proba-% T3 S# i- O. F1 a% H; [. ]7 V
bly more common than the rare case report in the
' b- ~. f. J+ w) tliterature.4& L( w9 J( `! A1 l% A' I1 O
Patient Report
9 U! {5 m2 P# [* |: aA 16-month-old white child was referred to the
7 I; \; c" L, ~- F4 mendocrine clinic by his pediatrician with the concern
4 s3 q9 A* K9 b8 \+ S" nof early sexual development. His mother noticed" x7 Q. A1 U, A3 r( p
light colored pubic hair development when he was
/ k. O5 y6 v8 J* A* B% u. kFrom the 1Division of Pediatric Endocrinology, 2University of0 P8 N! {! g# F  B6 p
South Alabama Medical Center, Mobile, Alabama.7 w. [: V! X  @) r4 ]" u" K
Address correspondence to: Samar K. Bhowmick, MD, FACE,6 R, Z; H, q9 B2 D
Professor of Pediatrics, University of South Alabama, College of/ N* I5 T& n& F
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;' f: c$ F) n3 \
e-mail: [email protected].* G1 b% t, U- y$ E
about 6 to 7 months old, which progressively became
) E/ F  u9 w, t/ _, R5 ndarker. She was also concerned about the enlarge-8 U5 [1 r: N7 r, k: }, Q5 J" Y
ment of his penis and frequent erections. The child- D  r" A, G) x* y0 x2 j" ?9 `2 h
was the product of a full-term normal delivery, with& A. B: ?) Z, K  [' n% y
a birth weight of 7 lb 14 oz, and birth length of" e5 x3 T) p: z$ w8 d
20 inches. He was breast-fed throughout the first year6 A% T3 n7 _) o
of life and was still receiving breast milk along with. X9 Q0 F; ]7 u1 k! V) n' j
solid food. He had no hospitalizations or surgery,! J2 Z, j. I1 Y  n' {) Y' ?
and his psychosocial and psychomotor development
8 _  k) z$ c' O7 v! O) R5 ewas age appropriate.1 u7 m* D# Y3 r
The family history was remarkable for the father,9 u3 r3 j, k" ?6 V
who was diagnosed with hypothyroidism at age 16,2 \% F$ w/ F$ o
which was treated with thyroxine. The father’s
5 |3 `0 \0 F  e+ theight was 6 feet, and he went through a somewhat/ Q/ Q# ^3 j. p: {' c% Q
early puberty and had stopped growing by age 14.
# Y/ t, i* j+ c2 @, O0 MThe father denied taking any other medication. The
4 j+ H. n. {/ n' K7 F$ t3 T. Ochild’s mother was in good health. Her menarche
( S/ s0 \) \7 }8 P0 Iwas at 11 years of age, and her height was at 5 feet
! w* n. G$ w: y& y! K( K3 X5 inches. There was no other family history of pre-
& f/ S( |$ z; [8 scocious sexual development in the first-degree rela-% v% w/ ~3 U# A% ^4 Z
tives. There were no siblings.
: O1 m7 A2 u" H) d, gPhysical Examination/ L# r2 l* P6 _0 v
The physical examination revealed a very active,! R3 v4 r2 P- ^( X" Y0 B6 l7 ~% p
playful, and healthy boy. The vital signs documented" z" ]5 g5 g+ T0 s' b; R
a blood pressure of 85/50 mm Hg, his length was( F7 E6 `) h# v$ A& e. K! R
90 cm (>97th percentile), and his weight was 14.4 kg
- Q9 ]" X; d# t' D# O(also >97th percentile). The observed yearly growth
. s7 L, w+ p( _& l7 [* t1 {. h/ xvelocity was 30 cm (12 inches). The examination of$ }( d7 ^; F( k# c- y4 G9 x6 ]( \7 b
the neck revealed no thyroid enlargement.1 i# x5 r5 |, J5 Y  ~
The genitourinary examination was remarkable for( r) R7 e6 x: B; G; m/ t
enlargement of the penis, with a stretched length of; x/ D" l" C# T2 ], [7 j! k* `
8 cm and a width of 2 cm. The glans penis was very well( q9 q+ b4 ^% N& W( j# T
developed. The pubic hair was Tanner II, mostly around
( l# u5 d  R3 D8 ~0 l- N' U1 [1 H540/ c# w4 j" \) J# J5 A( G- U  X6 \
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from5 S& }" n  y& N1 ?7 z* h: J. U. n
the base of the phallus and was dark and curled. The  S! y: ], A( A  e+ ~: _2 D
testicular volume was prepubertal at 2 mL each.
# w$ L: t3 K+ V3 I6 [4 XThe skin was moist and smooth and somewhat
" [6 W6 O- q% t" Z4 j: x& s. Ioily. No axillary hair was noted. There were no
% A- v  f. O( ]* Labnormal skin pigmentations or café-au-lait spots./ ]( |# I7 r$ y1 m; A$ {& ?
Neurologic evaluation showed deep tendon reflex 2+
0 z/ p% Z" s! {5 i" ]bilateral and symmetrical. There was no suggestion
; p" n3 s9 ]" I) Z5 Vof papilledema.' V# k& t% O% V- U! Z
Laboratory Evaluation
4 A" n+ K( s  o& F! c* nThe bone age was consistent with 28 months by, ?6 a$ I8 f. c* U4 y
using the standard of Greulich and Pyle at a chrono-
! y* I# A8 K1 j6 f* b8 slogic age of 16 months (advanced).5 Chromosomal6 l; b/ R0 [; g3 }2 U: J
karyotype was 46XY. The thyroid function test) p6 [  P2 q: C( A- v) o- Z
showed a free T4 of 1.69 ng/dL, and thyroid stimu-) x$ M; j4 F  b; Y; E+ L
lating hormone level was 1.3 µIU/mL (both normal).  L4 n( W6 [) w. [
The concentrations of serum electrolytes, blood
- s1 n7 f. c+ G8 eurea nitrogen, creatinine, and calcium all were* Q/ F( l% s1 u' x. Q% j7 e8 S" j
within normal range for his age. The concentration
' s* g  W. ?! Jof serum 17-hydroxyprogesterone was 16 ng/dL
- c' L' K, d2 r5 a9 c5 v- n(normal, 3 to 90 ng/dL), androstenedione was 20
( y* n" \; O% [3 ing/dL (normal, 18 to 80 ng/dL), dehydroepiandros-" U0 k3 H1 v' v2 r3 W- g
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
  Y; d5 [9 b3 q! Z/ ~8 l1 J9 r5 W4 n% Tdesoxycorticosterone was 4.3 ng/dL (normal, 7 to
7 `8 E. I4 Y! P7 z6 q3 B; {0 \  o49ng/dL), 11-desoxycortisol (specific compound S)
% m/ F/ o; m8 d% Y% M1 v8 `% awas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-$ g9 j/ c) p* d5 ^- o0 [
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
9 H# `7 Y9 L6 ^& @, |9 {9 O. ctestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
4 L4 u- y" b3 {# ~/ b: jand β-human chorionic gonadotropin was less than
( C( M: ?" [6 b5 mIU/mL (normal <5 mIU/mL). Serum follicular
# y$ J: w  F8 P& [stimulating hormone and leuteinizing hormone7 C$ r, w# J: e# P1 Q& n) _
concentrations were less than 0.05 mIU/mL2 X9 Y5 v5 F2 _, p1 |) q
(prepubertal).% d/ P/ u" ~) g- [8 O
The parents were notified about the laboratory
/ W. P+ m$ @- }4 R! P; Presults and were informed that all of the tests were
2 ?2 H5 B7 C0 T4 _normal except the testosterone level was high. The
; v, e. G6 s& i# E. V; ufollow-up visit was arranged within a few weeks to% o! `' e- ]! g0 e1 c) Z
obtain testicular and abdominal sonograms; how-
8 W' d' E+ E! d  ~ever, the family did not return for 4 months.
% c9 C  _3 h+ \* jPhysical examination at this time revealed that the
5 p9 Q- V6 J0 schild had grown 2.5 cm in 4 months and had gained0 y$ d2 S# i& G% M/ g
2 kg of weight. Physical examination remained
1 p2 P& U. n- q9 Bunchanged. Surprisingly, the pubic hair almost com-8 T& Z! M% e. o+ Q
pletely disappeared except for a few vellous hairs at
! K  q, T7 E. N' P4 B% C1 gthe base of the phallus. Testicular volume was still 2
2 q2 V# J7 x2 r  nmL, and the size of the penis remained unchanged.# Z# j3 M# C6 K9 {" d( b
The mother also said that the boy was no longer hav-1 w% s, @2 M2 O6 e6 w3 ?5 V
ing frequent erections.2 h  r* X0 D6 l& o9 a
Both parents were again questioned about use of
/ D' O% E8 @) o( y# \' ^3 kany ointment/creams that they may have applied to
# Y6 d* @' r- C- E7 s1 Rthe child’s skin. This time the father admitted the% s0 w: t% d- _/ k2 D# c- m
Topical Testosterone Exposure / Bhowmick et al 541
2 N/ D& `* X/ W& @: iuse of testosterone gel twice daily that he was apply-
! k& w+ F5 d8 S9 Uing over his own shoulders, chest, and back area for6 X; h) R% F. B4 `/ }
a year. The father also revealed he was embarrassed
' Y% b4 P3 D, x" m0 \& _to disclose that he was using a testosterone gel pre-4 {5 ]; y8 q* m( `; A* [
scribed by his family physician for decreased libido
# K+ ?+ @6 Z# asecondary to depression.
+ p4 W& ~) G1 X0 xThe child slept in the same bed with parents.3 ^# A, S* G5 m! B; Z5 h
The father would hug the baby and hold him on his
- M! j, N% z( M. |5 G0 mchest for a considerable period of time, causing sig-" y1 Y2 {2 t& K4 k0 ?+ x0 h
nificant bare skin contact between baby and father., t6 ~6 a- F6 j) ^* f% \
The father also admitted that after the phone call,2 s% @6 S. t  {& R+ M/ o, F
when he learned the testosterone level in the baby( |, ?) A* |- K" G
was high, he then read the product information
+ Q/ Q1 E+ }% p2 B0 ^packet and concluded that it was most likely the rea-
) N  X6 Z$ `4 v* f" Nson for the child’s virilization. At that time, they
+ e* I5 p6 I* odecided to put the baby in a separate bed, and the
' O! v, ~* s6 u' M7 @father was not hugging him with bare skin and had
8 u, ], s: Q: g- S9 H0 xbeen using protective clothing. A repeat testosterone
# L4 k( }# N8 o. [1 h& C2 Utest was ordered, but the family did not go to the3 e& v7 S% l+ [" I- m- ^- n
laboratory to obtain the test.
1 `/ w/ H5 `* RDiscussion% p6 f) Z5 |& t1 p& w3 _
Precocious puberty in boys is defined as secondary
% A* d/ |" J& Z) S3 _& |4 ssexual development before 9 years of age.1,4
; v# c. u" p4 A1 M3 R1 CPrecocious puberty is termed as central (true) when
8 S. O4 r) L  G2 `# X7 t& _it is caused by the premature activation of hypo-! Y2 D; [) O% \( M3 Z7 Q4 o
thalamic pituitary gonadal axis. CPP is more com-
. N( G2 A. }3 Vmon in girls than in boys.1,3 Most boys with CPP$ V, M6 E. w5 M1 z$ E; u
may have a central nervous system lesion that is5 P$ M3 G( U, k% {8 s8 V
responsible for the early activation of the hypothal-
9 [% {" s: Q/ ?1 z4 ]4 @5 \1 {amic pituitary gonadal axis.1-3 Thus, greater empha-: c8 x1 ^" v( }9 t- y
sis has been given to neuroradiologic imaging in' l2 _+ P& f* B! `6 v
boys with precocious puberty. In addition to viril-
: I# V) s5 d' w3 O# l4 g' cization, the clinical hallmark of CPP is the symmet-; G$ x& u! k! `& d) Y
rical testicular growth secondary to stimulation by) K) ]# {( d  ?; b
gonadotropins.1,3
% t8 h- Z: E: O' e9 CGonadotropin-independent peripheral preco-  N6 S8 J- e" ?5 \! Y2 ?; |
cious puberty in boys also results from inappropriate
6 y- {0 R, x1 _, g" W% H' xandrogenic stimulation from either endogenous or
7 V; i2 n" C0 }9 kexogenous sources, nonpituitary gonadotropin stim-
9 Y" N4 X6 k! k. O9 N/ C& Julation, and rare activating mutations.3 Virilizing
$ g' u& _/ W& v. p9 Gcongenital adrenal hyperplasia producing excessive# H4 g0 f' A5 _; j: k
adrenal androgens is a common cause of precocious$ x- w& a: X  O+ h
puberty in boys.3,40 T4 z+ J" A) d" S) _- z7 a+ v" [9 E
The most common form of congenital adrenal
+ S, y, I4 S. A: t4 s. whyperplasia is the 21-hydroxylase enzyme deficiency.) u% t1 v% R7 n1 R% Z8 J# F$ Y- u
The 11-β hydroxylase deficiency may also result in
3 U; N& A6 O/ z+ i5 U) ?excessive adrenal androgen production, and rarely,- G; K  z8 H/ J- Y
an adrenal tumor may also cause adrenal androgen1 u0 M1 e  Q8 t& |, o4 u- b
excess.1,3
  ~- S6 l6 a) v) Q* E2 \at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from* q# N. M1 D4 `4 t
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007& W0 I9 b" m9 U" W3 z( G2 ~$ }
A unique entity of male-limited gonadotropin-
( F3 S7 S9 d" s  Uindependent precocious puberty, which is also known4 W$ }1 ?' N  o9 b2 V
as testotoxicosis, may cause precocious puberty at a
$ t7 y! u' n7 |5 V# z0 L2 wvery young age. The physical findings in these boys( r8 x. z. y, e5 g# j- ^9 ^
with this disorder are full pubertal development,7 x" r1 `% J( w# J/ ?1 l1 C* F. ]
including bilateral testicular growth, similar to boys
8 o- T7 Z5 B6 |& Qwith CPP. The gonadotropin levels in this disorder
* [/ `6 r" L! {( n4 Z- Z+ B5 ^: L. }are suppressed to prepubertal levels and do not show
. j  Q. u1 R+ b* u) Ypubertal response of gonadotropin after gonadotropin-: Y# B0 B- `9 U! b# p5 T7 P
releasing hormone stimulation. This is a sex-linked; E9 i3 L  l6 Q; q* S8 h9 ^- B
autosomal dominant disorder that affects only/ w- d; c& N9 D- s% J4 s2 c; l
males; therefore, other male members of the family
+ I2 ~0 k& Q3 X) Z; [) ~6 q% D9 xmay have similar precocious puberty.3: R$ |/ `8 q* c$ ]: d5 i2 U
In our patient, physical examination was incon-
9 G0 i" h) t* I' [& W+ I0 Psistent with true precocious puberty since his testi-
" P- {" c( t( f& z4 ncles were prepubertal in size. However, testotoxicosis3 C2 m$ u( c% A. v/ R1 [+ {$ Y
was in the differential diagnosis because his father
5 I2 z: N, k( D! j- Vstarted puberty somewhat early, and occasionally,% c/ T$ `6 U2 J, O) ?: C" j
testicular enlargement is not that evident in the5 c) x2 Z& |6 A
beginning of this process.1 In the absence of a neg-2 \- D5 Y2 G1 C
ative initial history of androgen exposure, our, D: k! ?* g) C1 J1 q
biggest concern was virilizing adrenal hyperplasia,
1 Q( v& S6 x. _* u0 jeither 21-hydroxylase deficiency or 11-β hydroxylase
4 R2 h/ T3 {1 G9 A; A. |" Sdeficiency. Those diagnoses were excluded by find-
( V) V1 K1 ~6 M3 v( iing the normal level of adrenal steroids.. k/ E8 w8 J3 z: }. `
The diagnosis of exogenous androgens was strongly
/ Q" a" A1 E" G% s: nsuspected in a follow-up visit after 4 months because8 D0 q  h" Y+ a3 T7 G
the physical examination revealed the complete disap-
/ _) d' f8 M. d; f7 _) npearance of pubic hair, normal growth velocity, and
, m. t$ i( E8 V- j5 wdecreased erections. The father admitted using a testos-! v1 O2 w8 N6 c4 c, `! [3 n; R% `
terone gel, which he concealed at first visit. He was" L- z) B. a2 d  \
using it rather frequently, twice a day. The Physicians’
9 _1 o5 a1 y& _  x+ J( v6 ZDesk Reference, or package insert of this product, gel or
, |9 U* j$ R/ V3 p( P6 r; Ccream, cautions about dermal testosterone transfer to) w6 Y. e( g& R
unprotected females through direct skin exposure.
" ~7 }: ?- y4 x9 z; e# z# p, n3 Q# ~Serum testosterone level was found to be 2 times the
' t# W! Q* X7 ~1 x* ~+ P9 Y8 L6 |6 [baseline value in those females who were exposed to
. j' ?( ^; M  Q) x% ~even 15 minutes of direct skin contact with their male
! t. J; c0 [( a4 m8 |1 Ipartners.6 However, when a shirt covered the applica-
; T" Z0 @: V3 z( A1 T- P5 `tion site, this testosterone transfer was prevented.
2 m8 ]" i1 A5 ^  VOur patient’s testosterone level was 60 ng/mL,* A! \1 ?) e$ b8 U# i
which was clearly high. Some studies suggest that
( K7 _: o( w+ bdermal conversion of testosterone to dihydrotestos-  u! X- c/ |$ m* }2 k- W' `  B8 f
terone, which is a more potent metabolite, is more6 R; i$ b4 J! r# ]8 v( v( B
active in young children exposed to testosterone: n/ ~5 M, {# D& T+ J+ `& j
exogenously7; however, we did not measure a dihy-: U. o' g% C& t
drotestosterone level in our patient. In addition to
4 i$ e& J/ _% e6 w6 @) t4 avirilization, exposure to exogenous testosterone in; E* v7 O5 J. B$ c' T) Y
children results in an increase in growth velocity and$ U' O8 R' P, i
advanced bone age, as seen in our patient.
# j/ J: ]. v4 }The long-term effect of androgen exposure during
' n) T+ h% w+ E  ^early childhood on pubertal development and final
, w7 ~3 X3 R6 P  K) ?adult height are not fully known and always remain
" G* |8 B4 @; |6 m. X5 {a concern. Children treated with short-term testos-& u' k, @& t  X  H2 ^8 O9 }5 u) o
terone injection or topical androgen may exhibit some' W9 S! C5 Z( s
acceleration of the skeletal maturation; however, after3 A( \* `; H$ ^" w+ @7 K* q" E
cessation of treatment, the rate of bone maturation
* G0 ^) V4 F* b9 W/ |- ^decelerates and gradually returns to normal.8,90 T3 e; C3 S2 f/ Y: v
There are conflicting reports and controversy
( g- P/ E% g8 X6 h5 [over the effect of early androgen exposure on adult
( e7 K! R6 Z5 Q- [penile length.10,11 Some reports suggest subnormal
1 }$ x+ {4 W8 `& A" Y& L  g! C2 Nadult penile length, apparently because of downreg-
' \  b& E6 M' c- Lulation of androgen receptor number.10,12 However,
2 r1 M3 [/ O5 F3 O# T: y, \' ESutherland et al13 did not find a correlation between
9 d9 H( r; i# J# R% [; j: ]childhood testosterone exposure and reduced adult9 Y" K* J( F* W( I  {
penile length in clinical studies." P3 x& _, N9 ]- P7 `; @
Nonetheless, we do not believe our patient is# c9 \" L( r/ c8 D9 i" B
going to experience any of the untoward effects from
; K9 L9 `/ s/ o* N8 ntestosterone exposure as mentioned earlier because. S; j7 S8 G( \& m* {
the exposure was not for a prolonged period of time.
4 }- ^; e; B% I, ~% H7 E* @Although the bone age was advanced at the time of1 G# N) T: j0 ~2 A- b
diagnosis, the child had a normal growth velocity at& ~! \" F% U* k- Z9 f; Y3 J
the follow-up visit. It is hoped that his final adult
& f: d) r7 f1 y: m* H( gheight will not be affected.% B0 Q, V/ _7 t# @' w
Although rarely reported, the widespread avail-
5 b5 P( w0 [/ g' t. Z0 E5 vability of androgen products in our society may
# e! L% I; b6 ]/ cindeed cause more virilization in male or female
3 l7 v# s4 W' u) v, Pchildren than one would realize. Exposure to andro-
- Y$ x1 L$ l* D5 _" j; agen products must be considered and specific ques-! [6 |( x+ w3 g5 ]& l8 c% C( j+ j. E
tioning about the use of a testosterone product or# X4 T. b( m! v. ]& g
gel should be asked of the family members during
, M$ L$ T2 {' N4 Q$ Q$ Q' M& D, a7 ethe evaluation of any children who present with vir-
3 m: l, `9 M8 e" hilization or peripheral precocious puberty. The diag-1 I4 S* o& X, D7 P3 H9 Z' \
nosis can be established by just a few tests and by% g2 v; h9 J( {9 {. j
appropriate history. The inability to obtain such a
! ^7 y" W8 K7 `* ]/ Z$ t, s, khistory, or failure to ask the specific questions, may
$ w0 y8 T$ k# {& @( hresult in extensive, unnecessary, and expensive. X( P. z1 B. q/ b4 q, x8 x
investigation. The primary care physician should be
. k, C5 s* z9 h8 y! Caware of this fact, because most of these children
# \7 l5 K; @6 t1 V+ `may initially present in their practice. The Physicians’$ A6 d* D& T$ `. s7 w9 y/ d
Desk Reference and package insert should also put a
* t& Z6 N0 K& ]1 g9 B* Iwarning about the virilizing effect on a male or) u  C7 {/ a$ I3 {+ P. H- Q8 K
female child who might come in contact with some-
$ ]$ r# Z& W" P/ ^; |4 Sone using any of these products.
* r1 k6 U* G. a7 E- b6 [References6 W3 h, b6 q1 t- q! M2 e
1. Styne DM. The testes: disorder of sexual differentiation& G% f, y0 b) F7 A
and puberty in the male. In: Sperling MA, ed. Pediatric4 S& C: r* [% a$ p! S8 m1 k
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
/ Y# S# E5 o2 |1 o2002: 565-628.0 t8 {, Z7 _. }' W
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
  |7 ^- ]6 x4 I" G1 N6 N7 Y: }" Hpuberty 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
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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
4 o3 }: K6 K" E+ y; J5 c1 D5 Y" P) B
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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