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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% m- A1 C/ T0 }' S
Boy Induced by Indirect Topical
/ r! Q# |+ B2 F! N9 JExposure to Testosterone& z" e& P: A3 j; A) y2 s( g! J+ ~" M
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,22 s  \" h0 y- G& g& L+ t: |* \
and Kenneth R. Rettig, MD1
" h% r* F% Z4 o1 M1 w' \+ e: @Clinical Pediatrics
, L& X4 }5 V4 b# I/ C/ L! x. b( j) rVolume 46 Number 6
$ Q7 C: S: s& r+ ~: kJuly 2007 540-543. W5 C! S  i5 [2 R( Q
© 2007 Sage Publications
6 _/ u+ M2 |6 X3 s5 k7 j10.1177/0009922806296651
9 J/ p, D+ A5 W8 zhttp://clp.sagepub.com$ A9 r& @8 T6 ~
hosted at
1 Y, W- r5 t( L; Bhttp://online.sagepub.com
& b5 C: \4 \( [  C9 yPrecocious puberty in boys, central or peripheral,
+ T9 ~0 w1 L& [is a significant concern for physicians. Central
$ R! g' \& U3 F; C$ B$ f% mprecocious puberty (CPP), which is mediated- u- E& J* n8 |' M  X
through the hypothalamic pituitary gonadal axis, has
3 i( ?, R4 q$ x6 P5 f3 Ea higher incidence of organic central nervous system0 k& x6 d5 g) E2 B1 [8 L
lesions in boys.1,2 Virilization in boys, as manifested# w  K8 _3 j! g- o, O! w6 ?8 P  f) _' K
by enlargement of the penis, development of pubic6 t5 e+ f3 |1 k* Q- g
hair, and facial acne without enlargement of testi-. G7 Z  G0 F2 L0 S& X
cles, suggests peripheral or pseudopuberty.1-3 We: G$ y4 I$ h  U+ n
report a 16-month-old boy who presented with the; Z2 W7 E. q4 ]. j; z$ |
enlargement of the phallus and pubic hair develop-
! l2 Q, L8 V8 j7 oment without testicular enlargement, which was due8 k4 Z) L0 X" G$ |
to the unintentional exposure to androgen gel used by
/ j' |. s) j1 C6 L$ Athe father. The family initially concealed this infor-. d' q) B& [" x2 P& r: c
mation, resulting in an extensive work-up for this1 r- x. u# x8 s* Z1 d9 y9 W
child. Given the widespread and easy availability of
' D0 Z1 o4 @; K; A- F1 mtestosterone gel and cream, we believe this is proba-' B- J, Q2 P7 k  v% r5 o1 w5 l
bly more common than the rare case report in the
) }5 y! ]/ x8 F$ j, wliterature.4% f) S7 o- S) q( B- k; a9 ]* I( e7 p
Patient Report
9 u& S* O. d3 l& Y, @A 16-month-old white child was referred to the$ ?/ |  r) J4 e- ^  c$ l
endocrine clinic by his pediatrician with the concern5 N+ |6 Q" P* W. l" }
of early sexual development. His mother noticed, `& a$ L# W2 y9 [7 g0 U0 [
light colored pubic hair development when he was
+ N& Q) [2 Q7 N$ {From the 1Division of Pediatric Endocrinology, 2University of
1 x4 d- B9 Y2 o1 y  U* hSouth Alabama Medical Center, Mobile, Alabama.
1 Z5 F) _. P7 m5 ?; P) n5 nAddress correspondence to: Samar K. Bhowmick, MD, FACE,
5 \1 j5 e& q% F$ `5 Z7 oProfessor of Pediatrics, University of South Alabama, College of  }/ g; K$ O; H0 I
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
/ n# H3 e; M" ~7 L" ye-mail: [email protected].
8 j( o$ m% M- Z& v. g% qabout 6 to 7 months old, which progressively became8 L9 P# t5 B, \2 }9 m6 W) k
darker. She was also concerned about the enlarge-4 C7 b" [0 B% U0 l% s7 G
ment of his penis and frequent erections. The child
# f4 j  a+ n) o( c/ Cwas the product of a full-term normal delivery, with! D' ^( n: Z6 k( q8 E9 V0 G' w1 }
a birth weight of 7 lb 14 oz, and birth length of5 R( g, l; P5 ~7 D3 [
20 inches. He was breast-fed throughout the first year
7 z. S0 X- A" cof life and was still receiving breast milk along with
3 }% T7 `+ s, j) p% qsolid food. He had no hospitalizations or surgery,
, b/ R/ `9 O! y( B  Band his psychosocial and psychomotor development2 K; b. \* r; I* K
was age appropriate.
: R4 l! a" a9 f: g: P4 {% u" Y( u: K4 iThe family history was remarkable for the father,
' A# X+ S% g! N; _) I* wwho was diagnosed with hypothyroidism at age 16,
) ~" c: `" y( l* k$ p# ~  B6 pwhich was treated with thyroxine. The father’s8 m. e- w3 i' W$ y
height was 6 feet, and he went through a somewhat: @) q& U2 S4 W# ]' k) Q6 x
early puberty and had stopped growing by age 14.
6 Y6 H2 m- w' D  D0 CThe father denied taking any other medication. The$ u6 Z' G" r2 C5 N; f: I; B* ~
child’s mother was in good health. Her menarche7 V; C$ p: f3 E; ?$ `+ A  j; d6 [
was at 11 years of age, and her height was at 5 feet; x- p) @* {3 v. w  \% @' }( w# Y
5 inches. There was no other family history of pre-
& _* R& \" p2 }/ Ucocious sexual development in the first-degree rela-4 ~) K) d* T$ ?& p
tives. There were no siblings.
5 _8 V5 U* p( F2 hPhysical Examination
- f& Q6 S8 Y2 d, g/ \. WThe physical examination revealed a very active,' D9 A9 j- W' I  M+ [% ~
playful, and healthy boy. The vital signs documented" j/ a% n8 ]' t0 \& y$ u5 n3 _  u
a blood pressure of 85/50 mm Hg, his length was' L; c/ u6 T) Y$ K! n& ]
90 cm (>97th percentile), and his weight was 14.4 kg% ~: X; }  M+ f) w
(also >97th percentile). The observed yearly growth
4 J- [5 t: G+ i! V% K5 kvelocity was 30 cm (12 inches). The examination of
% `% m, P1 g! C; D/ Vthe neck revealed no thyroid enlargement./ a' Z5 ~8 F. F! _8 ^9 S0 ^
The genitourinary examination was remarkable for! ]/ G& ~" p8 a) Y' q5 k4 W
enlargement of the penis, with a stretched length of
; |# }8 O) q8 _, O" C2 f$ X9 H8 cm and a width of 2 cm. The glans penis was very well& P' i; e- r4 W) s# b1 R  ?  ?) L0 t; `
developed. The pubic hair was Tanner II, mostly around
" o, d/ {* _; W8 Q1 u! t# w. u540. e7 x, x1 Z* V
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
: s: l9 d6 F: \4 Uthe base of the phallus and was dark and curled. The
5 Q9 R6 A1 G& [* O4 q: f9 j  F: Mtesticular volume was prepubertal at 2 mL each.
6 B# N9 c/ L5 ]7 h$ ^! y8 {The skin was moist and smooth and somewhat+ i: C) I" {; \0 e2 X
oily. No axillary hair was noted. There were no
% I, C+ w/ ~8 g+ I) Jabnormal skin pigmentations or café-au-lait spots.
1 \! m' T9 c* s2 Z9 R4 KNeurologic evaluation showed deep tendon reflex 2+. i- |8 @9 {& e6 U& a! t. z
bilateral and symmetrical. There was no suggestion) r2 p9 v4 N* r+ Q3 r8 y( q
of papilledema.
% z3 R0 U% F4 [1 Y+ LLaboratory Evaluation: r- b& |! i4 Z
The bone age was consistent with 28 months by' d4 ?. `9 u. I* M5 |+ r
using the standard of Greulich and Pyle at a chrono-
- O+ C: e0 i+ t3 k3 `logic age of 16 months (advanced).5 Chromosomal3 X% k: E& R1 C  D  ~; v
karyotype was 46XY. The thyroid function test
1 [9 s0 z8 m, n% kshowed a free T4 of 1.69 ng/dL, and thyroid stimu-% e2 ~8 S: z; K: C9 g7 t1 i% C
lating hormone level was 1.3 µIU/mL (both normal).
, R+ F) Z5 O, W& [) d2 E& A5 fThe concentrations of serum electrolytes, blood4 W" {+ j9 C1 M" U+ h# C: Q: R
urea nitrogen, creatinine, and calcium all were: R" q7 v6 S2 ^9 A
within normal range for his age. The concentration' [/ e1 f1 P* W+ X. ]
of serum 17-hydroxyprogesterone was 16 ng/dL/ z* R$ L- y4 {( @8 p
(normal, 3 to 90 ng/dL), androstenedione was 20- D1 L" U/ i2 P& H1 ^* n$ A* U
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
  U1 X0 z! {" m* M- ?terone was 38 ng/dL (normal, 50 to 760 ng/dL),7 U6 A) I+ `% I/ a/ H. {
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
) o4 z) H4 ?* N0 [2 S; ~49ng/dL), 11-desoxycortisol (specific compound S)
1 U: |8 c& g: Q* m  e6 d7 fwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-8 F" d9 F+ R$ J, H! ~
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
& A. u" M$ k) _/ Q& E1 Xtestosterone was 60 ng/dL (normal <3 to 10 ng/dL),1 l. z4 M- T& H4 E
and β-human chorionic gonadotropin was less than
2 F' v. P! _0 S( }5 mIU/mL (normal <5 mIU/mL). Serum follicular
' n; e/ z# _6 j' d& Wstimulating hormone and leuteinizing hormone0 d2 G: m. G5 K; c# o  ~
concentrations were less than 0.05 mIU/mL7 S( _5 r: R& @; W4 t  P
(prepubertal).6 V  ~( @" ]1 G1 ^
The parents were notified about the laboratory1 F' [$ l4 L9 e7 y$ X3 G0 R
results and were informed that all of the tests were  \7 P% }$ c* B' W! f
normal except the testosterone level was high. The: c" H: ]$ I/ Q- K! D
follow-up visit was arranged within a few weeks to
5 D+ f2 I' u* v7 n8 Iobtain testicular and abdominal sonograms; how-" N9 [- K! S. z' S  }. e" R
ever, the family did not return for 4 months.
: s- z9 ]( }3 v$ B2 @- L+ yPhysical examination at this time revealed that the, F: h8 Y4 P- ~; E$ _
child had grown 2.5 cm in 4 months and had gained
# i9 P6 s$ Y- U) e2 kg of weight. Physical examination remained
% U% U; ~. S- H: ~unchanged. Surprisingly, the pubic hair almost com-9 z  r6 R0 r% C% z" M+ B
pletely disappeared except for a few vellous hairs at4 H; d7 K/ H  r. |; Y
the base of the phallus. Testicular volume was still 2
- l/ t7 \6 o* n& ^mL, and the size of the penis remained unchanged.% N: p% v8 G* }/ o% k" m
The mother also said that the boy was no longer hav-
' H+ H% Z8 u" e: f$ t1 ]ing frequent erections.
# B: j% L+ M/ `0 b- B' u2 v; I' XBoth parents were again questioned about use of& ]5 T; a3 V% {& u/ s4 ?
any ointment/creams that they may have applied to
  o8 Z3 F' W1 Q' \: W$ dthe child’s skin. This time the father admitted the% J: n+ f' _; J$ n# K3 ?2 S
Topical Testosterone Exposure / Bhowmick et al 541
; u% O0 u* c; l6 g8 puse of testosterone gel twice daily that he was apply-
4 y. H4 P; D7 ~  e1 Qing over his own shoulders, chest, and back area for
) z, ~! H$ f& W! K, Ra year. The father also revealed he was embarrassed
/ O( s8 C0 B% i7 r! _to disclose that he was using a testosterone gel pre-
0 k+ z; ~) v9 c' }" |4 S1 X7 Bscribed by his family physician for decreased libido
9 h# U* z# F7 L  c+ J+ nsecondary to depression.
  e# }- M9 P! JThe child slept in the same bed with parents.
& V0 ^/ o, G6 d" R9 B$ ]8 gThe father would hug the baby and hold him on his8 `: C+ J" E. r0 J& {5 [
chest for a considerable period of time, causing sig-& N1 O1 m' c) O7 u- y0 I
nificant bare skin contact between baby and father.
& h' g! S( ^, b% EThe father also admitted that after the phone call,4 k9 Z: U( a& _
when he learned the testosterone level in the baby. A9 b$ t# Q- K' v; ]% v2 d; s* |
was high, he then read the product information
/ S: j1 F3 a& c8 g% q, Y/ bpacket and concluded that it was most likely the rea-- P! o5 i2 ]& d
son for the child’s virilization. At that time, they% m1 V8 t; G* C' [5 \
decided to put the baby in a separate bed, and the
2 J9 Q' W  F1 w% r1 c2 C0 `9 ]father was not hugging him with bare skin and had; Y- J% j; U$ i' L; b
been using protective clothing. A repeat testosterone
9 |2 W! D0 j& a3 I! B+ V) ~test was ordered, but the family did not go to the8 u* N+ f: P$ g4 k5 R. P# Q
laboratory to obtain the test.
; m+ n6 m* z& ADiscussion; r' L) F* Q4 ?3 s
Precocious puberty in boys is defined as secondary' i$ {8 u' c0 X
sexual development before 9 years of age.1,47 p9 v% f6 ^; S! R. z
Precocious puberty is termed as central (true) when
* p8 Y+ \% ^; sit is caused by the premature activation of hypo-
1 i! }; {  g/ K' Athalamic pituitary gonadal axis. CPP is more com-& p. F' C# g1 w5 Q. S
mon in girls than in boys.1,3 Most boys with CPP
) g" R- x1 N" B+ c' bmay have a central nervous system lesion that is6 |8 I, F( z; o( l1 Y8 F
responsible for the early activation of the hypothal-
+ U9 ?4 D  o3 _& x& \amic pituitary gonadal axis.1-3 Thus, greater empha-0 r0 U* N3 n1 C2 J, b+ l/ \
sis has been given to neuroradiologic imaging in+ x, p; d' O# \0 a
boys with precocious puberty. In addition to viril-0 ?- U; a& F: }  M$ u
ization, the clinical hallmark of CPP is the symmet-, r+ B5 m8 Z/ u' f3 Q2 e2 L' |
rical testicular growth secondary to stimulation by9 o9 z5 k) t. b& g. K5 R! U
gonadotropins.1,37 A: _0 V  d$ ^, l
Gonadotropin-independent peripheral preco-
, y# W. r; b5 T& m1 o: Z+ D; Dcious puberty in boys also results from inappropriate
3 D( s& K4 Z6 L6 I; l- {2 }5 m( pandrogenic stimulation from either endogenous or- P  z% a5 u1 `5 {8 G$ {# j- {
exogenous sources, nonpituitary gonadotropin stim-, t% g. ^  R! U2 Z
ulation, and rare activating mutations.3 Virilizing
" G; Y( y( u' N; f* Zcongenital adrenal hyperplasia producing excessive
0 g- J9 n6 ~, |( Gadrenal androgens is a common cause of precocious
; t( n! L* G1 _7 @) fpuberty in boys.3,4
# i+ Y- i  p! {. o1 E& k! E; X$ mThe most common form of congenital adrenal8 I$ n& t0 m0 \" L4 V
hyperplasia is the 21-hydroxylase enzyme deficiency.; {3 x4 C; q  i6 e: I7 [
The 11-β hydroxylase deficiency may also result in# ^; s: w2 J4 L- D3 h" g7 i5 t
excessive adrenal androgen production, and rarely,1 ]% N. T/ X! ?/ g( ^8 a! n7 J6 N
an adrenal tumor may also cause adrenal androgen, b8 y9 Y! \4 u
excess.1,30 X* _' X2 v$ G9 b
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from2 q0 q' v2 @2 m$ b' Y2 G
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007! R6 }% l; \% T% E. L; E0 Q1 G* W7 @
A unique entity of male-limited gonadotropin-
" T) T! b3 _5 _3 w8 [! mindependent precocious puberty, which is also known1 G5 J2 T* G5 b: @$ @6 l* x* R
as testotoxicosis, may cause precocious puberty at a
. W+ S) W( M$ B/ tvery young age. The physical findings in these boys9 p% i3 u. h6 y2 [+ K
with this disorder are full pubertal development,
5 @1 X/ |  n, r0 z) _$ i# \/ bincluding bilateral testicular growth, similar to boys
' `/ H9 V+ c9 V' Uwith CPP. The gonadotropin levels in this disorder" P* H4 c; ~3 |+ S
are suppressed to prepubertal levels and do not show6 P- R/ P" a; r( n( b* D6 E( z6 {
pubertal response of gonadotropin after gonadotropin-
+ n! ?3 z1 u/ Z' ~8 D- hreleasing hormone stimulation. This is a sex-linked; L) x3 S" H6 p
autosomal dominant disorder that affects only- Y. s' n' E' S% G8 K: ^
males; therefore, other male members of the family, O: X6 C: ^$ t% V! m9 |
may have similar precocious puberty.3% {* f9 q; }% ]# g
In our patient, physical examination was incon-
1 f: m/ f% P. m7 z, Vsistent with true precocious puberty since his testi-
( E) C% @9 }6 g# j( Bcles were prepubertal in size. However, testotoxicosis
6 B) G4 w( L2 Rwas in the differential diagnosis because his father# l3 w+ F. ?$ I! }  ~$ p
started puberty somewhat early, and occasionally,
# G4 ]+ D& m5 G* _! ~testicular enlargement is not that evident in the5 d/ ^: @+ j& l4 w* t) A% K& G( n
beginning of this process.1 In the absence of a neg-
6 l8 g% p; K5 G- G1 mative initial history of androgen exposure, our8 l) N. H1 @. P/ U. D( v3 c/ t$ L
biggest concern was virilizing adrenal hyperplasia,+ z3 S9 `/ u/ ?: z7 V( x" L' z; j7 K
either 21-hydroxylase deficiency or 11-β hydroxylase# M2 j) b8 u1 }: C; e" n/ A
deficiency. Those diagnoses were excluded by find-
# f3 \% G7 r! F" ting the normal level of adrenal steroids.$ |6 A+ e' x. y7 Z
The diagnosis of exogenous androgens was strongly7 P) T( ]8 \& T: n6 b3 v& w
suspected in a follow-up visit after 4 months because
; b8 D+ X  b9 h7 \  D) \the physical examination revealed the complete disap-4 C% \" s, u3 u
pearance of pubic hair, normal growth velocity, and
, c7 F4 X0 A4 g! z3 }' t; ^* Ddecreased erections. The father admitted using a testos-
5 d8 r. f& }5 x5 ^$ _7 ]6 B/ hterone gel, which he concealed at first visit. He was
) \/ R" W' Z1 l+ y$ ]2 ]% b% @using it rather frequently, twice a day. The Physicians’1 ]/ D2 o$ y, w
Desk Reference, or package insert of this product, gel or
' X% V9 ?! @9 S! ^cream, cautions about dermal testosterone transfer to0 i  r2 T* B5 w* _' E. m
unprotected females through direct skin exposure.* Z! e9 f4 T1 X. d9 t1 K, A8 {
Serum testosterone level was found to be 2 times the* ]' h- ?1 b7 o- j0 `4 s- w
baseline value in those females who were exposed to
- A- l9 e4 t1 K' S% ~even 15 minutes of direct skin contact with their male
! b- q' r. c% N( [& d) b# cpartners.6 However, when a shirt covered the applica-: z+ k$ U. Q5 C
tion site, this testosterone transfer was prevented.  _' r  t8 z4 R3 K+ \0 _
Our patient’s testosterone level was 60 ng/mL,6 ?# ^2 D$ u1 w4 A
which was clearly high. Some studies suggest that# }9 w( J  p  v" \$ D$ m
dermal conversion of testosterone to dihydrotestos-% E1 [$ q8 v1 [2 X5 b
terone, which is a more potent metabolite, is more2 B5 W6 V! ^  U; C) C
active in young children exposed to testosterone
7 `0 y4 `( \- J$ ?9 Vexogenously7; however, we did not measure a dihy-
9 N' ^  M8 W* U# Q$ t, ]. M3 bdrotestosterone level in our patient. In addition to) K: f7 f% v4 {0 y" K$ q
virilization, exposure to exogenous testosterone in: K# |* W/ {( C- x  E7 o
children results in an increase in growth velocity and( {+ U+ O! ~5 N; i; t  K. {  {4 a
advanced bone age, as seen in our patient.
* `0 e* \( c3 t; O% t/ ]2 oThe long-term effect of androgen exposure during
& P" l$ ]* _+ Oearly childhood on pubertal development and final
( n) c3 }2 T" nadult height are not fully known and always remain
8 ]/ ~( Y0 K- za concern. Children treated with short-term testos-& z6 P$ X, x, X4 J
terone injection or topical androgen may exhibit some
4 [  W/ i7 I; Uacceleration of the skeletal maturation; however, after* \  \$ C/ m! T) c) P
cessation of treatment, the rate of bone maturation
) b) v& {6 c# `: Ddecelerates and gradually returns to normal.8,97 p3 p) M; N$ T& Z$ j
There are conflicting reports and controversy
% e# M! a% N+ m- D$ i6 E6 R1 a; oover the effect of early androgen exposure on adult9 r! o1 i2 y1 O. P3 G/ b
penile length.10,11 Some reports suggest subnormal* p) w* ?& X. }! }8 h. w0 V
adult penile length, apparently because of downreg-" f0 G7 m* ~, [+ l4 a2 ]) w4 t( a- U
ulation of androgen receptor number.10,12 However,1 U2 V4 f; J5 |4 Z, R0 \4 b3 ^9 |$ `
Sutherland et al13 did not find a correlation between
- X% S, @( f1 g5 C, bchildhood testosterone exposure and reduced adult
6 P- k7 }; o* y( Y" a0 U, jpenile length in clinical studies.+ V. W( G( U( r" N& J
Nonetheless, we do not believe our patient is% b+ |" p$ u' ^5 k, Q! A; D% E$ h
going to experience any of the untoward effects from: V( J: y0 B2 |; v1 q3 m
testosterone exposure as mentioned earlier because
+ q3 k; r; i4 z' _( S+ F) \8 E" P$ mthe exposure was not for a prolonged period of time.
3 |+ T/ G) p) f* k; k+ P" kAlthough the bone age was advanced at the time of+ Z' ^+ q: b/ `' Q
diagnosis, the child had a normal growth velocity at/ w+ z; }* d) G+ \+ K- y4 y6 k
the follow-up visit. It is hoped that his final adult
( z7 D5 Y# l/ n4 _height will not be affected.8 L+ D  S$ H% y- g3 m% P
Although rarely reported, the widespread avail-8 B6 s& V& H" Q
ability of androgen products in our society may9 o# Q; y; b* b1 k! i8 }. ~3 p
indeed cause more virilization in male or female
+ ]- q& D, S; F; Q' F8 @children than one would realize. Exposure to andro-
: y1 R1 ~1 c3 X% G0 l# p: Ygen products must be considered and specific ques-) L0 K2 k5 n+ V) p) D/ J
tioning about the use of a testosterone product or0 {7 T' B/ p/ X8 _$ F8 E! b6 t
gel should be asked of the family members during
) s6 p3 f4 x) U5 ?the evaluation of any children who present with vir-; m& J& _- R, a0 n  F* m
ilization or peripheral precocious puberty. The diag-
; B" E# ]' F* @' U2 bnosis can be established by just a few tests and by
* o# e' D& T, Q& F9 g7 _& h5 M' X. L' Lappropriate history. The inability to obtain such a
6 D$ L( p% x& s; ]history, or failure to ask the specific questions, may3 i- e/ D' `- D7 i- \
result in extensive, unnecessary, and expensive9 m% \6 v; \1 Y/ o/ g
investigation. The primary care physician should be
9 T4 p) m( Q) E5 Faware of this fact, because most of these children
) a1 H& ]5 |2 S5 r7 z. rmay initially present in their practice. The Physicians’
2 ?) ]) s( C) o4 p3 X3 {Desk Reference and package insert should also put a4 r0 J( a+ j3 i/ C" l  e
warning about the virilizing effect on a male or
) h7 {% P7 o5 L, ^' r4 afemale child who might come in contact with some-
' r& H" x- j  q9 f# I+ sone using any of these products.2 V% ?. Z' F7 J$ R( j4 d, i, |
References
4 e4 m# E- B% e. t1. Styne DM. The testes: disorder of sexual differentiation: ^/ Y8 q/ F& O$ V8 ^
and puberty in the male. In: Sperling MA, ed. Pediatric
/ m: F; H. p5 Q: z5 tEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
: B" f3 t/ s1 _. T# K2002: 565-628.( Y. L$ x) {7 W( s
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious7 r2 e2 _* {$ s6 {% ^
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
) c- z* r/ y" z) [1 m- ]Boy Induced by Indirect Topical
. ?0 T4 Y8 \+ S9 X9 q: l  Y- LExposure to Testosterone
! ^: Q- q" c8 q) DSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,22 D6 f0 r. @. k7 }; `
and Kenneth R. Rettig, MD1: }  B3 _0 ?* y
Clinical Pediatrics( T& [# o. M, ^
Volume 46 Number 6
: M$ s! H4 k+ v' k. u0 I# B3 Q  e. LJuly 2007 540-543
. \# c" B) D, |2 K6 b, i7 ]4 K© 2007 Sage Publications
0 X, ?! r1 m; B10.1177/0009922806296651
& n( C' T; {- V: n& Chttp://clp.sagepub.com+ J6 v# s6 Z3 Y- U0 v+ X
hosted at
. S1 E. H* U# `: {! W" y2 ghttp://online.sagepub.com
6 a: f8 d! C& c( E/ u8 i1 nPrecocious puberty in boys, central or peripheral,
* f( K9 x% L- H  {# [is a significant concern for physicians. Central( m2 R* T$ `( k3 [# H* s
precocious puberty (CPP), which is mediated
" U0 z" B3 {( K$ Z2 U" ~through the hypothalamic pituitary gonadal axis, has' F9 F8 Y; q2 [$ ?
a higher incidence of organic central nervous system
0 w$ O; p; {8 C2 {( ?& w" s$ C3 S1 wlesions in boys.1,2 Virilization in boys, as manifested  n+ Z2 I7 L; O
by enlargement of the penis, development of pubic
, Q6 `; P6 A3 W. Q' Yhair, and facial acne without enlargement of testi-" p; `9 ]1 [$ D5 G1 H( v- }
cles, suggests peripheral or pseudopuberty.1-3 We
0 }% s. T" \8 ]: ?0 y2 D& Mreport a 16-month-old boy who presented with the5 C. \  o8 |6 w! E
enlargement of the phallus and pubic hair develop-& n* Y0 v6 N4 L
ment without testicular enlargement, which was due; W" a; A7 x+ f+ b9 ^( \( C
to the unintentional exposure to androgen gel used by3 _# @2 b+ I7 V8 f1 P( t  r( G
the father. The family initially concealed this infor-
# _: f: @  H7 K4 Cmation, resulting in an extensive work-up for this2 N& f6 z4 K: ~4 Z6 |9 e3 m
child. Given the widespread and easy availability of5 S9 B' y. r( Z% [6 v4 d
testosterone gel and cream, we believe this is proba-
4 A; M- P0 a" l2 Q" }bly more common than the rare case report in the8 k+ l" H! v0 ?4 u5 @2 }
literature.4* L. Y- ~7 ^  L: T
Patient Report# E8 x* E% h# a2 Z
A 16-month-old white child was referred to the
# ^# q) N% j  Rendocrine clinic by his pediatrician with the concern5 Q; O/ o/ n8 b" Q" I. S! j
of early sexual development. His mother noticed
0 U" w2 T6 e- C8 G5 W7 m- U: Y* B7 Alight colored pubic hair development when he was
" D/ W/ z$ A$ d( r& V$ u# vFrom the 1Division of Pediatric Endocrinology, 2University of
4 q& Q+ }, c: |( ^5 f1 RSouth Alabama Medical Center, Mobile, Alabama.5 F, G7 V; w8 z- c% K6 y
Address correspondence to: Samar K. Bhowmick, MD, FACE,6 j, K1 I2 F/ {+ Y- n; m9 s
Professor of Pediatrics, University of South Alabama, College of' B1 R2 a1 S& @; A5 L8 W; m# i
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;0 o4 C9 V' l8 H: e# D- O
e-mail: [email protected].+ J* f2 T) F& g+ Q9 f% u" {
about 6 to 7 months old, which progressively became5 b) U& n% V. P! E8 ~( |
darker. She was also concerned about the enlarge-
3 y1 k: D  N; F0 T6 n. ^* G! V4 yment of his penis and frequent erections. The child
- C: }6 a" C' h: J# X. w3 Gwas the product of a full-term normal delivery, with$ ~+ E8 c0 |: v' h3 T5 N7 L5 n
a birth weight of 7 lb 14 oz, and birth length of
1 a& L3 V0 W7 ^) A- u3 z; F20 inches. He was breast-fed throughout the first year" q; T2 |! R; G. Y: p3 ^% [
of life and was still receiving breast milk along with4 n- p; T4 V) S- A' Y* o( G% L
solid food. He had no hospitalizations or surgery,8 G" O/ [7 Y: D$ r
and his psychosocial and psychomotor development3 a) d/ q! P* w. b& Q
was age appropriate.
  T+ l- O+ \" ^/ z: c! ?3 bThe family history was remarkable for the father,
# C2 Z, S8 l' N4 y2 Q; E/ ewho was diagnosed with hypothyroidism at age 16,
% A& B* e+ c# P# J9 E# vwhich was treated with thyroxine. The father’s8 q/ X  N- T8 `
height was 6 feet, and he went through a somewhat, b% z# i- |5 H
early puberty and had stopped growing by age 14.
0 p5 ]9 c- ?( d( NThe father denied taking any other medication. The
' }4 y! V% s! o2 J! f, ?child’s mother was in good health. Her menarche
+ `2 n  O3 b$ M7 x+ Uwas at 11 years of age, and her height was at 5 feet& {# U+ |% G) T+ R
5 inches. There was no other family history of pre-
2 s0 s& H: y! [. Ycocious sexual development in the first-degree rela-
- o1 H  s/ ?. S' b) gtives. There were no siblings.5 ^/ V  e0 A7 q/ d
Physical Examination3 c# F2 ?+ ^& t, f/ Z. m, I  o
The physical examination revealed a very active,
0 V+ E. j! {. B+ Iplayful, and healthy boy. The vital signs documented
# U! K: k7 h' o- u% ^' u* z% Ma blood pressure of 85/50 mm Hg, his length was& ?8 l' r9 K9 E. b0 v) e/ ]: n# w: a
90 cm (>97th percentile), and his weight was 14.4 kg; L6 w9 V% p! x' T# @8 |
(also >97th percentile). The observed yearly growth. P  o) \; k7 x( l" V$ ?' n
velocity was 30 cm (12 inches). The examination of- X" B2 W% A6 n1 p3 `3 k0 {; C8 M
the neck revealed no thyroid enlargement.
4 P4 K' i0 q0 |9 X2 N# GThe genitourinary examination was remarkable for
& M$ n4 i2 N+ z; K6 uenlargement of the penis, with a stretched length of
6 E! s$ j# m# B1 G" ?9 M  f* ^8 cm and a width of 2 cm. The glans penis was very well
+ m7 w9 _9 T2 N  T+ I6 Udeveloped. The pubic hair was Tanner II, mostly around5 S. l8 n4 N8 M- x% e  _; A
540
* v! b4 V& K/ H9 ^# A% `& y1 iat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from$ f* p; `: k+ d+ g
the base of the phallus and was dark and curled. The" J9 r& g7 D* Z5 r. e
testicular volume was prepubertal at 2 mL each.5 n; A' I& h- \- }7 N3 u7 N! Y
The skin was moist and smooth and somewhat
+ t- ]. e! C5 W- P3 Z* Qoily. No axillary hair was noted. There were no" l' F) F* `5 K2 C4 S% s! J/ B
abnormal skin pigmentations or café-au-lait spots.8 a3 ]$ v# f, ~6 V
Neurologic evaluation showed deep tendon reflex 2+( a1 S2 U) C8 L! F
bilateral and symmetrical. There was no suggestion
4 q7 {/ o% g4 y9 eof papilledema.  W; }2 v) {$ t/ Q/ {6 b% n  r
Laboratory Evaluation
7 j5 U( g) s, I: z2 RThe bone age was consistent with 28 months by
6 ]; R: Q/ l7 {2 Tusing the standard of Greulich and Pyle at a chrono-3 ^% K- m: N, M* e9 k
logic age of 16 months (advanced).5 Chromosomal
) m; D* v4 M7 Q! j' N8 L/ y5 Ckaryotype was 46XY. The thyroid function test: F8 P$ s9 m* b0 i
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
% x$ h9 I$ @' O  Nlating hormone level was 1.3 µIU/mL (both normal).9 [/ \9 ]2 I  i1 s+ I: h$ k
The concentrations of serum electrolytes, blood
  {2 w, c1 h' O5 aurea nitrogen, creatinine, and calcium all were
! {0 _0 Q( u  q0 `. iwithin normal range for his age. The concentration
% Z: \+ q& U0 s" e% Rof serum 17-hydroxyprogesterone was 16 ng/dL
8 @" L( y# I1 x% v(normal, 3 to 90 ng/dL), androstenedione was 20
, J, ?/ U( d7 A- ], zng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
6 }( P- ~! {) A/ P8 b2 Gterone was 38 ng/dL (normal, 50 to 760 ng/dL),
+ W% _: V! X5 X- o3 ddesoxycorticosterone was 4.3 ng/dL (normal, 7 to
) Z  O1 U0 R8 S( O2 w" A49ng/dL), 11-desoxycortisol (specific compound S)
9 g5 w& r* L6 b. E1 Y" Hwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-, N, w3 |4 L' H" J+ A' \- J
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total5 d) o* }6 c1 O. s( K( g: Q
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),2 Y$ @) G9 c; G  W
and β-human chorionic gonadotropin was less than
6 o1 Y  a1 k' R. e5 mIU/mL (normal <5 mIU/mL). Serum follicular2 ~( Y0 H, N' Q! t# m& J
stimulating hormone and leuteinizing hormone
" a2 s& K9 `1 h& r! H* O* ~concentrations were less than 0.05 mIU/mL* y  @' m7 A, h, `+ x. V
(prepubertal).9 g/ l  I4 [/ A1 b
The parents were notified about the laboratory. e$ _  b6 @, v' X
results and were informed that all of the tests were
, \6 R7 Z" m6 \/ knormal except the testosterone level was high. The
( k7 |( @+ H6 e2 [7 Jfollow-up visit was arranged within a few weeks to
3 P  k+ m) @4 G- |/ \* f) }! W( x% Fobtain testicular and abdominal sonograms; how-3 o$ K3 L2 L! H( V
ever, the family did not return for 4 months.' t6 T, I5 B7 V0 x
Physical examination at this time revealed that the9 h" ~/ Y+ A3 N0 }8 e9 x; e( A
child had grown 2.5 cm in 4 months and had gained
: w" Z4 t7 m7 A) `( E- x0 k" W2 kg of weight. Physical examination remained
6 a" d$ A7 u( t0 q! w8 d  Y1 [! tunchanged. Surprisingly, the pubic hair almost com-& v  Z. j  ?' {: b7 G3 S) K
pletely disappeared except for a few vellous hairs at* O0 D5 R6 y' S1 c' u1 ^
the base of the phallus. Testicular volume was still 2, c" q" ]0 N3 ~* d
mL, and the size of the penis remained unchanged.
  t3 g: [* J6 H% o- p1 ?The mother also said that the boy was no longer hav-) d- X! S, L8 @$ E( |- Y
ing frequent erections.
- X/ z% o0 J0 W% [Both parents were again questioned about use of# r3 ^- I' ^* m
any ointment/creams that they may have applied to
9 o/ G6 k2 }% Q/ c! i2 q& w" Lthe child’s skin. This time the father admitted the6 H3 t  j% T, g7 |- m# I
Topical Testosterone Exposure / Bhowmick et al 541- n& y  v) |$ Z' \9 N% m" r6 [
use of testosterone gel twice daily that he was apply-0 ?; B, c$ W! N$ E3 W
ing over his own shoulders, chest, and back area for
( Q; o( K- d8 G( ma year. The father also revealed he was embarrassed
3 X% r3 s6 J& L1 G1 Pto disclose that he was using a testosterone gel pre-
4 \* B8 [3 I4 k" e8 dscribed by his family physician for decreased libido
5 W6 b1 U* _0 T' m+ T9 w9 M- X/ tsecondary to depression.3 X0 u6 c0 t4 h" s' E
The child slept in the same bed with parents.
/ T8 F& V8 X6 ]/ EThe father would hug the baby and hold him on his
; s( _1 u9 ~4 o6 i" Bchest for a considerable period of time, causing sig-
( v8 {0 s4 m3 Y6 z7 ~$ x) Y4 f- jnificant bare skin contact between baby and father.
+ j6 u  z7 t* a9 q' d0 @The father also admitted that after the phone call,
% q( `; s+ R8 v, Mwhen he learned the testosterone level in the baby
+ O% I; C2 d. L1 u7 j$ |) Dwas high, he then read the product information9 a7 @: R- f5 E2 l) [) y7 g
packet and concluded that it was most likely the rea-
6 x! b) K5 W; E( v: zson for the child’s virilization. At that time, they* Z; ~+ p# R& c* d# Q; s1 k
decided to put the baby in a separate bed, and the4 w- k: ]$ E, q! y; P+ S+ \$ p
father was not hugging him with bare skin and had
0 v! _/ W& \2 y' S* U8 c: U" Jbeen using protective clothing. A repeat testosterone9 R  G% H/ o0 z2 t" U' d  Q* t
test was ordered, but the family did not go to the
3 v2 O4 j1 @. V4 q# E# [! t+ J" Blaboratory to obtain the test.
: b" Z* \1 W/ C  `+ K' MDiscussion
+ \; ?; Q9 Y* [  N% N0 u9 Q( ?. oPrecocious puberty in boys is defined as secondary
% h7 e1 W) H; ysexual development before 9 years of age.1,4' ~1 ^* T# M' t
Precocious puberty is termed as central (true) when
1 G6 [! h' k4 H# r5 K3 s* fit is caused by the premature activation of hypo-
9 h  M+ l" h3 Q$ l# H2 ethalamic pituitary gonadal axis. CPP is more com-' M' g4 w) U+ O( R
mon in girls than in boys.1,3 Most boys with CPP" T; Q* s- h( u, i
may have a central nervous system lesion that is
- Y( S, M% {1 f; gresponsible for the early activation of the hypothal-
) J! X# ~1 p/ h9 E( iamic pituitary gonadal axis.1-3 Thus, greater empha-
1 C+ d1 K4 k/ R& V& r9 Isis has been given to neuroradiologic imaging in8 a2 |4 q) B" b6 P
boys with precocious puberty. In addition to viril-8 C& z9 F- V: C1 H
ization, the clinical hallmark of CPP is the symmet-5 r$ u, K: N% l  w- E
rical testicular growth secondary to stimulation by
; l9 k' c' R) E; R/ p6 Pgonadotropins.1,33 x9 _8 Y- e: f
Gonadotropin-independent peripheral preco-4 u& G: v8 C2 i, _. c1 v
cious puberty in boys also results from inappropriate
3 r1 }3 ^: @$ y6 A5 V2 a0 D1 vandrogenic stimulation from either endogenous or
! E+ F# v% q0 b: Q# F) L6 |exogenous sources, nonpituitary gonadotropin stim-( W3 ^4 D8 F" y  m
ulation, and rare activating mutations.3 Virilizing
, [0 d. I- h) q1 `congenital adrenal hyperplasia producing excessive
+ H& S& N! J5 R& m& Nadrenal androgens is a common cause of precocious
' N0 c1 c. h$ N! k* o1 o) [6 S; Opuberty in boys.3,4
+ u! m3 ^9 F: t% l% Q# \The most common form of congenital adrenal, H* ]9 g- C) L; V# M: l% e
hyperplasia is the 21-hydroxylase enzyme deficiency.) K1 Y/ P3 K& ?. U9 E
The 11-β hydroxylase deficiency may also result in
. c- \" b! K7 f. w- W8 ^+ K# texcessive adrenal androgen production, and rarely,
8 s  p5 b+ a! k0 L0 d5 S5 `$ {# nan adrenal tumor may also cause adrenal androgen
2 g4 J7 S5 J$ eexcess.1,36 Y0 t$ b3 ~0 h7 X3 y: ~
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from( ?, o9 R2 k. j- _$ l' f! r6 r4 C" J
542 Clinical Pediatrics / Vol. 46, No. 6, July 20075 g4 ?' J6 l1 I* w5 q9 f
A unique entity of male-limited gonadotropin-
/ b& g4 M, d# k9 Eindependent precocious puberty, which is also known2 w# x1 t4 [5 V  n0 J' L
as testotoxicosis, may cause precocious puberty at a; ]- N/ @4 s8 i) v* R# [, ]
very young age. The physical findings in these boys
/ [! Y% u3 |) X1 {1 h+ Swith this disorder are full pubertal development,3 h8 s5 {) q% q9 |
including bilateral testicular growth, similar to boys
- k) v- D% N& d3 i# f! _( R9 |with CPP. The gonadotropin levels in this disorder/ d+ M5 H% O5 g( N/ d
are suppressed to prepubertal levels and do not show1 l3 M. D9 R, O
pubertal response of gonadotropin after gonadotropin-
" Y2 V# n1 x+ G* i( mreleasing hormone stimulation. This is a sex-linked
* ?" \" C9 M. t; u) bautosomal dominant disorder that affects only
4 R. t3 g9 W+ U( i( `) [males; therefore, other male members of the family
) W0 z' W, ]5 }7 N! Kmay have similar precocious puberty.3
. h4 G' T! f' M  ~In our patient, physical examination was incon-/ P( H, M. |" s! a: W. P0 i
sistent with true precocious puberty since his testi-
" p: Z$ N' Q  [6 z0 O# w% B0 G0 Icles were prepubertal in size. However, testotoxicosis
8 x8 p; I0 U* ~" l2 Kwas in the differential diagnosis because his father
/ N7 g) g" j3 rstarted puberty somewhat early, and occasionally,
0 h  X2 h& r5 C+ Y( rtesticular enlargement is not that evident in the
. d9 {" k: I6 a+ f# C+ D8 U# vbeginning of this process.1 In the absence of a neg-& p4 Q0 ]# F+ F3 G+ K. T
ative initial history of androgen exposure, our4 l( e# J) o. \. `
biggest concern was virilizing adrenal hyperplasia,5 M  |% e2 K' `. F
either 21-hydroxylase deficiency or 11-β hydroxylase
# r9 u/ H* @. b$ r1 N- zdeficiency. Those diagnoses were excluded by find-- Z1 B* U$ b! M+ b
ing the normal level of adrenal steroids.# S+ N4 }6 b" P- J- }* x/ N/ V
The diagnosis of exogenous androgens was strongly6 V3 @! L; w( S" h5 U0 r: Q3 k9 r
suspected in a follow-up visit after 4 months because0 P* Q8 j0 F% O4 b
the physical examination revealed the complete disap-
# H% S( {% R. ]3 N2 qpearance of pubic hair, normal growth velocity, and8 D5 Y9 m4 d- I1 s' m3 F
decreased erections. The father admitted using a testos-
& ~1 \5 n) e  ?4 f) k8 T& ]" lterone gel, which he concealed at first visit. He was
; f- S. b/ ?8 ^! y/ @using it rather frequently, twice a day. The Physicians’6 f( p8 w: G4 {8 C
Desk Reference, or package insert of this product, gel or
( F8 ]. p# s8 ^cream, cautions about dermal testosterone transfer to# @/ S: x7 b" G* |7 M0 |0 L
unprotected females through direct skin exposure.
9 ?6 V8 _2 D( O0 [0 cSerum testosterone level was found to be 2 times the
, u! U  N$ A+ s& Rbaseline value in those females who were exposed to* o8 g. `6 f/ l5 t2 e4 b
even 15 minutes of direct skin contact with their male
& A! ~3 H$ @$ e# o3 v1 I5 apartners.6 However, when a shirt covered the applica-
" ^6 j/ |$ A$ |2 l) T5 Rtion site, this testosterone transfer was prevented.% K: g8 f/ q+ y1 L. [  }' L/ C1 e
Our patient’s testosterone level was 60 ng/mL,
  b5 f  b7 S& D7 g& I8 M7 ?1 _, K( Twhich was clearly high. Some studies suggest that& O3 I3 x% x: C! v
dermal conversion of testosterone to dihydrotestos-- W5 I( i0 U; X, C9 L9 Z
terone, which is a more potent metabolite, is more
! u8 K' O$ r  P/ v; W  B- Dactive in young children exposed to testosterone
7 z: }# I% G+ y7 ~5 Zexogenously7; however, we did not measure a dihy-7 `, U) r0 P3 Q7 H* t. J3 @" }4 {
drotestosterone level in our patient. In addition to
- F3 ^2 B7 F" F) {  j5 avirilization, exposure to exogenous testosterone in. ]# G. e" W: |9 ]$ N3 ^
children results in an increase in growth velocity and, z4 J4 p* G* ^6 B0 B2 N9 R
advanced bone age, as seen in our patient.; @9 T4 z' F" T- E4 d+ e$ i& t
The long-term effect of androgen exposure during- ]! d5 X/ Q" m2 S7 u
early childhood on pubertal development and final
' f$ B5 _/ Q6 d! N1 @$ C1 sadult height are not fully known and always remain* \! i+ v# w: [2 C8 ]( B/ Q! q
a concern. Children treated with short-term testos-
" ~+ {- o# |: y# v6 ?terone injection or topical androgen may exhibit some% Q* P5 u- e8 H% @5 Q
acceleration of the skeletal maturation; however, after
8 d1 {$ [; U, B. Rcessation of treatment, the rate of bone maturation
6 @" P- C! }  Ddecelerates and gradually returns to normal.8,9" c' b" }2 k( y3 {" Q5 g& {
There are conflicting reports and controversy
2 j3 T# h3 j! h. E) Rover the effect of early androgen exposure on adult
) P6 b+ E# }8 c1 c% M7 N( V5 k4 Openile length.10,11 Some reports suggest subnormal$ x$ m7 I3 J3 o6 A
adult penile length, apparently because of downreg-6 Q' k0 a3 N; ?* y3 ^$ J% \
ulation of androgen receptor number.10,12 However,& O$ Y' a0 m- S% W
Sutherland et al13 did not find a correlation between; b3 x( z& ^! H' s: c1 e
childhood testosterone exposure and reduced adult( z) _8 {  ]% D9 f
penile length in clinical studies.
- Z5 O4 R1 N- x; l5 E- QNonetheless, we do not believe our patient is
; E& x$ c! d+ ~going to experience any of the untoward effects from
+ s  Z8 J* D' X3 \) ~* ^4 \testosterone exposure as mentioned earlier because5 Z" e. B1 |0 ]8 t$ o( P
the exposure was not for a prolonged period of time.7 Q6 O2 Q4 i: Q7 B; H
Although the bone age was advanced at the time of: z. P9 _3 l7 J
diagnosis, the child had a normal growth velocity at# Z& O& q1 l/ _+ Z. @
the follow-up visit. It is hoped that his final adult& h+ a7 f: M! m2 l3 E
height will not be affected." {5 I# }4 T" A
Although rarely reported, the widespread avail-7 B( D6 b( m/ n) Q
ability of androgen products in our society may1 c# u% |; h. J  o
indeed cause more virilization in male or female. P2 W) k9 S9 ~& @8 ~
children than one would realize. Exposure to andro-
; v! P/ J4 X, n8 k: [& Ygen products must be considered and specific ques-
4 x6 ?6 }, [0 ^: ?) ?3 t6 p  Rtioning about the use of a testosterone product or9 z4 ^; b! ~. }
gel should be asked of the family members during
, V8 Q8 d- Q/ Y" U3 Hthe evaluation of any children who present with vir-
: ^* N/ s" Z: Y3 @: Y4 d0 Vilization or peripheral precocious puberty. The diag-
0 r0 k* W  @) q" u2 Inosis can be established by just a few tests and by" C1 x, L6 t5 T( l
appropriate history. The inability to obtain such a
) C* N2 Y0 B1 D7 Dhistory, or failure to ask the specific questions, may
5 |  @1 O9 Z8 m8 {. D, cresult in extensive, unnecessary, and expensive. h; g8 @6 o; c0 y% ~) k% I
investigation. The primary care physician should be6 `: ^+ T0 k0 Y% e
aware of this fact, because most of these children  x, w4 w8 U) t5 `
may initially present in their practice. The Physicians’
: v. o: o; V4 I  {' ~: eDesk Reference and package insert should also put a% F/ U* {/ W2 P1 F; [' @
warning about the virilizing effect on a male or
- [& T6 I1 R  N  }3 ~. R, }! p- v" }. yfemale child who might come in contact with some-
4 d) R+ F3 F* t! kone using any of these products.
8 E  U3 e. ]% NReferences; b6 N3 E/ d0 W* l  @' I
1. Styne DM. The testes: disorder of sexual differentiation
1 C" O: T& J# ?4 r) pand puberty in the male. In: Sperling MA, ed. Pediatric
. a5 x: h* p! l* P) cEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;  e) M# ?3 z2 D* \
2002: 565-628.1 V/ N$ m+ O  B5 \7 M8 E6 x( c
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious* ~* q) U- _# J
puberty in children with tumours of the suprasellar pineal
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感謝大大的辛勞分享!我會繼續在WK關注大大的文章!
發表於 2025-1-11 22:18:01 | 顯示全部樓層
女厕偷拍辅导班主任尿尿老师的逼很嫩还有一点
發表於 2025-1-17 16:31:39 | 顯示全部樓層
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加入VIP,享受高級特權宣傳賺金又升級,超級棒
4个什么样的?
發表於 2025-1-19 02:41:05 | 顯示全部樓層

, Z0 ]) J. C& ~. m1 }: i3 r  `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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