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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
& ~2 V& @* P- ~9 U( r4 uBoy Induced by Indirect Topical7 R) r& I7 B/ [- y9 E* F
Exposure to Testosterone
2 D' l  a8 ]9 M; \. b( x' c4 jSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2" `. s. T& P: f  U
and Kenneth R. Rettig, MD1
' j" l2 t3 I$ g4 u7 H# gClinical Pediatrics+ N  \2 O+ A3 q& P, I, `* e3 y
Volume 46 Number 6
3 r" b) F' A) j- U# ^& B2 uJuly 2007 540-543- b3 X# i0 j5 U5 W8 B  d2 p
© 2007 Sage Publications
* I; H) X2 @. S/ f6 M6 r10.1177/0009922806296651( }$ F" n) S1 L  `, x9 s: Q
http://clp.sagepub.com
7 Y7 i4 R+ _$ b# D, zhosted at8 n! @5 k& {: k
http://online.sagepub.com% G& h  B: i0 t' w
Precocious puberty in boys, central or peripheral,0 v7 ?' q# C+ }9 Q
is a significant concern for physicians. Central
, R& o0 }; U* e- a  ^' p. xprecocious puberty (CPP), which is mediated
: F* K7 X; l' x) d3 pthrough the hypothalamic pituitary gonadal axis, has
# |  K6 \6 X8 ^/ {a higher incidence of organic central nervous system
2 r8 p( I% [; @7 ^0 i: ]lesions in boys.1,2 Virilization in boys, as manifested
# C# M$ j/ w7 c. |" \  qby enlargement of the penis, development of pubic
+ D1 x2 w% Z5 u9 X* U, y! i6 @hair, and facial acne without enlargement of testi-
  u% R, q' Y7 ^4 ?& hcles, suggests peripheral or pseudopuberty.1-3 We9 B7 ?0 i' J9 r: v0 C) n7 V) B
report a 16-month-old boy who presented with the5 r! ^4 o1 a  \
enlargement of the phallus and pubic hair develop-0 P. u3 }! \# W" v. z
ment without testicular enlargement, which was due
7 c' H: z9 ^( c( Ato the unintentional exposure to androgen gel used by* D9 E* C1 C, u# I& A1 [
the father. The family initially concealed this infor-
& _0 A2 @- Y& N- mmation, resulting in an extensive work-up for this2 F, h3 N' K0 ^; Y! ?
child. Given the widespread and easy availability of
! T9 B  Q5 P) ]: ?/ R: Q  I/ {7 b1 jtestosterone gel and cream, we believe this is proba-0 n. N: B: G+ u; U
bly more common than the rare case report in the
: m7 t# l* O: a* K7 q% s6 P- U* f( k% @literature.4
+ V& F9 ^0 H9 @: wPatient Report
) W. F7 Y8 \$ ?% L- p$ MA 16-month-old white child was referred to the# F8 y# r4 a4 v/ K7 g. N; y
endocrine clinic by his pediatrician with the concern
  a. Q. A; _( b  D- ]of early sexual development. His mother noticed
5 r6 K: i+ |' _1 l; {, l# B9 c; Nlight colored pubic hair development when he was* R0 M% j' l! [7 B" @, |8 d
From the 1Division of Pediatric Endocrinology, 2University of
" X+ u* V. u4 \! q: H1 WSouth Alabama Medical Center, Mobile, Alabama.
* f7 h5 R5 u  Q0 v& wAddress correspondence to: Samar K. Bhowmick, MD, FACE,1 g' g  {( }" Q# h; D
Professor of Pediatrics, University of South Alabama, College of8 M/ D& O" H1 P9 E5 c
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
8 s: W' T+ X- O( j+ z$ We-mail: [email protected].
- }( A: G" y, Q: y, Z( C+ I0 b# Jabout 6 to 7 months old, which progressively became  Z) X0 ?5 `' P1 i7 i( I' N
darker. She was also concerned about the enlarge-) \0 c! m  U0 a; o/ A. l
ment of his penis and frequent erections. The child( c3 j. @2 A5 Y- c
was the product of a full-term normal delivery, with
7 [5 \. t/ {% ~; m) F: E0 s) _a birth weight of 7 lb 14 oz, and birth length of
" }8 N5 G+ @# M: x20 inches. He was breast-fed throughout the first year
$ c  v7 D( d- U, z, C% Hof life and was still receiving breast milk along with
. U' ^/ J3 a( M9 g* Esolid food. He had no hospitalizations or surgery,
8 _9 c( l2 ^8 A8 j( gand his psychosocial and psychomotor development
* z' |0 d( p8 X' f7 Q) W8 qwas age appropriate.% {: L# h8 G! j6 }& |
The family history was remarkable for the father,
+ M1 m; h7 f+ }! p& xwho was diagnosed with hypothyroidism at age 16,1 F( ?8 G6 {' u
which was treated with thyroxine. The father’s1 C" `: B. {% H
height was 6 feet, and he went through a somewhat
+ B: L9 @& \5 ~; E. @& pearly puberty and had stopped growing by age 14." K! F3 Q$ O4 H9 H5 X
The father denied taking any other medication. The6 H; r/ |1 z/ }# ~3 F
child’s mother was in good health. Her menarche% m$ x  i; V) x) ]3 a4 u% R
was at 11 years of age, and her height was at 5 feet
( D" J/ t# l$ m6 @5 i* [4 P5 inches. There was no other family history of pre-
/ ^; b1 ^5 E0 K' Icocious sexual development in the first-degree rela-
5 A! C* j8 M5 y$ Rtives. There were no siblings.
+ F3 I9 P1 G1 a+ W5 D$ \9 ZPhysical Examination+ S" {7 I1 c0 l
The physical examination revealed a very active,' C6 o0 F' s4 I) G5 |
playful, and healthy boy. The vital signs documented" u' y+ `2 L1 W4 E# h4 |4 x5 I0 H$ @
a blood pressure of 85/50 mm Hg, his length was0 p0 D  ]/ o2 y2 \& [9 h
90 cm (>97th percentile), and his weight was 14.4 kg, q6 c4 |6 q" z" I( C
(also >97th percentile). The observed yearly growth
+ @* b$ S4 U$ M$ n: _2 n  W5 V8 jvelocity was 30 cm (12 inches). The examination of1 a6 A$ S! D' b" i( J) _
the neck revealed no thyroid enlargement.7 O% {5 x$ T1 O/ b
The genitourinary examination was remarkable for
/ P# o( _( w7 s7 P. U  z/ penlargement of the penis, with a stretched length of
( a, h/ c; c+ p0 E4 l1 r8 cm and a width of 2 cm. The glans penis was very well
! [) N3 |7 b" @6 mdeveloped. The pubic hair was Tanner II, mostly around3 G4 X# h/ U/ ]) [7 }% i
5409 I0 n5 B. x6 R0 Y. L
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from2 [! u+ ?) K9 ?" u
the base of the phallus and was dark and curled. The
% T$ q0 G* V. C7 X9 Y  Qtesticular volume was prepubertal at 2 mL each.+ X, d& i1 C# I
The skin was moist and smooth and somewhat2 V$ P9 m! s% G0 c4 j6 g
oily. No axillary hair was noted. There were no: X# T, w6 C. f
abnormal skin pigmentations or café-au-lait spots.1 S, A  |' ^, A( w
Neurologic evaluation showed deep tendon reflex 2+2 e. ?7 x3 `  _
bilateral and symmetrical. There was no suggestion
; O# s& P3 `3 Fof papilledema.
1 R) P) \' @, k" M' |9 bLaboratory Evaluation
; H( |6 B, d3 i5 f+ x( dThe bone age was consistent with 28 months by
) G6 _9 P% |3 r4 _, U0 _: Xusing the standard of Greulich and Pyle at a chrono-- i8 K( A( f2 d# f" y
logic age of 16 months (advanced).5 Chromosomal$ c0 A6 k( w' I4 S0 M# h3 ]) `; t; d
karyotype was 46XY. The thyroid function test' m- r1 W8 _$ \0 p( t
showed a free T4 of 1.69 ng/dL, and thyroid stimu-& U6 |$ z: B: U; i( T4 j
lating hormone level was 1.3 µIU/mL (both normal).( u$ n/ N) s: p0 y% C1 H
The concentrations of serum electrolytes, blood; G' `4 l: V  |+ b6 l
urea nitrogen, creatinine, and calcium all were# b$ [. `7 l' R; u( ~
within normal range for his age. The concentration& I0 s9 T( n2 t2 G1 }
of serum 17-hydroxyprogesterone was 16 ng/dL
6 a* ^: \  T+ E- T(normal, 3 to 90 ng/dL), androstenedione was 20
- p3 ], @9 [; Z; V; T+ M( Nng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-1 ?% ^* V8 _* T* W- O
terone was 38 ng/dL (normal, 50 to 760 ng/dL),6 `' J% H. o9 i/ x9 P8 l) m$ {
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
/ I8 [* n4 w* n* M( N2 K+ \49ng/dL), 11-desoxycortisol (specific compound S). J7 t9 t7 L4 d5 m0 b/ z
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
; W( a$ i& K/ A4 D: dtisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
$ I7 \% _" M% p) `1 ~. ptestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
0 e' W# \* o  b) gand β-human chorionic gonadotropin was less than, h2 K9 f5 ?0 @9 N* \2 p: d
5 mIU/mL (normal <5 mIU/mL). Serum follicular
7 y+ g+ e/ f; y2 Hstimulating hormone and leuteinizing hormone4 S4 i! }' l! i1 G
concentrations were less than 0.05 mIU/mL
/ C+ d& h& y" `7 m/ _(prepubertal).
$ z9 N4 y4 B! R5 SThe parents were notified about the laboratory/ r; U! X/ k, ?
results and were informed that all of the tests were4 k  x' x" h9 O1 \8 n
normal except the testosterone level was high. The
: O" {3 Q; t) `. Q( j: L# T9 }follow-up visit was arranged within a few weeks to
- I2 _' t1 L9 ]- p9 G$ iobtain testicular and abdominal sonograms; how-
) K/ }& w- N1 S& `ever, the family did not return for 4 months.2 \; P( ]/ d9 l" `( Y. H  P# O
Physical examination at this time revealed that the1 o7 q/ ~) u4 a
child had grown 2.5 cm in 4 months and had gained
$ [3 y# D9 t, w8 f2 kg of weight. Physical examination remained, N% j/ Q1 j  z$ s
unchanged. Surprisingly, the pubic hair almost com-8 _9 a( B7 h) ^( ~
pletely disappeared except for a few vellous hairs at' j: w# }1 Q: p7 W! s1 k5 [
the base of the phallus. Testicular volume was still 2: ^* c- {0 E3 `/ H# k" o- J
mL, and the size of the penis remained unchanged.
/ F9 w, B8 x' KThe mother also said that the boy was no longer hav-, b" d4 S( K/ W  ~9 d) S0 |4 M
ing frequent erections.+ O# x9 c( f  c9 {3 f
Both parents were again questioned about use of
" i/ D( `. I6 i  G' {$ P" \any ointment/creams that they may have applied to% q/ G. ^; r( [2 c% ^
the child’s skin. This time the father admitted the: Y+ t' T+ d. W  b4 l+ w
Topical Testosterone Exposure / Bhowmick et al 541
( n1 t! _5 i7 w; S) p' A% I7 u" ?' b/ Ruse of testosterone gel twice daily that he was apply-
: k7 c  ^- g: p, fing over his own shoulders, chest, and back area for' {8 V5 U/ X* y( V/ F
a year. The father also revealed he was embarrassed6 Y& O1 J1 W$ f: b. P
to disclose that he was using a testosterone gel pre-2 R* M% v  i% r6 a
scribed by his family physician for decreased libido: [" D( R5 L( |1 q" b( o
secondary to depression.: z/ [& a) p8 s; r
The child slept in the same bed with parents.4 E/ J/ Q1 V% T9 J1 i
The father would hug the baby and hold him on his' C5 J6 O; g: i8 U! t
chest for a considerable period of time, causing sig-
/ T3 p- u7 ~' K  m0 }6 W4 L+ U0 {nificant bare skin contact between baby and father.
$ Q9 f5 a9 E0 @( K/ w$ }The father also admitted that after the phone call,
% ]  E" t: p% m7 U7 ?: c+ dwhen he learned the testosterone level in the baby$ h; L  g6 ?3 v4 m2 `
was high, he then read the product information
' x# H* ~/ H6 F" O0 {7 b% Gpacket and concluded that it was most likely the rea-
* y" K: \2 y. C/ {# S* a* b1 vson for the child’s virilization. At that time, they
2 @: E: L6 h  `% ]decided to put the baby in a separate bed, and the
" C/ [+ g, P  c* Ofather was not hugging him with bare skin and had
1 _4 l8 `- x2 P, l/ {been using protective clothing. A repeat testosterone
5 p* ^" O: K0 A9 z0 vtest was ordered, but the family did not go to the, p' u  B, g/ I5 L" ^
laboratory to obtain the test.
- V3 O2 D7 T, K2 \7 HDiscussion
* \9 a2 J/ S' t1 h" Y9 MPrecocious puberty in boys is defined as secondary2 e4 \$ `' j6 k  ?3 A
sexual development before 9 years of age.1,4
) @8 l; S5 t' iPrecocious puberty is termed as central (true) when
! T8 c( R: I( w/ e8 a- K9 [* Git is caused by the premature activation of hypo-
$ x) @; |, y5 i& Tthalamic pituitary gonadal axis. CPP is more com-
+ v* ?2 P  U* }mon in girls than in boys.1,3 Most boys with CPP
1 Z8 q: u5 K5 W  q( ~$ k5 Y+ r) Q# O6 {may have a central nervous system lesion that is3 W+ j2 h4 J5 c9 {7 {8 O
responsible for the early activation of the hypothal-
  ^5 {8 W3 c& S( n3 P( yamic pituitary gonadal axis.1-3 Thus, greater empha-
9 D; e6 m0 L5 qsis has been given to neuroradiologic imaging in
$ H% `& B' ]2 W+ F1 i0 ?9 Zboys with precocious puberty. In addition to viril-
3 j1 c# [" K* A4 Oization, the clinical hallmark of CPP is the symmet-
/ o2 L( B- }- U  o' Arical testicular growth secondary to stimulation by  s! T- f3 M3 o, J% E6 O) l
gonadotropins.1,3( O" J2 S2 U. s# x, H/ o8 q
Gonadotropin-independent peripheral preco-
2 \' R% `3 Z9 k9 Fcious puberty in boys also results from inappropriate  [' V& ?  Q7 |/ p
androgenic stimulation from either endogenous or. P4 A4 ?# i) R4 \
exogenous sources, nonpituitary gonadotropin stim-9 M+ @) b7 ~! q- l/ H
ulation, and rare activating mutations.3 Virilizing
# [& M5 i/ }( s- ?$ W6 @congenital adrenal hyperplasia producing excessive* V4 O$ \+ y& `9 b3 V7 X  a) M% j% e
adrenal androgens is a common cause of precocious' a# R) z* u3 F# X6 _% L2 f* G, y5 z5 }
puberty in boys.3,4- U8 W- h$ d9 f1 J) }8 K
The most common form of congenital adrenal
. X# Z  M+ T& r. }1 _3 fhyperplasia is the 21-hydroxylase enzyme deficiency.! J: M0 n! G3 {& ?1 O
The 11-β hydroxylase deficiency may also result in
. F, [2 w" _2 @% I5 V2 T# b" a1 u$ {excessive adrenal androgen production, and rarely,  b( R+ ~* P5 ]- {& O' _! D
an adrenal tumor may also cause adrenal androgen
+ a; ?! J. ~: O3 D4 Y, C7 ]; Bexcess.1,3
( u% O- V  T6 Eat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from+ \) C0 {! ~/ f+ ?% s% c
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
% G9 O, N: v7 eA unique entity of male-limited gonadotropin-
' A  i# h; H5 y6 w% gindependent precocious puberty, which is also known0 y, A3 m; v2 x2 Z) ~9 P
as testotoxicosis, may cause precocious puberty at a
, }: z& n$ J1 d; E4 tvery young age. The physical findings in these boys
5 u3 ~' B2 r- n1 _9 B8 k! uwith this disorder are full pubertal development,
8 r, X: g- c' |3 _3 f+ iincluding bilateral testicular growth, similar to boys; W8 t" g5 c% f# {& |
with CPP. The gonadotropin levels in this disorder- W3 Z- u( X: @7 i$ S
are suppressed to prepubertal levels and do not show/ R6 H9 N3 F( }
pubertal response of gonadotropin after gonadotropin-
5 i% p# `% K7 s% Wreleasing hormone stimulation. This is a sex-linked$ e' N6 j; }( W* l) j8 H4 W
autosomal dominant disorder that affects only# w$ M& p1 T. _  Y5 d# g
males; therefore, other male members of the family
1 i3 V. V* C# P. q8 Fmay have similar precocious puberty.3
, O* D  j/ e4 L. a; z3 aIn our patient, physical examination was incon-
8 k" [. z6 M# esistent with true precocious puberty since his testi-
( c  v: a% ]: p2 L3 [; W/ |cles were prepubertal in size. However, testotoxicosis% Y2 h7 B, p3 Z7 m  s
was in the differential diagnosis because his father. |6 z! z) ~: u( e! C. }2 s
started puberty somewhat early, and occasionally,+ l% t5 q! f4 c1 a; l: l
testicular enlargement is not that evident in the4 H# j  a" M, \
beginning of this process.1 In the absence of a neg-9 u0 G6 o) ?) I$ V% N9 q
ative initial history of androgen exposure, our
* c$ p, Y) @& [# tbiggest concern was virilizing adrenal hyperplasia,$ V( z7 E, V% W8 i7 R# o
either 21-hydroxylase deficiency or 11-β hydroxylase
! g- A2 C7 G; K( `deficiency. Those diagnoses were excluded by find-& L; E5 Y) j# [
ing the normal level of adrenal steroids.
5 ~. g3 S5 |  d+ f$ g6 Y/ O* fThe diagnosis of exogenous androgens was strongly( t  M- Q! I! |
suspected in a follow-up visit after 4 months because
3 g* _7 k& o% @$ X3 O& U+ wthe physical examination revealed the complete disap-
8 O8 R3 e0 n2 r7 s8 d) f' }9 x, lpearance of pubic hair, normal growth velocity, and0 T6 d4 T2 I6 ^  |5 W( M2 @( [
decreased erections. The father admitted using a testos-
7 y9 e1 `& A# ]" V" wterone gel, which he concealed at first visit. He was. \4 O6 r( A: c. s( T
using it rather frequently, twice a day. The Physicians’/ l4 q3 V, R* k1 B$ g6 R  Y! E
Desk Reference, or package insert of this product, gel or7 |2 h+ I5 _- }2 u% \
cream, cautions about dermal testosterone transfer to) \6 ]3 t9 }* s4 N
unprotected females through direct skin exposure.4 ]/ i0 @0 W# [* Z
Serum testosterone level was found to be 2 times the
7 R0 z1 \, L4 }, Q, Z3 |baseline value in those females who were exposed to' F/ o7 a  p9 v+ `# N
even 15 minutes of direct skin contact with their male- N+ x3 O$ Y8 K4 V& H
partners.6 However, when a shirt covered the applica-
2 E/ C: D# p- t2 L2 X! u% j8 mtion site, this testosterone transfer was prevented." R$ X" \9 q. p& B1 X; I
Our patient’s testosterone level was 60 ng/mL,
) U' q6 x' H9 T! ~3 X! M7 F: ^* i! fwhich was clearly high. Some studies suggest that
. t' r* b: l; Cdermal conversion of testosterone to dihydrotestos-
3 Y/ u4 F0 Q3 |" Uterone, which is a more potent metabolite, is more
/ v( s0 g# k& p) |" g. ractive in young children exposed to testosterone
* V3 o6 ?% n! c/ k; sexogenously7; however, we did not measure a dihy-
; j8 s# [! T* l: A* Hdrotestosterone level in our patient. In addition to7 c% D5 G$ d# s0 \
virilization, exposure to exogenous testosterone in
# s% P* D. ?) e) {children results in an increase in growth velocity and3 a, r; c* e  X2 b& F2 o: b
advanced bone age, as seen in our patient.
3 D9 a9 r- ?7 a5 K' tThe long-term effect of androgen exposure during! Y6 f" j0 W( V0 w3 p
early childhood on pubertal development and final
# ^2 q+ H1 p7 _) a9 r3 cadult height are not fully known and always remain
8 S& X( j3 l6 ^  t1 s4 Ja concern. Children treated with short-term testos-
+ i3 P7 B$ _' M4 O( C$ iterone injection or topical androgen may exhibit some6 k8 T5 q+ Q1 w* `* ^- t
acceleration of the skeletal maturation; however, after
2 o; P' ^  P5 m! J) v( @cessation of treatment, the rate of bone maturation
. n; d: m7 ?7 S7 D# }2 E2 Z, m' ?decelerates and gradually returns to normal.8,9
' d0 a3 C+ a" l2 y% Z) E( yThere are conflicting reports and controversy
  D+ k' z, x2 m1 H. pover the effect of early androgen exposure on adult( {9 y! ~* |) o/ Q$ a' ?  t
penile length.10,11 Some reports suggest subnormal2 X8 x0 f2 k) e
adult penile length, apparently because of downreg-0 a  p5 Y1 @5 {
ulation of androgen receptor number.10,12 However,
5 t' u9 k8 K, N$ p% c: c9 f$ OSutherland et al13 did not find a correlation between
7 X7 e% \5 \4 ?childhood testosterone exposure and reduced adult& {; M6 U& _4 ^- Y
penile length in clinical studies.5 U8 x1 P8 i( f4 r: F0 t
Nonetheless, we do not believe our patient is, u8 R, V8 D) c* s/ _0 F/ I9 X, \
going to experience any of the untoward effects from" e% V+ g( p& ^
testosterone exposure as mentioned earlier because7 a! |( _" Y6 w! W
the exposure was not for a prolonged period of time.# o7 O% X5 V' W
Although the bone age was advanced at the time of
2 H7 i: e8 K+ o2 Q5 Y' ?: K3 N; sdiagnosis, the child had a normal growth velocity at1 ~8 }* Y8 C. A5 J
the follow-up visit. It is hoped that his final adult
. n7 L9 b% a1 _, {' H. wheight will not be affected.
- {8 V# p9 @+ N# F- P; l' `- KAlthough rarely reported, the widespread avail-
/ a* S1 x, _. A4 aability of androgen products in our society may
8 U! a) D: a& Y/ `. {: Vindeed cause more virilization in male or female
& B1 P! }% K" v- }6 rchildren than one would realize. Exposure to andro-( y! f! B# B. v
gen products must be considered and specific ques-; X- N, I; Y8 v- G# H! H
tioning about the use of a testosterone product or# v* P* }7 V; K. Y! c; |8 x8 @! D
gel should be asked of the family members during
1 c5 a8 m, K6 Xthe evaluation of any children who present with vir-
1 ], A) |8 \! U+ Rilization or peripheral precocious puberty. The diag-/ u  j. ~8 @1 n9 U; \
nosis can be established by just a few tests and by
/ i7 ~5 X1 g+ {7 a. l+ Sappropriate history. The inability to obtain such a# |- P8 x5 ~3 A8 `4 i- D" T% Y
history, or failure to ask the specific questions, may
5 U/ }. c, Q8 ?, A. |result in extensive, unnecessary, and expensive
! n: B+ ]5 `% S' Ainvestigation. The primary care physician should be
3 l' l# v: o+ Xaware of this fact, because most of these children# h+ E/ ^" {: M9 f- \+ t. `8 b8 j: Z# W: J
may initially present in their practice. The Physicians’
9 K1 ?! H; [% s9 V# q  l; cDesk Reference and package insert should also put a- v3 l$ f! b8 M) `# M/ w# G0 U
warning about the virilizing effect on a male or
9 A3 c* _/ p% ?female child who might come in contact with some-
* @& A5 E) F0 {* Sone using any of these products.1 z2 X+ h0 P7 h4 K# J$ \
References
+ B+ ?1 j- o. A: @% o+ O0 E2 X1. Styne DM. The testes: disorder of sexual differentiation5 X# p/ A1 m8 J2 Y
and puberty in the male. In: Sperling MA, ed. Pediatric
- Y6 B- S4 V+ @Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
- D5 v/ t7 B3 u5 o  c, T  m2002: 565-628.
- S8 x3 ~% n9 l- D% C3 b& i; t2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
0 B. |1 h- ?- K' U" Z; Xpuberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old1 }  ^  e% K1 M6 k- f
Boy Induced by Indirect Topical4 H% P% @! o! V! X" q5 D
Exposure to Testosterone4 u4 r5 Y9 |; C) ^- Z
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
+ ]& y& ~  a* h" k" P! U1 u/ P2 ?and Kenneth R. Rettig, MD1/ p% ]% k/ N& m3 D2 B7 ^
Clinical Pediatrics6 o) E8 J$ f" z3 ], T
Volume 46 Number 6/ C) t7 M0 D* n# n; u& k
July 2007 540-543" T/ O0 e+ D# L. t
© 2007 Sage Publications2 O! n4 x, `3 M/ C6 J- A$ z- m1 a
10.1177/00099228062966516 O& j+ ~4 U) K& _* V; r, V
http://clp.sagepub.com8 N( a0 F- }* ?! ^6 [
hosted at/ Z' [5 U# ~& J" o
http://online.sagepub.com
3 P# r; t& ^  Q# F9 q" F* \4 h! PPrecocious puberty in boys, central or peripheral,* u2 w( K' u: s. i  `/ r# y& G( i5 F
is a significant concern for physicians. Central& P8 X2 u0 d  M; {4 D+ I! Z2 B
precocious puberty (CPP), which is mediated9 g9 J5 Y4 _+ T" n# T
through the hypothalamic pituitary gonadal axis, has. W( n$ w7 y3 t
a higher incidence of organic central nervous system3 v% _( ?' A, ^: y+ T8 w5 `4 y
lesions in boys.1,2 Virilization in boys, as manifested
2 g/ ]( _7 e* E* Q4 Oby enlargement of the penis, development of pubic" _1 j- y' y7 X; b+ X) @# A
hair, and facial acne without enlargement of testi-
* J: @) {2 L+ _$ @cles, suggests peripheral or pseudopuberty.1-3 We- e6 x$ g) C. Z; ]; v* C
report a 16-month-old boy who presented with the4 z; B) ^8 q3 [' A/ F% {( w# [
enlargement of the phallus and pubic hair develop-; ]0 P) ?7 f: B& a8 m
ment without testicular enlargement, which was due
/ ~: A5 f: T( [to the unintentional exposure to androgen gel used by, U) w( t4 x- E7 L9 w6 Y8 }. \
the father. The family initially concealed this infor-; @# G$ @: E2 W+ f! U% H
mation, resulting in an extensive work-up for this
; _8 w* e2 R0 _- Q% d/ Tchild. Given the widespread and easy availability of$ W) {3 V; h' h/ Q% v$ _9 ]' h
testosterone gel and cream, we believe this is proba-
4 a7 S+ G! @- C3 R: v& bbly more common than the rare case report in the5 R# D9 V1 e; Q" [5 e$ ?- m: v0 l
literature.48 H  ]& f) S/ L8 R/ }( Q# ]  z
Patient Report
# T* ]/ }) k$ f, a( R: S3 AA 16-month-old white child was referred to the$ _7 n, n1 t* s- i
endocrine clinic by his pediatrician with the concern
; R  w& \8 B4 Q# m, K9 T7 eof early sexual development. His mother noticed
3 B" [" L' |3 h+ y9 g' [light colored pubic hair development when he was
7 k8 J- D2 \3 Y" o" Y8 Q$ ~From the 1Division of Pediatric Endocrinology, 2University of
! W8 \# n1 f4 Y; mSouth Alabama Medical Center, Mobile, Alabama.
. H3 Z  V* U/ @$ CAddress correspondence to: Samar K. Bhowmick, MD, FACE,9 \( Y; Z4 \- {: h, M( y+ v3 d
Professor of Pediatrics, University of South Alabama, College of1 y4 W2 {4 p, A6 u
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;# U9 o5 g: n; v, B3 F9 u  C
e-mail: [email protected].: e6 R+ G& o) z
about 6 to 7 months old, which progressively became
4 x: q: w) K* F! Udarker. She was also concerned about the enlarge-
6 m+ F2 ?$ H2 D2 o/ C7 [& Rment of his penis and frequent erections. The child
  M9 h% g% z0 Q* pwas the product of a full-term normal delivery, with
+ X9 S0 }* Y, l2 H) i) Ja birth weight of 7 lb 14 oz, and birth length of( Q1 y7 V6 C) l7 |9 Q1 _. u6 D
20 inches. He was breast-fed throughout the first year
$ s" l& E8 w7 L, ^5 R7 kof life and was still receiving breast milk along with$ z% d* Y0 ?. a0 L  U; I& b4 R
solid food. He had no hospitalizations or surgery,3 Z7 ^+ j- x8 A  ^8 b3 ]
and his psychosocial and psychomotor development
% B9 h7 Z0 s8 Jwas age appropriate./ a& a/ H3 x- g8 V7 h/ E
The family history was remarkable for the father,
# x% L# I+ Z3 j# W6 V' ~who was diagnosed with hypothyroidism at age 16,# i' q5 u" ~  I( m9 g& ~/ x& m' d
which was treated with thyroxine. The father’s9 a1 c5 r2 S8 ^$ ?8 X
height was 6 feet, and he went through a somewhat
. z. _8 Q- |; hearly puberty and had stopped growing by age 14.9 O+ c  k* K7 u. R
The father denied taking any other medication. The. q) s: M8 [/ e7 j1 b# R2 n
child’s mother was in good health. Her menarche
$ o; D$ s5 u( |  Qwas at 11 years of age, and her height was at 5 feet, R  Q( E, ?( y3 w4 s
5 inches. There was no other family history of pre-& v& T8 l# c, `! y/ V7 {
cocious sexual development in the first-degree rela-' C) U  A+ u+ F
tives. There were no siblings.
2 G8 D- G0 v  }$ A: b. S1 u" o" zPhysical Examination  l) B4 b8 p2 m4 d) ]3 `
The physical examination revealed a very active,
% D0 ?$ j/ {& M; x3 g9 a  H/ b* Splayful, and healthy boy. The vital signs documented
7 M) ~' n) v1 ^a blood pressure of 85/50 mm Hg, his length was
" @$ ~0 o: f& A' V# Z# ]90 cm (>97th percentile), and his weight was 14.4 kg7 G- K5 q) I. U
(also >97th percentile). The observed yearly growth% C- Z6 D8 p* Z# v& @# G
velocity was 30 cm (12 inches). The examination of. z; e0 t+ u- u  ~- T- P! E
the neck revealed no thyroid enlargement.
5 W0 c9 \& c; m( iThe genitourinary examination was remarkable for
7 {/ L; x& @* W9 q. r( wenlargement of the penis, with a stretched length of
" n. |) D3 d- Q5 N8 cm and a width of 2 cm. The glans penis was very well1 K. x& ]7 }( W5 W8 {
developed. The pubic hair was Tanner II, mostly around
1 f3 B% x8 R1 q( S540% {7 z8 @  P; p: q" o$ g/ w
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from: K* ~5 T1 A! @4 r! e, Q: N0 h  a
the base of the phallus and was dark and curled. The
6 ]3 g+ E3 E) b3 z; `# M( ~testicular volume was prepubertal at 2 mL each.6 k  u/ G: I: j9 v6 [( H/ q$ L* @
The skin was moist and smooth and somewhat
" C8 A3 u1 d/ Toily. No axillary hair was noted. There were no2 I' K9 L: r3 N( N- C& j$ W$ g9 k
abnormal skin pigmentations or café-au-lait spots.. N4 v$ K9 ]$ c  c
Neurologic evaluation showed deep tendon reflex 2+( K9 n  B0 F, Q8 V
bilateral and symmetrical. There was no suggestion
% ?$ Z+ t. z+ w" N! ~of papilledema.
$ {8 }. a3 ~3 e& \" o; X5 ELaboratory Evaluation
; o+ ?5 J2 |, l& C  O7 aThe bone age was consistent with 28 months by! C$ O' b: Y7 S' L; \6 _
using the standard of Greulich and Pyle at a chrono-
( Z8 K, A( g9 C- {- r% d4 [logic age of 16 months (advanced).5 Chromosomal; u) f8 J" J3 D! p- s
karyotype was 46XY. The thyroid function test+ M+ G5 B% f: W$ G: U
showed a free T4 of 1.69 ng/dL, and thyroid stimu-  n6 Z5 q  Z% e; \
lating hormone level was 1.3 µIU/mL (both normal).! W2 m* W6 c1 R# q$ [+ s
The concentrations of serum electrolytes, blood; F" }& R3 p2 C$ Z9 S
urea nitrogen, creatinine, and calcium all were
# M( T& S7 X) }; ^  ?within normal range for his age. The concentration" Q. \0 F0 G5 [' h
of serum 17-hydroxyprogesterone was 16 ng/dL
1 @( Y- y/ O8 `# O) Q4 |(normal, 3 to 90 ng/dL), androstenedione was 20
$ f  I; l, c/ \5 g7 i: N/ W, zng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
( ^/ v+ [, D/ }7 o% Cterone was 38 ng/dL (normal, 50 to 760 ng/dL),
1 ]" V( y% v" c3 T9 V: q* hdesoxycorticosterone was 4.3 ng/dL (normal, 7 to5 A9 P. b. w6 V+ q9 {4 S# V9 Y2 \
49ng/dL), 11-desoxycortisol (specific compound S)2 n" P; o" T7 H( J- E- k' p
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-) Z, v, \2 l5 d
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
1 n3 a9 h9 ]% Atestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
3 ^- ?& I% ?) V% D3 P1 p! Oand β-human chorionic gonadotropin was less than
% Z7 U# f* S* Z% g! {9 g0 b5 mIU/mL (normal <5 mIU/mL). Serum follicular6 e1 k$ b- Q2 r: S& V( v4 V
stimulating hormone and leuteinizing hormone
! z/ E4 l( O) [) r! g- ~( `: Z+ d$ Sconcentrations were less than 0.05 mIU/mL1 D! m4 @" Z5 ?' N
(prepubertal).. ]# S8 H+ M% P6 Y/ o" q
The parents were notified about the laboratory
, A- `2 ]3 {# t0 S! z" U* mresults and were informed that all of the tests were) z& Q$ e8 \& v2 W+ h3 v, j; `
normal except the testosterone level was high. The
- z' z5 y9 V2 V) n7 t% g( i8 tfollow-up visit was arranged within a few weeks to0 `5 {. Z, E' \( R! o
obtain testicular and abdominal sonograms; how-, X; b0 E% c  Q" ]0 y
ever, the family did not return for 4 months.) m# \/ a0 X8 }2 w! Z0 {
Physical examination at this time revealed that the
5 |' r' G7 i- C$ Vchild had grown 2.5 cm in 4 months and had gained* C/ ?) a% D8 \+ S# l4 {& Y5 |
2 kg of weight. Physical examination remained7 J  N3 @/ C; F; I% D
unchanged. Surprisingly, the pubic hair almost com-
9 b4 j% x* K0 G( }3 P1 M3 P' b$ upletely disappeared except for a few vellous hairs at
0 {& j& r- i  |the base of the phallus. Testicular volume was still 28 j7 f& Y, i% Q/ ^- e% l! X
mL, and the size of the penis remained unchanged." ?2 \* a% t) p) t" B
The mother also said that the boy was no longer hav-8 |/ z) n/ X: |2 J; t# \
ing frequent erections.
4 e/ `7 u, L7 R- o* O- `Both parents were again questioned about use of5 J+ h4 d$ K( B* O0 E
any ointment/creams that they may have applied to3 }$ s% V$ ^" b5 ?
the child’s skin. This time the father admitted the  B- ]4 b( |* {$ |
Topical Testosterone Exposure / Bhowmick et al 541
8 F3 u* G4 v6 j% u, duse of testosterone gel twice daily that he was apply-
# f2 S  G3 C- r' f: Iing over his own shoulders, chest, and back area for$ a8 \  e% y) {8 m/ k
a year. The father also revealed he was embarrassed, w/ y. l' c$ T3 V
to disclose that he was using a testosterone gel pre-
& X+ _7 H6 a, ascribed by his family physician for decreased libido3 X& w3 Y! F& J$ D+ @! Z: h
secondary to depression.4 M" S7 w/ P4 O3 d' g' A8 q' W, V8 u
The child slept in the same bed with parents.7 T1 Y. H& ~0 w
The father would hug the baby and hold him on his
5 X. Z& O  R. h3 [# [chest for a considerable period of time, causing sig-
* W" S+ {7 D) u2 \7 y6 znificant bare skin contact between baby and father.0 q7 e% k3 {" \
The father also admitted that after the phone call,1 l  q2 o9 S; j$ y1 q
when he learned the testosterone level in the baby
2 ?# n$ P5 B* x2 Vwas high, he then read the product information: \* Y2 ~: f0 y+ R" z, O' _
packet and concluded that it was most likely the rea-
; a5 b4 v9 x5 d  e2 Vson for the child’s virilization. At that time, they6 b; q0 b; r7 `4 N# _: U8 \
decided to put the baby in a separate bed, and the
  G; a! ]* x( k, efather was not hugging him with bare skin and had/ z3 T$ O1 F" u  @$ [. L
been using protective clothing. A repeat testosterone! v3 j) `5 @7 ~3 R7 N' [* w
test was ordered, but the family did not go to the3 p- n) q  F% `; k( U( O
laboratory to obtain the test.
8 q9 J& W' z$ u7 ]. K( CDiscussion
, a  q# d/ K0 HPrecocious puberty in boys is defined as secondary
% B; ?5 e6 [+ ]: x; i3 K8 I) {+ Qsexual development before 9 years of age.1,4
( {3 R$ L7 z6 ZPrecocious puberty is termed as central (true) when
! g" k0 H6 L$ e5 c5 iit is caused by the premature activation of hypo-; c4 m0 K* ?7 x, f9 _
thalamic pituitary gonadal axis. CPP is more com-$ `0 P% o2 d0 x( L: m' L: m
mon in girls than in boys.1,3 Most boys with CPP7 _( o6 c2 S2 b
may have a central nervous system lesion that is
/ Q: H* P% L, Q: F. |$ w+ Q$ B, lresponsible for the early activation of the hypothal-* @: u8 n8 k2 t% w4 r4 N6 F! z
amic pituitary gonadal axis.1-3 Thus, greater empha-
+ Q1 M6 z2 C+ f6 F5 O* Z9 J# Tsis has been given to neuroradiologic imaging in
' V7 n% c: a) @2 @) T) F& hboys with precocious puberty. In addition to viril-0 i* I2 c  O6 i6 L# q; G
ization, the clinical hallmark of CPP is the symmet-$ x5 @: s, k7 I9 Q" o) G6 M8 z5 A; Z$ V
rical testicular growth secondary to stimulation by
' D- O. i6 f: l& }* Z- ugonadotropins.1,3
, l; K9 ^1 G3 s. ?5 CGonadotropin-independent peripheral preco-
5 J) |! T; y- B0 w. u8 J; K+ e* H% lcious puberty in boys also results from inappropriate
) m8 S, u3 i9 w- X0 W( Xandrogenic stimulation from either endogenous or
- b% W, R. T' D5 l  E" c0 C, Dexogenous sources, nonpituitary gonadotropin stim-3 J8 Y- b! s& @+ p/ q- ~
ulation, and rare activating mutations.3 Virilizing
# B5 {2 o" |/ X6 B% zcongenital adrenal hyperplasia producing excessive
1 t/ I' p' p4 a9 w4 tadrenal androgens is a common cause of precocious/ w2 G: Q+ ~  p
puberty in boys.3,4, F7 S+ Z+ O( W# @/ B
The most common form of congenital adrenal7 M2 E5 p/ s: v( ^) M% O% I" B
hyperplasia is the 21-hydroxylase enzyme deficiency.7 n* n1 v! N9 [4 M3 E+ j
The 11-β hydroxylase deficiency may also result in
" t* l  m, ~. q/ c( ]excessive adrenal androgen production, and rarely,& t$ b' h) a/ ^6 v; z2 v
an adrenal tumor may also cause adrenal androgen
9 v  I1 _' [8 e8 l0 q! cexcess.1,3  @: i0 w7 O3 P9 H5 |6 [
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
, X. W3 H* X, c( u* p6 y- b542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
/ N; j. |. t7 W: y, TA unique entity of male-limited gonadotropin-
0 M+ m& f/ [4 x2 Jindependent precocious puberty, which is also known* Y% C/ O; ?0 `  E( s) }$ L8 X
as testotoxicosis, may cause precocious puberty at a$ D! P3 D9 `0 H, W1 B7 _8 T2 {
very young age. The physical findings in these boys) Z$ ]* ?/ F4 w$ j9 f
with this disorder are full pubertal development,( z* D9 F) U$ ]( _+ h& q0 f/ d  |
including bilateral testicular growth, similar to boys1 I' [. W7 g( A
with CPP. The gonadotropin levels in this disorder
# p: ]6 X) F) ?( b8 ~are suppressed to prepubertal levels and do not show
; |6 O2 [1 d$ {5 ^$ ^6 @pubertal response of gonadotropin after gonadotropin-
  @) e4 w. t7 ]& ureleasing hormone stimulation. This is a sex-linked
* A5 T: T' f! Wautosomal dominant disorder that affects only
' G( \6 s3 p9 M9 ymales; therefore, other male members of the family  r# f( j/ _, K2 ~$ `2 O; f
may have similar precocious puberty.3
2 V! O* O0 ]; Z1 d2 o' q. Y# c! _In our patient, physical examination was incon-
! _/ e7 k; Q7 Q3 \sistent with true precocious puberty since his testi-; K: a. n9 ~. j/ O/ ~6 n; B
cles were prepubertal in size. However, testotoxicosis) l9 M3 Y2 Q* Q3 y+ ?0 a8 _3 E
was in the differential diagnosis because his father  z% y7 ]7 o% A$ q4 Q7 Y
started puberty somewhat early, and occasionally,
0 o& M- G! ^8 Y3 V% H* atesticular enlargement is not that evident in the6 z8 H0 E. B/ a4 W1 B' f' h' r* t5 D! G
beginning of this process.1 In the absence of a neg-
  ?( G. V6 Q* Y& O* _6 iative initial history of androgen exposure, our5 |) t) N: y7 Q! ]; D1 P
biggest concern was virilizing adrenal hyperplasia,0 P2 A! P6 z9 ?$ Q, X0 N/ w
either 21-hydroxylase deficiency or 11-β hydroxylase' ^. s# q$ V; s6 ^
deficiency. Those diagnoses were excluded by find-% C1 X) R. @! Y
ing the normal level of adrenal steroids.* {$ E' a$ \7 p- D" t
The diagnosis of exogenous androgens was strongly/ O; L" H3 A5 t1 j: \4 U/ U
suspected in a follow-up visit after 4 months because
& w. V" \  G# t/ b; j+ G, wthe physical examination revealed the complete disap-- c6 N( r( _* M$ q* _
pearance of pubic hair, normal growth velocity, and  \8 V- [7 D8 r. P% \2 A  \
decreased erections. The father admitted using a testos-8 [/ {. _; t" {0 H3 H$ `: A# E
terone gel, which he concealed at first visit. He was
9 X7 t8 Y: K+ z+ Eusing it rather frequently, twice a day. The Physicians’
- X5 s' q$ a% n6 I9 g7 A) K( ^Desk Reference, or package insert of this product, gel or* n! A; E; M) i- p
cream, cautions about dermal testosterone transfer to0 O* Y. f( X6 X4 G* d
unprotected females through direct skin exposure.3 F" K2 b, I% l& e& p* s
Serum testosterone level was found to be 2 times the
$ M# R9 ]$ @1 @" V4 p1 @baseline value in those females who were exposed to7 s* M! N1 j' \% w
even 15 minutes of direct skin contact with their male- m  c9 C5 S. H5 C1 S
partners.6 However, when a shirt covered the applica-
! T+ n" r0 ~) ^0 ]( Jtion site, this testosterone transfer was prevented.0 I& E& c/ N8 z, F9 T
Our patient’s testosterone level was 60 ng/mL,
1 h5 n( r5 |& D' K) l5 Cwhich was clearly high. Some studies suggest that
4 _+ c  t% _8 h0 X7 T) H8 ldermal conversion of testosterone to dihydrotestos-
0 x2 z% e. v' ^5 S; oterone, which is a more potent metabolite, is more3 |! f% A1 L+ l$ T" M8 B* y; A
active in young children exposed to testosterone
( r* R, [& ^8 V1 B# Y$ M- Lexogenously7; however, we did not measure a dihy-
/ e% k& @; O4 L% |drotestosterone level in our patient. In addition to4 Z% j0 ?2 ~7 `2 G1 j, L' A
virilization, exposure to exogenous testosterone in
& O& M! L+ p  B" `& D& Q, k' Xchildren results in an increase in growth velocity and
' `" q8 E. p3 U* K" {+ f- |$ ^advanced bone age, as seen in our patient.8 Z) n) x; D* z* s' X* |$ B# D( A( }
The long-term effect of androgen exposure during0 Y$ d; E! K3 p& b5 W: Z; h
early childhood on pubertal development and final0 J+ D: Y) A6 u/ Y1 C
adult height are not fully known and always remain8 G  _2 i9 W- N
a concern. Children treated with short-term testos-' j# i1 L. O  x7 E8 _
terone injection or topical androgen may exhibit some
2 h8 b- C$ f+ Kacceleration of the skeletal maturation; however, after
+ m- \7 W9 p- e2 ?! ucessation of treatment, the rate of bone maturation) @/ s8 F1 x+ g
decelerates and gradually returns to normal.8,9& n1 U+ p" S- b% h
There are conflicting reports and controversy
: g/ W% [" K( [* \5 Iover the effect of early androgen exposure on adult4 `% G5 A" z! U7 b
penile length.10,11 Some reports suggest subnormal& I. M( R$ T3 p3 r" Y) L3 _( d6 L
adult penile length, apparently because of downreg-; {; v" M+ g0 t' n; l4 `1 Z8 g7 I
ulation of androgen receptor number.10,12 However,5 L& b( }) `; }2 |$ \. E6 w
Sutherland et al13 did not find a correlation between2 Z) B& u8 s5 `7 I2 S
childhood testosterone exposure and reduced adult
' G9 P3 r% @/ }' I  `* vpenile length in clinical studies.! z8 V/ e' W% X) b
Nonetheless, we do not believe our patient is
2 b& j! ~; k4 C. Agoing to experience any of the untoward effects from
' X7 O% Z9 f* T) Y) v, w1 ptestosterone exposure as mentioned earlier because) E: q: e1 U! W6 H5 Y. Y
the exposure was not for a prolonged period of time.
' p1 m1 H7 q: c; Z3 }. ]3 T, bAlthough the bone age was advanced at the time of
) A. s, Y* I! [& p  Z3 h  a' C+ Xdiagnosis, the child had a normal growth velocity at
1 u' V/ {( o+ a9 uthe follow-up visit. It is hoped that his final adult( E2 p/ F( C: S8 Z* v( t
height will not be affected.' I' v. O2 C7 V8 E
Although rarely reported, the widespread avail-
: y* @- C/ J! G- l. n# Fability of androgen products in our society may
$ k0 [3 x- ?. l9 Cindeed cause more virilization in male or female
  m8 c  S9 Q% W: E5 D' `/ U% @& ~+ Lchildren than one would realize. Exposure to andro-: d' b* G$ f) M1 w$ r" b
gen products must be considered and specific ques-
/ {6 a% A$ ^$ h, U  y. _tioning about the use of a testosterone product or
/ P; e1 [4 H, R) S/ o: d+ `gel should be asked of the family members during2 k' A; U& F) _& K
the evaluation of any children who present with vir-( P  V/ l$ D( b3 X  Z' B
ilization or peripheral precocious puberty. The diag-
/ X' M2 I" X6 P9 @9 d+ |* b1 X+ ?nosis can be established by just a few tests and by- I5 w$ O" ?( _# z8 G- p/ W
appropriate history. The inability to obtain such a
4 ~& d% b* D# xhistory, or failure to ask the specific questions, may# k: N5 X! e& v8 j" M# U  p
result in extensive, unnecessary, and expensive, H6 R3 ^6 T' t3 X* t" i
investigation. The primary care physician should be% r0 Z! Y% ]+ V9 s! ~) m6 G( N
aware of this fact, because most of these children9 n3 D& Z! v( H" }
may initially present in their practice. The Physicians’
7 C7 @7 [  i6 ~  [# |2 h5 cDesk Reference and package insert should also put a
0 y* T# m* ^  \: Q6 Jwarning about the virilizing effect on a male or: ~* Z6 j& S: v% I# i6 O
female child who might come in contact with some-
; x' S4 s: j9 Pone using any of these products.: a3 W- R! x9 j- C# q$ m. {% b
References
0 g; p# W7 T2 L2 N7 r% v1. Styne DM. The testes: disorder of sexual differentiation
3 U+ D4 p( i; n; d5 s) I; Fand puberty in the male. In: Sperling MA, ed. Pediatric, B% G% t# o* v2 c8 N
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;  F2 W& h1 W1 b, b! @
2002: 565-628.
; W) l5 M& }6 t9 f2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious- m. L. q: u. A5 L* [) }3 N
puberty in children with tumours of the suprasellar pineal
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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
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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

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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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