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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-Old7 s* G  j" y2 X1 Z
Boy Induced by Indirect Topical
2 {* l+ s2 D* P! h4 ^0 ^. iExposure to Testosterone
& ^1 S; V0 Y! \2 f8 G7 H- O2 PSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2: Y, t/ x& m' `8 l- V- y- t
and Kenneth R. Rettig, MD1
6 L+ _8 E7 h( R8 N$ J9 iClinical Pediatrics
: ^6 W% u0 }* Z6 d7 A9 iVolume 46 Number 6
& _. z( |) h- G5 L* |July 2007 540-543
+ I  `' p' n- z1 h( k© 2007 Sage Publications
8 j+ T2 B& Q3 K# E! `10.1177/00099228062966511 ]: _- w$ c# ~& L) O2 R
http://clp.sagepub.com3 u/ i& \8 ]$ [) Q5 S( [
hosted at& |/ z; D" h( `# y: x' a
http://online.sagepub.com7 r; N# Y* t" e  ^/ d3 }0 ]
Precocious puberty in boys, central or peripheral,
0 J' e7 Q$ I* Bis a significant concern for physicians. Central
! g( m# y! |7 {8 }9 X" mprecocious puberty (CPP), which is mediated, Q1 L0 p, O  w3 M& o. [/ k4 e
through the hypothalamic pituitary gonadal axis, has
' W' P! R/ N# J8 l+ u; Ua higher incidence of organic central nervous system
( E" E+ |: H0 Clesions in boys.1,2 Virilization in boys, as manifested
5 r5 x% S. C4 c, {. \by enlargement of the penis, development of pubic$ S# e+ ^& w: l8 m
hair, and facial acne without enlargement of testi-  ~  c+ G/ f1 X0 x) _
cles, suggests peripheral or pseudopuberty.1-3 We
& I3 ~6 k$ g( d! ?+ Ereport a 16-month-old boy who presented with the
( X, |0 F; I0 e5 L8 C  wenlargement of the phallus and pubic hair develop-/ f+ D; V- L3 C6 k6 ~
ment without testicular enlargement, which was due* ]' V) B3 s; f. c" \
to the unintentional exposure to androgen gel used by
& a6 H5 J) O2 K: i9 B! Z8 hthe father. The family initially concealed this infor-
0 y6 r' Y' ?- F. J# x/ ~mation, resulting in an extensive work-up for this
/ I1 X- Y) N( r  Ochild. Given the widespread and easy availability of& T0 H* Z. ^8 _3 s# L  v
testosterone gel and cream, we believe this is proba-9 q" ~0 r. x( Z4 B& O' O0 d$ v1 F2 M
bly more common than the rare case report in the
1 ]" q/ d: `# t  m  aliterature.4
5 O/ s- U$ Z- z6 XPatient Report5 a! I' b: _3 ?9 o! P- [. e/ U, D
A 16-month-old white child was referred to the
# p  `4 V% S; Y* p  \' oendocrine clinic by his pediatrician with the concern! T/ ]- p' T% P+ Q8 F5 {
of early sexual development. His mother noticed
! J; p6 ]8 E* i+ [2 P3 E8 ?, t  ~light colored pubic hair development when he was
) ^8 e. ~7 {# g6 {# J+ \! ?From the 1Division of Pediatric Endocrinology, 2University of, W4 X: `1 ?5 s# R6 M
South Alabama Medical Center, Mobile, Alabama.8 W+ Z7 R; |9 E
Address correspondence to: Samar K. Bhowmick, MD, FACE,
" f3 V" h* u; z; C) wProfessor of Pediatrics, University of South Alabama, College of. T8 Z: F; J8 S5 p* L: C( N  ]
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;" b/ G3 z) _9 ~: d: V8 @
e-mail: [email protected].
/ n$ @8 x7 h, @& v8 Kabout 6 to 7 months old, which progressively became
4 O% Q- `; f6 n7 Q. S4 H) xdarker. She was also concerned about the enlarge-
  \6 R4 X& M8 S4 U2 p& jment of his penis and frequent erections. The child( q0 V: `$ b- T) T0 l. B# R& Q: P
was the product of a full-term normal delivery, with* Z# w; P( v) P  O! ^  k7 X( ]
a birth weight of 7 lb 14 oz, and birth length of$ N- O$ w( |2 A6 F/ }7 N
20 inches. He was breast-fed throughout the first year- y& e, c# P" e
of life and was still receiving breast milk along with5 M9 l1 Z4 h% c  q0 W
solid food. He had no hospitalizations or surgery,- S) R( s+ q! O- H
and his psychosocial and psychomotor development2 i3 o6 A. X& O. O0 g( C6 e# r8 v
was age appropriate.
$ E# f7 v! ?3 h# A. ?5 uThe family history was remarkable for the father,  b  ^2 r; L' a- Y3 L) e# U" B) u: a
who was diagnosed with hypothyroidism at age 16,
$ R4 w3 o, N4 h" {( iwhich was treated with thyroxine. The father’s
- V- t- M! W8 O7 r! Nheight was 6 feet, and he went through a somewhat
9 C1 q7 D! X: W$ Z, Yearly puberty and had stopped growing by age 14.
& Z% e# r4 Y/ q. V& `The father denied taking any other medication. The
( P. \/ f1 V" F9 V' rchild’s mother was in good health. Her menarche# H. k- A. y5 Y9 J
was at 11 years of age, and her height was at 5 feet1 F6 D( E5 @- a: L# Y
5 inches. There was no other family history of pre-
4 `7 V( k5 Q9 {3 Q! Fcocious sexual development in the first-degree rela-* e; q+ W  T, ~7 ?" y
tives. There were no siblings.* L* b+ R* {- X5 H: ?
Physical Examination; @9 g4 u" P; o; h0 F& I% |. Y
The physical examination revealed a very active,
4 B( b1 ^% |, m/ p% ~& H- Qplayful, and healthy boy. The vital signs documented0 `! z4 N% ?! a; x0 [8 G; ^
a blood pressure of 85/50 mm Hg, his length was/ c7 l' X+ m. |$ N. G# {+ o; C
90 cm (>97th percentile), and his weight was 14.4 kg) z, R# g. }5 C- P4 K/ o8 b6 G
(also >97th percentile). The observed yearly growth9 R) V  X1 p2 J. O0 K9 z
velocity was 30 cm (12 inches). The examination of
& x( s" S/ {3 m. M" B. n  \the neck revealed no thyroid enlargement.+ r8 b9 h/ p* T8 M, q" P: g
The genitourinary examination was remarkable for
% `- A5 A& G6 u! ]6 o* p1 Senlargement of the penis, with a stretched length of
9 {& p8 V$ A- [; I9 N' n2 s8 cm and a width of 2 cm. The glans penis was very well5 A- e, W9 V; {  W6 |$ g; {
developed. The pubic hair was Tanner II, mostly around
3 g6 f5 C# N0 J. S" [( F& X540" ?3 h/ ~! x" B- o2 b: ~) i/ V; O
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
2 K8 Z' `4 e) s" K# Y+ }. B) x' Dthe base of the phallus and was dark and curled. The
- r+ r6 Q) e3 |testicular volume was prepubertal at 2 mL each.) q  ?+ `' Z) y9 F! i7 M, q' F  _0 v+ A
The skin was moist and smooth and somewhat
0 p5 ^8 u2 v- M9 K  q7 H0 noily. No axillary hair was noted. There were no
+ ~7 i& z' n( e  o6 P9 Yabnormal skin pigmentations or café-au-lait spots.
' Y3 Z5 G; s) N% x; g1 W. M' P! H: dNeurologic evaluation showed deep tendon reflex 2+
+ ], ^" n: J& u2 \bilateral and symmetrical. There was no suggestion4 ~# s- \% f' R) r6 Z+ U& ^: G, c
of papilledema.
# Z- a( U" \& J0 ELaboratory Evaluation
; H) ~% Q3 i/ l; KThe bone age was consistent with 28 months by8 K5 |4 ^/ @8 @/ p
using the standard of Greulich and Pyle at a chrono-  x) a) a+ v' F$ ^+ W( B
logic age of 16 months (advanced).5 Chromosomal+ j+ f1 M3 n3 o
karyotype was 46XY. The thyroid function test
- O7 Q9 u' u) c7 e0 e$ ]0 m" wshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
' e/ U& ^; F' C" `  C: R6 t0 |lating hormone level was 1.3 µIU/mL (both normal).% B- S2 D4 J# w, r
The concentrations of serum electrolytes, blood
3 _; n( U; q( @urea nitrogen, creatinine, and calcium all were
! J% X" r5 S, M# s7 Dwithin normal range for his age. The concentration
; g$ J' Y2 K  K+ Rof serum 17-hydroxyprogesterone was 16 ng/dL
( m& \; r* p- O0 h(normal, 3 to 90 ng/dL), androstenedione was 20
$ {$ M8 L+ `( Vng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
3 @4 a" K; `. U  ^& F$ Cterone was 38 ng/dL (normal, 50 to 760 ng/dL),! n& s: g+ T# \  B# q7 X6 V; A- G
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
* T- ~! ?$ {2 G49ng/dL), 11-desoxycortisol (specific compound S)
3 [' ]* \( J$ L8 {8 e2 u( n+ ?6 b# xwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
: F: D$ D1 u6 }  G& _+ Utisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
. A) Z0 _- {! q; |1 s3 wtestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
8 g% ^: Q" C+ E' K/ C! Mand β-human chorionic gonadotropin was less than
3 z$ C8 G/ Z+ K' k7 P" S: G. e5 mIU/mL (normal <5 mIU/mL). Serum follicular
! D# a& [" [! o/ V/ pstimulating hormone and leuteinizing hormone" r+ Q6 ]7 W$ w0 U
concentrations were less than 0.05 mIU/mL
! T8 n- t: O" c6 ?% ~(prepubertal).  q8 [; d3 _* y. S0 M' s
The parents were notified about the laboratory
. O  a5 h4 W4 ^% t" M/ e- Gresults and were informed that all of the tests were- n/ D& V; q7 o
normal except the testosterone level was high. The) g1 u: F; d& Z' o
follow-up visit was arranged within a few weeks to
  |5 z2 N) d' `obtain testicular and abdominal sonograms; how-
3 @/ ]  B0 f/ e0 n7 j$ Lever, the family did not return for 4 months.
- x) l( j% D& X2 l* ^5 |Physical examination at this time revealed that the
5 Q7 Y/ ^' L/ V5 j+ }& g9 Nchild had grown 2.5 cm in 4 months and had gained( E, c" q) P8 O9 u
2 kg of weight. Physical examination remained; Q4 m1 c9 v$ [/ U' a; v
unchanged. Surprisingly, the pubic hair almost com-; `  [4 h+ U, M, O1 i
pletely disappeared except for a few vellous hairs at* x2 k7 d" P) u' n6 C, V& ?
the base of the phallus. Testicular volume was still 20 Z7 ~6 C- {. O: v
mL, and the size of the penis remained unchanged.2 P# ~) W; W' f! `: q& L* B( S- @
The mother also said that the boy was no longer hav-# v( ?2 {+ ]1 i0 I' J& Z
ing frequent erections.' e. c- s; L( t+ f1 q- j; m# Q( G# `
Both parents were again questioned about use of
6 u3 q, C! ]) G  \2 wany ointment/creams that they may have applied to
& o. I/ i% y$ e2 Jthe child’s skin. This time the father admitted the& i3 h  b! J6 g5 I
Topical Testosterone Exposure / Bhowmick et al 541
+ z. V: f( m$ d) J1 z7 h" ?% Tuse of testosterone gel twice daily that he was apply-
8 o" \/ y5 c0 N; }' v- ming over his own shoulders, chest, and back area for
- c# [2 `9 h7 A& j) Za year. The father also revealed he was embarrassed4 J! d0 l" u' z1 d
to disclose that he was using a testosterone gel pre-
+ ^& W" X0 V. b& b: y/ oscribed by his family physician for decreased libido0 w, p) X; L; p+ E: F: K+ y
secondary to depression.7 j% v, T5 V+ C# v1 z
The child slept in the same bed with parents.
# v' N6 P1 s4 T' d- x& J; IThe father would hug the baby and hold him on his  G* g0 X$ T0 W
chest for a considerable period of time, causing sig-
; }% l. ~4 B5 Q7 w2 }3 z9 Vnificant bare skin contact between baby and father.% |8 n7 ^; m: J4 Q& G+ Y
The father also admitted that after the phone call,
+ e6 B& ?. P8 M/ O$ `* B/ Y( g3 kwhen he learned the testosterone level in the baby" B2 [9 T% b- j* d% I
was high, he then read the product information
0 I& H$ X$ q4 Z  ?! R8 l% S0 Ipacket and concluded that it was most likely the rea-
: H* R6 G3 b) nson for the child’s virilization. At that time, they6 n# V* P/ M& @$ ^. i% F6 x
decided to put the baby in a separate bed, and the& l+ j/ X, {0 S/ k$ u6 ?
father was not hugging him with bare skin and had
9 c% i1 `& }( c% S4 Ubeen using protective clothing. A repeat testosterone" C7 W) Z  N9 K: z
test was ordered, but the family did not go to the
' i( `2 F' F) I. Tlaboratory to obtain the test.
6 `2 A8 V7 M8 g, d: n, J% dDiscussion
$ @! n* T& p- ^7 H/ FPrecocious puberty in boys is defined as secondary
2 h" e3 y. M# e& Z+ \7 X( D7 lsexual development before 9 years of age.1,4
0 Y) k0 b) M7 E' Z3 {7 yPrecocious puberty is termed as central (true) when- v# k3 u3 w- X, M& L8 Z
it is caused by the premature activation of hypo-
" p- w0 ^4 U9 w" d- U; z5 Z2 Gthalamic pituitary gonadal axis. CPP is more com-
6 R6 J2 D+ C+ a: K/ Fmon in girls than in boys.1,3 Most boys with CPP
& e4 E7 i6 b4 W) Vmay have a central nervous system lesion that is
# v* v) B1 `( p0 ~responsible for the early activation of the hypothal-
: q0 K; j4 p# t( b, [amic pituitary gonadal axis.1-3 Thus, greater empha-
+ q' }) M: t: ]' Fsis has been given to neuroradiologic imaging in
7 x8 h: O0 q8 H9 [, h( Uboys with precocious puberty. In addition to viril-
: n$ [8 i" b& P; E* X5 Zization, the clinical hallmark of CPP is the symmet-
' P) A- H. X" Y) q2 w( zrical testicular growth secondary to stimulation by$ B2 I9 d& l8 G4 n  g9 C& F: a
gonadotropins.1,3
$ D0 e4 P& T5 l/ w- X% X0 IGonadotropin-independent peripheral preco-: P! t* [+ r# P) i  t
cious puberty in boys also results from inappropriate( ?9 j8 Y- h& @' V
androgenic stimulation from either endogenous or
# E4 t" U0 D0 m, l* k$ bexogenous sources, nonpituitary gonadotropin stim-. R5 Y: Q$ L1 u5 p
ulation, and rare activating mutations.3 Virilizing
2 ~3 J- U) C2 H  i6 H: bcongenital adrenal hyperplasia producing excessive
1 G7 X# W6 E0 Z- ]9 `adrenal androgens is a common cause of precocious
1 f9 I! i, {' g' D5 [" dpuberty in boys.3,4
7 G: C6 l, d' W; f8 y" O2 `The most common form of congenital adrenal
* ]9 }' d( `2 Q) R! H/ `+ dhyperplasia is the 21-hydroxylase enzyme deficiency.8 g1 V% U+ K0 C3 [0 \
The 11-β hydroxylase deficiency may also result in
7 c5 w5 p4 @) \' r) U$ ?. P8 X; O5 a8 kexcessive adrenal androgen production, and rarely,
, `6 n9 e+ p8 m5 E. Can adrenal tumor may also cause adrenal androgen, \, R9 A9 a/ d- [
excess.1,3
( ?- S$ \8 s  O4 d7 Y5 d) |at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from* r& v" D  G0 v$ e
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
0 F- E- R# C3 E8 @$ g5 UA unique entity of male-limited gonadotropin-. E0 U5 d7 n: I( `! f
independent precocious puberty, which is also known
% \# W9 y: t; ]% c. ras testotoxicosis, may cause precocious puberty at a
( ]; \' t8 y! S, m) |2 u6 Vvery young age. The physical findings in these boys
: a0 H# E: O# ewith this disorder are full pubertal development,
1 B+ C7 N* F2 Hincluding bilateral testicular growth, similar to boys
, p- V) J9 T+ j& w8 zwith CPP. The gonadotropin levels in this disorder$ u& C) F' U- M. H2 ^
are suppressed to prepubertal levels and do not show# X. {+ l. x  P, i" {; k5 r, `+ _
pubertal response of gonadotropin after gonadotropin-
! J8 I: p* H# E9 ~9 Z6 lreleasing hormone stimulation. This is a sex-linked' N+ Z+ i7 ~  s2 v2 F7 ?1 b
autosomal dominant disorder that affects only" T* O$ ~# L, Z, n1 Q% _
males; therefore, other male members of the family1 E. O7 D9 }, ^* t' T4 b! ^: Q0 P
may have similar precocious puberty.34 J' P) |$ d3 m* F
In our patient, physical examination was incon-
: }9 ~. P1 I* {sistent with true precocious puberty since his testi-$ @5 d1 z3 f  s& |- p+ Q0 \
cles were prepubertal in size. However, testotoxicosis6 |, h6 f( Q/ K$ ]
was in the differential diagnosis because his father
+ y; l1 l  Z( O+ {. Ustarted puberty somewhat early, and occasionally,2 p0 E) d6 a  A% g$ m
testicular enlargement is not that evident in the
9 j# j/ l- `6 M7 {5 e/ K. d" @beginning of this process.1 In the absence of a neg-
- U6 S+ {3 j7 i# Oative initial history of androgen exposure, our$ K) U$ r& i+ [% u. H& U- {
biggest concern was virilizing adrenal hyperplasia,% j2 }/ c* {6 O+ P
either 21-hydroxylase deficiency or 11-β hydroxylase" o1 \4 D: Q1 r
deficiency. Those diagnoses were excluded by find-
) y+ |1 e; S4 ^. _& Wing the normal level of adrenal steroids.
# ~- r0 J8 L3 B* \5 ZThe diagnosis of exogenous androgens was strongly, E5 d/ N% Y0 u$ {
suspected in a follow-up visit after 4 months because4 [" ^9 }: f4 b6 t( }
the physical examination revealed the complete disap-- N3 R# ^( h  x1 e4 p( e2 Y8 W
pearance of pubic hair, normal growth velocity, and
# o' d% ?8 b* H6 q3 ]6 Jdecreased erections. The father admitted using a testos-9 [  Q% u  ~' l6 m0 V' S2 G
terone gel, which he concealed at first visit. He was; Q# O* M& ~5 S* A9 v
using it rather frequently, twice a day. The Physicians’8 q3 C) B5 i0 H* U7 s% x5 R  I
Desk Reference, or package insert of this product, gel or) \- v. @8 ^6 a/ N; P: D
cream, cautions about dermal testosterone transfer to( ~& K/ ~7 s! `+ j/ e8 X8 e
unprotected females through direct skin exposure.* x- t3 o: w. U3 @8 `: x
Serum testosterone level was found to be 2 times the% Q) R+ ?: V! U  N9 p( Z
baseline value in those females who were exposed to3 d! A) I% q- C3 m5 J
even 15 minutes of direct skin contact with their male
1 Q. F& j* F6 @3 k1 zpartners.6 However, when a shirt covered the applica-4 M! B1 ]4 G3 `6 J* a0 e* k) n
tion site, this testosterone transfer was prevented.* W% z- ~8 E* j+ Y- U* ]
Our patient’s testosterone level was 60 ng/mL,
# u5 p  ]6 f( L8 S+ P+ M: O/ T: Uwhich was clearly high. Some studies suggest that
: M: Y+ S  D- C* D1 ?! f$ jdermal conversion of testosterone to dihydrotestos-. f+ K& V% c2 p
terone, which is a more potent metabolite, is more! K. X. l9 b) N6 J# m
active in young children exposed to testosterone5 {  v2 K& G) k% M) M+ h
exogenously7; however, we did not measure a dihy-
; i  B0 V1 p0 W8 cdrotestosterone level in our patient. In addition to) c5 s$ F; z+ s7 _' W
virilization, exposure to exogenous testosterone in
8 E& d: }7 {( S- T6 Tchildren results in an increase in growth velocity and
) i- O, N- k) B5 c* dadvanced bone age, as seen in our patient.) x# O0 w) f, @3 w
The long-term effect of androgen exposure during
$ q& d& G7 X, K# \" o+ w  ]early childhood on pubertal development and final
; L  O) U0 B: P: |" _adult height are not fully known and always remain
9 M1 {' O* K- d5 b4 ^; ^9 Sa concern. Children treated with short-term testos-
: u) Z9 n+ z8 D$ ^+ X! tterone injection or topical androgen may exhibit some* R2 ], {4 I$ B: ?" Q- {; l5 D
acceleration of the skeletal maturation; however, after5 Z; y& ?* I% `4 I
cessation of treatment, the rate of bone maturation$ N, I8 {$ k4 R$ N- \( Z9 E2 v
decelerates and gradually returns to normal.8,9
# Y6 F. o; A& B5 L% B' oThere are conflicting reports and controversy! S! {, Q+ |0 H) |
over the effect of early androgen exposure on adult
5 w3 i7 }/ P3 _penile length.10,11 Some reports suggest subnormal' a& L" p1 m* p/ ~
adult penile length, apparently because of downreg-
" H! Y! m' v( }6 S: }0 O% bulation of androgen receptor number.10,12 However,
9 M) H9 i$ |9 RSutherland et al13 did not find a correlation between
3 X" {! T8 C' `6 _& B9 A0 Wchildhood testosterone exposure and reduced adult% E# F7 s! C3 _  x+ K: W
penile length in clinical studies.
1 U2 Y) D1 m. e. ^" T! m; MNonetheless, we do not believe our patient is* r+ `6 v+ `: A, u7 Y
going to experience any of the untoward effects from
( B) Q5 {) ?: e0 B/ Ltestosterone exposure as mentioned earlier because& {( R6 B; {+ i" n
the exposure was not for a prolonged period of time.
! N7 n6 ?2 W) z: a1 _, Q. h3 j, bAlthough the bone age was advanced at the time of
3 |' Q- `/ Y: p7 {7 I* v: Z; Sdiagnosis, the child had a normal growth velocity at
, y+ ?) R3 S7 M5 W# }the follow-up visit. It is hoped that his final adult
0 J3 a7 u) n- O2 lheight will not be affected.
3 g7 F4 l% V$ m: iAlthough rarely reported, the widespread avail-6 L' V4 z0 L7 `" }7 _' l! a
ability of androgen products in our society may. Z# l$ v/ o( a3 j) {+ G, v
indeed cause more virilization in male or female
( d5 r9 _7 `+ ochildren than one would realize. Exposure to andro-
) C' ~" R0 E" c, u5 \, `6 Igen products must be considered and specific ques-
! h- e6 q) G$ y$ F* ptioning about the use of a testosterone product or
" U3 Q+ b/ ]) L8 d; g2 sgel should be asked of the family members during
( e* b2 b3 b; athe evaluation of any children who present with vir-
6 D' P2 r2 ]7 w. c7 H8 Cilization or peripheral precocious puberty. The diag-
2 f7 Q. r* {9 n) W5 Qnosis can be established by just a few tests and by
- h( Z% N+ Q: Q  u) i5 L" Cappropriate history. The inability to obtain such a/ U& {, b& K: e* C
history, or failure to ask the specific questions, may1 V0 ^1 U# b+ Z( p6 N
result in extensive, unnecessary, and expensive
: J0 j2 t$ t3 L* j; S, e, y' W7 |investigation. The primary care physician should be6 j; q! E2 A+ L* y# W
aware of this fact, because most of these children
6 _; W4 u) ]  v4 S1 p- N$ gmay initially present in their practice. The Physicians’
% [" W) J1 Q7 d) tDesk Reference and package insert should also put a" S" I2 V/ V) T# O3 q3 U
warning about the virilizing effect on a male or
, {: R- b2 A% `! _4 `female child who might come in contact with some-2 K6 Q8 D# i7 T. F
one using any of these products.
$ I# Z; u1 _( p( u7 I; UReferences% p- q+ @& R" O: f  j1 v7 N* W
1. Styne DM. The testes: disorder of sexual differentiation. R  q7 M$ }* G, e5 a7 y  b
and puberty in the male. In: Sperling MA, ed. Pediatric
4 I6 l  N' ^5 u4 S/ ~4 tEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
9 I! e# h+ Y5 B" i+ C2002: 565-628.2 x+ g% R, {( P( c( e! ]; ?5 G/ k8 @
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious" I3 a/ [6 g5 ^+ z
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old& G! A/ U; q' C1 B
Boy Induced by Indirect Topical, C, u' G  M7 b8 [* N2 V
Exposure to Testosterone
" q4 R0 `7 j( {( `+ D3 s( USamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,29 e' [# w( q2 H* s
and Kenneth R. Rettig, MD1
. S' E5 h) k2 ]- b* A8 t0 jClinical Pediatrics
$ Z9 |3 B. l0 k0 q5 X2 c" J% tVolume 46 Number 6( v3 }9 ~0 M( {5 a
July 2007 540-543
. L1 p& e" g+ s6 ^© 2007 Sage Publications+ O- P+ T4 n$ C% g0 _) I. Q
10.1177/0009922806296651# N& |; P! Q# Q# e
http://clp.sagepub.com
" K; g& t- W" ?1 l7 ]1 Jhosted at9 C5 I: P; z6 _" g$ E! ?6 r' B
http://online.sagepub.com$ O2 ^+ C8 _- u  _* b# O5 t, q
Precocious puberty in boys, central or peripheral,  j7 G* k- a6 ~, U' B
is a significant concern for physicians. Central4 e) m9 z# q. ?# _
precocious puberty (CPP), which is mediated3 j2 \' Q  X& J5 B0 u! ^5 w
through the hypothalamic pituitary gonadal axis, has, g' b. s2 L" V2 q- x
a higher incidence of organic central nervous system" d5 E* w) i: ]8 J, `% l3 O8 ]# t
lesions in boys.1,2 Virilization in boys, as manifested
: ^2 Q8 A6 @6 t/ sby enlargement of the penis, development of pubic( w8 p) D. N) ?1 O/ c
hair, and facial acne without enlargement of testi-1 ]' F6 b, i) {( a
cles, suggests peripheral or pseudopuberty.1-3 We, @" ^9 l8 e6 w+ r; E& [
report a 16-month-old boy who presented with the1 a! [3 D  C& v7 Y4 n+ G
enlargement of the phallus and pubic hair develop-
+ y" p9 p: J& r9 Q% ?ment without testicular enlargement, which was due0 h5 m3 r$ x# s7 t
to the unintentional exposure to androgen gel used by7 T$ F. M, a$ m1 x+ J
the father. The family initially concealed this infor-
0 t5 ~3 F$ O8 d. k% ?mation, resulting in an extensive work-up for this2 L, e# _3 H* l% v  |4 R
child. Given the widespread and easy availability of. b" C$ W) m. j' G" K/ I5 `
testosterone gel and cream, we believe this is proba-
  k+ r" n" J, Xbly more common than the rare case report in the
9 H3 ]6 v: c5 w' j" j1 S% m- Oliterature.4' A) k- L& q$ k, ]+ X9 ]% }) S
Patient Report
( O+ {9 t4 U% i, NA 16-month-old white child was referred to the
; ^, x% ^6 S& N3 H7 U. ~( rendocrine clinic by his pediatrician with the concern) t9 t! s2 ^& A8 [
of early sexual development. His mother noticed5 N7 d$ Z) Y2 z
light colored pubic hair development when he was
1 R- i) Q$ C; ^! P9 g$ OFrom the 1Division of Pediatric Endocrinology, 2University of+ t9 n  j  d" R  G  ^3 k! l9 H: t3 R
South Alabama Medical Center, Mobile, Alabama.
" a1 e, A) a6 s: \Address correspondence to: Samar K. Bhowmick, MD, FACE,4 B# `' d+ _: @0 J; `
Professor of Pediatrics, University of South Alabama, College of
% n8 w( Z( N  y9 W$ `- b5 J- g" DMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
7 M1 k9 O7 W$ F8 `e-mail: [email protected].! E" k- W  Y) b; P& b
about 6 to 7 months old, which progressively became3 L0 d1 r# t& _4 ^) p1 Y
darker. She was also concerned about the enlarge-, k7 }4 `9 {! B2 r6 l9 m
ment of his penis and frequent erections. The child2 R4 ]' k& y. a$ p1 P# u  e0 c  F
was the product of a full-term normal delivery, with
, Y# I5 J0 U1 k5 ea birth weight of 7 lb 14 oz, and birth length of, ~7 z# W5 H! u/ t* j; n2 u, y
20 inches. He was breast-fed throughout the first year/ }- |! F" E% m7 j/ b  _$ Q8 J7 x
of life and was still receiving breast milk along with, P2 a/ F9 |; p& b
solid food. He had no hospitalizations or surgery,
8 o' ^$ T& f4 q  K5 S: g/ ~and his psychosocial and psychomotor development
4 |1 N1 V- t& D& Hwas age appropriate.
) u; g* h+ A# J: \3 K5 [The family history was remarkable for the father,
9 _7 r9 j, p# P  P: \% }2 _who was diagnosed with hypothyroidism at age 16,: `  B' u* v& }& X( e' n
which was treated with thyroxine. The father’s4 T2 @/ J' ~( E( M  V/ e( w
height was 6 feet, and he went through a somewhat" ^6 @) ~1 g8 i- C) j
early puberty and had stopped growing by age 14.
+ e0 n1 B: M7 J' S# I( h+ |The father denied taking any other medication. The9 T" K0 k: m8 \2 r$ T/ e5 ]
child’s mother was in good health. Her menarche' @0 F2 H9 w0 d0 a# B  X' R7 S
was at 11 years of age, and her height was at 5 feet
; b( a% q" f/ a5 inches. There was no other family history of pre-' {9 b0 l1 \3 B+ P
cocious sexual development in the first-degree rela-3 y8 ^$ Q+ m5 q7 M4 v% D9 L
tives. There were no siblings.
! q; W7 m1 ?* `: j+ J1 fPhysical Examination
& a$ u& V+ @+ J4 P3 SThe physical examination revealed a very active,
; i2 x6 c' R( ?5 Lplayful, and healthy boy. The vital signs documented2 g' i2 L  s# c; j+ _; j# ^
a blood pressure of 85/50 mm Hg, his length was; e3 t! U* z% h8 f8 g4 x
90 cm (>97th percentile), and his weight was 14.4 kg
8 B1 T* u, t! O# K$ I(also >97th percentile). The observed yearly growth
5 {" I2 q7 g% N. a7 r3 }velocity was 30 cm (12 inches). The examination of
- _4 w7 {  d7 o8 othe neck revealed no thyroid enlargement.
; `' ]1 g" Q* _$ P3 R9 d" u* KThe genitourinary examination was remarkable for1 E0 a5 X/ a3 q( ?7 ~. V/ i8 L
enlargement of the penis, with a stretched length of$ p  S9 w" o7 G" Q
8 cm and a width of 2 cm. The glans penis was very well
. |; e2 O& H  @; o  Udeveloped. The pubic hair was Tanner II, mostly around  }- ~* `1 Y( C" O
5408 f/ n% n8 _# Y% P3 @& i5 P
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from* A* j7 C- S- Z! s
the base of the phallus and was dark and curled. The
5 j8 @+ K' b# w8 M8 k6 w+ `3 c! Ztesticular volume was prepubertal at 2 mL each.$ y% {7 N9 a% w. h5 Z" a; U
The skin was moist and smooth and somewhat. G, [( P9 L2 f
oily. No axillary hair was noted. There were no& k" b& X- ~8 I/ X
abnormal skin pigmentations or café-au-lait spots.
5 Q0 ]/ T, j4 w- K! jNeurologic evaluation showed deep tendon reflex 2+
& m7 }- Q3 L: |4 q* A3 Pbilateral and symmetrical. There was no suggestion7 \( c1 T) W9 W7 ]7 b
of papilledema.4 d7 ]  r0 g2 u& z& S
Laboratory Evaluation
: {: p( X' g: c( @2 g7 t7 _$ oThe bone age was consistent with 28 months by
) r. t) M& T5 t! r- a( _using the standard of Greulich and Pyle at a chrono-# {0 j& V. U" ?% ?+ L1 C
logic age of 16 months (advanced).5 Chromosomal0 z9 e# J: U( _0 x7 j' o( \* d
karyotype was 46XY. The thyroid function test
, C( b$ @1 L) u$ l% yshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
- I- _) c1 i- \# n6 S7 Xlating hormone level was 1.3 µIU/mL (both normal).1 p6 s+ r# \0 N' m4 h* A
The concentrations of serum electrolytes, blood5 V" j% B) P6 i8 m
urea nitrogen, creatinine, and calcium all were! H- Y" N/ e* f. M# Q! a4 k
within normal range for his age. The concentration
' r: S6 C' c+ E- ^# |of serum 17-hydroxyprogesterone was 16 ng/dL
- |) E2 y7 F7 Z) U(normal, 3 to 90 ng/dL), androstenedione was 20- Z+ ~5 Y* b8 `; ^6 v8 e
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
! m0 E7 v( K( M( e# ~terone was 38 ng/dL (normal, 50 to 760 ng/dL),% p7 I, V5 Q$ ?
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
' U6 @* Y1 Z  s  Q$ f* f# n7 N49ng/dL), 11-desoxycortisol (specific compound S)
3 ^+ r2 D$ l( `- Vwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-' w1 o/ Q3 Z% ^7 i
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
# |  W: |8 k5 g9 y5 E- Ftestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
) ^- G! K  J, Rand β-human chorionic gonadotropin was less than: w$ [( ]+ D6 l" R, r$ d( m% g* m
5 mIU/mL (normal <5 mIU/mL). Serum follicular
0 v2 @( N* b7 {  K0 ostimulating hormone and leuteinizing hormone( h0 g1 y* ?1 A! E" ^: Y
concentrations were less than 0.05 mIU/mL; s# C; F4 u$ c! p- M
(prepubertal).+ T/ X' _) c/ N9 e7 I
The parents were notified about the laboratory
3 X" f; l* K0 {- s8 Vresults and were informed that all of the tests were/ `: Q* Y9 y! V; N4 L
normal except the testosterone level was high. The4 N6 ~, R, ?6 n4 A# h
follow-up visit was arranged within a few weeks to% M" j4 _; w/ \8 b" r
obtain testicular and abdominal sonograms; how-+ s8 Q* A* P% f' U& f1 C& k
ever, the family did not return for 4 months.
/ d  W3 U3 h9 X5 n8 C% z8 R0 vPhysical examination at this time revealed that the
; V2 ~' T& _* k9 n% Tchild had grown 2.5 cm in 4 months and had gained$ b* V/ A% K: s7 N
2 kg of weight. Physical examination remained
, m: i$ [9 P! {: t0 z8 J, W# xunchanged. Surprisingly, the pubic hair almost com-
1 k" e9 v' a8 d: {9 Epletely disappeared except for a few vellous hairs at. }0 ?# t- t( j0 m/ r; R# _, {$ ~
the base of the phallus. Testicular volume was still 2
) r: W( N4 N6 P9 a) umL, and the size of the penis remained unchanged.; U' F- {- ?, e; p9 i" o: e
The mother also said that the boy was no longer hav-+ ?0 b* F* r6 k2 H6 J  Z
ing frequent erections.
7 s" x2 ]9 L6 S* T  [. X) ^; O! p9 vBoth parents were again questioned about use of! q) ~+ r: }+ Q9 X. G/ q) {
any ointment/creams that they may have applied to. d, m# y2 h$ `0 v% S
the child’s skin. This time the father admitted the
5 C2 q" f9 W8 |. o+ hTopical Testosterone Exposure / Bhowmick et al 541( {0 H! l3 a; ~
use of testosterone gel twice daily that he was apply-
4 ^% N9 [; [/ b% X9 F3 B& w9 fing over his own shoulders, chest, and back area for
2 U0 x0 Q, ]5 ?5 Oa year. The father also revealed he was embarrassed
0 e- g$ r1 y5 N! Wto disclose that he was using a testosterone gel pre-
  c$ H9 g" S1 d4 ~- @scribed by his family physician for decreased libido. K# z- p, I- N
secondary to depression.
$ T& @0 m! Z( @/ y( i$ qThe child slept in the same bed with parents.3 N. @7 u  p* l. j" s0 A
The father would hug the baby and hold him on his
' k1 i6 K. `, m/ T4 z( d9 vchest for a considerable period of time, causing sig-
/ F9 M7 C+ ]7 i; Vnificant bare skin contact between baby and father.2 O  S5 q, I5 T% q  L
The father also admitted that after the phone call,, z/ C/ a7 ?+ _' X; t+ Y
when he learned the testosterone level in the baby! S6 K9 E: F( h5 g  B" Y2 \
was high, he then read the product information
* C. H  c5 O8 Rpacket and concluded that it was most likely the rea-
9 I3 B; O9 q. N/ P3 B; P$ Mson for the child’s virilization. At that time, they& Z2 k2 r! `' r0 D8 _+ B! {
decided to put the baby in a separate bed, and the
. z4 L: m4 c" B" M/ l2 Ofather was not hugging him with bare skin and had$ X  v( z; G  u7 P9 y/ w: U' r) ^* |
been using protective clothing. A repeat testosterone
9 q6 v& S7 _6 `4 u* Wtest was ordered, but the family did not go to the
3 q' h! R% l# d- F" }! @laboratory to obtain the test.# X6 y6 @) ]6 Q- x! t
Discussion
& N7 Y) P# h9 V# k) p- HPrecocious puberty in boys is defined as secondary& ], C( |! t. T3 A
sexual development before 9 years of age.1,4
$ T9 t" u4 A! W4 xPrecocious puberty is termed as central (true) when- H( r) A" V3 `* j2 t
it is caused by the premature activation of hypo-: L0 }! A+ B" l% J" J; `
thalamic pituitary gonadal axis. CPP is more com-, i/ }& w6 I; t$ F5 @
mon in girls than in boys.1,3 Most boys with CPP" A$ O" K1 Y/ i( [5 e  B5 U
may have a central nervous system lesion that is* J; X4 u  ]4 d
responsible for the early activation of the hypothal-
" I4 R" a/ s; K# o3 i; k5 p1 Pamic pituitary gonadal axis.1-3 Thus, greater empha-$ c5 q) j$ Y  g4 H: T. L. ]+ P4 k
sis has been given to neuroradiologic imaging in
3 I3 y& _/ }9 r0 N0 c6 A. L  sboys with precocious puberty. In addition to viril-1 B6 b; E0 `% t
ization, the clinical hallmark of CPP is the symmet-
8 C9 p5 S  @5 j) zrical testicular growth secondary to stimulation by
+ N% s- O9 T3 i/ Ygonadotropins.1,3& C- I- i7 H8 z) Y2 r) r4 O
Gonadotropin-independent peripheral preco-
4 i+ {" w- @0 f0 r/ z0 \cious puberty in boys also results from inappropriate6 B8 P: K5 |% c' O
androgenic stimulation from either endogenous or
/ C  G" w0 M- \: m. V8 E1 _exogenous sources, nonpituitary gonadotropin stim-+ G% Q! P+ \" r& g# I$ E" F
ulation, and rare activating mutations.3 Virilizing
: W+ |2 d- W. I. }7 E) Qcongenital adrenal hyperplasia producing excessive" J- R* P, [# ~7 B$ E  J
adrenal androgens is a common cause of precocious
: g) a8 N, i8 l' M+ w3 tpuberty in boys.3,4: h9 L2 v6 T" _1 X) ^) l2 ?7 F/ E
The most common form of congenital adrenal
3 m0 w5 S7 _$ o9 n; N" }hyperplasia is the 21-hydroxylase enzyme deficiency.
3 S$ g# `" r3 i9 W/ mThe 11-β hydroxylase deficiency may also result in3 x! t( v: j& h
excessive adrenal androgen production, and rarely,
% p) \0 |" |0 ^/ p: Y1 R9 T/ Q1 ~# fan adrenal tumor may also cause adrenal androgen% U' @0 ?% [0 `0 |8 D
excess.1,3
5 a) |; `0 u- I. w; d3 [at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from! s) S$ @. ?5 w. R1 v
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
0 i" ^. Z) C3 M  c( u2 H& Z' iA unique entity of male-limited gonadotropin-
8 X- f5 C; q# @. Windependent precocious puberty, which is also known
) E$ T* V) ^9 d" N: M, @$ Was testotoxicosis, may cause precocious puberty at a& y4 a/ F  D) A- _/ c
very young age. The physical findings in these boys
+ K! ]& M# t- q# h0 l7 g" \+ Q4 Kwith this disorder are full pubertal development,
) H; u! P5 v1 o: r0 t9 N: u2 `# {2 Nincluding bilateral testicular growth, similar to boys& n) _$ V0 Z% |& y/ z+ U" t
with CPP. The gonadotropin levels in this disorder
5 y( N, J) n! m2 ^. x2 z! Nare suppressed to prepubertal levels and do not show  d  J% ~4 m9 Z/ N
pubertal response of gonadotropin after gonadotropin-( b; ?* X8 d3 q6 d7 P( Z
releasing hormone stimulation. This is a sex-linked6 K; w+ r1 ^6 f
autosomal dominant disorder that affects only
  w) U2 f; X% V' l/ X/ hmales; therefore, other male members of the family
1 K  }1 ?! \" B6 gmay have similar precocious puberty.32 W6 p4 \+ t) {9 q. s8 w
In our patient, physical examination was incon-
, I' ^" W4 G" z! `2 Xsistent with true precocious puberty since his testi-" U+ @2 {# }3 x
cles were prepubertal in size. However, testotoxicosis8 O4 P- u2 m- f/ E2 z, G
was in the differential diagnosis because his father
0 R3 b, ]. M' W% D' M8 D7 tstarted puberty somewhat early, and occasionally,- `$ e4 l* X7 `. a) K. Z
testicular enlargement is not that evident in the7 C9 W+ v* i1 m: S  i9 a% O5 v
beginning of this process.1 In the absence of a neg-
9 P# y" N2 [- }3 V0 k6 T& Pative initial history of androgen exposure, our" [* Q/ a5 I# ]/ N- K) B. Y, D$ r
biggest concern was virilizing adrenal hyperplasia,; K3 y6 \+ j4 m5 j
either 21-hydroxylase deficiency or 11-β hydroxylase
: t) W* i+ |/ {" Zdeficiency. Those diagnoses were excluded by find-
* y7 {, x" h; G( @# l" Cing the normal level of adrenal steroids./ n7 ^8 M% b& E# h/ k; k% h' c
The diagnosis of exogenous androgens was strongly
! l( O: P( G: D3 H8 b. Ssuspected in a follow-up visit after 4 months because
$ u; m6 w1 ?; o6 g2 L. I& sthe physical examination revealed the complete disap-
& Z' k, V4 T( B0 U) Y* jpearance of pubic hair, normal growth velocity, and
+ q% p, b- T# p5 Sdecreased erections. The father admitted using a testos-
/ {" b3 c+ d4 E$ [8 T) u: S) Fterone gel, which he concealed at first visit. He was0 I! s1 p, r. z# G  I
using it rather frequently, twice a day. The Physicians’
* `7 X) x  ^% E$ H' J; c- G" `& ^# hDesk Reference, or package insert of this product, gel or& a( x: R' j# k& E- i1 s
cream, cautions about dermal testosterone transfer to! v! l9 a6 d! L* `7 [- K
unprotected females through direct skin exposure.
* p& i2 X5 n9 z: S% X. vSerum testosterone level was found to be 2 times the
' P$ J1 _3 P3 c* E) ubaseline value in those females who were exposed to
2 H' [2 ?5 M% J& {: weven 15 minutes of direct skin contact with their male" u* F( T  [& m* a: r& B7 u' v
partners.6 However, when a shirt covered the applica-% y' X: @4 |: V+ k0 C) x
tion site, this testosterone transfer was prevented.
$ E1 X  P1 j  m' s* ]7 [' @' i7 |Our patient’s testosterone level was 60 ng/mL,
+ i3 a% W* L# ^; mwhich was clearly high. Some studies suggest that, A& s# {  z. W4 d- F
dermal conversion of testosterone to dihydrotestos-8 C# j# c: |' P. \) H; c
terone, which is a more potent metabolite, is more
7 q1 _; M" {3 Q! W. Jactive in young children exposed to testosterone3 i. r9 ~" I; c
exogenously7; however, we did not measure a dihy-8 s4 r5 y  c; V* U1 P5 |
drotestosterone level in our patient. In addition to3 u1 e: h" t% m+ C7 p" M: v+ Q3 ~
virilization, exposure to exogenous testosterone in5 s9 U$ _/ ]0 z' g
children results in an increase in growth velocity and
1 ^4 D2 [6 A4 B- @* Z0 }6 ~advanced bone age, as seen in our patient.1 n$ D$ Y! m7 Y  H: Q  i+ s5 w
The long-term effect of androgen exposure during" U, [! V) K1 r( i
early childhood on pubertal development and final
# S% J% X3 q9 S5 i$ Q2 Q1 [2 Iadult height are not fully known and always remain& a  E2 j3 x5 i" T8 j
a concern. Children treated with short-term testos-
( J2 K" |2 A% p. lterone injection or topical androgen may exhibit some2 |% u" e3 k/ x$ |  S( A
acceleration of the skeletal maturation; however, after, s  R, `4 u* e1 T  J
cessation of treatment, the rate of bone maturation/ u+ k2 r/ i9 G2 V4 W( [
decelerates and gradually returns to normal.8,9
/ @' V: N6 _% Z8 \- D' E0 GThere are conflicting reports and controversy
: U1 a$ D. r, [' w; y8 {" P# jover the effect of early androgen exposure on adult1 ]& X" M1 h; v
penile length.10,11 Some reports suggest subnormal$ q1 }% o' F' X0 o$ k5 y8 c  q9 g
adult penile length, apparently because of downreg-! k9 u- \0 `  F' b) R
ulation of androgen receptor number.10,12 However,
9 W9 _8 V! O8 ]; QSutherland et al13 did not find a correlation between
  T3 x4 r( l/ D5 p" l. Z5 I5 Wchildhood testosterone exposure and reduced adult7 K! n9 w' h+ i/ s  L
penile length in clinical studies.
) q; O" H: o, K5 C$ R$ U9 ?: Q" LNonetheless, we do not believe our patient is: P, `0 T9 I* E. S6 J
going to experience any of the untoward effects from
7 [! g  v( r1 W* t$ w- v8 \testosterone exposure as mentioned earlier because* Y7 s7 `8 l9 }3 W0 s  T
the exposure was not for a prolonged period of time.* k- {& \5 o: D' `7 _& _! c' |
Although the bone age was advanced at the time of
2 s4 a6 M& W; |1 p/ [' Q$ jdiagnosis, the child had a normal growth velocity at
$ D, g2 H6 A0 M" U; t9 E7 G) Uthe follow-up visit. It is hoped that his final adult
6 v) v0 p( u% r7 [. Fheight will not be affected.
9 h  o* n: X. A  H/ KAlthough rarely reported, the widespread avail-
% _2 K* z- d" X1 {( v% Hability of androgen products in our society may
5 w( J; p# x$ Kindeed cause more virilization in male or female0 q# ~1 T6 d9 |3 D+ O/ b6 E
children than one would realize. Exposure to andro-3 B! L5 U" O# _+ r
gen products must be considered and specific ques-
  X4 B9 e. J/ p6 V1 W* f& Q, Stioning about the use of a testosterone product or  o  r$ W& E- G. W3 ~8 \! O
gel should be asked of the family members during5 \: t5 v' v1 z2 ?; r' P% _) N$ p
the evaluation of any children who present with vir-( {& d7 B$ T6 W
ilization or peripheral precocious puberty. The diag-4 {5 p( ]: G* C, K& E1 N
nosis can be established by just a few tests and by
, B  ^; d, o1 L! V3 O$ F6 x: n4 aappropriate history. The inability to obtain such a; L: z/ Z# j( ]. K" m5 \, ~
history, or failure to ask the specific questions, may; [$ |& ?/ Q, h
result in extensive, unnecessary, and expensive
& s, m9 ^% t( o. f# Xinvestigation. The primary care physician should be
. e7 }1 a! v$ A9 A. o0 i8 R1 \aware of this fact, because most of these children
* }( h" f1 _& Y' Amay initially present in their practice. The Physicians’
/ q2 p  U' V6 T# j- Z0 F# P' C' j# BDesk Reference and package insert should also put a
& ]0 q" e- c: t- h  f% Dwarning about the virilizing effect on a male or
; E$ H$ w* H' J+ ^  W- s4 Afemale child who might come in contact with some-
2 y( ~  p8 _0 Cone using any of these products.
6 p4 ?' S: t7 k# l6 L- ?' ~+ |References) \) T0 X) H# j/ c' X1 U
1. Styne DM. The testes: disorder of sexual differentiation
& a3 v+ c5 r( N% D* t4 Land puberty in the male. In: Sperling MA, ed. Pediatric  N- ]# @7 i; y
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
; @. j9 B9 n; o- W2002: 565-628.
9 h' `; H( E2 J! l  j! {2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
: P+ R$ [, H* X- z3 ^% Xpuberty in children with tumours of the suprasellar pineal
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這個我收藏了!謝謝分享!WK的資源越來越豐富,這少不了大大的辛勞!
發表於 2025-1-10 10:43:39 | 顯示全部樓層
VIP精品區,資源無限好賺金任務區,輕松賺金幣
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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
VIP精品區,資源無限好賺金任務區,輕松賺金幣
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

* Y" l8 P3 q; `' t$ ~4 h/ u% ?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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