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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  j/ J9 j* M1 T+ s7 H* c
Boy Induced by Indirect Topical
# }/ }* d. o3 Z$ a9 @Exposure to Testosterone- o7 {2 T- @' ]  O7 _$ U
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2: L6 `; |. e) [" j1 D
and Kenneth R. Rettig, MD16 F- T: t0 `7 Y
Clinical Pediatrics: U6 Z/ T& Y/ s
Volume 46 Number 69 o0 x' Z% x1 J. l
July 2007 540-5433 x2 h5 q5 G+ G( i8 V0 V$ Q
© 2007 Sage Publications
6 g: H' i9 E, o6 b4 e, I7 v10.1177/0009922806296651
. t# `; U/ \: _! K4 H& P$ Lhttp://clp.sagepub.com
$ [+ W$ {6 V) e' w' q6 Thosted at
. r! c4 a# G( N/ [( w  Ghttp://online.sagepub.com; J% `: r4 L; `+ m8 |
Precocious puberty in boys, central or peripheral,
/ i. ^* D6 m5 F3 `* O' A4 sis a significant concern for physicians. Central
1 p+ {1 q/ P  s, b9 o) b' B, ?precocious puberty (CPP), which is mediated
, y8 v0 K% V+ @& v3 x0 V+ d& pthrough the hypothalamic pituitary gonadal axis, has
& W, e" R- H# L, j* ka higher incidence of organic central nervous system
5 M# _2 q, o6 R. Clesions in boys.1,2 Virilization in boys, as manifested2 A) _2 Q7 X* ^
by enlargement of the penis, development of pubic$ g6 u9 U" j' x: I9 N* ?
hair, and facial acne without enlargement of testi-
( E* X! F$ D6 y+ Zcles, suggests peripheral or pseudopuberty.1-3 We/ T1 A& p. b" f2 o8 _5 u
report a 16-month-old boy who presented with the+ I2 A2 T% A$ D  w% A$ ~
enlargement of the phallus and pubic hair develop-
+ j. m) {; z, fment without testicular enlargement, which was due/ e! x, [0 m3 T4 n9 Y4 ]! H5 k$ m& p
to the unintentional exposure to androgen gel used by
0 d+ w& {& {8 R! x. mthe father. The family initially concealed this infor-
  T3 `/ q( R1 a% c0 k# u$ emation, resulting in an extensive work-up for this! q; F( {5 q4 U0 J, j3 s
child. Given the widespread and easy availability of; u: u) \( D8 T5 i: ?. Z0 a
testosterone gel and cream, we believe this is proba-( N& B% V2 v" I2 l
bly more common than the rare case report in the
7 L# O2 l$ p+ S1 nliterature.42 M( K. B+ ]: C" o& P" S% Y# ~
Patient Report
# c, K5 N( {7 ?  P, Y2 H, {5 jA 16-month-old white child was referred to the) W0 J& }: s0 J2 Z. q
endocrine clinic by his pediatrician with the concern
& T: M6 K: j1 k* |  d4 f( Cof early sexual development. His mother noticed
% b7 O5 K3 M6 k% v6 `light colored pubic hair development when he was6 o5 E! v% x7 ~/ |) g5 a/ ?( B7 x
From the 1Division of Pediatric Endocrinology, 2University of
6 F# b5 u4 G' qSouth Alabama Medical Center, Mobile, Alabama.( C. a. @- J% g, z
Address correspondence to: Samar K. Bhowmick, MD, FACE,9 w! X7 M5 `; E/ ?" @; Z6 j$ R
Professor of Pediatrics, University of South Alabama, College of
& V- Q, j9 I7 U* l% ], z  _. y: |4 gMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;0 z2 Q& f* L* g  g
e-mail: [email protected].
2 j3 U8 f# O9 n, N) G5 cabout 6 to 7 months old, which progressively became) Q' M5 I# y0 ]" g: M
darker. She was also concerned about the enlarge-
: H0 ]$ Q+ g6 U2 S7 o( x. B2 J: |ment of his penis and frequent erections. The child
- q$ w3 m6 H. ~3 Jwas the product of a full-term normal delivery, with
$ \% @% {8 X. m- X& @& ?a birth weight of 7 lb 14 oz, and birth length of) h2 E" Q' b$ C  [6 B6 t9 m
20 inches. He was breast-fed throughout the first year
7 d6 T$ t' j+ k, G  ]* T% Dof life and was still receiving breast milk along with
. _+ |& D) R0 l4 K; K/ _( Hsolid food. He had no hospitalizations or surgery,
# V, K1 g5 G3 J! ^7 X% F. l+ N5 d: qand his psychosocial and psychomotor development
, y7 @+ b. v( t/ a7 c! F. ywas age appropriate.
1 I0 f1 N8 y" h8 F& HThe family history was remarkable for the father,$ P% q) l8 |3 T- l$ c( y* F) ~
who was diagnosed with hypothyroidism at age 16,
, s  q% \. H$ k: W+ x: I" X  pwhich was treated with thyroxine. The father’s
/ v, g" i5 h4 h' C3 }& }2 zheight was 6 feet, and he went through a somewhat% e+ W  J/ ~) a$ j
early puberty and had stopped growing by age 14.
% y. ]: H* X1 S' X1 Q# H$ bThe father denied taking any other medication. The' {- Q  l9 V' f# P# G
child’s mother was in good health. Her menarche; H! F% M3 }  T' a4 Y
was at 11 years of age, and her height was at 5 feet% j- m4 Z# p) b% Z7 u
5 inches. There was no other family history of pre-: s" z! F( t! `: s; v
cocious sexual development in the first-degree rela-
% Q& s* R4 A6 E  ntives. There were no siblings.) W/ O. [/ s; [9 G4 w
Physical Examination! F) ^  o2 Q$ y. ]; o8 |+ R
The physical examination revealed a very active,/ j% [( z2 R1 P7 W7 y4 ]
playful, and healthy boy. The vital signs documented1 A( @9 \, w& L% a3 I
a blood pressure of 85/50 mm Hg, his length was
5 f# A" ?) G5 m) g4 \' @90 cm (>97th percentile), and his weight was 14.4 kg9 y+ O5 d1 Z/ }0 b1 A3 {+ v
(also >97th percentile). The observed yearly growth
: S. j2 S$ ^7 A5 Ivelocity was 30 cm (12 inches). The examination of
( }3 i" _) v6 U3 Uthe neck revealed no thyroid enlargement.
' |* m  H$ F; l: r2 iThe genitourinary examination was remarkable for
* Q) r  h# ?% Z* c2 {enlargement of the penis, with a stretched length of: ~# A9 q8 D; u5 |1 P) G& N0 g  W
8 cm and a width of 2 cm. The glans penis was very well5 ^$ G* L% @& g  s) ^
developed. The pubic hair was Tanner II, mostly around  b0 `1 E9 x! M6 D1 R+ [% r
540
% n6 \. ^# W7 I5 O) i$ `at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from! j0 j2 X0 j/ J0 Q
the base of the phallus and was dark and curled. The1 N1 `2 X+ G. J2 t
testicular volume was prepubertal at 2 mL each.$ M' Y- [3 M# V3 k8 ~0 R
The skin was moist and smooth and somewhat$ E7 G! a" y4 f: \* k4 \- ~. t
oily. No axillary hair was noted. There were no
( L6 B7 ^: w: c; O6 q- T; r9 eabnormal skin pigmentations or café-au-lait spots.
$ X1 u- z  q$ Z; I" \: eNeurologic evaluation showed deep tendon reflex 2+
+ I; L, e$ E4 I/ R, H/ D3 `bilateral and symmetrical. There was no suggestion1 S8 F/ V* J7 I
of papilledema.- o3 I, _3 G0 z
Laboratory Evaluation
8 d# }- Z, K3 qThe bone age was consistent with 28 months by
$ j6 v' |  I5 B# ~3 q! `! M' q9 }using the standard of Greulich and Pyle at a chrono-
8 X, I2 S2 L6 ^8 ]& l/ xlogic age of 16 months (advanced).5 Chromosomal
' B, A' i* |9 W7 ]( {0 ukaryotype was 46XY. The thyroid function test
8 i! W% r! z; lshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
; f/ O. K+ M( e: a! v/ l! Plating hormone level was 1.3 µIU/mL (both normal).; g: B* Y& V9 n" i' D0 j* _
The concentrations of serum electrolytes, blood
/ Q* }1 G6 Q/ Murea nitrogen, creatinine, and calcium all were- j; t4 |+ Q/ ?. q1 }6 ^
within normal range for his age. The concentration% D+ _1 V6 \* Z
of serum 17-hydroxyprogesterone was 16 ng/dL
& X/ T, L; X0 D& Y0 e7 v( w. q(normal, 3 to 90 ng/dL), androstenedione was 20: h8 f  I  x5 W9 ?. s: o! F
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-2 W/ _4 }2 U( N6 }
terone was 38 ng/dL (normal, 50 to 760 ng/dL),8 o8 G8 W! d7 `7 m+ @! G
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
' m) i; G5 m" R. R6 ~49ng/dL), 11-desoxycortisol (specific compound S)9 g; G5 c; D# M4 H$ \7 V8 Y
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-* E, w: J* L5 g. W) i
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total0 x0 ^, r# H. W" _
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),9 u& y* ^; Q0 o  {, V' @
and β-human chorionic gonadotropin was less than
+ a: k# ^. ~9 F5 mIU/mL (normal <5 mIU/mL). Serum follicular
( r2 d' v% j7 u0 dstimulating hormone and leuteinizing hormone6 B4 F+ f: _5 W8 e! F7 R$ U
concentrations were less than 0.05 mIU/mL
- W1 n, D! n% ](prepubertal).
2 F2 [# ^" T$ T* FThe parents were notified about the laboratory" P7 @% d3 U3 S' k: M* e7 Q. e$ P
results and were informed that all of the tests were' h& o5 o# ]+ p% ]
normal except the testosterone level was high. The
! o) @. I2 \2 |% @follow-up visit was arranged within a few weeks to
/ g8 y, s: z! R8 u# Yobtain testicular and abdominal sonograms; how-8 B6 @1 I: ^, {) ]) S  {# A$ R! e
ever, the family did not return for 4 months.4 H( e6 F; U0 {. _& u) T
Physical examination at this time revealed that the
' ?; Q& }4 e1 M; |child had grown 2.5 cm in 4 months and had gained0 k) A* x% M+ l3 I6 C7 U
2 kg of weight. Physical examination remained
6 ^  M8 v( [7 h. e1 E/ L( O' {! tunchanged. Surprisingly, the pubic hair almost com-$ ^% t% I/ E- p8 K/ x; L
pletely disappeared except for a few vellous hairs at0 ~: X9 R9 n' v- ^5 h/ ~# l
the base of the phallus. Testicular volume was still 2
2 t+ g# K  C6 T$ u: n* H2 UmL, and the size of the penis remained unchanged.
7 h/ q# `  X1 W# \1 W1 x# jThe mother also said that the boy was no longer hav-* @0 s/ K. E) v  v, Y  g; N- D
ing frequent erections.; p$ b8 ?  @/ S+ F0 J
Both parents were again questioned about use of
6 S9 L+ x5 [4 [) O- A$ |1 ^any ointment/creams that they may have applied to, B* Z, ~0 t! I6 F, e0 }
the child’s skin. This time the father admitted the
: F8 L, q* j  _Topical Testosterone Exposure / Bhowmick et al 541. L& e- T6 `; Y) o
use of testosterone gel twice daily that he was apply-' X1 L, i7 n5 ^* h
ing over his own shoulders, chest, and back area for) Z  Y9 y0 c" a( R5 C
a year. The father also revealed he was embarrassed( L- v2 }" |, \7 I7 U9 G9 f
to disclose that he was using a testosterone gel pre-6 U+ J' ?& ~& L# k. L2 U
scribed by his family physician for decreased libido
# y8 J, o, x: \secondary to depression.) V+ K) A2 b1 t! b/ \, Q3 V
The child slept in the same bed with parents.
( N5 [3 c9 ]: E( JThe father would hug the baby and hold him on his6 {, J3 t9 h+ \0 p! S1 k; J
chest for a considerable period of time, causing sig-8 @* K5 e% O+ |* \4 a, O
nificant bare skin contact between baby and father.
/ x0 n: U/ s4 ^The father also admitted that after the phone call,- m( V, X1 y! E% Z* b! s
when he learned the testosterone level in the baby
6 ]! ?6 u5 k+ Fwas high, he then read the product information
0 k" O* z7 B6 b  j: ~packet and concluded that it was most likely the rea-. e" c8 i9 R" L0 E$ [4 [
son for the child’s virilization. At that time, they
( C. @; J# p( V, L# udecided to put the baby in a separate bed, and the! ?( {' e5 X. V7 j4 y! k" P4 d
father was not hugging him with bare skin and had- V/ N: ?) f3 l7 |" h
been using protective clothing. A repeat testosterone
3 {  O* ^6 J. q) otest was ordered, but the family did not go to the
' B$ M. h: A: h: U# Elaboratory to obtain the test.$ a& T; ?3 V( }- I% }
Discussion
. \- P, _/ k, Z+ M& NPrecocious puberty in boys is defined as secondary
; R! X  s# r! i* X: J: Msexual development before 9 years of age.1,40 l* v, _' l: T2 _
Precocious puberty is termed as central (true) when3 n! e1 O5 l0 z
it is caused by the premature activation of hypo-
, o% O) g' J! G1 Hthalamic pituitary gonadal axis. CPP is more com-+ K" v7 k, A  v  {
mon in girls than in boys.1,3 Most boys with CPP$ W4 u2 ~+ c4 i' A6 ?+ b# K
may have a central nervous system lesion that is7 D1 M% q9 H; v: F
responsible for the early activation of the hypothal-
/ K- k: |; Y) Y$ }7 Ramic pituitary gonadal axis.1-3 Thus, greater empha-: ]9 i2 K) E, D8 q4 S
sis has been given to neuroradiologic imaging in
$ \# ]# o' p: d7 z6 b: n4 {! ?boys with precocious puberty. In addition to viril-2 r+ T& }9 m1 j2 n; N  u
ization, the clinical hallmark of CPP is the symmet-
/ g  r; W# Z0 c7 M  x: _rical testicular growth secondary to stimulation by0 ?' _2 {. h$ P# x3 |/ g8 W
gonadotropins.1,3! k/ N# |% J( ]2 ]. F8 I2 |
Gonadotropin-independent peripheral preco-
% I5 w$ x3 E/ R% {* S+ ]( V4 [) gcious puberty in boys also results from inappropriate, Z8 m( g6 \' `4 `8 g* Y) R
androgenic stimulation from either endogenous or
" e% b( ~  d" i+ _9 C. Qexogenous sources, nonpituitary gonadotropin stim-) K* T/ G0 w! r& q' g( m
ulation, and rare activating mutations.3 Virilizing; c$ h  X& S: S4 w8 K" U% ]; {
congenital adrenal hyperplasia producing excessive  F0 _4 G: L7 b
adrenal androgens is a common cause of precocious
$ o5 |$ Q( }; y5 U4 ~, U4 Mpuberty in boys.3,4
' P7 o  }6 c/ o" tThe most common form of congenital adrenal2 S2 g% k2 r/ G5 D7 Z, k( F: V/ q$ Q7 Q
hyperplasia is the 21-hydroxylase enzyme deficiency.* }- o7 D2 b7 _5 `) F5 a1 r
The 11-β hydroxylase deficiency may also result in1 q& b- i: [% P( {$ E# C
excessive adrenal androgen production, and rarely,( {8 C# `$ @# Q
an adrenal tumor may also cause adrenal androgen
0 o+ e6 Q, e# E  A. O4 lexcess.1,3) U9 q5 |6 ^2 K. r# {" @) ~: O
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
+ X+ V+ a7 T* x$ u542 Clinical Pediatrics / Vol. 46, No. 6, July 20073 Q' }- |/ u% `: U. _1 \1 i& m# E7 U
A unique entity of male-limited gonadotropin-; B4 r0 [1 p8 y2 }9 V2 i5 y# q
independent precocious puberty, which is also known9 k5 X) y) i( _
as testotoxicosis, may cause precocious puberty at a: N0 V+ V- ?. k7 [+ l/ ]9 C* u
very young age. The physical findings in these boys
& k. r8 b& `+ ~+ k7 y! _with this disorder are full pubertal development,! h: M% C9 u8 r9 ]% U6 t
including bilateral testicular growth, similar to boys, j# R1 q* Z& `9 }1 ]' F% H# i1 X
with CPP. The gonadotropin levels in this disorder- e+ @5 E+ W' g
are suppressed to prepubertal levels and do not show4 \6 Q6 u8 j3 p) g
pubertal response of gonadotropin after gonadotropin-
% y  |7 `& z! g" O7 ^8 Xreleasing hormone stimulation. This is a sex-linked
2 r. C' \$ `' X$ b+ qautosomal dominant disorder that affects only! y9 D8 \' Q& r& V# J- U! z
males; therefore, other male members of the family4 g* |5 O7 ?) {7 V( Z
may have similar precocious puberty.3  U. R. m! y  O
In our patient, physical examination was incon-0 J+ A/ {& {6 r% b
sistent with true precocious puberty since his testi-- r* M. u2 q: _1 |  |* p, \
cles were prepubertal in size. However, testotoxicosis. F( T' }4 v8 m0 O# E
was in the differential diagnosis because his father1 P! k! h1 m1 F: n3 ?
started puberty somewhat early, and occasionally,% U) j$ @" A; C4 t  G) g. [9 t) [
testicular enlargement is not that evident in the
; S) x  C( K5 [+ k9 \6 bbeginning of this process.1 In the absence of a neg-; ^6 V4 W( s. b! L  A' D
ative initial history of androgen exposure, our
8 ~7 I6 Y* O$ u! Jbiggest concern was virilizing adrenal hyperplasia,/ A4 t6 ^, [* S+ ]9 w$ A
either 21-hydroxylase deficiency or 11-β hydroxylase
3 }/ _3 n6 H5 H' E6 l+ A0 C$ Mdeficiency. Those diagnoses were excluded by find-
, [1 O% [; X% h3 I4 H1 {ing the normal level of adrenal steroids.) Z$ y/ D6 C$ x$ j9 E" d
The diagnosis of exogenous androgens was strongly1 f8 K# b7 K; j: ^) ]5 Y, P  @
suspected in a follow-up visit after 4 months because
6 L1 U3 s& E3 ]- Athe physical examination revealed the complete disap-1 F4 `: V% G$ d& S- d
pearance of pubic hair, normal growth velocity, and
' I- x7 M8 o: Q" t8 O* W$ `decreased erections. The father admitted using a testos-
" p  Z5 _' o3 B7 T4 \% j, Fterone gel, which he concealed at first visit. He was% ]* v  f$ {; S
using it rather frequently, twice a day. The Physicians’
3 [* J& U9 n7 J2 A6 f* @/ [Desk Reference, or package insert of this product, gel or1 b5 T0 ~1 t9 \& t
cream, cautions about dermal testosterone transfer to9 C* N6 d  E. |; k$ H8 b
unprotected females through direct skin exposure.
! W, i+ |$ T' O1 {Serum testosterone level was found to be 2 times the
, r; U: v$ H+ f& o& `  e% ]baseline value in those females who were exposed to* s+ }" E7 ~/ L2 C% e
even 15 minutes of direct skin contact with their male
0 p4 `- [( h* `/ ppartners.6 However, when a shirt covered the applica-
, k$ \9 p% Y" e7 ^tion site, this testosterone transfer was prevented.
) ~- X, F) e8 y7 C1 b8 L& ^Our patient’s testosterone level was 60 ng/mL,
. A1 D: }7 h8 _; W0 {+ z: Ywhich was clearly high. Some studies suggest that/ E" e9 B2 L+ @* d4 I% J" K
dermal conversion of testosterone to dihydrotestos-
( o5 t& k* A: o1 pterone, which is a more potent metabolite, is more9 E' ]" |+ j+ e
active in young children exposed to testosterone
5 T* p( W0 [8 |+ d# Uexogenously7; however, we did not measure a dihy-
9 `5 K2 n9 O/ T5 y& j% M0 ndrotestosterone level in our patient. In addition to3 k* T0 B& s& V6 q  ]7 g! r
virilization, exposure to exogenous testosterone in9 v( u. {. E" b! F$ x" Y
children results in an increase in growth velocity and
8 g6 b9 N( S4 g- Vadvanced bone age, as seen in our patient.
* `4 N5 s- ?$ v5 gThe long-term effect of androgen exposure during0 J0 V& P  F2 X# _
early childhood on pubertal development and final
) @+ G) O" K- n! V, Gadult height are not fully known and always remain
! N7 U: T% {# N$ M8 }4 ], aa concern. Children treated with short-term testos-
& K- M) ?( C8 ]- Sterone injection or topical androgen may exhibit some- d  Z( z4 n% i. A) R
acceleration of the skeletal maturation; however, after
# E5 a& _9 `1 G" Y/ }$ a0 P- rcessation of treatment, the rate of bone maturation
. V9 X& E$ t# x6 _4 f6 `2 Xdecelerates and gradually returns to normal.8,9+ ^- [( e- O& b; g& V2 Z
There are conflicting reports and controversy
% _+ c. `! q6 c( L+ Uover the effect of early androgen exposure on adult5 v7 H2 d3 w2 t$ N# E7 T' E) R+ ~& @$ ^
penile length.10,11 Some reports suggest subnormal5 {9 v# g* ^" D$ @$ Z
adult penile length, apparently because of downreg-1 D; g' K$ h; b8 b; Z) Y
ulation of androgen receptor number.10,12 However,
. ~4 t3 d: M) r3 JSutherland et al13 did not find a correlation between' S% r, c' J4 p9 S
childhood testosterone exposure and reduced adult
* w; L# Z' P6 x% Rpenile length in clinical studies.- U9 `& s3 e7 F, z* r9 Q
Nonetheless, we do not believe our patient is- g/ y4 m1 O( N. M, _
going to experience any of the untoward effects from
$ D" C& Q8 Y( c2 R* Q  Ltestosterone exposure as mentioned earlier because/ ^; z* w% [( V5 E0 N4 N8 f. j2 X
the exposure was not for a prolonged period of time.
. d* A, ]+ f' }( _; o, wAlthough the bone age was advanced at the time of  P+ n4 A9 \3 b% T* }5 }, S
diagnosis, the child had a normal growth velocity at
2 s3 M6 h2 _9 Y! p& L) j9 _+ bthe follow-up visit. It is hoped that his final adult; s5 s8 J: [6 U" s6 d
height will not be affected.) I$ a( E. j! z5 h
Although rarely reported, the widespread avail-" Q/ K6 q& O2 }1 D! I; ^  l. x# n
ability of androgen products in our society may
) H1 |+ P2 O& g0 R" iindeed cause more virilization in male or female0 K5 ^! a- f' H# Z' B1 j4 C& I
children than one would realize. Exposure to andro-- O/ M& l6 P1 V/ p. }$ e9 d
gen products must be considered and specific ques-  s. x: F0 p% u% |# D
tioning about the use of a testosterone product or+ h/ _5 F+ t( g+ K
gel should be asked of the family members during9 ]+ Q  l- P% g8 \7 `3 F
the evaluation of any children who present with vir-5 \1 O4 `- T6 d8 g7 L7 D
ilization or peripheral precocious puberty. The diag-9 e2 x) h0 Y2 o! f0 G
nosis can be established by just a few tests and by' o% ~$ G" O2 m( b$ o5 s
appropriate history. The inability to obtain such a- d9 c, K: o' v8 E+ n% K/ {
history, or failure to ask the specific questions, may
/ a' O. g6 R& L5 K* Wresult in extensive, unnecessary, and expensive
+ q; d- `5 x. _/ J- w2 y6 W9 _investigation. The primary care physician should be
& R; ^, J2 q9 z6 Waware of this fact, because most of these children6 b+ ^* Z: Y; c& i/ a9 i# M
may initially present in their practice. The Physicians’* v0 i$ l. U8 r; }
Desk Reference and package insert should also put a
1 b& s& g: W5 A  Kwarning about the virilizing effect on a male or9 C( a- V: F4 P! m# E# I
female child who might come in contact with some-
6 I$ ^" r9 r  m( L  ?6 F" yone using any of these products.
0 U3 b3 g8 G  S4 jReferences
4 h' c( W3 B3 a: I# _1. Styne DM. The testes: disorder of sexual differentiation
' P7 f* [* |3 Nand puberty in the male. In: Sperling MA, ed. Pediatric& v0 \& O" n' p: {% F
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
. p# y" N% h$ |: K' u7 E( W2002: 565-628.$ B  a7 U3 c3 s
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
$ H* ?) ~6 L: _$ K" J- ?puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old* u0 l# A/ T7 K& G  _* A
Boy Induced by Indirect Topical0 I! I  l6 f" s
Exposure to Testosterone5 ]/ Z" C7 m: X  u5 c6 `. K
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
) q7 p& _" K: A& J% \7 oand Kenneth R. Rettig, MD1$ C& ~9 q! v3 V9 I* S0 m
Clinical Pediatrics
2 h) _8 Q) u) o, n$ z* k+ WVolume 46 Number 6. Z6 j, J! X$ n3 P
July 2007 540-543: s3 w' v  R6 v7 T
© 2007 Sage Publications& L) O  a2 t. a1 P/ k
10.1177/00099228062966510 z# N6 D+ e% f) C+ O" `
http://clp.sagepub.com7 X1 f' e# Q/ X( A* @* l" W
hosted at+ E7 i. U$ l) ?& j4 c
http://online.sagepub.com
5 b  q. I( ^; p+ {$ JPrecocious puberty in boys, central or peripheral,
' S& P4 a( `# h/ b  v$ cis a significant concern for physicians. Central
  u$ E! [' Y+ G7 U( W2 x. x0 |" _precocious puberty (CPP), which is mediated2 k' o& U  }; `5 m. D8 t5 K7 s" i
through the hypothalamic pituitary gonadal axis, has* l8 |0 W) K4 V0 n' T/ z; g
a higher incidence of organic central nervous system
- }, _$ r, D4 U; G7 Plesions in boys.1,2 Virilization in boys, as manifested% M0 I$ L% @# f7 q0 m; Z; D* h
by enlargement of the penis, development of pubic9 T: q! b5 n0 T
hair, and facial acne without enlargement of testi-8 S# c- `! @' C- U% w
cles, suggests peripheral or pseudopuberty.1-3 We
, ~2 K* M& X' E3 ureport a 16-month-old boy who presented with the/ L1 j% b0 }; T0 C7 H
enlargement of the phallus and pubic hair develop-
* X, O5 R' ^$ \% c, J1 Sment without testicular enlargement, which was due
. T( b( G1 N; ~) T, g6 w/ ?: }! Ito the unintentional exposure to androgen gel used by
8 w  h! U( J& @. sthe father. The family initially concealed this infor-/ ]$ I8 t" G+ g: X
mation, resulting in an extensive work-up for this
$ A" \' x5 ?; H# qchild. Given the widespread and easy availability of
' J. E. N$ Z1 U7 M  ^/ H* wtestosterone gel and cream, we believe this is proba-7 R( S, Q) [: E# P2 i$ G0 ^
bly more common than the rare case report in the
+ C/ W  Z$ a  Pliterature.4
  d2 R, T  o. D: a, a8 APatient Report
3 D4 v; J: \& \% o  OA 16-month-old white child was referred to the
6 Z# D0 j$ e- Q' [endocrine clinic by his pediatrician with the concern) N, p" e* r/ y5 B. c' n" ?8 {4 s
of early sexual development. His mother noticed" r7 ?3 Q" }; m9 j4 m' A2 ]
light colored pubic hair development when he was
2 ^. d* k* A2 x$ B0 F6 DFrom the 1Division of Pediatric Endocrinology, 2University of
8 e) i4 |' d6 B) dSouth Alabama Medical Center, Mobile, Alabama.
) D! e! u1 [; }0 v5 d' X& ~1 P! ?& @Address correspondence to: Samar K. Bhowmick, MD, FACE,
5 J5 N* b8 F. x0 I' Y9 ~3 AProfessor of Pediatrics, University of South Alabama, College of
7 e0 _- X0 M/ p$ VMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
% K- V4 b  U7 r# s# b. ~9 ?$ @e-mail: [email protected].: l! ?( d0 J, T& P
about 6 to 7 months old, which progressively became2 z, \: Z6 p, h; _! T: @
darker. She was also concerned about the enlarge-# B& y: ~- T, M: e$ g
ment of his penis and frequent erections. The child
- @% @5 n' M6 r# m' gwas the product of a full-term normal delivery, with7 _6 |3 r) F* f2 n5 K, L& Y
a birth weight of 7 lb 14 oz, and birth length of
" S) ]: v2 n  v  ^6 g. W0 u+ U$ |20 inches. He was breast-fed throughout the first year7 |' o4 g2 B/ k" g6 ?3 }9 l* _
of life and was still receiving breast milk along with6 I) _* w9 D4 _4 s& N% |
solid food. He had no hospitalizations or surgery,
6 D; X% |- }, G: {5 F8 Q0 `+ Y4 mand his psychosocial and psychomotor development
4 G* L( x5 L  p) u, g3 Xwas age appropriate.8 I% z2 v0 k$ j: n! L' ]
The family history was remarkable for the father,
2 S+ N. I0 L! P1 u- d" Iwho was diagnosed with hypothyroidism at age 16,$ T% P6 u  u  W: E# V, y6 C
which was treated with thyroxine. The father’s0 Q, q* H& g: N/ z9 a
height was 6 feet, and he went through a somewhat
' O2 M# T$ n7 m2 o# pearly puberty and had stopped growing by age 14.
' I" }. f" {, `# e) A5 EThe father denied taking any other medication. The
4 u+ u3 K7 E$ b# P/ K+ @8 u# gchild’s mother was in good health. Her menarche
# V/ m5 p1 G0 S, M, Dwas at 11 years of age, and her height was at 5 feet
3 C/ y/ _' P# K0 E! n0 e' f9 A5 inches. There was no other family history of pre-3 C) c/ l7 G: w. A
cocious sexual development in the first-degree rela-
8 g+ U9 [  _0 G3 l) r/ E: atives. There were no siblings.. a7 }! d6 @( {# s/ y" V/ ~0 p/ l
Physical Examination
7 k, y2 }/ o  z5 U+ U$ JThe physical examination revealed a very active,
2 Y7 l+ n( X8 E1 hplayful, and healthy boy. The vital signs documented
7 y* V# {, j& ~* x: A1 @a blood pressure of 85/50 mm Hg, his length was
% G% ^0 i6 w; Y; _% m- W2 `; I7 j90 cm (>97th percentile), and his weight was 14.4 kg( u& O- o: [0 H& h3 a1 G
(also >97th percentile). The observed yearly growth! o) {2 w; ~5 L: ?& n
velocity was 30 cm (12 inches). The examination of9 n- I" d; |. E" _# u9 x1 ]) I
the neck revealed no thyroid enlargement.0 p/ j( [* r1 d1 s* B9 I* e
The genitourinary examination was remarkable for' s& j& L) v' P& }
enlargement of the penis, with a stretched length of% L8 ^8 I! P& _/ z) b- f
8 cm and a width of 2 cm. The glans penis was very well
9 [% F* o4 d* |/ ]: [5 O: ndeveloped. The pubic hair was Tanner II, mostly around" a2 C/ n- I4 {9 n
540$ N& H2 m3 ~% k4 b# m7 G$ {9 b" Q  ^
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from$ {0 a, f- T+ m
the base of the phallus and was dark and curled. The; y/ {9 J, f+ A+ K0 N5 g- Z  D6 L
testicular volume was prepubertal at 2 mL each.' A2 V5 H* z# j  L( M
The skin was moist and smooth and somewhat
) l# p+ A* _5 m' `7 c( r3 eoily. No axillary hair was noted. There were no" \- L2 j' l  \+ B. N
abnormal skin pigmentations or café-au-lait spots./ O, p) v- K- a& d6 p) }  u
Neurologic evaluation showed deep tendon reflex 2++ \; O; U, Z$ ?  Z$ z
bilateral and symmetrical. There was no suggestion3 s7 l4 j9 H" }5 F* o" C
of papilledema.
: w7 e9 p5 B$ M  P! sLaboratory Evaluation  h5 L  |9 {1 M% l# J
The bone age was consistent with 28 months by/ g. v! M5 f4 @4 M! I4 c
using the standard of Greulich and Pyle at a chrono-0 q  v. Q8 n, Z+ \
logic age of 16 months (advanced).5 Chromosomal5 |$ Y0 m4 Q- X* I0 V; R
karyotype was 46XY. The thyroid function test' R7 w) y, ^' n/ b3 [
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
: b3 s" N3 A2 [/ m: K1 Nlating hormone level was 1.3 µIU/mL (both normal).& f0 D2 j& q+ l1 f4 O0 h+ A
The concentrations of serum electrolytes, blood/ j' }) e+ Q' S! Q( O
urea nitrogen, creatinine, and calcium all were# e4 p3 d& C$ K8 z2 Y; D5 F
within normal range for his age. The concentration" w& B2 L+ v+ O' C1 O
of serum 17-hydroxyprogesterone was 16 ng/dL7 o+ s. `4 M, |  g
(normal, 3 to 90 ng/dL), androstenedione was 20) [  t, k. r0 f
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
- c( m. f; D, e5 R  O  }# E) jterone was 38 ng/dL (normal, 50 to 760 ng/dL),
% X. R8 M! p. ^" x6 B/ Adesoxycorticosterone was 4.3 ng/dL (normal, 7 to1 B7 _5 c8 Q0 s" U& [
49ng/dL), 11-desoxycortisol (specific compound S)2 J" J' |; k6 @9 J4 Y8 l
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-  r5 |9 M# z  a6 a4 U$ K
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total' _# T& n/ u9 \7 F1 F; l
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),& I# S  D5 [+ }. E# F* c' `
and β-human chorionic gonadotropin was less than
) p- N* a+ A( V& y5 mIU/mL (normal <5 mIU/mL). Serum follicular+ U  H0 S$ @2 i  j" ~/ ^, N
stimulating hormone and leuteinizing hormone9 e4 Y. m& e6 R6 J
concentrations were less than 0.05 mIU/mL
* x/ K2 @6 g5 G7 [(prepubertal).
/ g6 B1 t- m# {! {/ AThe parents were notified about the laboratory4 ~7 {' f/ `# V0 r, Y4 g& m$ _' m
results and were informed that all of the tests were4 E- Q( u; {/ J9 _4 U+ L# F' j
normal except the testosterone level was high. The
* g+ _) \6 B1 G: s  Ffollow-up visit was arranged within a few weeks to
  E. B" U3 _  L) L! N" xobtain testicular and abdominal sonograms; how-& ~, G( G0 }# t3 p" S
ever, the family did not return for 4 months.
5 y, I- I# M( s2 [Physical examination at this time revealed that the& F& |" G: n# _0 B/ ~6 N* e
child had grown 2.5 cm in 4 months and had gained
+ g& A) ^1 e% s. I; Y1 v) R2 kg of weight. Physical examination remained0 D( \6 }! h9 b6 [
unchanged. Surprisingly, the pubic hair almost com-
. X3 w1 _; @+ `" X% z8 xpletely disappeared except for a few vellous hairs at4 W4 y2 l$ u' B2 w
the base of the phallus. Testicular volume was still 2+ L$ n7 m, U3 p; j( S* C6 E
mL, and the size of the penis remained unchanged.
  W5 w# A) b: n6 e/ Z  r$ h7 J3 @The mother also said that the boy was no longer hav-3 E- B; r, X& H+ ]* ~
ing frequent erections.4 z! v) s( P  a
Both parents were again questioned about use of, F3 z0 @# s7 E9 k
any ointment/creams that they may have applied to. Z5 q! f: C5 `- T, @: ?4 O4 y) i& g
the child’s skin. This time the father admitted the( P2 C- F+ D; n& X. U+ x5 G
Topical Testosterone Exposure / Bhowmick et al 541& S8 i. p5 K4 B9 D: y/ o
use of testosterone gel twice daily that he was apply-
, C- M- n/ N4 c) g' a" q/ eing over his own shoulders, chest, and back area for
! I- {8 R; x. sa year. The father also revealed he was embarrassed! Q4 u9 B! v& m1 {! j9 \
to disclose that he was using a testosterone gel pre-. Z$ c8 V5 k7 l2 l' x$ b
scribed by his family physician for decreased libido2 K/ v% ^! p0 `, ?7 A' y/ h8 ~) \
secondary to depression.
" X" X8 M/ a" W' U7 M0 H/ d6 nThe child slept in the same bed with parents.
. h) U+ X3 s$ M, V5 yThe father would hug the baby and hold him on his
3 M! s- q( b  R. f) U# Y+ Schest for a considerable period of time, causing sig-5 V6 n& z9 U* J8 b
nificant bare skin contact between baby and father.8 M  M5 w& c: z3 i9 u: u
The father also admitted that after the phone call,, v. ~3 O  E- z8 h; y' V' J
when he learned the testosterone level in the baby/ h" \9 h; i1 A. v3 q( l
was high, he then read the product information5 F1 j1 H8 r8 |  j0 w- Q
packet and concluded that it was most likely the rea-6 {! r5 [+ u% l
son for the child’s virilization. At that time, they2 d* f% N" }: D7 ]8 y
decided to put the baby in a separate bed, and the! b/ j0 {1 w, ^4 Z9 i% h
father was not hugging him with bare skin and had, p; h+ z1 r9 [  s7 L
been using protective clothing. A repeat testosterone
  m* r/ c+ b! C3 z/ C& c' Stest was ordered, but the family did not go to the
: S2 A6 }- @7 z4 g5 M* flaboratory to obtain the test.1 Q- I. c. d& Z$ i7 s
Discussion9 }8 F8 M. S0 K; e; J
Precocious puberty in boys is defined as secondary
4 r7 N. U* V' a& S- @sexual development before 9 years of age.1,4' o, l- W. B- l: H
Precocious puberty is termed as central (true) when" o7 v% ^1 f( g& s( b, q- M
it is caused by the premature activation of hypo-
# H( O$ b4 a# P, M/ @thalamic pituitary gonadal axis. CPP is more com-" u$ K, D3 a" b" w2 N
mon in girls than in boys.1,3 Most boys with CPP
8 Y* V( \) n3 @# I9 [5 Dmay have a central nervous system lesion that is( K8 E) m8 A+ h* [9 V
responsible for the early activation of the hypothal-
6 V8 k% {  G3 y) Lamic pituitary gonadal axis.1-3 Thus, greater empha-
9 e- n0 A# n4 Csis has been given to neuroradiologic imaging in' j" M# Y$ m+ {. M% W: ^0 X7 N5 E
boys with precocious puberty. In addition to viril-8 q5 w" e7 P: `/ n. c. v
ization, the clinical hallmark of CPP is the symmet-
/ j" g8 G: {0 ^# urical testicular growth secondary to stimulation by
0 U6 d. j* d% h% U, Z$ z; ?( xgonadotropins.1,3
$ ?$ f- \, G1 R( \$ d9 n- F: UGonadotropin-independent peripheral preco-
8 T/ z0 e! O; [6 Ycious puberty in boys also results from inappropriate
' u: [4 ^8 X' ^androgenic stimulation from either endogenous or' v8 c% M1 S6 r
exogenous sources, nonpituitary gonadotropin stim-3 l; ?- P4 W# b+ l
ulation, and rare activating mutations.3 Virilizing
: w# Z8 W8 `: o0 O# _6 F  fcongenital adrenal hyperplasia producing excessive
3 H* H8 o. {4 C- j) madrenal androgens is a common cause of precocious- W- U2 e+ G7 K9 X
puberty in boys.3,45 f4 i, |( d- f8 ?$ B
The most common form of congenital adrenal' M# d5 u% K6 F/ p
hyperplasia is the 21-hydroxylase enzyme deficiency.6 r' \  D+ m! s% W# }
The 11-β hydroxylase deficiency may also result in
/ F& y3 j5 V8 X& O$ g9 G" \excessive adrenal androgen production, and rarely,& D: i/ I+ l$ `4 l) W
an adrenal tumor may also cause adrenal androgen; H' \, @4 X) \. t" p$ ~
excess.1,32 @# K& b# K$ D1 c! h$ {. u
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
; ?. L: @$ ^. X  i- Y542 Clinical Pediatrics / Vol. 46, No. 6, July 2007" _$ _6 |" ^$ n( i
A unique entity of male-limited gonadotropin-
2 Y2 ]' B, L: F9 y0 @3 A) h2 bindependent precocious puberty, which is also known
: o) @" ~" s: x; qas testotoxicosis, may cause precocious puberty at a
# \1 V9 V4 f6 K6 x) C  Q4 y, Mvery young age. The physical findings in these boys
" Z& _! P! V- m! ~7 T: ]/ J3 {. {with this disorder are full pubertal development,
: G* ~* t( r  C6 ?  uincluding bilateral testicular growth, similar to boys
' I; x+ T9 W1 ^# Zwith CPP. The gonadotropin levels in this disorder* U  g3 y, d$ S
are suppressed to prepubertal levels and do not show) K2 e" h0 P' Q. g/ N
pubertal response of gonadotropin after gonadotropin-
' D8 k# W6 ]. `7 j, T0 Q9 ^releasing hormone stimulation. This is a sex-linked7 L7 h+ Z' B/ l0 Z% |$ U
autosomal dominant disorder that affects only
. c' |( O6 n$ E& P! n9 F. w! Z5 fmales; therefore, other male members of the family
& U" C2 l2 X+ n4 X- F2 |! B, O/ x) [may have similar precocious puberty.3  z1 Y) {! B- g. w& S" N/ Y( {! P
In our patient, physical examination was incon-. Q9 ]2 I9 k8 z! o
sistent with true precocious puberty since his testi-
! x  @% ?4 b2 M3 |  P! icles were prepubertal in size. However, testotoxicosis2 }0 t; x6 [6 z9 G& e! {9 b
was in the differential diagnosis because his father- W& g9 ?0 z6 j0 p, T2 q* C
started puberty somewhat early, and occasionally,
' E) m1 ]3 W; L3 o( Jtesticular enlargement is not that evident in the
$ w- o0 b; q, l: @1 C: l& nbeginning of this process.1 In the absence of a neg-3 l' P9 G# l2 W( s, B7 J
ative initial history of androgen exposure, our
6 r9 s: @0 c7 v) mbiggest concern was virilizing adrenal hyperplasia,  \/ f$ Z' i' z* m$ U' r
either 21-hydroxylase deficiency or 11-β hydroxylase# h! E) K0 r5 a% B
deficiency. Those diagnoses were excluded by find-
, ?2 l2 S2 s! D9 h7 V9 d$ Jing the normal level of adrenal steroids., q2 t; d! {( I- @# X7 t8 K
The diagnosis of exogenous androgens was strongly
9 r. H; h# }* k8 @( u3 hsuspected in a follow-up visit after 4 months because, m8 X  y1 }" N3 y) l
the physical examination revealed the complete disap-. X2 k6 y4 n5 j6 @% y! z
pearance of pubic hair, normal growth velocity, and+ Z# ^0 @5 I  ~/ W+ P# a- _
decreased erections. The father admitted using a testos-- X8 c9 B  y: j; B8 i
terone gel, which he concealed at first visit. He was
0 `; n: M9 A+ O9 Q3 H7 d5 susing it rather frequently, twice a day. The Physicians’7 e/ x3 D% {' I) b8 p
Desk Reference, or package insert of this product, gel or1 k% A9 y' X4 b* }
cream, cautions about dermal testosterone transfer to
# M2 `, t4 w* z8 w5 a4 M, bunprotected females through direct skin exposure.
4 u+ K. a# m5 t5 J5 [Serum testosterone level was found to be 2 times the
! ^& C  e6 P/ l! o5 a1 ~baseline value in those females who were exposed to
0 i% E$ ]( _5 p8 z+ v' Xeven 15 minutes of direct skin contact with their male
+ p% q' i$ O; i' D; n0 H$ Vpartners.6 However, when a shirt covered the applica-, r: Z. m* M1 t- y* S
tion site, this testosterone transfer was prevented.0 {- ~! {! p0 `: [* b1 x
Our patient’s testosterone level was 60 ng/mL,
; A$ i0 q- y9 r- Y! T0 y3 _6 twhich was clearly high. Some studies suggest that$ O; w6 Q9 M& n  ]" j, V# k. i8 i
dermal conversion of testosterone to dihydrotestos-
0 t/ ?3 G/ U5 Q% n% d5 N: R: lterone, which is a more potent metabolite, is more
9 r$ u; f/ G4 b/ ~6 @! s4 N, gactive in young children exposed to testosterone& G# H* ?3 G  w. S7 n7 ]
exogenously7; however, we did not measure a dihy-: P. l( }& T4 i7 j* R
drotestosterone level in our patient. In addition to! E# _$ p4 x8 E% @- H4 S) {8 L
virilization, exposure to exogenous testosterone in
9 d8 Y) }! T- K, t0 achildren results in an increase in growth velocity and
- O7 V. H" R, i( Oadvanced bone age, as seen in our patient.: q& b3 l8 ?9 d2 P
The long-term effect of androgen exposure during+ ?% Y( E1 c, I; ?- O- L# P7 v2 m
early childhood on pubertal development and final
. u% c7 H/ A- C2 F' jadult height are not fully known and always remain
/ p& L3 d, W% i" n; K# ^5 F) fa concern. Children treated with short-term testos-/ ~" h! x* S/ |* v
terone injection or topical androgen may exhibit some
6 b5 D: q; s7 Eacceleration of the skeletal maturation; however, after
3 c3 J0 ?) z3 n! Ncessation of treatment, the rate of bone maturation5 D) m9 c4 }5 `1 w. ^. `9 |
decelerates and gradually returns to normal.8,9' p) A2 ?7 i/ I
There are conflicting reports and controversy
, s4 U1 |& N/ H( m) Rover the effect of early androgen exposure on adult# [* y* n* _. L# \. b7 r
penile length.10,11 Some reports suggest subnormal1 K; p8 }4 p- A
adult penile length, apparently because of downreg-3 o- ^$ ^3 b) J$ T8 G  ^" B
ulation of androgen receptor number.10,12 However,2 J9 d/ W& S. D- C( p
Sutherland et al13 did not find a correlation between
4 M) S) k! ?& C. dchildhood testosterone exposure and reduced adult- A$ X" |9 U  @% ^$ ~
penile length in clinical studies.6 k1 M1 _8 K5 R
Nonetheless, we do not believe our patient is% K' J3 Q7 p+ g4 b) K. C- k
going to experience any of the untoward effects from
5 y; B0 z6 A' z$ n8 T. ]4 P% A3 X/ Mtestosterone exposure as mentioned earlier because# Z) z4 C" M4 q4 c
the exposure was not for a prolonged period of time.3 y! \) M  J' W# d
Although the bone age was advanced at the time of+ q4 I! a4 }+ H& @& A. t  t
diagnosis, the child had a normal growth velocity at7 P5 M4 N. u  x9 U6 \4 `2 z6 ~- Y$ i
the follow-up visit. It is hoped that his final adult8 J% c- r* g+ |* ]1 v* v5 \. b
height will not be affected.- v; f( a" B, q' L
Although rarely reported, the widespread avail-( W+ z# H0 S9 @
ability of androgen products in our society may
8 y7 s, R+ h" i2 w! Qindeed cause more virilization in male or female
! J& C* r+ l- y- pchildren than one would realize. Exposure to andro-
+ W* ]! a  K( {$ Q$ y- agen products must be considered and specific ques-
; Y8 h; i, ~/ d/ V& o7 M% U. Ltioning about the use of a testosterone product or
* ^9 k% x) n% `7 X8 lgel should be asked of the family members during
+ e7 r5 r1 ^# zthe evaluation of any children who present with vir-
. B0 d( @2 X9 g+ oilization or peripheral precocious puberty. The diag-9 [8 R3 U5 V- y
nosis can be established by just a few tests and by1 V( f' U- i" c5 ~/ ^9 P" }1 _
appropriate history. The inability to obtain such a
% V: I% a* R! S" o$ Khistory, or failure to ask the specific questions, may
) M7 Y# `8 ~  b! h) `) K& Yresult in extensive, unnecessary, and expensive
% K8 n7 B- M* h6 A) Q. x/ B$ [6 Iinvestigation. The primary care physician should be3 P! v$ o3 S" S8 {4 h% @
aware of this fact, because most of these children6 L7 ]  b0 G; O
may initially present in their practice. The Physicians’; F) U* V* g# Z8 O; ~" ?
Desk Reference and package insert should also put a
9 ~& E0 k' j# |: i3 ]+ ]: Uwarning about the virilizing effect on a male or
( c, k: J1 w: {female child who might come in contact with some-
) g2 R# J2 g1 N7 I& P0 Cone using any of these products.
# f6 ^; \5 m! AReferences
* `' e/ D! @6 e/ Z1. Styne DM. The testes: disorder of sexual differentiation
! q. z* u8 ?. V6 x  ^and puberty in the male. In: Sperling MA, ed. Pediatric
4 j6 b/ W- O; A6 u7 X7 IEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;: A0 Y9 X( v  n, l" \4 H. a
2002: 565-628.- s7 k" s0 ]( S' ]& l8 z0 K. H9 V/ z
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious5 K, _2 O; X5 z( h! A- E
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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4个什么样的?
發表於 2025-1-19 02:41:05 | 顯示全部樓層
& j: j3 c. R) w$ C
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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