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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
0 s7 m* G3 m: @# o5 T( a# {Boy Induced by Indirect Topical
$ r! P, y( X/ J0 N# T) FExposure to Testosterone. x* p4 o3 w: g# V* {  \. |
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2; b% s0 |' h7 _; M, M
and Kenneth R. Rettig, MD15 z  y, B; @# i2 S+ i3 _: H
Clinical Pediatrics6 ?, X' R% b( y$ @4 n
Volume 46 Number 6% j  U5 i, q( C; R0 q% `+ `. F
July 2007 540-543. Z& G' M0 Z1 v& _% f5 g
© 2007 Sage Publications; C: i3 ?7 |7 {1 F. |1 v9 m8 l
10.1177/0009922806296651
7 L$ ]- p. u6 N5 Q6 A4 Lhttp://clp.sagepub.com' P3 u8 ~. w' o  Y! \- m& w6 v
hosted at
! d' M1 b; E# j6 Z9 A$ ghttp://online.sagepub.com! Z$ n: }6 g; R. y+ _
Precocious puberty in boys, central or peripheral,. M# e5 e4 {  a; Q# u# ~+ J. @
is a significant concern for physicians. Central
* x. m, a( `$ y" Aprecocious puberty (CPP), which is mediated
% e! v! S1 T4 Mthrough the hypothalamic pituitary gonadal axis, has
  y9 F1 T9 U) I% ~& z* I; ?a higher incidence of organic central nervous system/ z& S0 W4 l0 i; ?  E
lesions in boys.1,2 Virilization in boys, as manifested& p3 d# i9 p6 E$ K
by enlargement of the penis, development of pubic
. |( n0 Y  K" [; @hair, and facial acne without enlargement of testi-
6 P' v* }: o! h* E& `8 [, j1 b" Scles, suggests peripheral or pseudopuberty.1-3 We6 P8 J3 U) i9 n# x" q
report a 16-month-old boy who presented with the1 P. b$ ?" g( i. M6 `
enlargement of the phallus and pubic hair develop-
* q, F, K7 c+ H4 Y* O4 Wment without testicular enlargement, which was due
% {) z8 E& U/ u9 X* Rto the unintentional exposure to androgen gel used by6 H* @! v" w3 d# T
the father. The family initially concealed this infor-
8 w, X  E: i6 }) nmation, resulting in an extensive work-up for this2 m) D# W# g- j+ M
child. Given the widespread and easy availability of/ b4 b3 \# M0 P; i; w( Z
testosterone gel and cream, we believe this is proba-
+ {! S% s3 n& r; X3 {& ^bly more common than the rare case report in the* q: o! d) H+ @2 \, X
literature.4
5 o% k# d, L% k8 h5 C7 G' I' lPatient Report2 w+ I. |+ h, i4 j9 g8 `! Y
A 16-month-old white child was referred to the
- K1 ]* x7 _4 c$ Z, `. e  G$ u* jendocrine clinic by his pediatrician with the concern3 N/ a8 [( T9 Q  o; i" Y% y' V
of early sexual development. His mother noticed0 P2 X) d% S) J- [
light colored pubic hair development when he was/ g0 C* P/ u, I- W: u6 V
From the 1Division of Pediatric Endocrinology, 2University of
" B+ h' b- q5 ~South Alabama Medical Center, Mobile, Alabama.
9 w- G, L& M( {# \$ j" w3 pAddress correspondence to: Samar K. Bhowmick, MD, FACE,
. T7 n3 o5 K9 ]9 k5 e/ @2 sProfessor of Pediatrics, University of South Alabama, College of
" n+ C* [+ h* r" f1 d1 N5 HMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;( A+ H, P/ G3 y7 f. p( B& z
e-mail: [email protected].; L. R( D+ n6 p" b/ b) Z
about 6 to 7 months old, which progressively became* Y) O! _4 p! Z7 s
darker. She was also concerned about the enlarge-/ M+ k  m4 {% ~4 B
ment of his penis and frequent erections. The child
& U* S0 \: ?' [4 E3 [; g% k% Lwas the product of a full-term normal delivery, with
, {5 f, F1 N4 _" F- Ka birth weight of 7 lb 14 oz, and birth length of
" |  s( o/ j4 |, |$ j- O20 inches. He was breast-fed throughout the first year
$ H, k# R3 ~3 @# Z# k' ^; {/ ^of life and was still receiving breast milk along with
+ H# z  s! |* d; isolid food. He had no hospitalizations or surgery,; R  _( X' P9 e) y5 h+ r
and his psychosocial and psychomotor development
0 M; Z# }$ I( b! }# x  @4 Gwas age appropriate.
! q3 T' o" R) |& @# cThe family history was remarkable for the father,
% Q3 S' R" e6 K! _- ?, Ywho was diagnosed with hypothyroidism at age 16,
5 ?& I- G' \+ S: b& Pwhich was treated with thyroxine. The father’s
& \0 b  L: V. t2 t! X0 Mheight was 6 feet, and he went through a somewhat
# M# P9 B2 L5 B. [early puberty and had stopped growing by age 14.0 L9 }/ p% U5 Y8 Z# t- ^$ \
The father denied taking any other medication. The$ a: m" p- |& f, ^: k
child’s mother was in good health. Her menarche  x- C. J: Y- Y4 i) ~
was at 11 years of age, and her height was at 5 feet
1 M2 [  B/ ~) R1 w6 ?% F5 inches. There was no other family history of pre-
3 t# a' e1 D) L9 h- p1 o6 d( q/ @0 s4 icocious sexual development in the first-degree rela-& K4 G. F& k) Q( J/ \3 J4 K
tives. There were no siblings.2 n7 j- D8 D. X8 w* x# @0 m
Physical Examination
5 v2 w0 K) P, \: G  QThe physical examination revealed a very active,
, x, e: p% ]" zplayful, and healthy boy. The vital signs documented7 H8 f! }6 Z0 t; F% L
a blood pressure of 85/50 mm Hg, his length was% \* ?. x( |/ `, a
90 cm (>97th percentile), and his weight was 14.4 kg
, H3 k3 K5 [0 t+ B. |  T4 V(also >97th percentile). The observed yearly growth
: o, m  y, B1 a) b8 ]velocity was 30 cm (12 inches). The examination of; [. F5 ?4 }5 I) X- y
the neck revealed no thyroid enlargement.  r* k* a6 v% K% {  R' l
The genitourinary examination was remarkable for6 u* R0 t/ I2 W4 `/ g
enlargement of the penis, with a stretched length of
( q, R( {7 B4 }6 \) l8 cm and a width of 2 cm. The glans penis was very well  a4 f  ^) o/ V: K$ s- O( y
developed. The pubic hair was Tanner II, mostly around' D# Z* m' W$ n6 d+ [9 ]$ v9 g
540
+ ?* _* z: G6 zat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from, m5 b* Z  L0 w$ a6 o0 T
the base of the phallus and was dark and curled. The4 b. i; y- c" s' i/ K; Y+ ^# B
testicular volume was prepubertal at 2 mL each.$ X$ i; Q4 W, T# o/ j
The skin was moist and smooth and somewhat+ \- `  S$ A# C5 n/ p( p
oily. No axillary hair was noted. There were no' F) x# Q4 ~9 H; u# w; P5 i5 U# f0 _
abnormal skin pigmentations or café-au-lait spots.
3 T7 |; v! D' H+ KNeurologic evaluation showed deep tendon reflex 2+
  c( x! f4 Y8 {5 q( o7 ]* X0 vbilateral and symmetrical. There was no suggestion1 q* o. S8 G, B  `# y; P
of papilledema.- K# Y6 R) F; L1 M* j! {$ Q# v
Laboratory Evaluation; ]1 w, c$ V6 [2 y! B0 D8 j
The bone age was consistent with 28 months by7 w! ~2 M( d+ w4 Q) G
using the standard of Greulich and Pyle at a chrono-
  L. c1 A8 r$ S- b" O: f( Alogic age of 16 months (advanced).5 Chromosomal
7 a4 b% t5 M3 ?karyotype was 46XY. The thyroid function test
: p* q2 s6 R4 n6 Nshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
2 r7 }2 _' h1 Q& l  I, Blating hormone level was 1.3 µIU/mL (both normal).  b4 m$ b& m. x4 H$ _& u
The concentrations of serum electrolytes, blood
# W9 @9 y$ E9 V4 Xurea nitrogen, creatinine, and calcium all were8 O- e7 |" b$ ~/ \/ Z
within normal range for his age. The concentration
" F& q# ]* L! \1 Gof serum 17-hydroxyprogesterone was 16 ng/dL/ L) [+ L* g, `( v- a
(normal, 3 to 90 ng/dL), androstenedione was 20
5 o- {( D2 n) o1 E4 Cng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
, U, Y8 H: @5 [3 Oterone was 38 ng/dL (normal, 50 to 760 ng/dL),
: q7 q9 ~9 j  X* ]desoxycorticosterone was 4.3 ng/dL (normal, 7 to
& |3 q& v. \9 j  }- r49ng/dL), 11-desoxycortisol (specific compound S)
5 `: G' t% e) J, o6 Mwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
! m5 {& _1 L7 X; D% d" Z4 Z$ xtisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
  b% ?- q3 Q. f1 R# [( ^. Ftestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
8 t- O4 N* O7 M5 P3 L0 Tand β-human chorionic gonadotropin was less than
- |0 `- E9 R% M4 r; e5 mIU/mL (normal <5 mIU/mL). Serum follicular
0 b0 |! o/ x/ Jstimulating hormone and leuteinizing hormone
2 k0 Y2 E2 S! {1 j1 e3 Kconcentrations were less than 0.05 mIU/mL
7 c/ b3 \' f1 E2 H" n+ C(prepubertal).
  w' l3 k9 p/ b  WThe parents were notified about the laboratory
+ e: p; A; a! o0 M5 h) qresults and were informed that all of the tests were
5 V3 @7 {8 l( a. qnormal except the testosterone level was high. The4 i+ `7 _/ s7 t3 d
follow-up visit was arranged within a few weeks to
' z/ H1 W% k5 r# _3 ?$ ^$ F8 Kobtain testicular and abdominal sonograms; how-! {$ K! J" E/ M/ H9 n
ever, the family did not return for 4 months.1 b$ L8 L& r) [
Physical examination at this time revealed that the
/ Z7 Y. d/ ~6 q0 O( L1 mchild had grown 2.5 cm in 4 months and had gained
4 i$ h& t3 _; c3 ~- C$ g( H2 kg of weight. Physical examination remained
& G) i7 o) T* k8 m" a5 s; ?unchanged. Surprisingly, the pubic hair almost com-
% Y' W, e) v% C6 V5 F7 u. Wpletely disappeared except for a few vellous hairs at
: P8 \: _( d8 I) Q9 R7 a0 ethe base of the phallus. Testicular volume was still 2
1 ?! e( r4 }3 m7 `" H$ XmL, and the size of the penis remained unchanged.
. ?. d3 n! M1 SThe mother also said that the boy was no longer hav-" R- H4 O/ C, Q
ing frequent erections.
1 x6 @) J+ O$ Y/ O; o4 z7 W  G0 oBoth parents were again questioned about use of
- X5 u8 ?5 z! F7 g/ cany ointment/creams that they may have applied to$ t$ ~9 O9 c: t: O, ~
the child’s skin. This time the father admitted the. N5 E" ?* d; h. G9 Q) F, q4 x# d
Topical Testosterone Exposure / Bhowmick et al 541' a- t  x3 @0 d1 S8 x7 D! b# Y
use of testosterone gel twice daily that he was apply-" z7 p9 g1 _+ \) ?, J+ y* H- z
ing over his own shoulders, chest, and back area for+ Z9 b) v1 Q6 |7 Z' i, [2 r0 m
a year. The father also revealed he was embarrassed; t1 C; H/ O7 _1 w' A+ U
to disclose that he was using a testosterone gel pre-
1 |! u& R+ a( b* ~scribed by his family physician for decreased libido
& M5 g$ S0 @6 P5 }3 B; q& \secondary to depression.' ^5 |0 F8 p! q) Z
The child slept in the same bed with parents.
/ [3 f' M- \7 w9 H8 f& vThe father would hug the baby and hold him on his% C8 z7 V! c' n$ S
chest for a considerable period of time, causing sig-* ~( O) Q: Z) d$ W
nificant bare skin contact between baby and father.
4 X# t$ ]) h, oThe father also admitted that after the phone call,9 s# r# I& C4 L
when he learned the testosterone level in the baby% K" i) P/ o: X0 @5 @) v$ q
was high, he then read the product information
: H5 Q7 M8 F- _! H, p, A1 Tpacket and concluded that it was most likely the rea-
* k6 r4 [- Y3 M& ]8 P  ^: t* |$ @son for the child’s virilization. At that time, they
( f5 C+ O& w" I6 ]1 Sdecided to put the baby in a separate bed, and the2 d/ s( Z  `, d2 M+ l. D
father was not hugging him with bare skin and had
! r9 ~5 m; S; v2 \been using protective clothing. A repeat testosterone
0 y  \/ X- }2 ^; P/ \test was ordered, but the family did not go to the, |+ C2 f; \' O1 {4 p
laboratory to obtain the test.
* T% n$ P" B6 QDiscussion
- S! L6 X- B( M9 N' J7 a3 CPrecocious puberty in boys is defined as secondary
0 h1 K2 d3 Q6 N; O4 B! gsexual development before 9 years of age.1,4
! J* V6 v  y1 ~+ n, TPrecocious puberty is termed as central (true) when( _/ @5 K0 F5 E7 F
it is caused by the premature activation of hypo-+ F* R9 r# p: ?
thalamic pituitary gonadal axis. CPP is more com-
- I3 b3 i+ _$ R" gmon in girls than in boys.1,3 Most boys with CPP
0 e+ U4 c7 R, _7 {" j/ Nmay have a central nervous system lesion that is
" R9 z" b  y* jresponsible for the early activation of the hypothal-
* S# _+ r8 a, Ramic pituitary gonadal axis.1-3 Thus, greater empha-; G" W) B% n0 T3 d6 ^
sis has been given to neuroradiologic imaging in
* n' |0 N3 ~9 r# X3 H9 Yboys with precocious puberty. In addition to viril-$ D" w* R6 g8 r- Q  ?/ N
ization, the clinical hallmark of CPP is the symmet-
0 w; ?. G+ Q+ w* j" Erical testicular growth secondary to stimulation by  x4 K( ]( R) a, B( }! @* n# J
gonadotropins.1,3" \7 d; j* N) N  \: R0 S+ g1 I/ U
Gonadotropin-independent peripheral preco-& L. d+ N6 `7 {
cious puberty in boys also results from inappropriate
. |7 G7 v6 M$ Uandrogenic stimulation from either endogenous or5 i9 E3 b% X; k: m3 f1 z; _
exogenous sources, nonpituitary gonadotropin stim-
& s/ r* n: ?1 ?  g% G- e% Yulation, and rare activating mutations.3 Virilizing7 ~- v0 T! C' g8 \) r2 {
congenital adrenal hyperplasia producing excessive% Z# R5 S6 x- B4 d; m
adrenal androgens is a common cause of precocious
, a% a# B4 z; y+ p. ypuberty in boys.3,4
9 S4 @0 e3 E0 r$ g; q* [7 t$ W' YThe most common form of congenital adrenal$ ^4 a3 k# L# H. D0 F0 W( s
hyperplasia is the 21-hydroxylase enzyme deficiency.
' H  L' b% Z* H% t# vThe 11-β hydroxylase deficiency may also result in4 J( w( \! [) q/ x
excessive adrenal androgen production, and rarely,, v: i2 E4 @  @4 \8 U8 e- q7 r+ j
an adrenal tumor may also cause adrenal androgen; R. o* F" t' W* V0 U! ~
excess.1,3* J+ A) H# h3 ]" q; k# ~% D
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
$ I  _" A0 D% p0 J, `0 Q. v5 ^542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
) z3 N2 s- m. V8 a% QA unique entity of male-limited gonadotropin-
$ n. I- W; B) H% p" P& E( mindependent precocious puberty, which is also known  @) U& a; _3 S
as testotoxicosis, may cause precocious puberty at a
, [1 J$ b3 p/ g7 Q' lvery young age. The physical findings in these boys
! Y: h& L; h& O3 a$ \( u; {with this disorder are full pubertal development,$ v, d+ C. H$ b6 V# ]
including bilateral testicular growth, similar to boys, r& c! n! G; U
with CPP. The gonadotropin levels in this disorder
9 i8 w2 l% A# e. w, qare suppressed to prepubertal levels and do not show5 \" ?& i2 h  I) u* q
pubertal response of gonadotropin after gonadotropin-
+ ^' c6 Q3 c4 F1 X8 E; ~$ o# V) qreleasing hormone stimulation. This is a sex-linked
* ~  |  z* t& |' n: mautosomal dominant disorder that affects only
; k1 u! Q9 g) X, y  A& _males; therefore, other male members of the family
. ]/ W1 }& V/ i% i& gmay have similar precocious puberty.3
; r( I) s3 `3 Y  g) Z, lIn our patient, physical examination was incon-
& t0 L- c, L/ H8 h6 F3 Zsistent with true precocious puberty since his testi-
+ b1 j4 w$ h# Tcles were prepubertal in size. However, testotoxicosis3 n  U$ A6 p* a& g
was in the differential diagnosis because his father+ [/ [2 j8 l; k, Z* J
started puberty somewhat early, and occasionally,
9 G% o3 g5 G8 u+ Z$ h5 htesticular enlargement is not that evident in the& e# L) A, X6 s
beginning of this process.1 In the absence of a neg-" j" W4 p- m" `' {: D. ~6 n8 |, d1 n
ative initial history of androgen exposure, our
+ i* a5 ^. K7 u9 K2 H  ]" S3 ~/ Ebiggest concern was virilizing adrenal hyperplasia,
* @3 n, c; j9 Peither 21-hydroxylase deficiency or 11-β hydroxylase
9 @0 F" m6 b% K, u# Y% Bdeficiency. Those diagnoses were excluded by find-
, c8 X, }7 G/ w% d  A; Hing the normal level of adrenal steroids.9 [6 w9 E+ ?$ y1 S/ M* G8 x
The diagnosis of exogenous androgens was strongly: C% T% p+ E0 i9 W% C5 ?
suspected in a follow-up visit after 4 months because) O# j+ J4 l& ~* d4 ~" N  c) ], W5 R
the physical examination revealed the complete disap-' \/ S$ W: F# P9 i
pearance of pubic hair, normal growth velocity, and5 ?1 Q' i1 K" R' |8 P: S. z
decreased erections. The father admitted using a testos-
3 q* t4 p* j$ s$ Y" Zterone gel, which he concealed at first visit. He was; J: @( D8 |9 P& n6 q) B
using it rather frequently, twice a day. The Physicians’
2 b7 e7 W4 N# c! V4 cDesk Reference, or package insert of this product, gel or0 R2 E7 E% D9 r. m0 a
cream, cautions about dermal testosterone transfer to
7 ~4 T1 ~, g$ O' y, X" Punprotected females through direct skin exposure.& u' N2 U* x# X- z$ s
Serum testosterone level was found to be 2 times the
9 t/ p5 }% d! b3 i6 k6 l; G7 vbaseline value in those females who were exposed to
5 ^2 y: I. j, ~4 [( h8 T8 Veven 15 minutes of direct skin contact with their male
; B0 G% v7 ?0 hpartners.6 However, when a shirt covered the applica-
! R) a  c# F$ d% ction site, this testosterone transfer was prevented.7 Z4 X6 s5 q6 Z+ ?
Our patient’s testosterone level was 60 ng/mL,
0 \3 `) p0 n/ d! x' w% @" Iwhich was clearly high. Some studies suggest that
. p( r5 G5 }- Rdermal conversion of testosterone to dihydrotestos-
4 ^6 P$ K' i. p! E( ?terone, which is a more potent metabolite, is more  U$ ]- f7 Q' i1 Q% l8 F% O
active in young children exposed to testosterone: e6 h7 U0 \, C: t
exogenously7; however, we did not measure a dihy-
5 E" s, j7 x  q& }( B0 a8 sdrotestosterone level in our patient. In addition to- s. B& W( i# j! w7 N% F1 c( B7 Q
virilization, exposure to exogenous testosterone in. B# e8 i) g# y  l, i" Z) D* ?5 R
children results in an increase in growth velocity and+ d- Z6 H! B3 q' F5 d" w6 K" h
advanced bone age, as seen in our patient.
5 j  J# h* b% c$ M' @The long-term effect of androgen exposure during7 W! N# e: F4 \5 ?) Z
early childhood on pubertal development and final. D' q6 e: s2 I1 f% ?; u
adult height are not fully known and always remain) `- q  U& u7 B$ K
a concern. Children treated with short-term testos-
% M5 V! A  F, l& @; A, Y2 Vterone injection or topical androgen may exhibit some9 T) r% B9 S) H+ D
acceleration of the skeletal maturation; however, after  X- a' Z% s& v5 |
cessation of treatment, the rate of bone maturation
9 w2 p3 O( o. ^3 _" z% u2 e% ~2 Gdecelerates and gradually returns to normal.8,9
0 b3 k; L  v, S0 j" A: J; ?3 r& T# oThere are conflicting reports and controversy& C' f4 t* H4 n
over the effect of early androgen exposure on adult
. T- b$ g; T8 F  z1 mpenile length.10,11 Some reports suggest subnormal
  B( B! U  Q, J$ q# f) I2 ]adult penile length, apparently because of downreg-
6 t7 ~- `0 @+ u; x" A$ E7 S" q, gulation of androgen receptor number.10,12 However,* J( U8 r4 ?6 b
Sutherland et al13 did not find a correlation between
: m, U! V/ |; ?' ~. xchildhood testosterone exposure and reduced adult( c$ |! a# t$ O; \2 `$ W4 d
penile length in clinical studies.  [: [. h1 B7 }# m
Nonetheless, we do not believe our patient is
. v: b1 A2 Q: v& O7 |going to experience any of the untoward effects from  L5 e" F) ]7 [0 h
testosterone exposure as mentioned earlier because
, b# f1 I: e; h' S! d+ ^3 I" a, Fthe exposure was not for a prolonged period of time.* l- N  t! y! k) h# M/ h1 m
Although the bone age was advanced at the time of
2 O6 x8 J) ~/ p3 rdiagnosis, the child had a normal growth velocity at( {2 h% M( i: |1 P1 n4 y
the follow-up visit. It is hoped that his final adult
' g  X& W- Z1 }& U% pheight will not be affected.( B# x; J1 O" H8 l7 L* I
Although rarely reported, the widespread avail-/ x& T& e3 k. K2 j0 }1 |! x; w5 ?
ability of androgen products in our society may
2 z. f2 A- z5 ]/ Sindeed cause more virilization in male or female7 b$ |4 s. G$ T1 V/ A$ m- w$ u% @
children than one would realize. Exposure to andro-" j' C: z# X; X
gen products must be considered and specific ques-
/ h* s4 d* i0 \9 M& dtioning about the use of a testosterone product or
7 N8 Y2 A0 `- K; zgel should be asked of the family members during
/ T. ?- ~2 Q# p3 v/ o, Vthe evaluation of any children who present with vir-1 N% {0 t  Q1 L& q, u8 `$ H
ilization or peripheral precocious puberty. The diag-
7 J& E' G7 O( z- _nosis can be established by just a few tests and by' R% G4 p  ~) O  q. O
appropriate history. The inability to obtain such a
) T4 |' [. @  G4 \history, or failure to ask the specific questions, may
. P- n7 _  H4 R, Lresult in extensive, unnecessary, and expensive
( t; ~( n4 z, B& u, o! }  \& Ginvestigation. The primary care physician should be5 L9 E7 L8 |: K6 K6 B5 Q, l
aware of this fact, because most of these children6 T5 D1 |! l- N6 S& D
may initially present in their practice. The Physicians’9 e) q2 K0 K) j' m
Desk Reference and package insert should also put a
4 `0 X0 ~: T6 Fwarning about the virilizing effect on a male or
1 f8 e* ~* D; |' o- C/ Mfemale child who might come in contact with some-( J1 P6 M" O( |& H
one using any of these products.
* m' q/ K0 r1 G7 Q+ F3 n: _' YReferences
( ]4 i7 w! F( U" `( y  G1. Styne DM. The testes: disorder of sexual differentiation- y% P. i( G/ W+ U
and puberty in the male. In: Sperling MA, ed. Pediatric
! c' K: M' Z+ E5 t; yEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
1 x& U) R* `' Y( L3 a2002: 565-628.
& W. P5 r7 A$ S# }* }2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious0 Y! ^5 `; \" H; B! C& y
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old9 f9 G5 a- X" ]" C* R4 T9 ^
Boy Induced by Indirect Topical* z* w4 p* N" H! a( r) W
Exposure to Testosterone: y! t% [4 u( g$ z; v. R# k5 i
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
, ?7 @; \, V& \+ Y& fand Kenneth R. Rettig, MD1
, d& V! U5 k) Z8 aClinical Pediatrics7 m6 q& @: E" {
Volume 46 Number 6" l; a3 B/ A3 Y2 s
July 2007 540-543
& y  U1 j7 \& `2 G4 ]7 |© 2007 Sage Publications
' U" ~7 o1 X; f10.1177/0009922806296651$ A& l& G; L( j& c9 ]+ V
http://clp.sagepub.com$ g* w% y7 }" K
hosted at" h' Z$ e! x2 `& G- q4 f6 q
http://online.sagepub.com' V" @/ u8 l" x: c" A
Precocious puberty in boys, central or peripheral,
! ~/ X! [+ R# @% f  N. F# `is a significant concern for physicians. Central0 \9 x8 m/ g9 D$ v& W
precocious puberty (CPP), which is mediated
% R% h9 J9 P) x8 i$ x. R* s. Kthrough the hypothalamic pituitary gonadal axis, has
% U; P/ k5 _% R4 [: a. qa higher incidence of organic central nervous system
0 p+ m% t6 P( N' F3 mlesions in boys.1,2 Virilization in boys, as manifested: Q0 `3 G2 \5 D( e$ w& ]
by enlargement of the penis, development of pubic
! x  y' U( r" a, N) o. V+ I" u# v( Dhair, and facial acne without enlargement of testi-
% B9 ~  i; O5 {& _; Ocles, suggests peripheral or pseudopuberty.1-3 We7 W. f) m0 y7 b1 @5 ~1 W
report a 16-month-old boy who presented with the
0 J5 x, a$ f- x! X* yenlargement of the phallus and pubic hair develop-
5 _# ^3 C& e+ E" E8 [! G9 H/ Iment without testicular enlargement, which was due
3 T) t6 y; y0 n5 I6 A- eto the unintentional exposure to androgen gel used by
: |4 ]4 x) w$ u  r$ P0 p; P8 athe father. The family initially concealed this infor-8 l; F: ]2 V  h
mation, resulting in an extensive work-up for this
  y! C/ l* ]% y3 w) Ychild. Given the widespread and easy availability of
% d4 Z& b# d/ p, j9 Rtestosterone gel and cream, we believe this is proba-
5 X  d, |& U6 U' f5 ^( ]$ {6 G* Cbly more common than the rare case report in the
/ k' j+ M/ V. x4 L- A5 pliterature.4
2 ^; {6 w0 `+ v8 `" \Patient Report
: d% @# a$ f7 S- }" u( J% y/ |A 16-month-old white child was referred to the
3 s/ d: h5 k: p( z5 F  Lendocrine clinic by his pediatrician with the concern
& W- _  E( V5 S1 u. x: R, ?- e' wof early sexual development. His mother noticed8 r' D. Y! u+ V$ I- S+ y6 E
light colored pubic hair development when he was
/ ~; P& c- V2 w% \* @0 W& bFrom the 1Division of Pediatric Endocrinology, 2University of* I% x1 b3 e. w
South Alabama Medical Center, Mobile, Alabama.* j* n- M1 q+ c% p
Address correspondence to: Samar K. Bhowmick, MD, FACE,8 ]0 F- n) X! R9 |) u0 R0 |
Professor of Pediatrics, University of South Alabama, College of
- b; G  F+ j  ^, `% J, R) `( K0 jMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
1 g; V) @, Q& Oe-mail: [email protected].
/ r7 D, K" U" eabout 6 to 7 months old, which progressively became  F2 Q  e. h4 i$ W9 n( {, u
darker. She was also concerned about the enlarge-  S, m/ y6 k+ f. [/ a* _2 l
ment of his penis and frequent erections. The child( W; @- k$ p8 }& i, Z+ b  C4 R
was the product of a full-term normal delivery, with
5 W" \% W! U& l" y8 C1 Q. ]a birth weight of 7 lb 14 oz, and birth length of
  [, \5 X! c) l( F2 q# b20 inches. He was breast-fed throughout the first year* r1 D; X  @* U$ D( R, ~3 D8 A9 o$ C
of life and was still receiving breast milk along with- S. P, J* t5 B( w
solid food. He had no hospitalizations or surgery,% R! \9 D1 O6 n
and his psychosocial and psychomotor development' k' a5 W) X: ~
was age appropriate.. v4 @/ S4 t1 g, Z9 ^+ l4 y9 j3 t
The family history was remarkable for the father,) W6 |" n7 o3 W
who was diagnosed with hypothyroidism at age 16,
6 S7 Z/ n# l: [4 y) d0 Zwhich was treated with thyroxine. The father’s
3 B: N3 S# [- ~1 }) Uheight was 6 feet, and he went through a somewhat/ v0 w9 W- {- K) I
early puberty and had stopped growing by age 14.+ y- _% \+ ]. ?! I4 W
The father denied taking any other medication. The
* o1 |0 s; L( D! achild’s mother was in good health. Her menarche
! ?1 o6 ^6 c- Q  U( pwas at 11 years of age, and her height was at 5 feet: Q- Y! l3 B& g* H
5 inches. There was no other family history of pre-* M# A5 U: f! `' g7 k9 o
cocious sexual development in the first-degree rela-
" Y& ^% C( Q$ B5 h. K! Htives. There were no siblings.
. d, ]* N- ^0 x3 B* A3 E) dPhysical Examination
( O4 ]9 T9 Q( a8 N3 H. _  p1 }The physical examination revealed a very active,7 I# C1 _& B8 M# g
playful, and healthy boy. The vital signs documented4 b* ]/ E# o+ d" N, e
a blood pressure of 85/50 mm Hg, his length was
* r8 r, \# B( V' P* T* Y90 cm (>97th percentile), and his weight was 14.4 kg- t8 x/ g2 z1 T. V, f
(also >97th percentile). The observed yearly growth
: Y& ?8 N5 |7 {velocity was 30 cm (12 inches). The examination of6 q8 b, b3 O  k$ m2 G: @( @
the neck revealed no thyroid enlargement.2 @, y0 G9 J$ Z; _7 d. H
The genitourinary examination was remarkable for
7 B( N2 A' }- C" tenlargement of the penis, with a stretched length of, p4 [2 Z; X% a; _8 n" T
8 cm and a width of 2 cm. The glans penis was very well: s: X8 L' P  c2 ]7 D' r3 `
developed. The pubic hair was Tanner II, mostly around
: M4 ]( d* w5 {9 ^0 H540
/ F, q; j  m  @1 T+ t- Y& mat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from3 h$ E3 b9 v3 y8 r4 T
the base of the phallus and was dark and curled. The
* d; U# G6 G' j2 ?testicular volume was prepubertal at 2 mL each.* e1 _: x, w  a/ m* S% j
The skin was moist and smooth and somewhat) [6 ?( c$ V+ A4 n. Y
oily. No axillary hair was noted. There were no7 E0 \' Q8 H0 L; [: c/ e' |
abnormal skin pigmentations or café-au-lait spots.2 o( H, H5 P1 Z8 d, M- F+ |
Neurologic evaluation showed deep tendon reflex 2+
+ B+ }3 ?  v! F, @& Fbilateral and symmetrical. There was no suggestion9 P4 g$ o! A3 B3 a# e* {7 J
of papilledema.
$ L2 ~( @! b/ x' k9 p1 hLaboratory Evaluation
+ w! f3 m8 N4 j) ?1 zThe bone age was consistent with 28 months by
  R6 ^: _+ x; l% Jusing the standard of Greulich and Pyle at a chrono-
% M7 D" n3 s2 [% ilogic age of 16 months (advanced).5 Chromosomal
: x' B: I% c' b- ekaryotype was 46XY. The thyroid function test
8 Z* i+ Z: I2 q: ?" B: O9 y- L/ }* Gshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
1 g9 Y8 o1 |+ \1 z: {lating hormone level was 1.3 µIU/mL (both normal).
0 k9 _5 W$ P" B6 CThe concentrations of serum electrolytes, blood# K, i) i$ Z7 ~
urea nitrogen, creatinine, and calcium all were* t: W9 O3 U) R- b
within normal range for his age. The concentration
8 E' N/ P# g; L* s4 F: h, V! `of serum 17-hydroxyprogesterone was 16 ng/dL
( _  H& z' r+ U- L! x( @(normal, 3 to 90 ng/dL), androstenedione was 20- J, y  m: p) H  O3 T
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
! m: O0 x3 z; s/ D. ?8 ^  ]3 wterone was 38 ng/dL (normal, 50 to 760 ng/dL),% R4 S6 k. W6 ]$ p( [3 i: A6 e0 i
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
6 Q" L" W5 O7 t5 F3 F6 _) Z/ }; _49ng/dL), 11-desoxycortisol (specific compound S)+ A" r6 E" T( m
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
5 H$ S* [$ p* u1 `. f7 K! R1 vtisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
* C5 y1 d- ?5 y, V* ?' `, I$ Etestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
3 m: A+ J; K5 ~- v3 H5 iand β-human chorionic gonadotropin was less than( k5 ~7 j+ X6 M( ~
5 mIU/mL (normal <5 mIU/mL). Serum follicular
0 g: u+ o7 Y4 _/ ?8 r% hstimulating hormone and leuteinizing hormone
1 Y" j# k2 c' S! L+ x- C6 {concentrations were less than 0.05 mIU/mL
+ B: _3 U3 }5 [$ A(prepubertal).& i6 u! I8 _) s& k  t
The parents were notified about the laboratory- Z+ ?% v" |$ _" k$ W
results and were informed that all of the tests were
. t! q7 E4 G5 p- rnormal except the testosterone level was high. The5 c6 e/ D9 b) y
follow-up visit was arranged within a few weeks to
% S, ~& S4 Z! ~/ G4 {* \7 l. d1 {obtain testicular and abdominal sonograms; how-! u! \5 y2 m4 ~& P2 g' {2 f
ever, the family did not return for 4 months.
; E" c1 H7 `" }3 w! yPhysical examination at this time revealed that the
6 n: l* c) R$ a% ~# j  z% Tchild had grown 2.5 cm in 4 months and had gained3 J  ~$ Q5 n' \. `- G$ }
2 kg of weight. Physical examination remained
9 m  U4 S0 l# e4 t; E7 Junchanged. Surprisingly, the pubic hair almost com-; w/ V- {* z) c5 `; `" w
pletely disappeared except for a few vellous hairs at
2 @0 U8 G/ |$ R4 u' a4 |( rthe base of the phallus. Testicular volume was still 2
1 c8 M9 e* r) e# f8 JmL, and the size of the penis remained unchanged.
( B9 w0 n1 f  Z  N0 e" a' [8 gThe mother also said that the boy was no longer hav-7 \* \# J/ ~" W  D7 _  u
ing frequent erections.* g! @. |2 X8 M" p8 F0 N: ~
Both parents were again questioned about use of
2 V0 \: z  B8 U' x* ?( V" many ointment/creams that they may have applied to
# J8 z5 v; Z, m) L9 G1 Wthe child’s skin. This time the father admitted the
' ]- K3 h& x+ E0 GTopical Testosterone Exposure / Bhowmick et al 541# O$ H) Q% j4 w- D  }) `8 J: L
use of testosterone gel twice daily that he was apply-. Q7 Y. I5 @9 ~) o4 R# k# T
ing over his own shoulders, chest, and back area for! b# p' j# X7 [0 l  }, @- [5 Y" ]
a year. The father also revealed he was embarrassed$ l" x- G: _1 y  C# ]( `
to disclose that he was using a testosterone gel pre-9 _% @- D. b' U. x7 |
scribed by his family physician for decreased libido
2 e( @2 a5 p5 s1 O: H9 Q1 tsecondary to depression.
( w3 t* q3 p9 S- Q0 qThe child slept in the same bed with parents.
2 S% Q* d3 g0 Q1 R, m9 T% EThe father would hug the baby and hold him on his( E9 W6 f3 t1 u; T" n! a, ~- P
chest for a considerable period of time, causing sig-
% z1 {% N; `# V3 v* Lnificant bare skin contact between baby and father.( ~) ~/ n. o% |6 D
The father also admitted that after the phone call,. G6 z# ~7 Y7 F+ h; l% C; |
when he learned the testosterone level in the baby# y/ P) N$ f# U  h2 i; O3 O
was high, he then read the product information$ z4 Z# I* T! u1 m& o/ f
packet and concluded that it was most likely the rea-
; F( x2 |, E- F% q& s- m. Ison for the child’s virilization. At that time, they
$ ~, h: ?/ u# Y1 \  {+ Odecided to put the baby in a separate bed, and the
- G- [6 w" y; k  Q( Y" U& J5 `9 R( afather was not hugging him with bare skin and had$ k/ S$ Y* @% J) O
been using protective clothing. A repeat testosterone
. _( Q% }( M8 m0 B+ Rtest was ordered, but the family did not go to the( g  w0 Q3 a7 L/ C2 }( k
laboratory to obtain the test.
% J4 v# B( h# y) H2 O7 }% {Discussion
$ y0 C/ {8 x% p7 pPrecocious puberty in boys is defined as secondary  t* P8 e" {! t6 i
sexual development before 9 years of age.1,4) q: J5 q7 a( U% ~
Precocious puberty is termed as central (true) when- |. G4 L0 R/ x% ]8 }: h
it is caused by the premature activation of hypo-: H* V; }/ B* U5 w: d5 n, t
thalamic pituitary gonadal axis. CPP is more com-6 M- r& k7 }2 j3 J$ ?
mon in girls than in boys.1,3 Most boys with CPP
. X# N+ P) s) D0 p  y' [may have a central nervous system lesion that is# {% n; l7 j& c4 t1 l9 [& N. L+ a
responsible for the early activation of the hypothal-/ s% q( ^6 n$ R1 K3 c* }- ^9 Z
amic pituitary gonadal axis.1-3 Thus, greater empha-6 `' g" z# N7 @
sis has been given to neuroradiologic imaging in5 U3 q1 A# z* l! {
boys with precocious puberty. In addition to viril-
- Y) X5 }' T) O; Z# L* f/ d$ ^6 Yization, the clinical hallmark of CPP is the symmet-
+ Q( x- ]- ?6 F# u; B) k2 [' xrical testicular growth secondary to stimulation by; ?7 h, ~# k3 A  M+ l
gonadotropins.1,3
' b$ u8 r9 r% L. u9 M) RGonadotropin-independent peripheral preco-
, k: y" E5 s. t/ v( O& Hcious puberty in boys also results from inappropriate* U% q, D! m( e+ X. h+ l
androgenic stimulation from either endogenous or0 ~0 q6 n7 {0 F( ~2 L
exogenous sources, nonpituitary gonadotropin stim-
; l; E1 O$ z$ L, i, x# xulation, and rare activating mutations.3 Virilizing' }! q% t- _) U3 ]5 s: @0 a# W  a
congenital adrenal hyperplasia producing excessive
) B0 M/ t7 f+ Yadrenal androgens is a common cause of precocious* O: o  k6 K. [' V# q/ q' R+ B, z
puberty in boys.3,4
2 J# i0 A; |; l/ p: T. {3 Z- KThe most common form of congenital adrenal
. [  P  t; N3 m+ _5 W# B. V# a& whyperplasia is the 21-hydroxylase enzyme deficiency.
+ f2 z  u( ?( t3 ?& `8 \7 hThe 11-β hydroxylase deficiency may also result in
! A2 x" q. X+ m6 }excessive adrenal androgen production, and rarely,% w) E$ a* n+ W- Q! }: o4 ]+ [$ o
an adrenal tumor may also cause adrenal androgen
4 r# D3 ?6 K1 |( {  P1 ]% wexcess.1,3: E, b' t; v& z$ d6 N1 \5 {! c
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from& Q# s+ o- V8 `7 \
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
+ M$ l) D$ |( D/ q' z1 ?A unique entity of male-limited gonadotropin-  X. p/ q# }5 l
independent precocious puberty, which is also known" j0 t; y4 ~& ?# t
as testotoxicosis, may cause precocious puberty at a
- c1 F8 Z% `; a" f' v- |8 Zvery young age. The physical findings in these boys& F3 `/ {$ F% \
with this disorder are full pubertal development,2 U4 a  T) A- b
including bilateral testicular growth, similar to boys
$ d' r# I3 }7 t3 T6 \with CPP. The gonadotropin levels in this disorder
/ ^+ Z( S1 P( Z- x/ [. {  f! Rare suppressed to prepubertal levels and do not show: |: U2 s% L! o# {4 c
pubertal response of gonadotropin after gonadotropin-
) l" G3 [- e7 r  Q( Z5 H' dreleasing hormone stimulation. This is a sex-linked
. Q' r# ~# y2 w2 Wautosomal dominant disorder that affects only1 r# U; U6 O& h2 ^/ [" Q! a) D& y8 a
males; therefore, other male members of the family6 I/ }) f! h( e
may have similar precocious puberty.3
2 I/ L2 K( Q  G% yIn our patient, physical examination was incon-
, S$ {- g8 U4 u5 }5 ~4 m/ z5 @sistent with true precocious puberty since his testi-" a/ B/ f- U" v
cles were prepubertal in size. However, testotoxicosis  j" u  J( f6 i2 [
was in the differential diagnosis because his father8 ]6 m3 z" c& s6 Z6 e# P
started puberty somewhat early, and occasionally,
- |6 N- n1 Z. Atesticular enlargement is not that evident in the
' w) B1 m5 ]* R: o0 Ubeginning of this process.1 In the absence of a neg-
; l' n4 _' v/ [; n7 b6 sative initial history of androgen exposure, our# m6 c1 X" o/ b8 }6 ]& T
biggest concern was virilizing adrenal hyperplasia,
5 k% K  M( L8 G2 ^either 21-hydroxylase deficiency or 11-β hydroxylase
, s  u1 F& X+ K/ N8 M) [deficiency. Those diagnoses were excluded by find-( I- F( `: X/ k
ing the normal level of adrenal steroids.! a% W. e4 d# F3 }+ H8 ~7 D0 X" F: x
The diagnosis of exogenous androgens was strongly
: b9 s$ U% ~/ C7 Msuspected in a follow-up visit after 4 months because- X5 T6 c( V5 [* |
the physical examination revealed the complete disap-
# i5 o6 P% k: Z) d: _: W: qpearance of pubic hair, normal growth velocity, and5 i5 k# Q) o# Q
decreased erections. The father admitted using a testos-  }) s7 X* e6 a2 k# \; V, G5 K
terone gel, which he concealed at first visit. He was
3 u) W/ O$ a, Y" H+ W1 A  s$ _: Fusing it rather frequently, twice a day. The Physicians’
; T) }. G! a+ pDesk Reference, or package insert of this product, gel or
4 [7 t; u/ f* T$ g- u$ U$ I3 Qcream, cautions about dermal testosterone transfer to! c: W& \( B; t* l( z8 x2 z
unprotected females through direct skin exposure.
& O5 |0 ]& _7 L9 p" o% `Serum testosterone level was found to be 2 times the
; w4 {1 ]8 D) O& Y0 `' Abaseline value in those females who were exposed to
% ~* ^0 I. @( w- _even 15 minutes of direct skin contact with their male( V0 s2 w; z: B6 B
partners.6 However, when a shirt covered the applica-
, w& j0 y8 U9 e2 k! _- ~tion site, this testosterone transfer was prevented.6 {; ^+ s/ n) O& B
Our patient’s testosterone level was 60 ng/mL,
) B* M/ q  Q2 O4 Swhich was clearly high. Some studies suggest that
# d+ @0 p% N! O8 X) s8 Sdermal conversion of testosterone to dihydrotestos-# ^+ Q7 S$ B/ Q) S- N' p, D
terone, which is a more potent metabolite, is more
/ F8 I0 V' {- I+ |# ~, factive in young children exposed to testosterone
) N1 S0 t* t1 `+ zexogenously7; however, we did not measure a dihy-# z; G: H- Y4 t" r; n
drotestosterone level in our patient. In addition to
* v- J& G3 [) u1 ^, Y: Qvirilization, exposure to exogenous testosterone in- j8 z& _+ r; G. G; @, Q
children results in an increase in growth velocity and
  C2 c: n" X, N. hadvanced bone age, as seen in our patient.& H% ?2 T/ t# V$ X/ @
The long-term effect of androgen exposure during
/ {4 b$ E8 q$ C* J, C) }9 fearly childhood on pubertal development and final7 @( J+ s! K" k
adult height are not fully known and always remain
: Y# e: `- M% |' a* B! ~5 r  la concern. Children treated with short-term testos-8 H& y9 a! h% E0 I3 @
terone injection or topical androgen may exhibit some- w: [" O) h+ v- ~3 h
acceleration of the skeletal maturation; however, after
. S6 C* O1 \" r6 Gcessation of treatment, the rate of bone maturation$ Z4 i4 C6 Y! ]8 B6 q
decelerates and gradually returns to normal.8,90 P, Y: v' b* C6 S6 ?: b" l
There are conflicting reports and controversy5 z( Y+ m! L7 Q' y& F- p
over the effect of early androgen exposure on adult- i7 x: f' f2 k! s5 n9 }( l
penile length.10,11 Some reports suggest subnormal
- u& q. `& ^, E6 V/ b& j" _adult penile length, apparently because of downreg-
, ^: B) }1 i9 ]' J# m3 }3 dulation of androgen receptor number.10,12 However,3 z8 I; N5 d# _2 J
Sutherland et al13 did not find a correlation between
  U* C/ ?$ I8 A- |$ }4 Gchildhood testosterone exposure and reduced adult
. m  ]" ~: {$ bpenile length in clinical studies.
, I8 d( P) c  ^- XNonetheless, we do not believe our patient is
1 h& _/ F# m0 E) Z4 g5 f9 I  E1 M# Pgoing to experience any of the untoward effects from+ @+ B8 P7 o7 O3 H
testosterone exposure as mentioned earlier because! U7 D5 ~$ I/ b' Q
the exposure was not for a prolonged period of time.
. W5 l, e' z  E3 Q5 q7 VAlthough the bone age was advanced at the time of% X. a; i4 D7 S* X: j9 W# J
diagnosis, the child had a normal growth velocity at
# l0 c5 N, r( W5 r+ s4 m% B3 Fthe follow-up visit. It is hoped that his final adult
( o" g+ j0 Y$ X" C4 |" w/ q) ?height will not be affected., M9 ]5 e. _0 `
Although rarely reported, the widespread avail-, N1 N. W8 I* \  n( e% i
ability of androgen products in our society may
- k* B* i; b) ~indeed cause more virilization in male or female
* K$ V( B6 W7 B' `; j' N: I; a; echildren than one would realize. Exposure to andro-" i+ y, p  J9 ]) Q* c
gen products must be considered and specific ques-
; _6 x" Q. h7 F# g8 q. \. Ktioning about the use of a testosterone product or3 G5 Z  z5 R9 K8 [3 t+ w0 G
gel should be asked of the family members during
9 d" l8 ?6 [- B( Sthe evaluation of any children who present with vir-
/ u1 z2 W" h2 e" \: rilization or peripheral precocious puberty. The diag-: i4 f- s" ^5 {, e
nosis can be established by just a few tests and by
' x# w; N+ y: b# R8 R. ?appropriate history. The inability to obtain such a
: d, y6 h: U* T* |6 E. }5 s; O" b5 v+ Fhistory, or failure to ask the specific questions, may8 U3 R+ L" B3 @4 y
result in extensive, unnecessary, and expensive
/ K. v5 B5 N: C5 j! y1 Ginvestigation. The primary care physician should be; w& s  Z' }+ E/ L/ s8 q' j% r
aware of this fact, because most of these children
# i. L4 o- g1 ~+ n; M1 Nmay initially present in their practice. The Physicians’2 R* Z5 W7 X" [9 q" R, s! u4 L
Desk Reference and package insert should also put a
* Z& X/ J" H5 [) s9 `& jwarning about the virilizing effect on a male or
/ A) Q6 E5 i8 W! M* c' Yfemale child who might come in contact with some-9 x# N6 s% v: V4 d
one using any of these products.4 J- U4 Y% v' k; B6 v
References
+ q+ |  W  v% C7 G- s* w* B1. Styne DM. The testes: disorder of sexual differentiation0 ?* l: b  F' ]7 Z' g( |) D
and puberty in the male. In: Sperling MA, ed. Pediatric
& S* l5 ~& b: S6 P/ d; `5 b5 CEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
4 r+ o  Y" Y; x/ m5 P2002: 565-628.$ d- Q% s! S1 z" p" I- Q# ~
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
* |& b$ K1 G: K4 Y; d8 Opuberty 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!

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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
加入VIP,享受高級特權宣傳賺金又升級,超級棒
感謝大大的辛勞分享!我會繼續在WK關注大大的文章!
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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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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?
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發表於 2025-1-19 02:41:05 | 顯示全部樓層
* L9 `6 r' @+ Y+ x% r1 |: K
精妙絕倫的精品,感謝啊!期待你更多更好的創作哦!

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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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