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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/ v- X$ ~8 B7 N# [; _; u0 G0 i
Boy Induced by Indirect Topical
8 E# H+ u' j& D. r) H5 kExposure to Testosterone
1 l" H9 `" F$ CSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2  A, D2 m9 c  H* Z! n" ~- f
and Kenneth R. Rettig, MD1
+ ]) e: @! k3 p" s6 eClinical Pediatrics
- o# s  s& m( U) |' xVolume 46 Number 6; |# b! I' E2 o( G& R! S; Q
July 2007 540-5437 D: Q. y( ]* g+ J- t4 m
© 2007 Sage Publications2 L6 W' Z/ y0 O5 g" Y" {1 O4 ?
10.1177/00099228062966513 p2 G4 ]/ C; L* a
http://clp.sagepub.com" x: q7 _! u7 p' b
hosted at3 R8 G4 _# e4 T, R
http://online.sagepub.com& X- P( D& u) s" ?- E' q
Precocious puberty in boys, central or peripheral,' y; S% H  m* i7 D) A% _) i
is a significant concern for physicians. Central$ @! _1 z6 o' U8 B9 `6 P0 E) U
precocious puberty (CPP), which is mediated
: E7 E* @/ b* I6 W/ W' q7 P: D8 qthrough the hypothalamic pituitary gonadal axis, has
' h( d+ w1 `0 v+ r3 N* Ma higher incidence of organic central nervous system8 U, K7 W7 t/ i0 R  U
lesions in boys.1,2 Virilization in boys, as manifested6 o3 I" W. d" X
by enlargement of the penis, development of pubic
' F2 y2 m6 F8 T* W/ `9 Jhair, and facial acne without enlargement of testi-
, l1 o4 p8 E1 f  S/ H. Zcles, suggests peripheral or pseudopuberty.1-3 We& Y6 T/ K/ @" |+ C5 _4 y3 V% [; p5 a+ R
report a 16-month-old boy who presented with the
0 O9 g9 y1 Z; Uenlargement of the phallus and pubic hair develop-
2 m5 l( D8 A! _$ V0 Cment without testicular enlargement, which was due
  M0 _; ?) K; pto the unintentional exposure to androgen gel used by
) v* ~! s2 `6 f" V( H9 e; ^the father. The family initially concealed this infor-
  y; a6 t  I0 X) y# `1 Umation, resulting in an extensive work-up for this
1 P1 F: v6 a! e% ?3 X* [$ E) u! Bchild. Given the widespread and easy availability of
9 }* o, U  N- ^* Vtestosterone gel and cream, we believe this is proba-7 b6 J7 k( i' |- I) f
bly more common than the rare case report in the
9 M3 ]7 n- I+ p! X) T$ I( G4 rliterature.4
' I3 }9 v' e  c& s1 pPatient Report
6 Y& c1 a: o# O! Z, b. N$ DA 16-month-old white child was referred to the  j0 \& m3 X( e3 Z- p1 b
endocrine clinic by his pediatrician with the concern4 w3 i. S/ c( V1 E6 b) b1 H
of early sexual development. His mother noticed: u5 D7 s* Y1 M
light colored pubic hair development when he was
+ C5 V7 I6 d0 t$ x% J3 L5 kFrom the 1Division of Pediatric Endocrinology, 2University of
- Z. X: H9 M" [/ a& Z' T( M) LSouth Alabama Medical Center, Mobile, Alabama.
# }, \8 N) b1 `) @Address correspondence to: Samar K. Bhowmick, MD, FACE,
6 Z! b! ~) P* E* g3 YProfessor of Pediatrics, University of South Alabama, College of0 w  u2 s3 C0 \, [8 a
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;5 K% c$ A6 f$ \9 Y
e-mail: [email protected].
9 K7 O1 S: O0 R- Habout 6 to 7 months old, which progressively became8 w  N3 e# P$ v# U) V% ~% N
darker. She was also concerned about the enlarge-
( \7 v3 K6 T0 u3 d2 @: r1 cment of his penis and frequent erections. The child+ W; J& v/ T* O. n
was the product of a full-term normal delivery, with. H% y7 e: y7 W. {: o, u
a birth weight of 7 lb 14 oz, and birth length of, p% m& ]  \: [/ h
20 inches. He was breast-fed throughout the first year
, d1 c5 V- i; x4 N. l) G% X4 cof life and was still receiving breast milk along with) g4 x+ Y0 ]% x$ f+ |% F
solid food. He had no hospitalizations or surgery,. y6 P; Z) L" u6 G
and his psychosocial and psychomotor development: C# I2 G1 \5 n7 M7 u, N
was age appropriate.
1 b" s1 c- M1 t* z$ {: }4 ?; gThe family history was remarkable for the father,
5 ^; f. r& C- h  G! M+ q$ Z. ^3 A% \who was diagnosed with hypothyroidism at age 16,
2 O% ]# |0 H$ r7 |! A/ E4 Vwhich was treated with thyroxine. The father’s
$ Y' l4 R+ n# N( dheight was 6 feet, and he went through a somewhat2 x5 J8 X8 ~8 m+ g( J
early puberty and had stopped growing by age 14.
' I# C* ?+ [7 g2 |! v) XThe father denied taking any other medication. The
/ M% S  b1 g4 j/ a8 P$ ~. jchild’s mother was in good health. Her menarche8 G+ D( M# q9 {- D/ S1 {' t- n3 v( K6 h
was at 11 years of age, and her height was at 5 feet, B3 s* J3 _2 e0 B
5 inches. There was no other family history of pre-" D2 I5 E" f5 A/ @9 J0 B3 Z/ k
cocious sexual development in the first-degree rela-
6 {7 b7 L& f/ Y& ftives. There were no siblings.
) t* t0 {- k, z" ]; x+ oPhysical Examination- t, A7 M$ v( a+ z* ~# F. r
The physical examination revealed a very active,0 ]( w% ?. m) _& V1 F1 W
playful, and healthy boy. The vital signs documented
7 M3 X$ _) V4 W6 u# Oa blood pressure of 85/50 mm Hg, his length was6 t* F6 l2 W& {2 H. M- N
90 cm (>97th percentile), and his weight was 14.4 kg5 @; E- z- C5 O6 h* J' Y2 |
(also >97th percentile). The observed yearly growth
+ N- X  E* o3 D, ^velocity was 30 cm (12 inches). The examination of2 m' S, C) k9 p. A
the neck revealed no thyroid enlargement.
) @& H0 s: C$ oThe genitourinary examination was remarkable for
  o+ r1 W# J2 u1 nenlargement of the penis, with a stretched length of  c2 y; F4 ^+ ~/ s% C
8 cm and a width of 2 cm. The glans penis was very well. q2 C" g# O) Z7 o
developed. The pubic hair was Tanner II, mostly around
  M. E4 w2 ]) L0 p& j540! W0 {# l1 F4 n+ e: x! n0 y
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
9 S* v" V: k8 k& a$ Y, ythe base of the phallus and was dark and curled. The
% N( D( \/ {: c* O+ ktesticular volume was prepubertal at 2 mL each.5 h! k( u( A: ]) T; ~9 Y& y" h6 e
The skin was moist and smooth and somewhat
" J; C  p& N& s6 @' C' u9 Yoily. No axillary hair was noted. There were no
. D/ E9 b! b( L: s3 b9 U/ xabnormal skin pigmentations or café-au-lait spots.
! ?- d5 X* x- _% U- b; LNeurologic evaluation showed deep tendon reflex 2+
6 |: ?! J% H' `  Ebilateral and symmetrical. There was no suggestion
8 P3 A: t, X; E% W5 Q( `# }4 Tof papilledema.7 r- R6 G8 ?4 ]) n; J# z
Laboratory Evaluation, Y' a3 `9 q% n) k; F+ U. c+ }/ H
The bone age was consistent with 28 months by( K' a# Z; G& J- x
using the standard of Greulich and Pyle at a chrono-8 y* b. ~/ H' N1 O1 R3 H
logic age of 16 months (advanced).5 Chromosomal4 d& I" f9 G  c3 G' {
karyotype was 46XY. The thyroid function test) Q, D# W2 T1 J8 q! g) H
showed a free T4 of 1.69 ng/dL, and thyroid stimu-+ @! o5 ?" d6 e( }& s. q+ Y2 k% P
lating hormone level was 1.3 µIU/mL (both normal).
; f7 H4 Z" p9 t( {! ?: w& `The concentrations of serum electrolytes, blood
3 R3 q* p! N# Q1 j& {" [4 xurea nitrogen, creatinine, and calcium all were
  N! z2 q! M8 B8 G4 `within normal range for his age. The concentration
9 |/ j0 m0 [4 J2 L8 ^of serum 17-hydroxyprogesterone was 16 ng/dL* j& x( @4 Y/ i% _  Q, @
(normal, 3 to 90 ng/dL), androstenedione was 20
# G! z9 H1 p! z! D$ d+ ?ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
* O% y7 g, d5 G5 f  E2 f* K, \& `terone was 38 ng/dL (normal, 50 to 760 ng/dL),6 P! i8 e! E; X/ c
desoxycorticosterone was 4.3 ng/dL (normal, 7 to, W& i" Y7 h; Q
49ng/dL), 11-desoxycortisol (specific compound S)
' j) Z' l- x; \* ]was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-* p3 z  F. n9 h/ e6 C" {- i6 |
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
& ?" h! a8 J7 }0 s4 c, htestosterone was 60 ng/dL (normal <3 to 10 ng/dL),2 }+ x# i8 s2 V5 n
and β-human chorionic gonadotropin was less than4 _' z. P: W. @3 l# b: A
5 mIU/mL (normal <5 mIU/mL). Serum follicular
7 z& G7 f# {3 F& M1 P# x/ hstimulating hormone and leuteinizing hormone
8 G8 _$ |+ a* l# }. m$ t6 {! cconcentrations were less than 0.05 mIU/mL' `' H7 A- A; }6 L8 O
(prepubertal).
9 b0 H% R( H2 f' B3 |0 X3 x$ FThe parents were notified about the laboratory( f, [! d8 h% [2 n7 S. L! K
results and were informed that all of the tests were
5 M; A# p9 u$ M& p* l9 I+ n) |, Fnormal except the testosterone level was high. The+ v% f+ n/ t' O% Y
follow-up visit was arranged within a few weeks to: o8 W. i' c7 e3 A4 k6 I
obtain testicular and abdominal sonograms; how-
* o0 t5 ~) P8 B. {ever, the family did not return for 4 months.
, q( _5 [/ ]+ g/ L$ PPhysical examination at this time revealed that the
5 ]6 G& p6 v8 p& ochild had grown 2.5 cm in 4 months and had gained
  Z! S3 m+ f8 f% j9 M+ p2 kg of weight. Physical examination remained% @5 U, z  ^( ^: _) N
unchanged. Surprisingly, the pubic hair almost com-) M4 f  m5 \( T- J
pletely disappeared except for a few vellous hairs at- O* x0 m* E; J" i# `- f
the base of the phallus. Testicular volume was still 2
& G0 s& A( t# ~6 LmL, and the size of the penis remained unchanged.
5 z  A0 Q; S8 F  \1 g4 `1 f- zThe mother also said that the boy was no longer hav-
+ b7 _( X. q9 _2 b% king frequent erections.* c" ~: F$ n; w. R3 ~: E( ~
Both parents were again questioned about use of5 r+ {) x  c! S
any ointment/creams that they may have applied to4 F! Q  T8 ~4 ]1 K1 E( e
the child’s skin. This time the father admitted the4 v+ |! X, \5 P& G/ b
Topical Testosterone Exposure / Bhowmick et al 541+ T3 a6 n; ?) v  J: h# D
use of testosterone gel twice daily that he was apply-4 @  M7 j7 }5 s6 G* o
ing over his own shoulders, chest, and back area for
, Y* D" O, U+ ]# @a year. The father also revealed he was embarrassed; B1 Q1 H9 |4 E
to disclose that he was using a testosterone gel pre-% v) u( n' r, F* E
scribed by his family physician for decreased libido3 @; ~8 T2 o* d7 a
secondary to depression.
% p1 b' }% @! _5 q8 KThe child slept in the same bed with parents.$ Q, E: Z% I, A. O- b' m
The father would hug the baby and hold him on his
7 h* ~* ]$ q+ j1 {4 s* ?chest for a considerable period of time, causing sig-8 w$ i2 C/ d8 X" a+ J  T. _$ g
nificant bare skin contact between baby and father.6 Z; I5 b' d3 X% Y& P5 F6 V
The father also admitted that after the phone call,) [' ~- k& W( N
when he learned the testosterone level in the baby9 x6 C  ]5 z6 y2 X
was high, he then read the product information; b$ T, x& V! z) [4 s
packet and concluded that it was most likely the rea-  u, L2 z) F9 {/ N1 M, i
son for the child’s virilization. At that time, they
' I2 a* f, l" }5 K3 G$ {decided to put the baby in a separate bed, and the4 S) `# n' Y1 y: `, C. J6 ?& D5 J
father was not hugging him with bare skin and had
/ e+ p' L: z8 X8 v. Gbeen using protective clothing. A repeat testosterone; x2 F, g# a; ?2 h9 q* _# T  J& {
test was ordered, but the family did not go to the) E- r. l) l: ?0 f: o
laboratory to obtain the test.) z7 L6 J* l( s9 Y+ ]
Discussion
( H- s7 N' l/ g9 XPrecocious puberty in boys is defined as secondary5 w. B# V& n: L3 J5 C+ ?. @
sexual development before 9 years of age.1,4
  D" |8 I6 H+ a1 o$ f$ [* u  APrecocious puberty is termed as central (true) when
0 R+ U7 W# x4 a4 D4 iit is caused by the premature activation of hypo-# \5 D8 x9 r+ `+ S+ H8 t
thalamic pituitary gonadal axis. CPP is more com-
; I, J2 {6 Z5 P8 F8 ]7 T, E5 g3 Y7 jmon in girls than in boys.1,3 Most boys with CPP
2 _6 q2 l/ [. W7 s5 s0 Z& cmay have a central nervous system lesion that is# d9 N0 A8 ]+ Z! I- r) {1 \7 ?
responsible for the early activation of the hypothal-
. L2 |. b- @" S6 kamic pituitary gonadal axis.1-3 Thus, greater empha-) x9 o7 j( I( l! c# {2 C" Q$ K
sis has been given to neuroradiologic imaging in  [. \/ e( C: `1 D& T1 O
boys with precocious puberty. In addition to viril-
& K1 Q% q1 F- kization, the clinical hallmark of CPP is the symmet-
& S+ K  f* p0 ]6 P0 e1 x! srical testicular growth secondary to stimulation by
9 e) l% S2 o* E: X% O; q' Ggonadotropins.1,3. |2 z( r6 Z, v
Gonadotropin-independent peripheral preco-
. c2 {: a9 U& E: d: T3 hcious puberty in boys also results from inappropriate. H7 i, u8 b+ Y
androgenic stimulation from either endogenous or+ a- B: q- J; Y( a" ~
exogenous sources, nonpituitary gonadotropin stim-
- w& J& h+ r* _$ O; Xulation, and rare activating mutations.3 Virilizing
$ ~) ?2 |' b% f* G) Ucongenital adrenal hyperplasia producing excessive
3 q  D8 h: ]- v- Y0 yadrenal androgens is a common cause of precocious# S* @, u! B% N. q
puberty in boys.3,4
' O3 w; C1 B% A$ gThe most common form of congenital adrenal2 w# i( t& v# m* t
hyperplasia is the 21-hydroxylase enzyme deficiency.) W0 D" X4 z5 Z9 U! u
The 11-β hydroxylase deficiency may also result in! w. K& q4 g! G  |
excessive adrenal androgen production, and rarely,5 w8 m+ T$ @2 |5 D) J; E
an adrenal tumor may also cause adrenal androgen
/ R- j: c( M, X& w6 ~' ^7 k' L3 g; ~excess.1,3
7 P2 i1 {; _$ u" g6 Jat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from  F6 S/ D/ N2 Z0 d+ _, v$ N
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
# i3 o' n* ]) _# `1 mA unique entity of male-limited gonadotropin-+ ^! H0 F( n$ w* F
independent precocious puberty, which is also known
1 r! O- i: _. Fas testotoxicosis, may cause precocious puberty at a8 d* j6 K& w9 C7 |' ~- L' \+ b
very young age. The physical findings in these boys
7 T. [1 e6 a6 bwith this disorder are full pubertal development,
! R$ E3 h, M$ H; `, aincluding bilateral testicular growth, similar to boys9 p% b# E) ?+ |
with CPP. The gonadotropin levels in this disorder+ T6 U* t/ ~7 j6 E& {! C+ q; E8 n8 T9 g
are suppressed to prepubertal levels and do not show
  [9 ~/ p2 p! f: D6 S. \$ V3 mpubertal response of gonadotropin after gonadotropin-- u  o9 a$ c! y& i0 O: P- ~! g9 g
releasing hormone stimulation. This is a sex-linked
# B' v& v/ U3 qautosomal dominant disorder that affects only5 R$ v/ o6 M% c2 G9 N3 f
males; therefore, other male members of the family+ S' {/ ]) M7 w1 o( s2 B4 J+ @
may have similar precocious puberty.35 W/ E- J, n& P5 P% q, X" r
In our patient, physical examination was incon-
* `( @# e; k) V2 J) x1 osistent with true precocious puberty since his testi-
4 L. V/ Z* Q. e( H* ?  s) hcles were prepubertal in size. However, testotoxicosis& V/ E) p( j( h$ {6 Y1 r4 \
was in the differential diagnosis because his father
6 p$ ~1 G. h7 ^6 E- c6 i2 istarted puberty somewhat early, and occasionally,
( Y6 k/ S; W: J- l$ S% ztesticular enlargement is not that evident in the/ r5 I' ~' `3 a6 V, t
beginning of this process.1 In the absence of a neg-
9 `$ g" l5 e  {% O( q5 C) Lative initial history of androgen exposure, our
5 e8 }, m9 ~0 W- W% }6 t" zbiggest concern was virilizing adrenal hyperplasia,) H1 d  j/ O# c  f
either 21-hydroxylase deficiency or 11-β hydroxylase
1 A: _/ j7 S' o/ b- rdeficiency. Those diagnoses were excluded by find-
, S9 p  q; t* bing the normal level of adrenal steroids.) _1 M. H% z+ q
The diagnosis of exogenous androgens was strongly8 K, b. ~6 K" T  m9 M+ D
suspected in a follow-up visit after 4 months because$ q' ^$ `; C2 q  a. U
the physical examination revealed the complete disap-
; m' v0 ?& p( W, l) m2 _, ]5 Gpearance of pubic hair, normal growth velocity, and
# v! v* N' P, z  P! o2 V! Ldecreased erections. The father admitted using a testos-. L( w# Y6 H; m5 ~% o/ ^4 D0 o2 k1 E
terone gel, which he concealed at first visit. He was/ \: z2 h$ C' Y5 A2 s0 ^
using it rather frequently, twice a day. The Physicians’
: }: N5 B; H7 f' `* LDesk Reference, or package insert of this product, gel or
* u# Z' @- w2 Jcream, cautions about dermal testosterone transfer to
* T% v( _( K+ G! {$ gunprotected females through direct skin exposure.0 Y. y; h7 I/ `' y% k
Serum testosterone level was found to be 2 times the
- {1 t0 [7 x! ubaseline value in those females who were exposed to" m% v9 I# C& h) Y: D3 @+ Y
even 15 minutes of direct skin contact with their male
0 ~0 u4 T) K- `0 |' g. @partners.6 However, when a shirt covered the applica-. e- I( U6 j% v- \7 c
tion site, this testosterone transfer was prevented.9 K; b0 ^5 [+ m- E+ w
Our patient’s testosterone level was 60 ng/mL,
) b: p+ e0 m" S% G8 w% }which was clearly high. Some studies suggest that# K! f& z$ g5 j
dermal conversion of testosterone to dihydrotestos-+ l" y  Q1 V# D  t, f: s8 |& f
terone, which is a more potent metabolite, is more+ ~. j  ?& A: K9 i( F- u& y+ ]
active in young children exposed to testosterone
; a1 B; i3 s0 |7 M2 B6 g2 q0 wexogenously7; however, we did not measure a dihy-8 e4 n7 c. N% C, t
drotestosterone level in our patient. In addition to" K9 B9 {2 y0 z7 D$ ?" ^
virilization, exposure to exogenous testosterone in
1 Z8 ^1 h+ n) E& s/ rchildren results in an increase in growth velocity and
  K, ^' B4 u! T' ^! [* s6 Cadvanced bone age, as seen in our patient., \8 ~6 F4 \5 C7 j7 ~" z. A
The long-term effect of androgen exposure during+ G! ~' s4 n( T; {! Z/ h! d
early childhood on pubertal development and final4 v9 O* q& ^; j
adult height are not fully known and always remain
" E" ^& O6 \: T7 r8 Ua concern. Children treated with short-term testos-
5 e3 M7 Z; ^: E$ |/ Iterone injection or topical androgen may exhibit some  b. u. n" B& e( a
acceleration of the skeletal maturation; however, after, c( E  `/ j9 L2 h: |; i& K+ |* p$ i
cessation of treatment, the rate of bone maturation
/ p# [1 W6 [# }  P- xdecelerates and gradually returns to normal.8,9
9 o  `+ y" v% W- jThere are conflicting reports and controversy: s* ]( z! A$ h8 K: L' ^: [' c  ^
over the effect of early androgen exposure on adult. Q8 {$ l. \. v( e* N( C6 g( s2 E
penile length.10,11 Some reports suggest subnormal% d- I7 ^' l$ n0 j4 o& G
adult penile length, apparently because of downreg-
& M! t$ g& [/ U0 D& ]ulation of androgen receptor number.10,12 However,1 e5 o" _$ Z( f, K4 F, F1 b
Sutherland et al13 did not find a correlation between
0 {; |( g% @: J& s9 y; kchildhood testosterone exposure and reduced adult3 z/ \3 e- h4 {8 ]
penile length in clinical studies.# g1 Z% ^/ @: u" R  Y/ o
Nonetheless, we do not believe our patient is
+ k: u$ R7 c! g. g$ Igoing to experience any of the untoward effects from$ u" i$ _* _- Y/ v# s7 l: f& X
testosterone exposure as mentioned earlier because
, R! B* v5 c; lthe exposure was not for a prolonged period of time.
3 _- C7 ]6 w% c! M& [; g, fAlthough the bone age was advanced at the time of1 n' m/ f: l1 O; g3 K0 ?
diagnosis, the child had a normal growth velocity at
# B/ Q: o: @+ f0 u& othe follow-up visit. It is hoped that his final adult
+ i8 N( \3 i% m1 F( i( d" t- h: dheight will not be affected.
) D' Z( q  v# U, g* L! Y& sAlthough rarely reported, the widespread avail-8 i' X% r8 y$ B/ n" V
ability of androgen products in our society may! ~, ?7 y% m: [; H5 L: V
indeed cause more virilization in male or female
$ T- H3 Z- ]( z. m7 [. Rchildren than one would realize. Exposure to andro-$ d/ \% R/ J; S+ E0 [5 G9 E
gen products must be considered and specific ques-
, w7 ]: @0 C! ~9 O2 a: K8 @tioning about the use of a testosterone product or
; }; ^: H% E. B" ~! a$ ogel should be asked of the family members during3 Z$ B" m, P9 z
the evaluation of any children who present with vir-
9 y2 N! q! e0 y: e$ r2 }, vilization or peripheral precocious puberty. The diag-
9 b2 |. O: u  i5 s& t4 W6 D9 W' fnosis can be established by just a few tests and by
* W* [* q6 \4 {+ P6 pappropriate history. The inability to obtain such a
% u/ {, @/ \& Y+ X6 Ghistory, or failure to ask the specific questions, may* m& L1 N/ E7 f2 b
result in extensive, unnecessary, and expensive
$ Y+ |3 R$ ?, q2 _: |investigation. The primary care physician should be8 ]$ v  R4 V' V  f
aware of this fact, because most of these children; A* p% o& b6 Q3 s
may initially present in their practice. The Physicians’3 q, K3 D$ f) Q* O2 Q' ^
Desk Reference and package insert should also put a
4 i5 Q8 N% w8 r: Twarning about the virilizing effect on a male or* _0 y& I; o% S1 r
female child who might come in contact with some-
' ^' N! v: x; Q" I% Zone using any of these products., _, Y- @3 d! D  M* Z7 T
References
1 Y2 n- J# H" q" W5 d) Q1. Styne DM. The testes: disorder of sexual differentiation$ ]" b2 G: [/ J/ [! q) m
and puberty in the male. In: Sperling MA, ed. Pediatric4 \; I6 l. D: r1 C4 W7 P
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
8 Q3 h. U' z7 ?- \; }9 P2002: 565-628.
4 ~$ i3 d6 A# M4 h5 A# |2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
( `/ V1 t7 Y* m4 \  ]1 K7 jpuberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
9 b) D& G# Q! \+ MBoy Induced by Indirect Topical: c* k6 D( F. L- q! E/ Z
Exposure to Testosterone
5 C- t5 ^' o5 i2 ?& A3 V' z7 @Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
5 \- z7 L, P; Rand Kenneth R. Rettig, MD1
1 \6 \% T7 T& sClinical Pediatrics, p2 L, b3 X! [$ z( ~3 q
Volume 46 Number 6
' V6 d0 e$ ^2 m8 m7 E8 i2 DJuly 2007 540-543
6 \; E; {& V8 O: p© 2007 Sage Publications) ]( ]" y/ v, w2 l
10.1177/00099228062966512 k' |- \# x# \: U1 q
http://clp.sagepub.com: D- O2 q" j) p! D7 x  Q2 c  i
hosted at+ L* X4 C% E! m! ^1 V1 E& L
http://online.sagepub.com
8 m* f% t' o8 o* APrecocious puberty in boys, central or peripheral,
3 P- ?: k! ~8 I. l" wis a significant concern for physicians. Central
! S+ Z! R* G1 Aprecocious puberty (CPP), which is mediated% i3 E4 f! C1 M4 y$ J! `8 X! [
through the hypothalamic pituitary gonadal axis, has
' U; G% Q+ Y" {% J0 D* ma higher incidence of organic central nervous system: n4 ?8 Q/ d- o2 e- q- I- t
lesions in boys.1,2 Virilization in boys, as manifested0 D& b7 Y7 B" \, d+ p
by enlargement of the penis, development of pubic
9 E3 q- _+ q# B) P7 A, Lhair, and facial acne without enlargement of testi-
, _; I' d4 E% x. j& qcles, suggests peripheral or pseudopuberty.1-3 We
' P$ @) U* r" B+ areport a 16-month-old boy who presented with the
- o% i4 R; E2 aenlargement of the phallus and pubic hair develop-
& N5 _- U1 a7 x* J- Ument without testicular enlargement, which was due" y' X4 F( n, H( z' o. b9 g% m
to the unintentional exposure to androgen gel used by
7 L+ d# |' Z: x, s' `! _the father. The family initially concealed this infor-
0 H5 I9 l$ Z2 H% ~; P  y' V/ h* Smation, resulting in an extensive work-up for this. T6 p( [% U1 {7 l! L3 R/ C6 p
child. Given the widespread and easy availability of
% x- ~- P" T8 F: O& Htestosterone gel and cream, we believe this is proba-
. W" y( E* f& k/ R2 F+ Ebly more common than the rare case report in the
$ `$ n: `0 Q/ F& B: Z: Vliterature.4; J; y2 c. V8 W7 i
Patient Report  m1 D# m, Z3 f+ I. U4 Z6 V1 h5 ?- q
A 16-month-old white child was referred to the- k* x- F. k/ Z. T8 A& H
endocrine clinic by his pediatrician with the concern
4 ?& P: B( \- b% U& A- kof early sexual development. His mother noticed1 ^1 c; R/ ]- D6 S
light colored pubic hair development when he was
4 u/ t+ T$ m7 o. v8 ?- K4 i! l) gFrom the 1Division of Pediatric Endocrinology, 2University of/ @( @8 X) Q# e' ?: c  N
South Alabama Medical Center, Mobile, Alabama.
1 Y" S* z# ?* q" lAddress correspondence to: Samar K. Bhowmick, MD, FACE,. f9 v% w4 y* h
Professor of Pediatrics, University of South Alabama, College of
* z- |0 ?1 B" j: I! ~9 E( B9 uMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
- y. t, K, p0 I2 S/ o- `! O5 _e-mail: [email protected].8 K/ z. F& L. S" f
about 6 to 7 months old, which progressively became
8 t8 m# T6 W+ E. C2 {1 zdarker. She was also concerned about the enlarge-! M9 |1 X; D. \, B3 s* d
ment of his penis and frequent erections. The child
7 v2 n, n! n1 q+ k2 C' Q) `) }was the product of a full-term normal delivery, with
* @' F) u" }3 d5 B! [0 H6 Z$ @a birth weight of 7 lb 14 oz, and birth length of  e# q0 U, B0 m1 J1 G
20 inches. He was breast-fed throughout the first year
$ k  e4 D0 W+ a4 c, K: U4 jof life and was still receiving breast milk along with' c( a; t, e, f# R; @
solid food. He had no hospitalizations or surgery,
( W+ z9 ~% u! S# E6 P7 Fand his psychosocial and psychomotor development
% E1 z3 {+ C! Z; }9 }- Swas age appropriate.
: @6 N3 p$ A' w0 }# I( Y, W! x" pThe family history was remarkable for the father,
) v: ~! c2 d; S  A4 zwho was diagnosed with hypothyroidism at age 16," Y" M  s2 Z; c1 v  ?; C
which was treated with thyroxine. The father’s; i/ Q7 D1 g6 E6 f7 h$ I. `
height was 6 feet, and he went through a somewhat0 k+ Y" h0 L( O
early puberty and had stopped growing by age 14.
- p' }+ x1 ?) [5 {5 X9 q4 \& BThe father denied taking any other medication. The0 U+ ]$ v& q% s! V, x+ I
child’s mother was in good health. Her menarche
* `8 `0 _: R3 S0 U5 ?was at 11 years of age, and her height was at 5 feet+ v0 B4 \; n  I4 c" {
5 inches. There was no other family history of pre-$ g0 b0 a/ x) |0 E, v* o5 d
cocious sexual development in the first-degree rela-9 s! Y7 P* y/ v8 O/ z1 h# U$ n
tives. There were no siblings.; [2 w$ z' I" B9 ?4 p, z
Physical Examination- K/ R/ [2 W# V9 T& V5 }
The physical examination revealed a very active,- N6 T# O/ G# Y- n, r" I0 U/ I
playful, and healthy boy. The vital signs documented
; Q7 O) }. E1 e& B/ Ya blood pressure of 85/50 mm Hg, his length was! I1 W% f8 w5 T  i1 j8 `
90 cm (>97th percentile), and his weight was 14.4 kg
9 @( a4 J) Y, L, i(also >97th percentile). The observed yearly growth( k# s) n' F5 {% m$ b
velocity was 30 cm (12 inches). The examination of
( }- ]: N% ]0 h$ w! p) @0 rthe neck revealed no thyroid enlargement.
: T$ y; W: n6 @8 ~4 ~The genitourinary examination was remarkable for
4 u: B, G- Q$ Penlargement of the penis, with a stretched length of
; t/ Q! U1 }. \6 P, [; U8 cm and a width of 2 cm. The glans penis was very well( R0 p  j& R4 V
developed. The pubic hair was Tanner II, mostly around6 ^' A+ m) s/ `/ v0 a
540+ x5 q' f, L# h" r
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from' _' w6 H# |' [% o) S
the base of the phallus and was dark and curled. The$ Z! I8 N7 G$ I. o
testicular volume was prepubertal at 2 mL each.% Q7 l. ]5 z# i6 r) ]
The skin was moist and smooth and somewhat
8 I5 p" p5 y& H7 k9 k* d# Zoily. No axillary hair was noted. There were no
# e- M7 z3 P! d% V; M! [abnormal skin pigmentations or café-au-lait spots.
* t$ V* n) B+ E+ S# ~2 l) A6 ]Neurologic evaluation showed deep tendon reflex 2+6 ?" `8 \9 k$ L
bilateral and symmetrical. There was no suggestion- @" v! ^8 ^6 J7 G, G
of papilledema.
: o. ~; v2 t% ]3 X3 PLaboratory Evaluation' x1 l5 d& v$ j. K8 J
The bone age was consistent with 28 months by6 B5 r! F0 t, W& h8 @8 J" S* u- l
using the standard of Greulich and Pyle at a chrono-8 n" ?6 @$ S" ?; x! t4 a  }
logic age of 16 months (advanced).5 Chromosomal9 x6 Z% d2 P6 R
karyotype was 46XY. The thyroid function test( k" ]9 |# y& }& H
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
3 j0 h2 E0 m/ Rlating hormone level was 1.3 µIU/mL (both normal).7 o  M6 Q' r2 R! S% l$ L
The concentrations of serum electrolytes, blood
/ m- _& T! d  ^urea nitrogen, creatinine, and calcium all were
+ B/ E8 ?* P3 x5 Dwithin normal range for his age. The concentration
$ A9 `0 Q1 u+ t3 Fof serum 17-hydroxyprogesterone was 16 ng/dL! Y6 }9 e' j2 s
(normal, 3 to 90 ng/dL), androstenedione was 20
2 w. q! [4 L1 x6 {ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
4 \1 \9 g) n1 v9 Q. e( `( _7 k7 [' Qterone was 38 ng/dL (normal, 50 to 760 ng/dL),+ c; c7 |1 D% M$ K! M& J2 b! h8 S8 U
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
) e0 I+ s8 D7 K5 d7 ^# f49ng/dL), 11-desoxycortisol (specific compound S)% H- W+ i/ Z2 s5 ~: u8 a
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-# N0 E4 h* a# h6 K$ X; [
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total& }; h. w) B. G" J+ t% h( c
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
% ^0 d6 B" f! Hand β-human chorionic gonadotropin was less than
, _$ ?1 Q0 [' f4 m7 ]5 mIU/mL (normal <5 mIU/mL). Serum follicular1 o8 d2 i: i7 H8 H% S6 `, \
stimulating hormone and leuteinizing hormone
6 |& w1 Y" f5 ]2 R/ Rconcentrations were less than 0.05 mIU/mL
& r5 ?/ T8 I5 y- W- T: g(prepubertal).. }7 T% n7 a+ j, B" {
The parents were notified about the laboratory
! S7 ]' f" d" O3 G( Lresults and were informed that all of the tests were, D2 q( r! A: O) n# x) h# N
normal except the testosterone level was high. The  q7 Z; Z) e, L9 u0 H* y
follow-up visit was arranged within a few weeks to
" [) l4 h' P) L: ]& m6 D; lobtain testicular and abdominal sonograms; how-7 f+ M7 G2 W! o
ever, the family did not return for 4 months.
! d+ L1 u6 d5 A3 I0 F9 mPhysical examination at this time revealed that the# l1 \) W; _) E4 F5 A! Z8 c) |& x5 S
child had grown 2.5 cm in 4 months and had gained" v, q, k# f, ?7 @4 m3 B4 H) ?
2 kg of weight. Physical examination remained
7 m/ e) G% @) @! o( ounchanged. Surprisingly, the pubic hair almost com-' E5 Z/ F, J% c1 F/ ]
pletely disappeared except for a few vellous hairs at- `9 {. d- \* r( ^
the base of the phallus. Testicular volume was still 2
6 E% r0 A$ a5 _5 NmL, and the size of the penis remained unchanged.
, U# {  p& K4 U9 Y+ G: w# ^The mother also said that the boy was no longer hav-
) B6 q3 j& E  D( b7 `! T& wing frequent erections.
7 J0 K" ~+ B$ _; R/ }Both parents were again questioned about use of# T& }4 W( J6 C$ @1 \1 W
any ointment/creams that they may have applied to
: \3 R' R. n2 N9 ~/ p; ^/ y7 Othe child’s skin. This time the father admitted the! C+ ?, v* ~8 O& A3 z
Topical Testosterone Exposure / Bhowmick et al 541
3 Y" e( `7 h1 A3 V& C7 L* xuse of testosterone gel twice daily that he was apply-
7 ?1 D; T6 L% Sing over his own shoulders, chest, and back area for2 {- H2 O+ `; u6 {1 }# G9 s) z: w. p
a year. The father also revealed he was embarrassed
+ T% `% z7 d. O$ }: \$ cto disclose that he was using a testosterone gel pre-
* Z7 s: |/ \! c3 L  J' Y4 i$ uscribed by his family physician for decreased libido" |4 U9 W' n* ^! @0 V. F0 w
secondary to depression.& l: }& k: M6 a, [7 W  p
The child slept in the same bed with parents.
' P8 b+ D# ^8 K* C; ^& x+ @The father would hug the baby and hold him on his
5 o3 x% D  g+ s) ~1 q( P5 Lchest for a considerable period of time, causing sig-  n* ^, [! I, u
nificant bare skin contact between baby and father.5 X+ r  B1 \+ [; z
The father also admitted that after the phone call,8 B! p3 B# @. N+ u+ O! ^
when he learned the testosterone level in the baby
8 t2 }* h8 A5 a3 r3 o- ]( Uwas high, he then read the product information
: z! i/ n: Y) p" M& \packet and concluded that it was most likely the rea-% u* b7 [( \! P# _
son for the child’s virilization. At that time, they
" D$ L9 F& \0 Ldecided to put the baby in a separate bed, and the
" ]) ?9 x7 U. Q8 u6 qfather was not hugging him with bare skin and had
: I7 D. [# K- D% Wbeen using protective clothing. A repeat testosterone
0 c* K- v0 d) ?9 k% wtest was ordered, but the family did not go to the2 }) Y  t0 A$ I' ~
laboratory to obtain the test.
, T+ `8 p6 e: S7 n% [; ]5 c# pDiscussion8 a: W" G0 x: ^
Precocious puberty in boys is defined as secondary
5 \+ g3 G3 s# n" ~2 ]" Zsexual development before 9 years of age.1,4
) z+ _  J: J  U+ Q1 S8 I& gPrecocious puberty is termed as central (true) when) w1 w% o: n$ J7 A3 _
it is caused by the premature activation of hypo-( P* x3 t6 Z8 p, z
thalamic pituitary gonadal axis. CPP is more com-
& O1 T5 ]5 j/ f% D1 pmon in girls than in boys.1,3 Most boys with CPP+ h" f8 u4 \# m6 K$ d- u
may have a central nervous system lesion that is
  w5 z' t$ T' O: Q. aresponsible for the early activation of the hypothal-( S+ P9 a8 `& `2 i. {
amic pituitary gonadal axis.1-3 Thus, greater empha-
& }% U$ \% N0 R% j- O: L/ F' Jsis has been given to neuroradiologic imaging in
8 a/ Z8 e1 X4 e5 yboys with precocious puberty. In addition to viril-1 U: M3 E8 [" }4 J. \+ @
ization, the clinical hallmark of CPP is the symmet-
+ T7 ~5 c0 V3 k: ]8 srical testicular growth secondary to stimulation by
, N4 d2 j  V% W8 N! f# F' U& Cgonadotropins.1,3
; V2 i0 e& M$ q' w7 bGonadotropin-independent peripheral preco-
- H7 q: l0 J( qcious puberty in boys also results from inappropriate* {& M# [) s' E5 U' d# z4 G. s) `
androgenic stimulation from either endogenous or
' T( n$ G# J0 u" Q! @: x5 Fexogenous sources, nonpituitary gonadotropin stim-
0 e7 L7 H& `' b: Fulation, and rare activating mutations.3 Virilizing7 U8 u, s" _. ~' D$ a  b
congenital adrenal hyperplasia producing excessive& x) f+ J7 [8 x! }0 {
adrenal androgens is a common cause of precocious
0 V% i" T/ Q- m$ Ppuberty in boys.3,4% C6 ]: _4 b2 W1 p* C* ~# }
The most common form of congenital adrenal4 ?. Q2 |3 g- \  B  n( s# W$ x  J
hyperplasia is the 21-hydroxylase enzyme deficiency.
6 P% [# c0 X) z0 sThe 11-β hydroxylase deficiency may also result in
* q, W& ~  @. G* v2 Yexcessive adrenal androgen production, and rarely,2 h# _8 H( v. Q' e0 ?2 c
an adrenal tumor may also cause adrenal androgen5 s' \4 o* B+ F4 G. g  a# @
excess.1,3
4 ~5 w( S/ k/ n& D- lat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
& Y$ Z! h7 u$ O9 e! u% t542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
9 E8 E0 F5 \3 w0 U0 @A unique entity of male-limited gonadotropin-1 E: d3 r  w- ]( J7 W& j
independent precocious puberty, which is also known: M% U# s+ m. Z
as testotoxicosis, may cause precocious puberty at a$ t. R" n5 |' y/ i4 S: [5 \3 D
very young age. The physical findings in these boys
/ r! }8 j4 b# }/ x# twith this disorder are full pubertal development,
( n2 Q1 ?3 h6 k9 zincluding bilateral testicular growth, similar to boys
) x) v% W; G; }8 `with CPP. The gonadotropin levels in this disorder' g+ x: S3 K: N0 k
are suppressed to prepubertal levels and do not show
2 ]! q5 I' [* t, X1 n! K* kpubertal response of gonadotropin after gonadotropin-
9 {" k+ w5 l0 R0 Q5 y3 B+ m3 Vreleasing hormone stimulation. This is a sex-linked- _/ P- v) a' \) O
autosomal dominant disorder that affects only
  C( W2 x. y0 f( [" F" \. emales; therefore, other male members of the family
, u! h+ A( S% Hmay have similar precocious puberty.3
8 e  d! M; t% \& s: o9 iIn our patient, physical examination was incon-9 |4 O2 N5 V  L
sistent with true precocious puberty since his testi-
0 K1 t* Q3 R' `$ xcles were prepubertal in size. However, testotoxicosis/ g0 ~4 w+ s: c
was in the differential diagnosis because his father
) }' {; |: f" X* v) g+ Ustarted puberty somewhat early, and occasionally,& L/ |; E$ B9 R/ F8 `, r, I" ~) |
testicular enlargement is not that evident in the3 [( R, t/ V6 T; Z7 j
beginning of this process.1 In the absence of a neg-" E  B! `3 F* ]' F3 h
ative initial history of androgen exposure, our
/ A' o  S* L' j8 k2 s: W  W* }biggest concern was virilizing adrenal hyperplasia,
) y( l- ?0 t' z5 ?0 aeither 21-hydroxylase deficiency or 11-β hydroxylase; W4 a7 J) |6 B* K4 r( \, d3 S
deficiency. Those diagnoses were excluded by find-% ]5 j& G5 g; a) W2 Z5 q
ing the normal level of adrenal steroids.
) G6 i/ c3 e7 p! c9 ?" v* U$ {( dThe diagnosis of exogenous androgens was strongly
* O% F& k: l6 T; N* R" h+ Xsuspected in a follow-up visit after 4 months because
, C: n/ _* ]& M% O) qthe physical examination revealed the complete disap-
- @6 V4 Z8 S, dpearance of pubic hair, normal growth velocity, and
! _+ j! t" t8 H1 edecreased erections. The father admitted using a testos-
* H) D' c) c7 D* E! q0 Kterone gel, which he concealed at first visit. He was
8 _" D0 I9 N. T4 ]( }! `0 Xusing it rather frequently, twice a day. The Physicians’6 i- M: C( o4 Z* M: _
Desk Reference, or package insert of this product, gel or
1 H; x$ G4 v/ w  Ccream, cautions about dermal testosterone transfer to
+ T4 \5 R" \+ Xunprotected females through direct skin exposure.
  s( F7 L* c3 |0 f1 }- r7 V+ ASerum testosterone level was found to be 2 times the! i$ A2 Q1 z/ k
baseline value in those females who were exposed to
( d- J& z1 v# Y% q! Y5 teven 15 minutes of direct skin contact with their male& h4 M$ E' b" c  H
partners.6 However, when a shirt covered the applica-
- H# V( Q' ], C! y5 x5 otion site, this testosterone transfer was prevented.
3 C# v0 N* }  x4 R0 }Our patient’s testosterone level was 60 ng/mL,
0 t2 O& v* G  U! R  Zwhich was clearly high. Some studies suggest that- q' K" z+ D% o8 |+ P  M. x
dermal conversion of testosterone to dihydrotestos-& Z1 g' k( X6 N( L0 l7 c, e1 O
terone, which is a more potent metabolite, is more
) r. o# u! p7 |: _active in young children exposed to testosterone' D5 W! Y  |- ]* l' k5 r6 d
exogenously7; however, we did not measure a dihy-/ q( D8 Z, Z+ q% s+ j* r" [5 y9 k
drotestosterone level in our patient. In addition to# M2 l( a1 B8 L
virilization, exposure to exogenous testosterone in
* o, U1 j% A: s& f: G& Bchildren results in an increase in growth velocity and2 A/ i# f. u* b9 h! `2 D- ?" c
advanced bone age, as seen in our patient.
5 m  d! p: D8 I. p- S  ~The long-term effect of androgen exposure during0 d  v" ~1 b1 I
early childhood on pubertal development and final
5 o! V8 h' K, xadult height are not fully known and always remain
/ z: u4 O* g2 ]- x; E8 fa concern. Children treated with short-term testos-' l, d: r0 w6 j, X$ u# I0 z, n, u
terone injection or topical androgen may exhibit some* v, g- a4 L% J* d2 x) O+ C% a6 n1 }
acceleration of the skeletal maturation; however, after+ M1 ^8 h$ w9 N; A' m* m, X* w) {
cessation of treatment, the rate of bone maturation- l. q7 N3 Z. e& l
decelerates and gradually returns to normal.8,9
$ S8 ?& v# i3 A* {* AThere are conflicting reports and controversy6 S6 k/ Y( Z$ ~: f8 t  u& }
over the effect of early androgen exposure on adult7 P6 q; l/ I& e& s" _4 n
penile length.10,11 Some reports suggest subnormal5 A" M) E* b. @
adult penile length, apparently because of downreg-
) q+ e" U- d+ r1 sulation of androgen receptor number.10,12 However,( d6 n1 l) _. V9 J
Sutherland et al13 did not find a correlation between
$ [; ^) c* R- f: xchildhood testosterone exposure and reduced adult7 y' a  T; c. @
penile length in clinical studies.
! ?2 |1 y; z7 C7 hNonetheless, we do not believe our patient is; l3 I- }4 v+ F( v: l2 m
going to experience any of the untoward effects from
; r+ @7 t9 R4 z# Btestosterone exposure as mentioned earlier because
7 K, K! C; k# m! dthe exposure was not for a prolonged period of time.
7 ~4 H5 }/ Q1 x) X4 rAlthough the bone age was advanced at the time of" E9 |, k! S8 L# G, p* i! n' `
diagnosis, the child had a normal growth velocity at
  K/ U* x% \7 e% tthe follow-up visit. It is hoped that his final adult
% [4 a0 z5 S  B' n" N6 |height will not be affected.. ?& q+ C1 L* J) p" j- w$ d
Although rarely reported, the widespread avail-
! o( x6 a3 u7 b& E2 v0 O# bability of androgen products in our society may; y! \! L# |0 N2 R" l8 H
indeed cause more virilization in male or female
7 l0 E2 O, \0 o* ochildren than one would realize. Exposure to andro-
" {5 G/ P$ B  \( v0 Ogen products must be considered and specific ques-
, A1 y- D$ |  e6 gtioning about the use of a testosterone product or
: H/ f& P% K+ v; f6 ogel should be asked of the family members during
  ^4 F* Q+ q9 {% ?2 J! \- [the evaluation of any children who present with vir-
2 a" h& G# b# ^! Zilization or peripheral precocious puberty. The diag-8 p% {; p) W! O7 G
nosis can be established by just a few tests and by
; z) b6 [' M+ n1 c5 Y- M& I7 e; F% oappropriate history. The inability to obtain such a% j' U! j& b3 l. k
history, or failure to ask the specific questions, may
# ]1 L, f' u# Hresult in extensive, unnecessary, and expensive3 w" c* l( b, x$ c+ o9 s& ~
investigation. The primary care physician should be' E. a0 }1 ~3 ~/ x2 c3 g- w
aware of this fact, because most of these children. x% f( J  `+ n8 l8 `8 @$ M8 N4 U
may initially present in their practice. The Physicians’+ S4 x% p: E7 \
Desk Reference and package insert should also put a: C# \5 |0 Y) K9 t! g
warning about the virilizing effect on a male or- Y. c8 L+ ?* E7 `7 |- C
female child who might come in contact with some-4 u/ g* J9 _" a2 a2 N
one using any of these products.# U: S) K9 Q9 g1 }
References
: s! B0 f' w: m7 U6 w1 r1. Styne DM. The testes: disorder of sexual differentiation
% d) C+ O' Q0 W2 B3 W' {and puberty in the male. In: Sperling MA, ed. Pediatric
' ^) Q0 Q! I. E) R, c# f& s, yEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
& \+ H2 q& L( p% T2002: 565-628.) J/ V" O& P& }& i
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious4 i0 G1 z9 ?$ w6 b& J' k  R
puberty 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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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

. S; t9 c4 B: w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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