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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
( p6 U3 M+ M0 a! VBoy Induced by Indirect Topical
# Z7 i: |# i& {$ [4 O# S4 O3 g& ~Exposure to Testosterone
: f7 Y& Z4 g! o4 j/ `6 c7 d. wSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
7 k0 B7 p. V: f( B% h: S. oand Kenneth R. Rettig, MD1, ?, U/ e3 y- d2 x% l- a0 B
Clinical Pediatrics
) i+ x7 Z! d% m( uVolume 46 Number 6- I: L4 J7 p7 W/ Q
July 2007 540-5435 m& v6 M3 L( _; j  B: I; [
© 2007 Sage Publications6 ^: y7 q: }: w0 W
10.1177/0009922806296651
( ~; Q! b. }. }6 n# Vhttp://clp.sagepub.com& z6 Q, L: S8 s9 [& E. K7 m
hosted at. |  P5 n! ]; Z- c$ t. Q* a1 l3 C# ~) q
http://online.sagepub.com
$ e: b; s7 l& bPrecocious puberty in boys, central or peripheral,# g* Z: \$ l3 d( Z. m
is a significant concern for physicians. Central
4 K% I+ V* p, z" H6 ?precocious puberty (CPP), which is mediated; l6 I# k! P- i
through the hypothalamic pituitary gonadal axis, has
9 ^- k6 I  t' E9 c: s; Pa higher incidence of organic central nervous system
# k9 i- _! B$ a" o# Vlesions in boys.1,2 Virilization in boys, as manifested. f7 b9 N- O) B* ^2 f) r
by enlargement of the penis, development of pubic* k3 e5 D: X2 w( W  c
hair, and facial acne without enlargement of testi-( h9 {! W2 I! h- h- I
cles, suggests peripheral or pseudopuberty.1-3 We; r& ^* Y3 H- n  d3 u
report a 16-month-old boy who presented with the
% P/ R7 m2 A: _2 i; p) h7 i( A" A3 Venlargement of the phallus and pubic hair develop-6 T- v# ?: ^8 w& j* T4 y- E
ment without testicular enlargement, which was due
2 h" |2 e5 `, {to the unintentional exposure to androgen gel used by
, r% v; w- M, e, b8 Q7 \8 mthe father. The family initially concealed this infor-. i, z' N) Z, k0 T/ `8 s
mation, resulting in an extensive work-up for this$ Z; O4 H  d1 j
child. Given the widespread and easy availability of: x0 U. e3 P$ {$ H( X/ ], g8 I0 ?
testosterone gel and cream, we believe this is proba-
$ ]4 H! \8 H6 |6 W/ {bly more common than the rare case report in the  y5 w3 G' k& D' u$ z, R6 Q% o
literature.4+ @5 n3 L6 \' B! h6 Y/ Z) J
Patient Report
  q) F: e+ s9 o3 G$ G( zA 16-month-old white child was referred to the
. a" K% [& j5 x+ v' Mendocrine clinic by his pediatrician with the concern
- k! O: R6 d) pof early sexual development. His mother noticed
  g9 u; `4 Z: m6 rlight colored pubic hair development when he was
: P8 ?6 l. }, i: Q. @$ [! Z/ jFrom the 1Division of Pediatric Endocrinology, 2University of
  L. o5 L  b0 N2 r8 m+ d: g$ zSouth Alabama Medical Center, Mobile, Alabama.7 y4 }( Z& J* G$ p% E! h! \( z
Address correspondence to: Samar K. Bhowmick, MD, FACE,, G; T6 Q, O- l
Professor of Pediatrics, University of South Alabama, College of' m1 q6 i3 r" m2 h
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
8 B5 }- N8 D, C5 me-mail: [email protected].7 r0 A. {' \2 T$ j
about 6 to 7 months old, which progressively became
7 x& P5 |0 B5 Pdarker. She was also concerned about the enlarge-
3 A. E) h& U1 U  m2 ?( T2 W* b4 m8 s( f% T3 \ment of his penis and frequent erections. The child
3 D' O& d  }' P; S+ k0 \was the product of a full-term normal delivery, with6 c5 v$ _9 J7 I0 g9 q
a birth weight of 7 lb 14 oz, and birth length of& A3 [( l  L9 H
20 inches. He was breast-fed throughout the first year6 N! c- ^1 b+ Q: z
of life and was still receiving breast milk along with
/ G  _, b# B  S5 i9 a! T0 Lsolid food. He had no hospitalizations or surgery,
; Q9 R  \1 h2 Pand his psychosocial and psychomotor development
! `- R. q/ ^6 h2 n3 p1 L( Lwas age appropriate.. g: R- R' t& z8 G" u) F. k5 Z8 G
The family history was remarkable for the father,# @% J. s& z7 M" \2 G) `+ i: x" N
who was diagnosed with hypothyroidism at age 16,
, {8 c7 Q6 w- c6 c6 e/ B( P6 Qwhich was treated with thyroxine. The father’s; s- H7 |, U' T8 ?2 E8 i* {
height was 6 feet, and he went through a somewhat7 j: c) b+ t. l( Z4 }
early puberty and had stopped growing by age 14.9 N2 a  X1 a2 U
The father denied taking any other medication. The
2 h: @. M  m& L; x  t! pchild’s mother was in good health. Her menarche, d. u5 ]6 ]. a) `9 f
was at 11 years of age, and her height was at 5 feet; A% T7 _4 M( S# q$ D
5 inches. There was no other family history of pre-0 b- `, D' x/ E
cocious sexual development in the first-degree rela-, @0 m6 U6 [' W! J! W% }: ?/ d
tives. There were no siblings.' {) R5 F/ a/ g/ t: y7 e
Physical Examination: g5 A7 [) }$ d1 `! T
The physical examination revealed a very active,
- v5 O6 j: e7 ]+ g" H+ O, s: zplayful, and healthy boy. The vital signs documented
. [% D( J; `* Y+ o! ]  Ka blood pressure of 85/50 mm Hg, his length was
) P/ S2 l" ]8 ~5 z  e( X90 cm (>97th percentile), and his weight was 14.4 kg& R  c; ^% U2 D3 J
(also >97th percentile). The observed yearly growth( y7 R$ [. ?. W, a/ L
velocity was 30 cm (12 inches). The examination of; y+ f( W8 r- a
the neck revealed no thyroid enlargement.
6 ?1 |3 q7 r/ mThe genitourinary examination was remarkable for8 d: ]# ?2 @+ D8 m7 S4 t$ P
enlargement of the penis, with a stretched length of
/ ^  m5 E8 I* }0 @+ _8 cm and a width of 2 cm. The glans penis was very well
/ i: }  k+ O& `developed. The pubic hair was Tanner II, mostly around
, v% ~- x( H$ V2 H540, T* I- U, {8 p: [4 g( ]
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from$ F8 m% D2 Q5 n# ^+ Q
the base of the phallus and was dark and curled. The
! H8 p9 f% b/ A" U. ptesticular volume was prepubertal at 2 mL each.+ k! v4 J& {8 ~; n
The skin was moist and smooth and somewhat7 L. y0 W9 E, U% ^1 H& O* _# Z
oily. No axillary hair was noted. There were no7 C4 _7 u: b4 t2 O8 i6 L% N, Y
abnormal skin pigmentations or café-au-lait spots.$ Q6 v* [$ Q. w" r/ j
Neurologic evaluation showed deep tendon reflex 2+$ V+ t; _2 _3 Q( k2 o$ u
bilateral and symmetrical. There was no suggestion  c1 \: U+ @+ C4 ^5 {' x  ]
of papilledema.+ B5 L  Y7 D7 Q
Laboratory Evaluation
0 D2 ?1 e3 D0 {) V" ~The bone age was consistent with 28 months by' M$ B$ x) p) [' G) N
using the standard of Greulich and Pyle at a chrono-+ V; Z# Y0 C: u3 q1 g$ F: \3 V* r3 L
logic age of 16 months (advanced).5 Chromosomal
  E! a7 k- d3 ]1 _2 d5 l) rkaryotype was 46XY. The thyroid function test
. r9 e/ p0 W6 w3 z+ |" Qshowed a free T4 of 1.69 ng/dL, and thyroid stimu-, Z3 F7 C7 K+ l9 C
lating hormone level was 1.3 µIU/mL (both normal).
  y( _/ H% f2 z! _The concentrations of serum electrolytes, blood
! q) v- v) E2 z) eurea nitrogen, creatinine, and calcium all were& T* x& w/ J+ l5 N
within normal range for his age. The concentration$ _$ H. B6 w9 [8 P! h
of serum 17-hydroxyprogesterone was 16 ng/dL
: G* `$ W/ `: u: e$ E3 C; b(normal, 3 to 90 ng/dL), androstenedione was 20
' C' G  F4 L. hng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
5 Y! m2 y+ M" Q' Uterone was 38 ng/dL (normal, 50 to 760 ng/dL),* O0 P% g# @* m
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
  ]0 [3 \. Y, l) I- K49ng/dL), 11-desoxycortisol (specific compound S)+ P/ {1 m& n! q- I2 c
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
8 r  l6 u7 B# V7 W) v5 {/ `  _& wtisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
5 v3 G/ w$ T3 ]: P3 ltestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
8 Y" S; i1 n2 x% h. S0 g+ qand β-human chorionic gonadotropin was less than- c) I: s, u3 ?: s0 x
5 mIU/mL (normal <5 mIU/mL). Serum follicular; H7 F2 w' y* H& }9 V( F* g
stimulating hormone and leuteinizing hormone2 K6 R! B" v2 k
concentrations were less than 0.05 mIU/mL
2 j; D% E! S, ]# Z1 w(prepubertal).
7 G% b/ F. H4 [) }The parents were notified about the laboratory, L% T2 G0 ]4 o& b5 i# B5 T
results and were informed that all of the tests were
/ V# w2 [$ E. a7 mnormal except the testosterone level was high. The9 I( }* l, p9 p% `& R4 N  \- _. H4 m
follow-up visit was arranged within a few weeks to7 e1 \5 `& M+ l2 z8 q
obtain testicular and abdominal sonograms; how-# @& j: t8 w1 w/ F. ?
ever, the family did not return for 4 months.
/ j- x% ?# V4 PPhysical examination at this time revealed that the
) m; ?8 `* E, w7 lchild had grown 2.5 cm in 4 months and had gained
" U# l% L! {: ?2 kg of weight. Physical examination remained
3 P& `* i& t, j1 j8 g' v* t; b' ]3 xunchanged. Surprisingly, the pubic hair almost com-
, s# @" \  t* W( Z0 L4 |: r8 m: Opletely disappeared except for a few vellous hairs at
7 d2 l9 h" x4 nthe base of the phallus. Testicular volume was still 2
- o. S, L+ [0 L  I; \/ dmL, and the size of the penis remained unchanged.
( T" f1 t+ [4 WThe mother also said that the boy was no longer hav-
3 q1 R: T& b/ ?- ?ing frequent erections.
: K  C; ]0 M9 s( a1 n6 m! m, FBoth parents were again questioned about use of
1 k9 A( T% W. ?3 a7 `any ointment/creams that they may have applied to
7 L2 S% {' k( a) g/ q  t$ N! ethe child’s skin. This time the father admitted the) H; q& s7 v* I" \3 p. [
Topical Testosterone Exposure / Bhowmick et al 541+ T' H( Y% H' u% O/ V
use of testosterone gel twice daily that he was apply-
3 o$ Z$ r3 s8 Aing over his own shoulders, chest, and back area for. F* Y  X! q- A0 F8 x
a year. The father also revealed he was embarrassed
- g/ I: q, `. U/ P  P; D5 l; Qto disclose that he was using a testosterone gel pre-
$ r2 P( |7 ^& e0 T; zscribed by his family physician for decreased libido
/ g4 Z% P+ l4 Bsecondary to depression.+ o8 S+ n4 ]6 W/ r
The child slept in the same bed with parents.
! w$ d: k% W/ b% [# l. TThe father would hug the baby and hold him on his
% w) U5 ~: U0 ?6 Qchest for a considerable period of time, causing sig-  p' }7 y: x. r* {1 |
nificant bare skin contact between baby and father.; N( _( R) a- t; t$ b
The father also admitted that after the phone call,
3 l1 L# S: F, B8 m) }4 c1 M! |when he learned the testosterone level in the baby
2 R, [! B& w5 o( ywas high, he then read the product information
% k: a1 t* u5 U8 C! c( xpacket and concluded that it was most likely the rea-4 n7 A  j2 W5 D! }8 b4 X* [; _
son for the child’s virilization. At that time, they
& {2 F- F/ _5 i, b1 _6 Qdecided to put the baby in a separate bed, and the
( c2 |- C8 R% c/ F, d- Wfather was not hugging him with bare skin and had2 p6 Y/ T  U, ]0 L# G
been using protective clothing. A repeat testosterone
1 Q. Q+ S  t8 ftest was ordered, but the family did not go to the9 o- x' s9 M* r' {7 V* x
laboratory to obtain the test.4 z: R" M9 F$ Z/ }1 ~( ?' q
Discussion
4 C1 h3 e' M+ |3 M' w# T1 sPrecocious puberty in boys is defined as secondary
% a. k) B  g) v- Z& l. vsexual development before 9 years of age.1,4
+ L8 e* D( s1 H+ fPrecocious puberty is termed as central (true) when
! m4 b% |+ z; c4 Z6 A3 q; g  M! dit is caused by the premature activation of hypo-# E$ k! f4 P5 c+ [
thalamic pituitary gonadal axis. CPP is more com-
8 a" [" ]% d- q$ }mon in girls than in boys.1,3 Most boys with CPP
. w1 E  O$ L: X' j4 j( H% \may have a central nervous system lesion that is
6 @4 }4 Y+ [3 d7 Nresponsible for the early activation of the hypothal-
' f! K! b; K3 N$ l' oamic pituitary gonadal axis.1-3 Thus, greater empha-1 n7 j; f% m$ x1 l! ?3 S+ `! G
sis has been given to neuroradiologic imaging in7 k; q) N( d, S* L
boys with precocious puberty. In addition to viril-$ o/ n7 \( |1 h3 R/ ]0 j" d
ization, the clinical hallmark of CPP is the symmet-' e' \9 b, S$ W" T
rical testicular growth secondary to stimulation by* Z: R1 z& V. d1 J% G/ w. K0 d
gonadotropins.1,3
: U0 Z7 F) s& v0 U7 }/ W, rGonadotropin-independent peripheral preco-
# i& p0 u" d; S7 b$ Lcious puberty in boys also results from inappropriate
& d4 k' f, Q6 t- ^5 nandrogenic stimulation from either endogenous or9 ~5 d! I  V5 k' N% z1 l
exogenous sources, nonpituitary gonadotropin stim-
% Y* i4 d3 x" ^) X- b! Xulation, and rare activating mutations.3 Virilizing
( k/ f, Z& F+ n' Hcongenital adrenal hyperplasia producing excessive
. ^, g$ W( O& g/ [1 Dadrenal androgens is a common cause of precocious- w+ D) `, ?- u7 B+ q
puberty in boys.3,4
+ O5 _9 b+ J% ^! m  Z0 gThe most common form of congenital adrenal
! x5 Z/ L+ Z+ ]' i8 ]hyperplasia is the 21-hydroxylase enzyme deficiency./ a! w( h" S* y0 y
The 11-β hydroxylase deficiency may also result in2 Q3 K- C3 \% C$ a+ C4 C  ~4 J% r
excessive adrenal androgen production, and rarely,
3 @) C% j$ [7 F+ Ian adrenal tumor may also cause adrenal androgen
8 l3 a% q) Y7 S  m4 `& F) I5 xexcess.1,3
; q+ C% D8 W" Hat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from2 i$ x. v6 x# G& e/ w/ F$ \
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007+ w3 r2 Y. |2 p$ |" H! Y
A unique entity of male-limited gonadotropin-, V" s0 G% H' E' Z+ z
independent precocious puberty, which is also known
7 E- ^  `3 P' }8 S. Tas testotoxicosis, may cause precocious puberty at a! n, N" T) J; ]
very young age. The physical findings in these boys" ^, V/ k, \. [
with this disorder are full pubertal development,
* {& L* J$ o+ Xincluding bilateral testicular growth, similar to boys4 z/ r. c" Q+ G  o
with CPP. The gonadotropin levels in this disorder
$ V4 D5 s* ]1 U4 l+ kare suppressed to prepubertal levels and do not show# V$ W( v8 T. L
pubertal response of gonadotropin after gonadotropin-8 h' N( j/ \  P2 e" L. o7 D6 U
releasing hormone stimulation. This is a sex-linked0 i5 H" ?+ ?! B
autosomal dominant disorder that affects only
9 U1 i! n* C9 C  H$ \males; therefore, other male members of the family
' D. a& v5 D  `5 V+ z- Cmay have similar precocious puberty.3$ Q8 N$ I: Z" ^8 I& @9 j$ K1 I
In our patient, physical examination was incon-& v. A4 y! I7 {* k5 O% h; O
sistent with true precocious puberty since his testi-
$ V: m( r) F* a, Z3 r* m9 H4 i  Fcles were prepubertal in size. However, testotoxicosis. p- {/ e4 z. s1 h
was in the differential diagnosis because his father
  M" G# C$ N* @started puberty somewhat early, and occasionally,9 Q$ `5 a0 Z5 P% S
testicular enlargement is not that evident in the& `( I- b& o; N
beginning of this process.1 In the absence of a neg-1 H4 D1 Z  J7 s$ X6 a' \% f# |
ative initial history of androgen exposure, our
: [9 l% k, e5 K; Tbiggest concern was virilizing adrenal hyperplasia,* v* {* m0 N7 L! {1 j) K
either 21-hydroxylase deficiency or 11-β hydroxylase
- h& Z% D& F# @$ c) Odeficiency. Those diagnoses were excluded by find-
+ u, e% F4 m# T* xing the normal level of adrenal steroids.
, ]! P# R, `5 o. X0 R- M( E9 XThe diagnosis of exogenous androgens was strongly3 x* N* d2 S. q5 M/ o6 l
suspected in a follow-up visit after 4 months because
' \" V4 P. b7 s. _% G3 i9 Qthe physical examination revealed the complete disap-7 `* D) e' S  a. I! G$ d( ]
pearance of pubic hair, normal growth velocity, and
- b$ P3 e6 W6 M$ R4 w. cdecreased erections. The father admitted using a testos-2 s( @5 A! A% J& \+ |' v
terone gel, which he concealed at first visit. He was( O! K: q7 G0 N
using it rather frequently, twice a day. The Physicians’
0 ~% u& h! v9 r0 R! fDesk Reference, or package insert of this product, gel or/ }+ V2 Q8 L( s! k% V
cream, cautions about dermal testosterone transfer to0 _$ M/ D: g* x: Y) I$ |# t( U) n+ a
unprotected females through direct skin exposure.  N' m+ x7 ?0 F8 P7 a) F2 I: t
Serum testosterone level was found to be 2 times the
5 j7 K9 C% t" P7 _baseline value in those females who were exposed to
2 d3 ^: z- `( t) v4 y. Deven 15 minutes of direct skin contact with their male, m8 U7 W! J3 @( M; Q, ]
partners.6 However, when a shirt covered the applica-( M! I9 u! @2 D
tion site, this testosterone transfer was prevented.
" {( }# q- ?6 k+ h. ?, kOur patient’s testosterone level was 60 ng/mL,* E4 i  R( i" f4 u. n
which was clearly high. Some studies suggest that2 E  b+ R5 k! ^3 L+ r
dermal conversion of testosterone to dihydrotestos-
: f8 w: g; Q# d" Rterone, which is a more potent metabolite, is more# E# M1 }2 K: u  ?% N+ {+ m( a
active in young children exposed to testosterone" f* {6 j0 I! `: \% I6 S+ R  G& f
exogenously7; however, we did not measure a dihy-- ]  _* a7 i& Z, ~
drotestosterone level in our patient. In addition to' [. i0 A9 X- ~& T+ G
virilization, exposure to exogenous testosterone in
# I1 z3 G7 e8 Ochildren results in an increase in growth velocity and% W# t/ W1 k2 [' `, W
advanced bone age, as seen in our patient.
; D* ^$ u* j- O" b7 T$ f3 A( xThe long-term effect of androgen exposure during
( e9 Q9 ]+ I( M2 o& eearly childhood on pubertal development and final
; B' \6 M3 X9 qadult height are not fully known and always remain9 ?. D  N' E, H* p# X! i
a concern. Children treated with short-term testos-
) P5 i# b& P' Wterone injection or topical androgen may exhibit some
0 Y3 X: `' `: D8 X  B) hacceleration of the skeletal maturation; however, after( \  l; D, U* h7 y3 s8 @9 h
cessation of treatment, the rate of bone maturation
+ u2 f) _6 Z  |decelerates and gradually returns to normal.8,97 i7 _9 x( f& L
There are conflicting reports and controversy( v- N3 n9 v, E4 l6 K
over the effect of early androgen exposure on adult; S% W7 R$ n/ y8 i! B: d
penile length.10,11 Some reports suggest subnormal+ L$ k; f# J! V; O0 M
adult penile length, apparently because of downreg-5 K6 _9 Z7 ~2 Y
ulation of androgen receptor number.10,12 However,; S2 L# H# Z. O) D# [9 K) j2 `2 g7 ?' R
Sutherland et al13 did not find a correlation between
+ ]6 p5 M- W5 D/ D# Tchildhood testosterone exposure and reduced adult" H/ B" R0 p7 p9 c
penile length in clinical studies.0 ?  L0 @. S! l4 z6 F! g- E( \
Nonetheless, we do not believe our patient is
/ c) B$ X: u* ], R3 igoing to experience any of the untoward effects from2 A3 q3 h% R( ~8 g+ Q) }+ a' B
testosterone exposure as mentioned earlier because
+ j& a# r7 y! dthe exposure was not for a prolonged period of time.  K" z- J- G8 ?
Although the bone age was advanced at the time of
% s, C! N" S$ R$ h3 p0 H3 D( k4 _0 Odiagnosis, the child had a normal growth velocity at
8 m. c% r1 D" J) d+ pthe follow-up visit. It is hoped that his final adult* z2 B& m2 F7 ^/ Q, F& c
height will not be affected." O& v. e9 h% V  k$ X
Although rarely reported, the widespread avail-
% Q6 `, o8 x+ cability of androgen products in our society may
' I. E: t- [: }indeed cause more virilization in male or female
8 k6 k5 E0 W- Y) t1 B3 Jchildren than one would realize. Exposure to andro-' ~- D6 Y" ]$ ]; {
gen products must be considered and specific ques-0 D" q# q& n5 c, _& A& A& y
tioning about the use of a testosterone product or
+ C1 {. `3 Y4 B; Fgel should be asked of the family members during
) K: B6 g0 X6 ^( t$ wthe evaluation of any children who present with vir-
5 A6 c$ E! s, D+ Dilization or peripheral precocious puberty. The diag-
7 A$ C* m7 h6 ^1 P9 b& f3 A% @nosis can be established by just a few tests and by
/ H+ V- @( ?% K; D, t, gappropriate history. The inability to obtain such a
5 r4 H: W8 ^3 F$ h" N& dhistory, or failure to ask the specific questions, may& j0 [1 D+ L" {# [8 l
result in extensive, unnecessary, and expensive
6 [' Y& Z; H- U% B$ D( W0 Xinvestigation. The primary care physician should be& @' I: W0 O6 D9 `8 k* {8 u9 r, ^, Y
aware of this fact, because most of these children
1 \+ P' ]6 N2 m& l' ]# Q7 G8 |& |may initially present in their practice. The Physicians’- U- C" _6 r$ T* M; ?
Desk Reference and package insert should also put a
7 C( M% a1 ]; S" R1 T; U$ S* Uwarning about the virilizing effect on a male or0 S. }9 T6 i- W) N( F8 A+ }3 N: F. e
female child who might come in contact with some-
" H/ E" c! }; Uone using any of these products.: L3 e3 @7 P6 G
References) |7 x  H' L9 O2 Z4 i6 W6 u$ X
1. Styne DM. The testes: disorder of sexual differentiation
6 W- ^9 c# Y% t/ e2 Q3 _8 kand puberty in the male. In: Sperling MA, ed. Pediatric
8 n5 j. P, v! i! z8 ?/ FEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;7 [: ?" i; s4 |0 _& ~9 |
2002: 565-628.6 R4 d+ g; l7 x5 {4 U7 |9 E
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious, N5 {7 ?# p/ t
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
$ W/ x/ X4 n4 s5 J* D" i2 T) @Boy Induced by Indirect Topical
) Z+ F  {" @) T  p% nExposure to Testosterone
3 ]+ R! w. C& U5 JSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
2 L+ Y" M; |  x6 j- g# x8 zand Kenneth R. Rettig, MD1: d1 z7 b$ X  e( Q/ z* `
Clinical Pediatrics* U; t4 N$ E) {2 L6 o/ n" ~
Volume 46 Number 6
2 \" E% V+ r. h/ m0 Z; g* ^) y6 g# SJuly 2007 540-543
0 G' x9 |& @( J# r  M( w# y© 2007 Sage Publications
, n9 V! w+ y% Y/ ]4 {10.1177/0009922806296651
( J; _; S$ V/ a1 h0 J7 D/ i" c- q# a5 ]http://clp.sagepub.com
: r: `4 I9 v! X) B% \3 \5 P: ?6 ehosted at9 }3 m7 H: M6 K' v: v2 i$ e, r& ~
http://online.sagepub.com& C- l& {1 g# H# s/ J- q1 p
Precocious puberty in boys, central or peripheral,
* m, o. ]' g% `* g  w5 yis a significant concern for physicians. Central
& k" H" W! Q' j6 s8 U- o7 Eprecocious puberty (CPP), which is mediated2 P- f, j0 w; d; w/ f  v' ?
through the hypothalamic pituitary gonadal axis, has7 a# v4 v9 R  T7 x3 u! G' X/ @8 J
a higher incidence of organic central nervous system8 i% o  a8 o. `
lesions in boys.1,2 Virilization in boys, as manifested# N' \2 f, a+ c8 {' G/ j5 S  K. A: A
by enlargement of the penis, development of pubic2 b1 G; p8 r( A  v1 i
hair, and facial acne without enlargement of testi-
$ i5 u: D6 ?. Pcles, suggests peripheral or pseudopuberty.1-3 We6 A1 T; m6 }: E1 p7 |/ `  D7 C
report a 16-month-old boy who presented with the4 r; _! u: y( M" N5 L
enlargement of the phallus and pubic hair develop-
" f6 {# N8 X3 M7 u8 h, Zment without testicular enlargement, which was due& j$ c+ F8 u" y$ I: j
to the unintentional exposure to androgen gel used by
1 L3 d+ v( {/ K  |( xthe father. The family initially concealed this infor-: @' G# a  t( ]
mation, resulting in an extensive work-up for this
" a; i5 x# ^. O% ~; i" n3 [+ Hchild. Given the widespread and easy availability of, Y0 m# e5 n3 [; n
testosterone gel and cream, we believe this is proba-
' `' M& v# H7 E7 c& b, Ybly more common than the rare case report in the: S; K, M" _# I3 W4 S0 K9 B
literature.4
8 e; f# J& p. s( f5 O0 aPatient Report( p+ i2 T5 y4 C: d3 ]# z4 X
A 16-month-old white child was referred to the
3 W# ?# P! h. bendocrine clinic by his pediatrician with the concern0 v: T) d; N+ N4 H( u
of early sexual development. His mother noticed
) {9 ~7 C4 k1 S# tlight colored pubic hair development when he was6 c% D3 a$ G$ f; p! z& Y
From the 1Division of Pediatric Endocrinology, 2University of8 m+ {, b$ `1 O  v. j: {
South Alabama Medical Center, Mobile, Alabama.
3 q9 O* \$ `3 q% l9 V3 S# J7 c( {) _Address correspondence to: Samar K. Bhowmick, MD, FACE,8 W7 E, T5 Q9 a3 E1 u. H
Professor of Pediatrics, University of South Alabama, College of
0 {& Q0 I0 q  Z9 w5 }, {! CMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
. d4 P2 v  p- w1 u& i+ f% i* p+ te-mail: [email protected].
0 j8 E4 k" x9 {3 Jabout 6 to 7 months old, which progressively became; G( F8 O: ?4 ^  b( `+ E9 Q* z
darker. She was also concerned about the enlarge-
' T& W, R* e% N1 U, ?# ?ment of his penis and frequent erections. The child$ O  ]4 v( R1 Q- g! L
was the product of a full-term normal delivery, with
/ v( H5 _+ `5 k# ^$ ^a birth weight of 7 lb 14 oz, and birth length of) U' a0 p5 r( V$ z  Z5 Y/ H
20 inches. He was breast-fed throughout the first year
# t8 S' S0 V! S8 P9 O8 yof life and was still receiving breast milk along with+ K3 M8 u. }& F7 Q% `4 S2 K% \
solid food. He had no hospitalizations or surgery,
  R0 r' K3 y6 w6 r' k$ J: eand his psychosocial and psychomotor development
7 E' W' P! N& L4 T' @was age appropriate.& J7 D- q6 A6 m& ]0 Z' \
The family history was remarkable for the father,
, G. J* @7 T1 L, _/ Fwho was diagnosed with hypothyroidism at age 16,
" S' P. s3 a0 S+ ^which was treated with thyroxine. The father’s5 P  Q0 u/ e: X5 O4 G( H; P
height was 6 feet, and he went through a somewhat$ d* i8 h0 g# q  y$ m1 ]& W
early puberty and had stopped growing by age 14.  E0 i% a: R+ M' D  y# l
The father denied taking any other medication. The# _" j0 I4 j  w: F# C- Y' W
child’s mother was in good health. Her menarche! y; z; W- o: Z
was at 11 years of age, and her height was at 5 feet
. m& \& Y# |/ L7 q+ U" E5 inches. There was no other family history of pre-
; D% O: u: x. }( [/ A! ?7 acocious sexual development in the first-degree rela-. ~2 ?& Y* v* H
tives. There were no siblings.( g% x6 E& ^3 B7 I& g* H: ^
Physical Examination* g& I3 w% d2 Q! Q
The physical examination revealed a very active,
) V4 ~! f6 J# G$ Q% {$ y7 [6 pplayful, and healthy boy. The vital signs documented
! ^* H* K* [. b. ^8 D, Ba blood pressure of 85/50 mm Hg, his length was" e. H: |8 m8 p" ~, w' h; `# D2 A5 r
90 cm (>97th percentile), and his weight was 14.4 kg
3 t! {4 x# N, F4 E/ u(also >97th percentile). The observed yearly growth
4 y7 A# @8 H0 _velocity was 30 cm (12 inches). The examination of
* W8 H$ N7 O( K3 ]the neck revealed no thyroid enlargement.4 @: J$ H4 X$ z% v' q! I' K* T
The genitourinary examination was remarkable for# P# c' n- M/ d/ c
enlargement of the penis, with a stretched length of
/ m$ c4 O$ C! Z0 Q; ?3 |( @8 cm and a width of 2 cm. The glans penis was very well
5 I1 U& S* A4 Q% t' pdeveloped. The pubic hair was Tanner II, mostly around
; {$ A% d3 D9 I2 W$ d4 a0 b) r/ L- `: K540
( L: ?) c: g& D  W$ Iat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from' u2 F8 v5 e2 h! }3 e9 t: H3 \
the base of the phallus and was dark and curled. The$ E3 w3 n9 _6 s2 j9 g" z" N
testicular volume was prepubertal at 2 mL each.
5 k" A! k1 ?* i+ |/ n  zThe skin was moist and smooth and somewhat, q9 H* y. e0 d) g% O7 I9 e
oily. No axillary hair was noted. There were no. S# Q3 u( }/ d2 q
abnormal skin pigmentations or café-au-lait spots.5 J6 K9 O# m# [! G+ x  E1 P5 L$ T0 W
Neurologic evaluation showed deep tendon reflex 2+
  X7 Z& V! }- R6 \3 Vbilateral and symmetrical. There was no suggestion! v) g+ Z2 K# ~5 ~
of papilledema.
5 X9 F: d# R. }" R- tLaboratory Evaluation
  c7 c' \* Z3 c9 \2 wThe bone age was consistent with 28 months by
. N- S6 v4 F& A+ H  z4 f% q" x4 G+ Ausing the standard of Greulich and Pyle at a chrono-
% z4 g1 A  }' a$ J' Glogic age of 16 months (advanced).5 Chromosomal" S7 {$ ^* E3 i) O
karyotype was 46XY. The thyroid function test
1 i5 i5 W; z& @) D( K1 J% b8 eshowed a free T4 of 1.69 ng/dL, and thyroid stimu-* _- L! A; y5 L# j5 J& _4 Y
lating hormone level was 1.3 µIU/mL (both normal).1 @7 l5 \( y! l- \( V
The concentrations of serum electrolytes, blood7 N. f/ p% v' a( B6 d
urea nitrogen, creatinine, and calcium all were! |& m- h+ ?6 L$ U6 V* Z$ g" L
within normal range for his age. The concentration* c; ^: [6 x6 k4 a8 V; Z# s
of serum 17-hydroxyprogesterone was 16 ng/dL
% _! R9 x# ]) p% i) [& V: [(normal, 3 to 90 ng/dL), androstenedione was 203 L7 R1 L7 m$ X+ U# u# ]
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
/ G. y( l) Z+ pterone was 38 ng/dL (normal, 50 to 760 ng/dL),3 |1 T' i! g+ Q$ I1 q
desoxycorticosterone was 4.3 ng/dL (normal, 7 to: n0 {. \" K! N1 b3 ]; b/ x
49ng/dL), 11-desoxycortisol (specific compound S)0 {3 f# F( B2 R& I) R8 [% p5 j, R
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-& E1 L, v' U* r& a4 O1 i
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total; r" ?  _( A" r3 v
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),3 \0 }* y; J& c& x" t( A6 k2 G
and β-human chorionic gonadotropin was less than" W' H# r+ l) v# Y7 M
5 mIU/mL (normal <5 mIU/mL). Serum follicular
6 N+ R* j' X& f, @- I" J9 Wstimulating hormone and leuteinizing hormone
4 q6 C' n) i6 v5 A6 p9 zconcentrations were less than 0.05 mIU/mL# {* C: I# N2 {" O& }3 v- D
(prepubertal).+ R/ d8 Z/ g% ]$ ^% ^
The parents were notified about the laboratory: W' s4 _- ?8 N, b$ C+ Z, g" x
results and were informed that all of the tests were7 G" m) q- k& u" H; ]
normal except the testosterone level was high. The- q" t. {* u: y' D
follow-up visit was arranged within a few weeks to) t/ [% h! C' B% ~0 r
obtain testicular and abdominal sonograms; how-
0 w6 x4 ]3 q" w# @0 never, the family did not return for 4 months.
3 L- x% G  k/ K4 n- N$ `. R/ JPhysical examination at this time revealed that the
: S' w& ?6 n$ ]; r. l+ F2 l7 r$ Rchild had grown 2.5 cm in 4 months and had gained
6 W! R9 q3 ?8 d0 w! L0 c0 q/ z2 kg of weight. Physical examination remained0 Q# z6 _% C/ j
unchanged. Surprisingly, the pubic hair almost com-0 g0 e$ O  {; N
pletely disappeared except for a few vellous hairs at
& o- p* \9 ?* _# P# q& kthe base of the phallus. Testicular volume was still 2" }* F4 s% ^. |9 A" B. @3 Z
mL, and the size of the penis remained unchanged.7 H, y. `2 h( T* u; k
The mother also said that the boy was no longer hav-) H- a% v0 W5 g* X% |# W0 f4 [: m
ing frequent erections.
) [( T: @' c7 s* G) mBoth parents were again questioned about use of
( i0 j" a4 c: l. D# _8 T& C5 Xany ointment/creams that they may have applied to3 V0 ^4 z: ?. x, u
the child’s skin. This time the father admitted the" x7 N: p) J  h+ C3 y1 B
Topical Testosterone Exposure / Bhowmick et al 541
/ ^8 y  j7 R3 S, ^" h% v1 h: ]- Suse of testosterone gel twice daily that he was apply-
. Q) ]" E; r4 k. X/ X; ying over his own shoulders, chest, and back area for
/ \1 f# Q5 j7 t) A) Sa year. The father also revealed he was embarrassed) U6 V- ~7 x/ ^& s9 d
to disclose that he was using a testosterone gel pre-- A# V5 H( U) D7 \  U8 Q
scribed by his family physician for decreased libido
" V: H3 t, j5 _9 E/ c/ _9 `; Wsecondary to depression.
% U: C$ R2 W, v8 ~The child slept in the same bed with parents.4 n5 J1 B- D3 D0 Q0 x
The father would hug the baby and hold him on his+ d; P/ D4 u- C# l: l) T
chest for a considerable period of time, causing sig-
) J# K: ?- E5 `, ~nificant bare skin contact between baby and father.
9 a3 Y8 k' y1 C( z4 sThe father also admitted that after the phone call,6 L. f) V  ~! k/ f8 D- X
when he learned the testosterone level in the baby1 d4 Y3 ^+ p: p3 T
was high, he then read the product information
* }7 D- F: @- Y* i0 npacket and concluded that it was most likely the rea-3 w- V4 u; J% b1 h
son for the child’s virilization. At that time, they
, g# r: S4 ]  s1 zdecided to put the baby in a separate bed, and the
( e7 q1 B- R/ v7 }father was not hugging him with bare skin and had( i6 T3 G% y8 @2 x5 N0 Y
been using protective clothing. A repeat testosterone$ l( g: v3 \9 [1 u7 z5 W; J
test was ordered, but the family did not go to the
  d4 Y# s" g* Ilaboratory to obtain the test.
. ?+ G3 ^) |5 X- q' `5 qDiscussion+ K; h% `1 l8 Y% K% G+ K0 z7 R0 g
Precocious puberty in boys is defined as secondary
1 Z- w, c4 P! Z5 a8 Nsexual development before 9 years of age.1,4# z, d7 w" h5 l8 p. q! N
Precocious puberty is termed as central (true) when5 x  K3 ~0 |+ M8 d* W
it is caused by the premature activation of hypo-6 D% a) p- S" H3 j- S! U+ n
thalamic pituitary gonadal axis. CPP is more com-9 Y2 B5 `# h  [! Q
mon in girls than in boys.1,3 Most boys with CPP
5 X; f; j5 u9 W2 L) w3 mmay have a central nervous system lesion that is% y: A$ E8 s- v9 C6 v' v( \( U
responsible for the early activation of the hypothal-
: ?, L* F( [& _1 s3 \amic pituitary gonadal axis.1-3 Thus, greater empha-
6 r! P: z/ l! Qsis has been given to neuroradiologic imaging in
3 Q# \1 I- M! p) ]8 Y1 ~boys with precocious puberty. In addition to viril-# h, L, E7 K+ \7 j- b
ization, the clinical hallmark of CPP is the symmet-
3 t* `. h4 g( Drical testicular growth secondary to stimulation by
) k  c1 G" `# |3 Vgonadotropins.1,3' s( K: }3 Z; S! t& z8 [
Gonadotropin-independent peripheral preco-
, H+ t8 M3 B  x4 ccious puberty in boys also results from inappropriate
) \: F/ `- u) `androgenic stimulation from either endogenous or; l+ `1 n7 f/ h% w# {
exogenous sources, nonpituitary gonadotropin stim-( m; A) P6 K  M6 p( T7 T* y5 R6 r: N
ulation, and rare activating mutations.3 Virilizing, I! D$ ?) ~; m! D; i! k/ K' K
congenital adrenal hyperplasia producing excessive
* w. z% O4 V: v* c, W$ k, Cadrenal androgens is a common cause of precocious
0 D! o3 [* i: `5 n2 cpuberty in boys.3,4
. u( F8 u6 c- E$ t( yThe most common form of congenital adrenal
4 j6 W9 K% ]5 I# L5 lhyperplasia is the 21-hydroxylase enzyme deficiency.# H# t! ^( n! K% W2 W* b7 b$ G
The 11-β hydroxylase deficiency may also result in1 }) X( v. [! q  H1 S
excessive adrenal androgen production, and rarely,
' r' A: p9 u2 ~$ X6 \0 `an adrenal tumor may also cause adrenal androgen
7 U& s: j* K6 F+ K( k' _  wexcess.1,3) X, _! W; ^1 ^/ s/ H& d
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from( T2 i- c7 z$ t# X) Y
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
; e' \. r: R# {  aA unique entity of male-limited gonadotropin-9 }: H0 U2 ^# r
independent precocious puberty, which is also known- P) [. [4 _8 e. K) j8 g- g8 Q
as testotoxicosis, may cause precocious puberty at a
1 @* ?0 f; }/ X% q1 z, Pvery young age. The physical findings in these boys
* I% J: q+ e  I- Q) dwith this disorder are full pubertal development,5 G% K# G; p. t( t' e
including bilateral testicular growth, similar to boys8 ]8 U3 v( ?  K: l' x
with CPP. The gonadotropin levels in this disorder! v: V8 b  F3 f0 G+ F2 T9 I! a6 Z) J
are suppressed to prepubertal levels and do not show
7 x3 Z- g& {0 {1 H% ~5 }6 Ypubertal response of gonadotropin after gonadotropin-8 b  ~, K) I$ Q% P+ r
releasing hormone stimulation. This is a sex-linked
/ m' M8 ^8 h7 a, H1 _7 lautosomal dominant disorder that affects only
& I4 s9 W; z4 D3 Amales; therefore, other male members of the family  @4 j; H: I4 [- I7 i7 F
may have similar precocious puberty.3" T% Y# U' ?/ f( Z. u8 d
In our patient, physical examination was incon-5 T7 ~7 }; B# V6 s# ]
sistent with true precocious puberty since his testi-
& f$ P1 n* P# P+ xcles were prepubertal in size. However, testotoxicosis
3 `8 x. I) v- f* _was in the differential diagnosis because his father
9 ]4 }' C! u  |started puberty somewhat early, and occasionally,8 O8 n) T  I, B/ E+ a
testicular enlargement is not that evident in the
, w' F) L* h3 V$ d' cbeginning of this process.1 In the absence of a neg-
! [) Z# F! A+ v. H+ @+ g1 x. V  Tative initial history of androgen exposure, our
$ }, x! ^, _1 P' f5 ebiggest concern was virilizing adrenal hyperplasia,3 q+ R# Q3 e4 e& _# I$ N
either 21-hydroxylase deficiency or 11-β hydroxylase
: K, o( K2 t+ A2 B( p% ]deficiency. Those diagnoses were excluded by find-
8 j' c" _% Z! I6 O; {; Sing the normal level of adrenal steroids." k* \7 ^0 N3 H9 d1 n- w  u! b
The diagnosis of exogenous androgens was strongly
0 ^' Q0 U8 Z* ^suspected in a follow-up visit after 4 months because( ~% f/ K" n0 D& |
the physical examination revealed the complete disap-; |; L& D+ c  \3 W& c/ Z
pearance of pubic hair, normal growth velocity, and! c& }4 q3 k  S" a
decreased erections. The father admitted using a testos-4 r9 G) [2 x7 [, ?7 \: |
terone gel, which he concealed at first visit. He was* p5 G/ g7 Q. r- ]% ]
using it rather frequently, twice a day. The Physicians’
' O. j7 ~  Q  f5 xDesk Reference, or package insert of this product, gel or
: K" x9 I- {( B- o6 ccream, cautions about dermal testosterone transfer to
$ Z/ B2 ^0 M$ {! M4 cunprotected females through direct skin exposure.
- {( \! U$ [4 i, s  b- J+ TSerum testosterone level was found to be 2 times the
/ d6 _5 M% D0 J- B' v# t, L: w: W5 sbaseline value in those females who were exposed to5 D& M1 R2 V  J5 W- }: h
even 15 minutes of direct skin contact with their male
' m/ p. ]6 O% `5 ppartners.6 However, when a shirt covered the applica-
# \; C$ H1 V5 ?* Ution site, this testosterone transfer was prevented.
& T" q8 m; L- i- H3 ~Our patient’s testosterone level was 60 ng/mL,
  q  e  X/ r( [7 |; Twhich was clearly high. Some studies suggest that
, G% P# ~! }1 O# u# D+ ^0 Wdermal conversion of testosterone to dihydrotestos-
' Q& P7 e  o/ Q% y/ a/ Nterone, which is a more potent metabolite, is more
" X% |) H4 E% ^! v9 ]* m$ Pactive in young children exposed to testosterone
0 Y- P) G! |1 P) ~, @: W) M4 ~exogenously7; however, we did not measure a dihy-7 x1 N, r& Q, ?( N5 {
drotestosterone level in our patient. In addition to* A3 Q+ g- b' M
virilization, exposure to exogenous testosterone in
2 I1 c3 d' Y, z6 b. wchildren results in an increase in growth velocity and
7 }9 _' h6 h% n% n3 S  Madvanced bone age, as seen in our patient.1 Y6 z9 E2 d4 `- x8 m2 v' O/ _7 U
The long-term effect of androgen exposure during" G. \% Q$ U, r; v: {, [
early childhood on pubertal development and final! Y7 C# ]- Y  b4 B+ P
adult height are not fully known and always remain
7 K! Y! a# x, Q+ A* _3 p; Da concern. Children treated with short-term testos-* L! v  y; }$ n0 C
terone injection or topical androgen may exhibit some1 \9 }0 I% ~6 W$ M5 p: O; n
acceleration of the skeletal maturation; however, after
/ O$ V9 K7 s& r3 b6 M: s& zcessation of treatment, the rate of bone maturation4 d3 t1 v2 Y/ o1 T( Q( f
decelerates and gradually returns to normal.8,9
+ r0 g/ S, j/ U0 {There are conflicting reports and controversy
  J$ z" E- F0 |: p3 Q- a% M, \over the effect of early androgen exposure on adult6 P2 z3 B. u; z9 a+ X4 i- f) M
penile length.10,11 Some reports suggest subnormal2 K! q- V. v( v; k0 R/ a/ X* J. c6 F
adult penile length, apparently because of downreg-4 T/ l! @8 X2 D, q7 S( Z
ulation of androgen receptor number.10,12 However,
$ J/ ?1 ^  p- F2 r& P4 ?& j5 tSutherland et al13 did not find a correlation between
( ^- y) u9 k% M7 ?childhood testosterone exposure and reduced adult6 L5 w0 i1 l! B. X% h! q
penile length in clinical studies.
, W  o9 |2 v. @& `& ^Nonetheless, we do not believe our patient is
, j+ U9 S% y6 S( {5 l" P) P1 ^4 Agoing to experience any of the untoward effects from( D" l9 X2 A* ]. t/ i4 S  u
testosterone exposure as mentioned earlier because- Z! [% M0 q# F4 G+ Q
the exposure was not for a prolonged period of time.
. `& K3 I8 O# V6 d3 Q  W' o' OAlthough the bone age was advanced at the time of0 ^- w0 n& V+ l
diagnosis, the child had a normal growth velocity at
) Z8 U9 i$ P0 n1 m5 P; R2 y" Wthe follow-up visit. It is hoped that his final adult. `& z; o9 T7 o; Q) W
height will not be affected.$ Q  H0 J8 O" ~3 o
Although rarely reported, the widespread avail-
8 B9 l! [" v% ~: B8 y! Rability of androgen products in our society may! B! @2 ~  F3 O# j/ D0 a
indeed cause more virilization in male or female5 ~5 k8 K) n) j& ^
children than one would realize. Exposure to andro-; a, d' ]9 q; v' Y
gen products must be considered and specific ques-
3 ?/ I+ n) C) {8 D; ^# u3 g, Ftioning about the use of a testosterone product or
8 k( |  d; v# Egel should be asked of the family members during
( `2 W) A& c/ y& [2 z1 a, K+ j* Othe evaluation of any children who present with vir-% Y- l6 |7 t# e0 ?
ilization or peripheral precocious puberty. The diag-3 d& V1 H3 \' a9 U
nosis can be established by just a few tests and by2 ~; R$ @& l9 H) }5 S4 p' V+ `
appropriate history. The inability to obtain such a
- f" X. D/ V. ~! B2 Ehistory, or failure to ask the specific questions, may" ]% ]1 f, O. T7 T) V
result in extensive, unnecessary, and expensive) N. q! ^3 _; [7 X
investigation. The primary care physician should be
* N% e3 x# X4 [% A; Paware of this fact, because most of these children! S1 r. ]$ h6 b# ^1 ?2 h4 u: ^+ f3 L
may initially present in their practice. The Physicians’
" F6 ?! S! D% |4 z% @Desk Reference and package insert should also put a
  [! y) U- P( n* J  Ewarning about the virilizing effect on a male or* P0 j: E# ]3 F! f! z6 m) Z. M, J
female child who might come in contact with some-" Z' q$ V$ e" q' |& [
one using any of these products.
9 a; r( c! u  {9 j7 }7 C) H4 KReferences# N$ g. p; X0 I/ V4 T, w$ e
1. Styne DM. The testes: disorder of sexual differentiation) z0 A5 s' ]$ ^1 o
and puberty in the male. In: Sperling MA, ed. Pediatric
3 K6 R! B9 g" `Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
4 u# N6 W5 ^! W1 V! @2002: 565-628.' }% L& T% y5 J8 M8 [3 `" ?, x; @
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious6 N2 y: p- j1 d4 Y' ]5 H/ y
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
VIP精品區,資源無限好賺金任務區,輕松賺金幣
加入VIP,享受高級特權宣傳賺金又升級,超級棒
4个什么样的?
發表於 2025-1-19 02:41:05 | 顯示全部樓層
/ B6 \( `( @7 S& D9 d' y) a) e
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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