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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 X# @% z0 h; O
Boy Induced by Indirect Topical; N; n' z' a& n0 G
Exposure to Testosterone4 [1 x( w. S* O) }" j
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,20 e) B+ o& N8 R! F6 H# ]4 l
and Kenneth R. Rettig, MD19 j% F! Q" l3 C2 |( M. r3 f
Clinical Pediatrics
% ]5 C- S# u% }. g  X1 B+ [. v$ m5 GVolume 46 Number 6. ?6 F: |* A9 u1 u0 Q9 s$ j
July 2007 540-543
5 _. o6 R  u1 H( \' [; I) w+ a; v© 2007 Sage Publications
6 B) e& M/ L! K* }10.1177/0009922806296651
/ V, D9 y- N6 l3 mhttp://clp.sagepub.com$ a1 Y3 ~7 C) J1 ~' f
hosted at; s/ o) M$ L8 r3 N, s2 W# d
http://online.sagepub.com: W' ?) `! s5 b/ H3 `, i
Precocious puberty in boys, central or peripheral,- W; U3 l  W7 G
is a significant concern for physicians. Central- r' {* i( ~% X; G, H
precocious puberty (CPP), which is mediated1 w2 q- d: ^( L8 l/ w5 c
through the hypothalamic pituitary gonadal axis, has
0 T# }9 n4 r3 J5 M0 a. t! f4 \; C- |a higher incidence of organic central nervous system
) d4 U! `7 T  ^lesions in boys.1,2 Virilization in boys, as manifested
% k* _* A/ ?* y( K* Uby enlargement of the penis, development of pubic3 z$ F5 {2 C% [
hair, and facial acne without enlargement of testi-; T: P- I7 Q4 h/ u+ `* d
cles, suggests peripheral or pseudopuberty.1-3 We- G3 Z& }" k: r0 e: m; X( `3 @
report a 16-month-old boy who presented with the
! Y/ R  T# ^4 {7 |% S, Menlargement of the phallus and pubic hair develop-
7 y2 ]8 N! T0 v0 ~$ A' Q5 }ment without testicular enlargement, which was due( h5 w2 h6 q% l; W+ v
to the unintentional exposure to androgen gel used by
- B  W- i8 A* I/ X; o/ R" s) _the father. The family initially concealed this infor-
' P  \: ~9 h+ q( Nmation, resulting in an extensive work-up for this
  j  x6 e: p; \* Mchild. Given the widespread and easy availability of
( p7 I  n3 b6 G, Gtestosterone gel and cream, we believe this is proba-/ ?) Z# ^( ^5 y$ n9 W
bly more common than the rare case report in the. y1 W- K3 [* D% a3 K9 C
literature.4
  E. g5 ^4 w; F) c/ c& U$ iPatient Report3 K( u& q' q& Q
A 16-month-old white child was referred to the
9 R  }$ A; Q  I7 ~endocrine clinic by his pediatrician with the concern
, P- Z6 o+ s6 V7 }) E4 a6 Lof early sexual development. His mother noticed+ s. \, u; l$ n
light colored pubic hair development when he was
, ~  F2 B+ S7 C! D1 ]From the 1Division of Pediatric Endocrinology, 2University of
; y+ [% M5 h8 Z2 BSouth Alabama Medical Center, Mobile, Alabama.
3 a: x( j2 j; n; ]& q& }6 @4 h" e3 VAddress correspondence to: Samar K. Bhowmick, MD, FACE,
- _: [$ l1 b1 R) z  f0 kProfessor of Pediatrics, University of South Alabama, College of, G/ h; Y0 j" F* e) M# {, g
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
1 N1 P8 k9 L8 ]e-mail: [email protected].
3 E! p. G9 a3 Dabout 6 to 7 months old, which progressively became8 ~2 s! q4 }6 U& ~  H9 k
darker. She was also concerned about the enlarge-
- q! @% }. y& i% gment of his penis and frequent erections. The child) F" T  A* q- L
was the product of a full-term normal delivery, with
" j7 N8 n8 {8 w  M! B( ^' J7 n3 {a birth weight of 7 lb 14 oz, and birth length of
! P2 \! N# @4 n20 inches. He was breast-fed throughout the first year$ C0 ?' g& N% \( X7 q/ m6 @
of life and was still receiving breast milk along with
4 E4 y0 H. O" Q, R* asolid food. He had no hospitalizations or surgery,) J5 ]" @" B1 w* R) C
and his psychosocial and psychomotor development
" W$ W6 x; ?- }& lwas age appropriate.9 l% E% V! S  S5 P% F
The family history was remarkable for the father,, Z% i) w- m& k9 k1 W, E
who was diagnosed with hypothyroidism at age 16,
- _& |( B8 v( d0 Q5 r6 owhich was treated with thyroxine. The father’s' y% Y: ?; T# e9 w. a' I$ H  s
height was 6 feet, and he went through a somewhat
- p! ^1 X2 X/ o$ d! iearly puberty and had stopped growing by age 14.; O3 p$ ?/ ?+ K1 `" P: W3 ^* F
The father denied taking any other medication. The
) k. r5 C* T2 \0 k+ y& S8 Pchild’s mother was in good health. Her menarche2 t" u, S' S( i7 k. o
was at 11 years of age, and her height was at 5 feet
2 w: M( ]- [3 S/ z5 inches. There was no other family history of pre-
! I* V* R% U' h4 j) z: I5 M8 \cocious sexual development in the first-degree rela-
/ x' \; k$ H$ c" ltives. There were no siblings.
$ Z4 @- i' h$ P4 VPhysical Examination. Z# H- s3 t; K1 ^
The physical examination revealed a very active,2 @8 X) w3 r$ @; o
playful, and healthy boy. The vital signs documented
4 L. w* c" }5 Q8 \a blood pressure of 85/50 mm Hg, his length was% L: D) Z- g3 W
90 cm (>97th percentile), and his weight was 14.4 kg& q. ~# J. o% ^. z- G- _) s
(also >97th percentile). The observed yearly growth' k+ N+ a" o; b
velocity was 30 cm (12 inches). The examination of: V+ W; p1 K/ Y" N/ P
the neck revealed no thyroid enlargement.
5 `% X/ W" |6 s( |4 w- y& _The genitourinary examination was remarkable for
! R5 J4 j6 A" m2 V) ?3 o1 L- ^enlargement of the penis, with a stretched length of
* s& j! k, ^! g: z9 `4 n& Y4 B8 cm and a width of 2 cm. The glans penis was very well' e  q0 j& t. ]0 O- n. W
developed. The pubic hair was Tanner II, mostly around- v. p6 m% i" U% y6 F# ^" N6 n/ d
540
7 m( G/ I( Q; M- H$ }at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from& Z( \2 ?: Z9 @& {2 v0 \) L8 m
the base of the phallus and was dark and curled. The
0 Q: H( k- _2 v( utesticular volume was prepubertal at 2 mL each.- ^1 h0 n- ]" V3 G* \
The skin was moist and smooth and somewhat4 r1 F4 F7 s: `
oily. No axillary hair was noted. There were no
# w# X3 [5 b# t& Z8 M+ W& jabnormal skin pigmentations or café-au-lait spots.- o" {2 a, P/ M) B
Neurologic evaluation showed deep tendon reflex 2+9 q& e6 z( f% F5 x- l
bilateral and symmetrical. There was no suggestion, b9 y- X% u) t, X/ P2 _2 W2 _
of papilledema.' ~9 |0 Q' C# `, `8 j# }4 ]1 A6 B
Laboratory Evaluation
) s" ^; t/ g$ @# ^- eThe bone age was consistent with 28 months by
- _  b1 v6 |6 Z, Gusing the standard of Greulich and Pyle at a chrono-% F5 ?& K% f; y7 K7 M
logic age of 16 months (advanced).5 Chromosomal) F, [2 u1 N' f$ W4 C8 V
karyotype was 46XY. The thyroid function test! q3 Z5 X; h2 L% o6 v0 d8 a$ [
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
( Z" ], s) U5 Mlating hormone level was 1.3 µIU/mL (both normal).% `' i1 e6 I6 i, }) u1 N
The concentrations of serum electrolytes, blood# C) m- |$ @' n+ S
urea nitrogen, creatinine, and calcium all were( L3 ]' p/ p7 o; l# w
within normal range for his age. The concentration. e9 b6 ~4 e3 |0 N
of serum 17-hydroxyprogesterone was 16 ng/dL
9 C, j, L6 d) t, X- C(normal, 3 to 90 ng/dL), androstenedione was 203 h% M; W" }7 }/ B
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-) j- m, d& h, P% T" Q, [# |* z
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
! Q2 R& l8 |: \( [  Pdesoxycorticosterone was 4.3 ng/dL (normal, 7 to, @/ O( b4 p: {' _: e9 h
49ng/dL), 11-desoxycortisol (specific compound S)
* c, \* J5 `* y' v4 [" ewas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-( E) K' l1 ?8 M* T  @9 b
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total4 W( B. l8 ~5 D0 M- U% Z
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),0 o/ b; _- A7 D( P" L6 x3 v& U
and β-human chorionic gonadotropin was less than: N; \2 |  l' B0 ?" Y( I8 `( C+ C
5 mIU/mL (normal <5 mIU/mL). Serum follicular$ f9 ?) m7 r7 ]
stimulating hormone and leuteinizing hormone
) y4 g3 X6 g5 l/ w/ H* v& Z, m$ Nconcentrations were less than 0.05 mIU/mL
; H7 B% t* v/ f" \3 }4 l7 y(prepubertal).6 w2 ?5 |: B, B4 r7 Z7 P! [
The parents were notified about the laboratory! l; q) F' y2 C6 p
results and were informed that all of the tests were
7 c' ]# ~& {# q* \normal except the testosterone level was high. The& H+ R5 X8 A; P  j- r; l! R+ ~
follow-up visit was arranged within a few weeks to
. l( G$ o% Z7 }8 x/ V$ J% pobtain testicular and abdominal sonograms; how-
0 o# Q- q( ?( N/ p: s" e8 R; Wever, the family did not return for 4 months.
9 U3 t- f- m8 H7 V1 jPhysical examination at this time revealed that the  Q! i  m# m& ?$ t9 ~; N
child had grown 2.5 cm in 4 months and had gained) H" H6 I& {7 M9 ]' E
2 kg of weight. Physical examination remained& U9 n0 X8 l& e) G& p% i
unchanged. Surprisingly, the pubic hair almost com-
# b" g$ a3 m& x. E# a7 [1 U! \* ?pletely disappeared except for a few vellous hairs at6 y  x3 k8 U  x3 ]
the base of the phallus. Testicular volume was still 29 l5 q! A' w. G2 j5 F
mL, and the size of the penis remained unchanged.
2 t1 M4 W( s/ f' ]2 \The mother also said that the boy was no longer hav-4 s6 v) J  q5 S- y0 N
ing frequent erections.
" k% j/ X& H  j7 p! mBoth parents were again questioned about use of8 p8 v5 h4 m* @( g8 Q7 q
any ointment/creams that they may have applied to& F" c: t, g" k; @
the child’s skin. This time the father admitted the0 E( Y+ s% r5 Q1 @, U
Topical Testosterone Exposure / Bhowmick et al 541
0 s  [* M7 [2 @( X/ w& e! i* Ouse of testosterone gel twice daily that he was apply-2 s5 Z" k% c. t- X: \1 a2 K
ing over his own shoulders, chest, and back area for8 {* `. O7 Y5 Z; Y( G' g
a year. The father also revealed he was embarrassed
) }& C! y. ]0 Q* x6 r6 xto disclose that he was using a testosterone gel pre-" e) N2 ]2 t+ h
scribed by his family physician for decreased libido, i2 r: |$ y! ]# J. o1 n
secondary to depression.
. D( ]4 Q  V4 E& k: r6 @9 tThe child slept in the same bed with parents.
3 ]3 k; n# p5 z" R% K2 w8 pThe father would hug the baby and hold him on his
$ d2 D8 U0 D( I0 f( O1 lchest for a considerable period of time, causing sig-
! r  O* w( V6 V4 g% a) [- Rnificant bare skin contact between baby and father.
( q- H# U4 h8 e+ EThe father also admitted that after the phone call,* ^# F! j% }4 ?% y% b/ l" T2 j
when he learned the testosterone level in the baby0 A4 o& F: W8 i2 G
was high, he then read the product information
1 y! l* F5 N3 Q2 Jpacket and concluded that it was most likely the rea-
! q0 d2 c( ~. |son for the child’s virilization. At that time, they8 G0 C& R0 ^( p5 u
decided to put the baby in a separate bed, and the+ l+ F7 w7 j) ?3 i9 N* d
father was not hugging him with bare skin and had* o0 w$ y4 y( U- l6 F* j9 w
been using protective clothing. A repeat testosterone
% n6 Y7 D+ l: |/ R( R: mtest was ordered, but the family did not go to the7 U7 O* }( @$ Y& Y9 s7 D4 q+ W
laboratory to obtain the test.
6 ]) a2 T5 m. \& D2 _% s: f8 Z5 JDiscussion
& t6 J# F  C) I+ e" APrecocious puberty in boys is defined as secondary5 _, S) k' o; T" g% G. `' b4 C
sexual development before 9 years of age.1,4) n4 [9 v; h( \
Precocious puberty is termed as central (true) when  o  U2 M0 n0 A. N! r; F6 u
it is caused by the premature activation of hypo-
+ ]( X. v: [) _thalamic pituitary gonadal axis. CPP is more com-
" X7 y6 L% r0 t7 qmon in girls than in boys.1,3 Most boys with CPP! @# L! w1 v. C/ p
may have a central nervous system lesion that is( G5 o0 E' i0 N& b: h3 x
responsible for the early activation of the hypothal-
9 ^5 q  G- s$ `amic pituitary gonadal axis.1-3 Thus, greater empha-: c5 C# T) z/ x/ y
sis has been given to neuroradiologic imaging in
3 y8 [* u3 \6 N* N+ g. |& j9 Q( Vboys with precocious puberty. In addition to viril-4 b" L) w" ?" |: b3 d
ization, the clinical hallmark of CPP is the symmet-
" p; Y+ g0 T+ I4 S1 s1 F# M; ^rical testicular growth secondary to stimulation by
8 v0 _- U" M" a/ vgonadotropins.1,3
! Z: _5 A9 P2 u7 w5 |3 w# p, UGonadotropin-independent peripheral preco-
  b# B) s% B( O; y* scious puberty in boys also results from inappropriate
1 c) p( u" D7 F. m  x+ Q$ \" c1 Iandrogenic stimulation from either endogenous or2 h, P: u; [( @2 F( c6 B" J
exogenous sources, nonpituitary gonadotropin stim-
$ A) Z& q( w0 S8 a( culation, and rare activating mutations.3 Virilizing5 Y8 q: n/ H' p. s# D+ _6 s. d$ _
congenital adrenal hyperplasia producing excessive% y0 g5 f! L& r7 o: H  o
adrenal androgens is a common cause of precocious
1 w6 E: a8 L; Q5 F6 D( i/ O& [puberty in boys.3,4) a9 q7 [1 g* ^4 S% h" l: z: p1 d# S
The most common form of congenital adrenal) _6 c2 e/ U) C  H' m
hyperplasia is the 21-hydroxylase enzyme deficiency.' ^: H- g0 W$ w7 E" m
The 11-β hydroxylase deficiency may also result in. D, w% s0 ?4 G7 r! ]  E
excessive adrenal androgen production, and rarely," h2 c- A1 e4 P" _
an adrenal tumor may also cause adrenal androgen
+ P" X" g, m' x* X. S' jexcess.1,3, U1 @; X% ]: v& G% ]8 H
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from  r! n& t( }/ C% N3 Q) e# z
542 Clinical Pediatrics / Vol. 46, No. 6, July 20078 Z9 o  N. D1 r0 g* l/ l9 r
A unique entity of male-limited gonadotropin-* J: }& g3 R7 G- Z0 _$ j8 o6 H
independent precocious puberty, which is also known0 E' j+ W+ ^" w( e, J$ O  u* }( ?% \
as testotoxicosis, may cause precocious puberty at a
$ E$ J8 a! o. Bvery young age. The physical findings in these boys
. q* T+ A5 r/ Y, G$ jwith this disorder are full pubertal development,* Y8 d5 C. T2 L. Y9 p8 V8 b0 x
including bilateral testicular growth, similar to boys
/ w& I- ~4 S3 @. K7 R! Mwith CPP. The gonadotropin levels in this disorder, o7 p% S/ A  l8 q# G
are suppressed to prepubertal levels and do not show# O* F) q0 ]. U
pubertal response of gonadotropin after gonadotropin-
' P0 r  A' |3 g/ f+ Y1 j8 Lreleasing hormone stimulation. This is a sex-linked& J+ m" s' [" s
autosomal dominant disorder that affects only
) n& u% R0 Y) F- B6 [2 V( l- ]males; therefore, other male members of the family) S3 O& r' {& d* }; f) w. @9 W
may have similar precocious puberty.3# j) R0 R% x  r
In our patient, physical examination was incon-- F! E& T4 y3 ~' v5 P& w
sistent with true precocious puberty since his testi-
- ^0 O) v" X3 e; ]: F' \( Gcles were prepubertal in size. However, testotoxicosis0 T1 o  @2 l- M  g! n. s3 O
was in the differential diagnosis because his father
. n/ }- k' ~4 c1 mstarted puberty somewhat early, and occasionally,$ G0 K2 [5 q5 x* v" v* ^
testicular enlargement is not that evident in the
; P( Z: c& G, L7 \beginning of this process.1 In the absence of a neg-
/ s  g  r0 G1 q  rative initial history of androgen exposure, our; m3 }5 x" h" X0 u& ^
biggest concern was virilizing adrenal hyperplasia,6 C+ [! ~  u, U
either 21-hydroxylase deficiency or 11-β hydroxylase
9 U: }  W) e* w' vdeficiency. Those diagnoses were excluded by find-& r- a6 }% t$ N' r; E
ing the normal level of adrenal steroids., b5 r% n2 Z. k0 e2 T
The diagnosis of exogenous androgens was strongly& X2 \% Y/ A! p; v$ V
suspected in a follow-up visit after 4 months because' D# K7 p- |! e& @" n
the physical examination revealed the complete disap-
+ y4 G8 F9 }4 g4 O* O1 zpearance of pubic hair, normal growth velocity, and
/ {, I  i3 }" a# {) `5 T" x9 i  ydecreased erections. The father admitted using a testos-
( B5 s0 o2 s0 ?% O* j) {1 Jterone gel, which he concealed at first visit. He was3 J$ t3 r4 C: {! f# v7 _% B
using it rather frequently, twice a day. The Physicians’0 }: Q2 K; u# d) U
Desk Reference, or package insert of this product, gel or6 D8 F, M  |) U$ n
cream, cautions about dermal testosterone transfer to
8 r8 y& T& D* Y2 E, o8 v: S3 Vunprotected females through direct skin exposure.
, e' Q; a( O3 F/ `- uSerum testosterone level was found to be 2 times the2 D6 X, Z- g! Q$ J2 f) t, L
baseline value in those females who were exposed to/ J1 T! G( T, C
even 15 minutes of direct skin contact with their male
) H0 J: J9 R) o, B" N  cpartners.6 However, when a shirt covered the applica-
2 i: c/ U* L: q. y* s' Dtion site, this testosterone transfer was prevented./ q+ _6 T. m. _3 h
Our patient’s testosterone level was 60 ng/mL,/ x) q. l) f6 ~$ ]6 K; h
which was clearly high. Some studies suggest that% y1 [# N, q( W; M+ M$ M
dermal conversion of testosterone to dihydrotestos-
8 t, D6 ]- O3 n3 K; j0 Kterone, which is a more potent metabolite, is more
# y; s0 {0 k/ ~7 W* bactive in young children exposed to testosterone
$ p2 e4 d/ r# Pexogenously7; however, we did not measure a dihy-: y. w) C, m3 D  x7 ~( m: e% g
drotestosterone level in our patient. In addition to
, _1 t# e. O0 t* S$ T9 V3 Avirilization, exposure to exogenous testosterone in
, t- @( Z' S# B6 Rchildren results in an increase in growth velocity and% u0 S& d; a  E& W$ w/ H$ A$ d
advanced bone age, as seen in our patient.
1 Y* R9 k5 O0 F; NThe long-term effect of androgen exposure during! y: D" B; f) ~( F9 S9 Q& R1 Z
early childhood on pubertal development and final
" H1 h: h3 v6 G' Uadult height are not fully known and always remain
& c8 D) d7 t8 o8 Z& e  ia concern. Children treated with short-term testos-& u# P' @$ `, P$ b5 H0 F. _
terone injection or topical androgen may exhibit some/ @3 |3 z  K+ p
acceleration of the skeletal maturation; however, after: r5 d" R) z1 {2 q* J/ y! g6 Q
cessation of treatment, the rate of bone maturation9 t' S1 j/ l  U5 v: G7 p
decelerates and gradually returns to normal.8,9
3 r: S; ^# K: S1 B7 }' xThere are conflicting reports and controversy* m4 R& c6 D7 O: j4 k% R
over the effect of early androgen exposure on adult# h4 ?) }+ a" Y* T
penile length.10,11 Some reports suggest subnormal" V, C* i# {9 m5 v* s- j" N6 q
adult penile length, apparently because of downreg-
) B! {/ f& i+ `ulation of androgen receptor number.10,12 However,7 Y0 J" `, `8 O! C# B7 f7 g' n
Sutherland et al13 did not find a correlation between
2 o+ d0 r3 x! Q1 ~. z: s, f$ x; \childhood testosterone exposure and reduced adult
* {: r& [5 b+ K4 g& jpenile length in clinical studies.$ L' e$ Q3 `7 i* O$ y+ @2 Z( ^
Nonetheless, we do not believe our patient is. ~$ ], J5 ]* `: @' V0 s8 i
going to experience any of the untoward effects from' u0 M6 E5 K! ~; h" O/ @3 F% Z
testosterone exposure as mentioned earlier because
/ L/ K# V- {6 n" L0 ]- F9 othe exposure was not for a prolonged period of time.% H% k( _. u! d
Although the bone age was advanced at the time of
3 A% }' L8 x$ \diagnosis, the child had a normal growth velocity at5 N; k+ R! K6 y+ @+ A0 |  ]. \
the follow-up visit. It is hoped that his final adult% {. x/ Z  I3 ~6 N3 N1 G1 ?. G
height will not be affected.3 z& L9 l9 y6 H6 k9 `1 d
Although rarely reported, the widespread avail-7 g$ j! Y8 W- K1 ~
ability of androgen products in our society may
# H# L) l- C9 U$ ?7 j! S* C! dindeed cause more virilization in male or female1 y$ K  a7 ~* }1 z* w% }  M
children than one would realize. Exposure to andro-! y3 u. T3 Z: Z5 f
gen products must be considered and specific ques-' C. ^% O7 c6 v& ]) e, B
tioning about the use of a testosterone product or
5 s4 V% ]9 L- o. r+ Bgel should be asked of the family members during4 Q& I1 s3 M9 W) k
the evaluation of any children who present with vir-
1 f) p; f3 z& K" k% J/ d. p/ j1 E, yilization or peripheral precocious puberty. The diag-
, P; \! W: ?+ K. J' ?! unosis can be established by just a few tests and by
# `, J6 o) Z. B8 Nappropriate history. The inability to obtain such a
; Y# P0 P) ^9 W( F% \history, or failure to ask the specific questions, may
& S1 K$ w* l) Z7 z. bresult in extensive, unnecessary, and expensive
/ J" l5 L5 b+ `3 h: Finvestigation. The primary care physician should be
" B, c) @0 p+ j8 y0 s0 }, Oaware of this fact, because most of these children
- o1 N! }9 l  W* vmay initially present in their practice. The Physicians’
: n4 A1 y: [) S  tDesk Reference and package insert should also put a
3 K6 N$ B7 e7 E; Z! E/ w) D0 ?4 J0 wwarning about the virilizing effect on a male or. j! g+ T! {1 K& v% m+ h) R
female child who might come in contact with some-) r: R1 o4 {; f6 e
one using any of these products., l+ r/ J3 h9 E! Z" K5 e- D
References4 C: p5 }3 B# ?, y- L6 t/ o
1. Styne DM. The testes: disorder of sexual differentiation
; q1 Y( c, |4 L0 J! w. J) N$ {and puberty in the male. In: Sperling MA, ed. Pediatric3 {: ?# I+ n5 [  B  d! n) A3 b' m) D
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;3 B" x% p. h5 j( [' f4 O% P- [6 D
2002: 565-628.% ^* i$ G" C; C& l
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious$ ^/ B2 e9 r7 x
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
8 p0 s# u0 ?* f  M* qBoy Induced by Indirect Topical
) `5 B, z- t, v$ z  w" ]Exposure to Testosterone
4 S1 }; P) Y4 s3 KSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2: d$ Q9 A' |% ]2 R7 R" D
and Kenneth R. Rettig, MD1
) N8 W* f+ x! k& B2 vClinical Pediatrics
8 X, s3 z7 U, S+ dVolume 46 Number 6
5 Z1 h7 ?2 {7 W, @2 p) R4 jJuly 2007 540-543
. J. H, p4 {7 p- j/ M  J2 C© 2007 Sage Publications) ^; y1 B/ _5 F) n# g. _
10.1177/0009922806296651
! D$ D' z$ S" |% phttp://clp.sagepub.com
" I" X. a( f* a* p6 u5 Ohosted at& j% a" ~. ^2 j( I# z7 R0 k/ S, w
http://online.sagepub.com
# P* n- d- @. W" IPrecocious puberty in boys, central or peripheral,1 \8 z% v. I. U1 _; B+ L1 w; q
is a significant concern for physicians. Central
# }2 Q0 O4 C% ?. H6 Oprecocious puberty (CPP), which is mediated$ [5 @- c0 x5 J9 x1 H6 {! {; h
through the hypothalamic pituitary gonadal axis, has
4 m. c! F8 J, L+ i0 ^a higher incidence of organic central nervous system$ M1 w9 q# o$ ]4 e, S" q. l0 l; r
lesions in boys.1,2 Virilization in boys, as manifested
- C" h& `& |" t& m0 G, A5 c" K# S# vby enlargement of the penis, development of pubic, p# `0 r0 K" v5 o7 e& o3 k0 l5 H
hair, and facial acne without enlargement of testi-( y# G1 U+ A5 F- i, ^" H
cles, suggests peripheral or pseudopuberty.1-3 We
) S, u% A4 c) i  v' treport a 16-month-old boy who presented with the
9 f0 l, L, X& X( lenlargement of the phallus and pubic hair develop-; j1 v/ |9 E- b
ment without testicular enlargement, which was due/ N- V6 d. ~7 o1 _5 o/ f( v- L) h
to the unintentional exposure to androgen gel used by
" q0 u0 u, C$ Y9 @( j& Uthe father. The family initially concealed this infor-- f! m) s+ s$ Y6 n! Y  K- k
mation, resulting in an extensive work-up for this
1 A# q% N8 X; i( p0 }6 p  G5 ~child. Given the widespread and easy availability of
/ k' G4 f0 a. G0 ]' z$ `: a5 Y/ Atestosterone gel and cream, we believe this is proba-0 w" ~- E% @# o2 i* d
bly more common than the rare case report in the. f7 z9 a, }8 ~( j
literature.4) v. `6 P# R0 S: F8 T# ^
Patient Report
* T7 i9 L: ?/ \/ NA 16-month-old white child was referred to the. J7 v; ^: ^" y
endocrine clinic by his pediatrician with the concern
$ J. k4 k9 S4 F+ j0 u& Hof early sexual development. His mother noticed" ?7 f7 {* l: f8 u6 `/ n
light colored pubic hair development when he was
. v. B* a) Q) B+ EFrom the 1Division of Pediatric Endocrinology, 2University of: D7 t1 G) I( k% I  Z! y
South Alabama Medical Center, Mobile, Alabama.$ G( b2 f8 N9 K5 f( i$ {# V: z6 i3 R
Address correspondence to: Samar K. Bhowmick, MD, FACE,
8 K4 u; _. ^# J4 b2 E. p% ~Professor of Pediatrics, University of South Alabama, College of
' G. t1 b5 ~, y2 M. q5 m: I7 o) V5 YMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;6 V6 K3 n" i( o  ?
e-mail: [email protected].
5 L* _( L) a3 _7 oabout 6 to 7 months old, which progressively became
% R! v* ]2 k  [7 C5 B; @. j4 Adarker. She was also concerned about the enlarge-
9 ^* h2 w4 o( ^2 X6 Dment of his penis and frequent erections. The child, [  z1 F7 F) z3 b9 h4 M
was the product of a full-term normal delivery, with& m' l. I+ q  ^4 {# P  u5 E
a birth weight of 7 lb 14 oz, and birth length of
8 D% P+ O& C# T, W! g% X0 e20 inches. He was breast-fed throughout the first year9 `8 l5 j) J- M
of life and was still receiving breast milk along with+ q4 A: N; N+ B7 z
solid food. He had no hospitalizations or surgery,
4 c6 m3 k! b/ M. Z" S) i; C, qand his psychosocial and psychomotor development
/ T( P6 A5 r8 K7 qwas age appropriate.
" l8 p. r4 O: M) V6 iThe family history was remarkable for the father,6 g, F8 d' x; r6 A+ i
who was diagnosed with hypothyroidism at age 16,( ^/ i$ F' ^% R( D$ @
which was treated with thyroxine. The father’s
  a5 W) l1 A! D% X6 J; pheight was 6 feet, and he went through a somewhat3 k: b0 K, f& I4 Q- P
early puberty and had stopped growing by age 14.# O5 L# N: C/ `8 e& Z1 a
The father denied taking any other medication. The6 L3 O, y, c1 X$ e0 C# q7 g
child’s mother was in good health. Her menarche
* b; a( O) w8 j% W, @: j" o# o9 swas at 11 years of age, and her height was at 5 feet
/ l- Z: G; x2 a4 M5 inches. There was no other family history of pre-2 \' ]: [+ d0 _# {5 b+ ], B7 h
cocious sexual development in the first-degree rela-" ^/ p' Q1 j. m5 u7 f
tives. There were no siblings.# Z; W; L3 m4 T3 Q
Physical Examination
+ j* S: }1 i4 P$ L- d( d) m  XThe physical examination revealed a very active,
& q4 c5 A  R4 x, gplayful, and healthy boy. The vital signs documented+ E: u: ^7 l  ]" r' d# N) {
a blood pressure of 85/50 mm Hg, his length was/ q# H. S1 r* A$ ^; M
90 cm (>97th percentile), and his weight was 14.4 kg* A% K. P' \" ~  l+ C; y3 T
(also >97th percentile). The observed yearly growth
; G. T+ \/ [' E; h6 @3 _9 Vvelocity was 30 cm (12 inches). The examination of( E/ B/ x6 x% r
the neck revealed no thyroid enlargement.. G- y' c! i' G$ X& a
The genitourinary examination was remarkable for/ g+ k# r" P- g. ]3 ?9 y5 ^( j: d
enlargement of the penis, with a stretched length of1 {! Q! }8 e* H! F
8 cm and a width of 2 cm. The glans penis was very well
7 P! ~! G  L0 |9 N  Wdeveloped. The pubic hair was Tanner II, mostly around+ M+ d, S: Y. f. n3 G6 h
540  j4 Q( J+ D7 r' ~
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from* j7 o# L" w* w. R# {
the base of the phallus and was dark and curled. The) e0 r/ _/ T: I. {" L( E
testicular volume was prepubertal at 2 mL each.. l8 G9 W. |6 t! d; _% W; J' z
The skin was moist and smooth and somewhat3 t& _- s! i8 f- L2 w8 b/ F
oily. No axillary hair was noted. There were no
. ^' x( k; e. `4 t( babnormal skin pigmentations or café-au-lait spots.
% A$ r' o! v0 j$ @) C) QNeurologic evaluation showed deep tendon reflex 2+1 v9 d9 I' U$ M1 p
bilateral and symmetrical. There was no suggestion8 K  y2 |$ R- j8 n
of papilledema.
) ]6 B7 E1 d- I- N. zLaboratory Evaluation
" t. p% X4 c$ ]( U: k  h6 ?* ^3 B  _) MThe bone age was consistent with 28 months by" D' |5 D& f- g8 U, c
using the standard of Greulich and Pyle at a chrono-
2 i1 ^$ s1 ?( Y# E( e, g% n* n& jlogic age of 16 months (advanced).5 Chromosomal) L8 `2 S' \, P, @' c
karyotype was 46XY. The thyroid function test
) }  U  \  |8 |+ e1 l# |% g# tshowed a free T4 of 1.69 ng/dL, and thyroid stimu-1 I' |- @: }0 S9 c/ r
lating hormone level was 1.3 µIU/mL (both normal).
# d1 w' ?, T; f9 tThe concentrations of serum electrolytes, blood
; j4 L$ s7 D* @: A5 g. vurea nitrogen, creatinine, and calcium all were! H6 e) e; G+ q% B
within normal range for his age. The concentration
8 Y  Z! n8 U/ Fof serum 17-hydroxyprogesterone was 16 ng/dL
4 q: h: J! a4 O8 ~( N% x% J(normal, 3 to 90 ng/dL), androstenedione was 20
* a# F, O$ g9 ^1 hng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
+ l% j9 G" k- h" `6 P! gterone was 38 ng/dL (normal, 50 to 760 ng/dL),3 X! s# K( G* S/ y; l
desoxycorticosterone was 4.3 ng/dL (normal, 7 to. M8 O: u, \! F# ~5 v# I
49ng/dL), 11-desoxycortisol (specific compound S)
0 W! y1 s! G5 M3 i/ p5 Pwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-+ r2 T5 J6 ~( U5 f! t
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total' ^+ j, A1 T" c
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
  I/ w. `, T& D/ Sand β-human chorionic gonadotropin was less than, U8 X0 r" d* m0 h* k
5 mIU/mL (normal <5 mIU/mL). Serum follicular! F; b1 ^# h' P# Z
stimulating hormone and leuteinizing hormone
* N6 n- c( p, S) zconcentrations were less than 0.05 mIU/mL, l) Q+ T% {7 R% S
(prepubertal).
% _- i+ m4 g% @0 u+ q- ~- E* ^The parents were notified about the laboratory
  A, C0 A/ K! h2 x1 v0 Fresults and were informed that all of the tests were' ]' X5 N/ L0 U( S3 Z/ `
normal except the testosterone level was high. The, C/ U" q( H- n; z$ q/ g
follow-up visit was arranged within a few weeks to* _7 }& o; I0 B0 z3 N) ?# e
obtain testicular and abdominal sonograms; how-) t' r1 `. B. M/ J3 w7 Q
ever, the family did not return for 4 months.7 w- P! j: n; J2 ~
Physical examination at this time revealed that the
+ O1 {) B0 k& s1 @child had grown 2.5 cm in 4 months and had gained' v- x/ }) A1 f# V4 O5 S
2 kg of weight. Physical examination remained
- K4 j$ d. I  Aunchanged. Surprisingly, the pubic hair almost com-
' V. l. e% z+ o" L# @pletely disappeared except for a few vellous hairs at
* T, }: ~9 g! y+ ]. M* r* F5 u; Kthe base of the phallus. Testicular volume was still 2, P; ^3 V; t) D/ |. s
mL, and the size of the penis remained unchanged.
  ^: g9 s# Y4 [/ @The mother also said that the boy was no longer hav-7 h. t8 }. T  a
ing frequent erections.
+ M0 @- T7 l& d, h1 r9 UBoth parents were again questioned about use of
4 X: ?# C& p) `* h  sany ointment/creams that they may have applied to" L4 o! ^4 I3 p# p& O
the child’s skin. This time the father admitted the2 {( _1 z- k/ i2 F0 W
Topical Testosterone Exposure / Bhowmick et al 541
: v! I) c; ?% O9 F9 p# y( ~0 muse of testosterone gel twice daily that he was apply-
" v& x' S/ E) |2 o7 X" H+ R$ xing over his own shoulders, chest, and back area for8 G  [6 U( l7 F9 J0 ?
a year. The father also revealed he was embarrassed" p$ y5 }/ o9 y; d3 c( ^
to disclose that he was using a testosterone gel pre-
# {) C1 [" ~' Lscribed by his family physician for decreased libido) ^, ?4 Q" F: q1 o" R
secondary to depression.
% ]% Q* l! z5 GThe child slept in the same bed with parents.' n# m1 u: U( W+ r: w
The father would hug the baby and hold him on his2 S9 r1 ]! \& M1 B' L' |, A! m
chest for a considerable period of time, causing sig-0 Q1 A8 U6 |6 R
nificant bare skin contact between baby and father.
/ {7 S. Z: k. y) o2 t  Y4 Y: n' ~5 @The father also admitted that after the phone call,
) o) ~! @( l7 `9 H$ U9 ~when he learned the testosterone level in the baby
; |2 N$ E4 o7 S  swas high, he then read the product information  x- |5 T0 G: @* S7 ]
packet and concluded that it was most likely the rea-
. V6 {9 K3 k2 {! y1 qson for the child’s virilization. At that time, they
) Z' a# h: y& I* g8 D+ @! xdecided to put the baby in a separate bed, and the
4 X! W5 t# J1 m/ Yfather was not hugging him with bare skin and had
. y0 H8 o( A4 J4 x# P, rbeen using protective clothing. A repeat testosterone
* g) r+ T8 E0 V" jtest was ordered, but the family did not go to the
0 |3 V9 w* ]/ P+ e& ]" zlaboratory to obtain the test.
' A: \+ t6 e9 L& tDiscussion
* [! T) t: v/ C6 X0 SPrecocious puberty in boys is defined as secondary8 G2 d8 x: ~+ d) _
sexual development before 9 years of age.1,45 T' a/ V  m- Q% T. p0 Q
Precocious puberty is termed as central (true) when
/ e" e# o0 |0 D: K# ]/ ^3 xit is caused by the premature activation of hypo-
1 }( o* }/ I. r" w9 o2 rthalamic pituitary gonadal axis. CPP is more com-
2 L3 O/ y7 W0 ?mon in girls than in boys.1,3 Most boys with CPP
4 P8 q. u4 k2 E  O7 nmay have a central nervous system lesion that is
! J) [' h1 `' T! E, S( j" sresponsible for the early activation of the hypothal-: q1 N- ^! X: Z7 |: p* D# I  D! _
amic pituitary gonadal axis.1-3 Thus, greater empha-
+ R% d2 h- l1 r7 O; u1 U4 nsis has been given to neuroradiologic imaging in. O# K: o! C# X7 d7 {3 A0 D/ f9 U
boys with precocious puberty. In addition to viril-
( B5 J' j) w/ z% ]ization, the clinical hallmark of CPP is the symmet-
% B9 ?8 y! H+ P3 h4 Y, |# ?" ~2 [8 Vrical testicular growth secondary to stimulation by& J% E9 [$ L0 [# `2 Z! z2 A; I
gonadotropins.1,3
6 Z% Q: B) L4 y/ h5 F# z! R4 n0 oGonadotropin-independent peripheral preco-
  a0 e9 K+ s9 j9 ?- Z6 T- e1 mcious puberty in boys also results from inappropriate; `& ~, [6 Z7 n- ~) C8 J3 _8 L
androgenic stimulation from either endogenous or* m! M9 ?4 j' a
exogenous sources, nonpituitary gonadotropin stim-4 s* B) G7 d- Y3 m: n+ Z
ulation, and rare activating mutations.3 Virilizing6 i! N6 H) J1 o2 @, i, t0 `
congenital adrenal hyperplasia producing excessive2 a2 H; Y: {% N/ R& J
adrenal androgens is a common cause of precocious3 ]! U3 l. u6 r% a
puberty in boys.3,4
( Q+ d2 h' t- V; s! FThe most common form of congenital adrenal
: i2 d. L4 p- ?: R% mhyperplasia is the 21-hydroxylase enzyme deficiency.
- S1 c& D+ O# T2 _" d" CThe 11-β hydroxylase deficiency may also result in& ?* B4 ~  x  P
excessive adrenal androgen production, and rarely,
; X+ T6 t) T; E' Pan adrenal tumor may also cause adrenal androgen
- Z% I6 c" ~5 m+ A4 v! |  F) pexcess.1,32 F* s. ~& G- b! V6 W) h/ @
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from! g# ^& ~7 [  F* |4 ^5 s
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
: j! l* k2 [4 \% L, x( L$ eA unique entity of male-limited gonadotropin-
! \  f' c. o. H3 lindependent precocious puberty, which is also known
8 {/ ]- S* N" tas testotoxicosis, may cause precocious puberty at a/ @) E/ y" v2 M# t8 j0 b0 h  N
very young age. The physical findings in these boys5 L  I9 X- C; y' T
with this disorder are full pubertal development,
- y( f! J6 B* y8 b. @: \including bilateral testicular growth, similar to boys" ^: ~3 G4 L( _; T3 T( m7 [
with CPP. The gonadotropin levels in this disorder
! l+ f* @% a0 M* Y: Z8 Q7 ~6 i( jare suppressed to prepubertal levels and do not show
8 e; u) U6 E0 {+ i1 D$ C3 W2 ]2 ~pubertal response of gonadotropin after gonadotropin-; `; z4 b/ E1 t7 o- ]9 |
releasing hormone stimulation. This is a sex-linked9 \' @; H/ g/ W
autosomal dominant disorder that affects only
# _, S; K) Y( R* M! x; E/ wmales; therefore, other male members of the family
* x. g) y  d' m! kmay have similar precocious puberty.3( `$ X) ~# ~" M1 B$ _% x; d( d7 i7 d
In our patient, physical examination was incon-
% q( {: `5 n' X9 lsistent with true precocious puberty since his testi-/ t+ J7 X& v: x1 r, A4 I* ]# ~* F' o
cles were prepubertal in size. However, testotoxicosis
, T+ t& I& }9 E% f5 G) ewas in the differential diagnosis because his father
0 Y, n' n* D$ b: V0 s2 F- H1 ?started puberty somewhat early, and occasionally,
# Q/ U1 |0 p2 R, R, e, u; Ctesticular enlargement is not that evident in the1 j4 F" G2 |6 y/ p$ C, Q
beginning of this process.1 In the absence of a neg-1 j/ Q- y( `2 w6 X. F) I& s; b
ative initial history of androgen exposure, our
  w0 j* a- c# C# S# P$ p5 Hbiggest concern was virilizing adrenal hyperplasia,- d6 A. y3 G/ Z+ m3 O: ^( h
either 21-hydroxylase deficiency or 11-β hydroxylase
5 D3 C6 i  k9 k0 Vdeficiency. Those diagnoses were excluded by find-
" }, `1 _  n3 H' V7 y( ming the normal level of adrenal steroids.
9 w* x' g0 {% y+ r5 f* KThe diagnosis of exogenous androgens was strongly
! r9 y% g0 X' R$ z% l- isuspected in a follow-up visit after 4 months because5 c9 u8 q# j* s0 {4 d3 g
the physical examination revealed the complete disap-) P* b) V& P( T8 D& Q  W1 n
pearance of pubic hair, normal growth velocity, and! T1 _/ S3 e3 L8 f
decreased erections. The father admitted using a testos-0 D( m4 t# _3 v8 S) C" \
terone gel, which he concealed at first visit. He was+ l. t/ z; v9 O& {$ g$ F
using it rather frequently, twice a day. The Physicians’- d) G+ {; q! V# A
Desk Reference, or package insert of this product, gel or
7 M) ], M: v9 i* Y3 {cream, cautions about dermal testosterone transfer to' k# E: z* a( a; A
unprotected females through direct skin exposure.
* n( ]0 q5 b: ]) ?. C" ^Serum testosterone level was found to be 2 times the1 T! B- \- f5 X' D# @5 j; b
baseline value in those females who were exposed to
6 |) B0 M, U) ~% N3 C/ |: |. Geven 15 minutes of direct skin contact with their male
2 R. m) N" h# v0 i$ Q# S* K3 `partners.6 However, when a shirt covered the applica-' M& h! D/ F" ~+ i8 f  T
tion site, this testosterone transfer was prevented.
0 ~$ w& n0 ^5 I* ^5 aOur patient’s testosterone level was 60 ng/mL,
  {2 m9 A, J+ y: o& `; U! B2 owhich was clearly high. Some studies suggest that; z# l" p' V! J+ x
dermal conversion of testosterone to dihydrotestos-
% @! K9 I% \* z3 g% fterone, which is a more potent metabolite, is more1 m* G4 \7 U1 M. H: P1 z& w
active in young children exposed to testosterone
0 F( I( P$ W2 B4 \$ T: k& Qexogenously7; however, we did not measure a dihy-
' z  b2 o- c5 {; S8 _0 W/ t, bdrotestosterone level in our patient. In addition to) _6 X& N& J  b% m
virilization, exposure to exogenous testosterone in
4 f' K/ w; l3 t+ @- ]+ jchildren results in an increase in growth velocity and) W' Z  E% H; l
advanced bone age, as seen in our patient.
) o0 U& y: M* o2 i0 qThe long-term effect of androgen exposure during8 U# o* f1 W9 H% B: g( i
early childhood on pubertal development and final1 c* u1 c4 @9 w8 ]6 F
adult height are not fully known and always remain
2 A5 m  d" [0 Q6 V6 Ua concern. Children treated with short-term testos-" j- F1 ^- Z+ K* R5 p) k2 k
terone injection or topical androgen may exhibit some
1 s% w6 r) u; K) h8 z7 Uacceleration of the skeletal maturation; however, after% h+ U" N, V* K) l. j
cessation of treatment, the rate of bone maturation& u* f3 C( G/ ]- q2 n, g
decelerates and gradually returns to normal.8,95 c' F7 e* v. X- i
There are conflicting reports and controversy4 j- Z6 M3 ]7 r9 g
over the effect of early androgen exposure on adult8 p2 L1 T6 W# |; x! B, @
penile length.10,11 Some reports suggest subnormal
# g  E- }: ?; h7 Y; qadult penile length, apparently because of downreg-
! `4 L8 f2 @7 [& v# \: j1 }0 dulation of androgen receptor number.10,12 However,6 |  t/ c  M( `/ a
Sutherland et al13 did not find a correlation between
: Q' z  G5 w& a6 vchildhood testosterone exposure and reduced adult
) E6 q; m5 n, C6 v" R" S+ Ypenile length in clinical studies.
7 _' G, q; f8 }Nonetheless, we do not believe our patient is
0 j" a& J% Q7 bgoing to experience any of the untoward effects from
9 ^% l' n4 l1 S! ~% [testosterone exposure as mentioned earlier because
! R- ]. p# @4 Z4 r& o$ rthe exposure was not for a prolonged period of time.9 J6 d3 L1 E8 l4 A/ d
Although the bone age was advanced at the time of
& q( o3 }( _, O1 P: x. Ldiagnosis, the child had a normal growth velocity at5 H. }/ G' \, D- y6 {& @5 O
the follow-up visit. It is hoped that his final adult
$ |: o& Y) y+ rheight will not be affected.
# M: _' A/ d. l  p) A/ }8 }4 a1 s; `Although rarely reported, the widespread avail-
$ X3 {, l) s: e8 Iability of androgen products in our society may- m: m6 U- d' |- z( L8 P% T  U
indeed cause more virilization in male or female" n4 x  i, R! d, V) @; I
children than one would realize. Exposure to andro-
3 x* R6 ]( r3 l- x2 L9 O/ [4 q0 w- Igen products must be considered and specific ques-
. \/ c3 Q! Z: U3 C" x& d! Itioning about the use of a testosterone product or% Z. p4 \, g+ Q6 m
gel should be asked of the family members during
# }  C% G( n$ t+ ~) \the evaluation of any children who present with vir-; s6 W6 c4 l5 J7 w% \: q8 |
ilization or peripheral precocious puberty. The diag-
% d# w/ z. j7 R9 onosis can be established by just a few tests and by
2 {5 o7 J; |2 t; }! \# xappropriate history. The inability to obtain such a
. W: J5 W3 d" P4 g* f$ Y0 dhistory, or failure to ask the specific questions, may& F& }0 `) p! F9 b( \. s; C+ X
result in extensive, unnecessary, and expensive1 H# B; E% ?' c$ }, S0 Y0 z
investigation. The primary care physician should be
8 S9 t' Z! \* uaware of this fact, because most of these children
& |2 ~7 B$ T; u  dmay initially present in their practice. The Physicians’
/ ^. }. F9 c) Y  HDesk Reference and package insert should also put a
0 b1 Q9 Z' d8 l/ ?" r* Pwarning about the virilizing effect on a male or! [5 {: w% V9 y5 S- V: H
female child who might come in contact with some-, P+ v: S* D8 s) m+ X9 V
one using any of these products.
8 X( Q* C. `- yReferences: B6 B( B- W) I
1. Styne DM. The testes: disorder of sexual differentiation  [6 ?8 \7 f* k: t: S0 D! E! l
and puberty in the male. In: Sperling MA, ed. Pediatric
6 x& i. o6 K+ L7 R& FEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;, ~  H: F2 y' t8 }/ S( n% d
2002: 565-628.6 @6 f2 h7 O5 M- B
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious2 n# u* r" K4 l! I  f- L/ W
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
$ e# ]- M% l; _
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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