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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
" a3 [4 _2 A5 J- t* ^1 b- FBoy Induced by Indirect Topical
7 K# o* O" s( AExposure to Testosterone
) m% C3 I# A, B; \! d: CSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
" @/ G3 w' T* Z4 ]* `3 l7 nand Kenneth R. Rettig, MD1" j3 t2 p4 @' ^7 p
Clinical Pediatrics& \8 p7 {8 p: t! e2 Q1 i! y6 F8 U
Volume 46 Number 6
! E2 q4 @% o- z3 X3 t3 h" XJuly 2007 540-543
8 m' F/ ^! b) y8 q© 2007 Sage Publications
2 M! P5 y# ^5 P3 p3 e6 C3 x! W9 W# R10.1177/0009922806296651
' Q4 c6 c4 _& w6 q7 [! whttp://clp.sagepub.com
. w) r* u7 y- qhosted at, o- p; g- x8 r; {! \8 X1 \
http://online.sagepub.com; ?2 k  n2 `% Z0 ~' P3 o5 v
Precocious puberty in boys, central or peripheral,/ h# n! l7 `0 J" I0 o: V2 F
is a significant concern for physicians. Central5 w5 I2 t0 Q2 ?4 P
precocious puberty (CPP), which is mediated
1 t8 t& W! t7 P9 d/ }& Rthrough the hypothalamic pituitary gonadal axis, has: \) U6 d6 e2 t+ l$ f! q0 P/ L7 F
a higher incidence of organic central nervous system
, m4 C8 l" H1 R- W7 j: llesions in boys.1,2 Virilization in boys, as manifested
: q7 I) N! G+ {# \  Oby enlargement of the penis, development of pubic8 g& q- _( O9 G5 }
hair, and facial acne without enlargement of testi-) o( q" I& ?9 C! j  B! H2 y
cles, suggests peripheral or pseudopuberty.1-3 We8 U6 J! g2 Z: f0 N- B5 w, Z
report a 16-month-old boy who presented with the( T) S3 u1 {* r; T* r
enlargement of the phallus and pubic hair develop-
( }& q/ i& M$ d& Cment without testicular enlargement, which was due
" o( }1 F% n) Tto the unintentional exposure to androgen gel used by
' u) c: a6 Q9 ]1 e# ], y  Dthe father. The family initially concealed this infor-; Z  Z" m3 x/ O8 N0 I
mation, resulting in an extensive work-up for this
9 d' G8 c. p& t+ Y( M% n6 T9 tchild. Given the widespread and easy availability of2 W+ m6 n1 y( A0 Q$ F, I7 ]$ C
testosterone gel and cream, we believe this is proba-$ Z- b  ^$ ~* B
bly more common than the rare case report in the' v7 k/ N4 p: H, n+ s' h& y
literature.4" f3 M: n- n8 J- Q( E
Patient Report
2 p3 z% f: j2 t$ w2 O/ XA 16-month-old white child was referred to the
. ~$ o6 I* V9 tendocrine clinic by his pediatrician with the concern8 j9 ?' t/ z9 [% [5 K3 K7 l2 q' ?
of early sexual development. His mother noticed
' l8 \- h% P3 @5 T& Q9 A: O1 V( clight colored pubic hair development when he was
4 D: t. G( G8 Q+ y( W8 A) TFrom the 1Division of Pediatric Endocrinology, 2University of
8 q' d0 d5 z7 @# sSouth Alabama Medical Center, Mobile, Alabama.
$ h0 R9 g( i6 U+ X8 gAddress correspondence to: Samar K. Bhowmick, MD, FACE,
, [! p$ W, ~  h0 |9 V6 z1 KProfessor of Pediatrics, University of South Alabama, College of, w2 x* Q& J" N" h/ c
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
  }0 `5 d% W* [: y  De-mail: [email protected].& e, l; [" N) _, f: C- H
about 6 to 7 months old, which progressively became; p/ O* d& Q1 C
darker. She was also concerned about the enlarge-
) P- \' f8 ^+ a2 S! ~( h  }ment of his penis and frequent erections. The child7 j! B* y9 e( d/ H1 s- n
was the product of a full-term normal delivery, with
5 [- E0 {# T- u+ za birth weight of 7 lb 14 oz, and birth length of
4 ~# ]# e/ n! _" M& [1 f+ q7 X20 inches. He was breast-fed throughout the first year
/ y1 Q  f7 ]2 q! Yof life and was still receiving breast milk along with
9 x1 E+ H) z5 D9 N1 Z$ osolid food. He had no hospitalizations or surgery,4 y2 L  v1 B: @+ K& j9 @
and his psychosocial and psychomotor development
0 G6 K8 B0 J* H7 [5 E2 \was age appropriate.; z: N3 k# H% H, S
The family history was remarkable for the father,# v% @- a: k1 _+ U0 q2 L
who was diagnosed with hypothyroidism at age 16,$ E2 U3 @/ j  U  L. l9 `
which was treated with thyroxine. The father’s
( e3 Y2 I$ v" T4 K$ u3 o& Iheight was 6 feet, and he went through a somewhat
  \% D" j; c! i* w8 L2 vearly puberty and had stopped growing by age 14.# M- f$ V: W( `2 Y( g
The father denied taking any other medication. The
2 Q5 i0 ]# }% Nchild’s mother was in good health. Her menarche$ h$ S& J4 l0 }$ {: N
was at 11 years of age, and her height was at 5 feet
+ ^# Y* q$ R5 Q2 X6 c5 inches. There was no other family history of pre-! o( G/ E7 H- o/ }8 S' N
cocious sexual development in the first-degree rela-! e0 F; X2 O3 T2 t: b- s5 [
tives. There were no siblings.0 q) V2 F$ T9 X" s3 m
Physical Examination
( O5 ?/ v8 I6 A; wThe physical examination revealed a very active,: }2 M1 }( Q4 [+ I' |
playful, and healthy boy. The vital signs documented3 P! S  M* O2 p0 S$ ]' ~% P) e
a blood pressure of 85/50 mm Hg, his length was
0 n( l' M4 U- _/ J" p8 C90 cm (>97th percentile), and his weight was 14.4 kg3 J( ]3 M1 E4 n! F1 a
(also >97th percentile). The observed yearly growth
* L) I2 r% U/ r# ?) Ivelocity was 30 cm (12 inches). The examination of: S; D) y5 m* B0 G0 L8 q- Q& f
the neck revealed no thyroid enlargement.! |* d! L9 v9 ~2 Z0 ^
The genitourinary examination was remarkable for
: V3 W4 b  M8 k; nenlargement of the penis, with a stretched length of
/ F! c: ]% i" D6 E' X+ n8 cm and a width of 2 cm. The glans penis was very well
/ H2 W* s9 N% U4 }0 b, v3 ?7 ]. Hdeveloped. The pubic hair was Tanner II, mostly around2 {3 v/ h1 p  g5 {8 y6 i, ~- b
5403 n, Y3 R4 p4 r* _% |
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
5 S! e- ]& u" xthe base of the phallus and was dark and curled. The
2 _* ?- ?" [. Mtesticular volume was prepubertal at 2 mL each.
3 W& C) @' r5 f7 e/ FThe skin was moist and smooth and somewhat$ m# m1 A0 }3 J0 v, |
oily. No axillary hair was noted. There were no
, U  C/ a' s+ D( g. V/ W% c! Tabnormal skin pigmentations or café-au-lait spots.
0 s* g  v+ r# O, h; ^2 o+ ?4 |Neurologic evaluation showed deep tendon reflex 2+1 t6 F; m$ M9 z$ ?( i" V$ a/ F; W
bilateral and symmetrical. There was no suggestion7 h2 M& R( X6 x  a. Z9 z
of papilledema.8 I6 r0 P+ z4 v9 `% R) ^6 x
Laboratory Evaluation
' [9 L3 E+ f( }. L% A6 {; DThe bone age was consistent with 28 months by
5 _0 `) y% e9 Y( Eusing the standard of Greulich and Pyle at a chrono-" C. O2 G+ `2 E2 _
logic age of 16 months (advanced).5 Chromosomal
0 D% k8 T( E+ z6 `' vkaryotype was 46XY. The thyroid function test
  \2 {/ E1 z  Mshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
7 x% M! E7 t/ S' _lating hormone level was 1.3 µIU/mL (both normal).5 U1 e; T7 {( ~+ {, p
The concentrations of serum electrolytes, blood
+ G; Z6 C' f/ wurea nitrogen, creatinine, and calcium all were
/ n/ s6 I  ~6 y* }3 Qwithin normal range for his age. The concentration$ ~, k0 k' k1 j9 S" C2 b, k9 O
of serum 17-hydroxyprogesterone was 16 ng/dL
; I3 O. v5 k% z/ O' X0 Q(normal, 3 to 90 ng/dL), androstenedione was 20
- g4 A% o0 l' D: i3 ?5 G" X) p' F  rng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
2 N. ~! o9 T9 M" l5 ?  \  K& mterone was 38 ng/dL (normal, 50 to 760 ng/dL),
, z- m  A7 n9 g" j2 Pdesoxycorticosterone was 4.3 ng/dL (normal, 7 to
9 C! R" k0 y% i9 v49ng/dL), 11-desoxycortisol (specific compound S)6 S" `7 F8 s- T2 V7 M
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
1 L6 v0 b- V2 \) P1 G* M- Wtisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
8 Q. V( h: Q4 p9 k, B) R" \# qtestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
1 f3 ^! B. V) V7 i* M/ Aand β-human chorionic gonadotropin was less than
1 L3 w) S) D, V# v4 G. ^5 mIU/mL (normal <5 mIU/mL). Serum follicular
' `* p" l" v- N! w) O7 wstimulating hormone and leuteinizing hormone& b, W6 S. V, t5 S
concentrations were less than 0.05 mIU/mL
5 _' P% I1 K; {* s' @(prepubertal).& ^- Q6 a6 @! f
The parents were notified about the laboratory
" l+ g8 q1 f2 L' \7 L* ^results and were informed that all of the tests were3 a# T3 k6 z4 C7 e4 N8 B9 E4 g
normal except the testosterone level was high. The+ [' b+ S  A) H* B  k0 H
follow-up visit was arranged within a few weeks to6 C; t' [7 _5 z3 u- a
obtain testicular and abdominal sonograms; how-. r9 n" `7 u# o9 [5 P
ever, the family did not return for 4 months.
" E' D0 ?5 k6 L! ^& _& K9 e6 e: lPhysical examination at this time revealed that the
5 z, @2 [. a" lchild had grown 2.5 cm in 4 months and had gained2 l) S- T- `4 e5 {2 R
2 kg of weight. Physical examination remained4 i. Q( z; ^& v; O4 F
unchanged. Surprisingly, the pubic hair almost com-# M. ^9 t& X3 a" Q6 }' k
pletely disappeared except for a few vellous hairs at
" A6 l+ o4 Y& W  r0 J7 ?$ Fthe base of the phallus. Testicular volume was still 27 ?' \2 O: x2 z/ T* _# s' G
mL, and the size of the penis remained unchanged.# H- |* S( {( e! G% }
The mother also said that the boy was no longer hav-
$ j0 {4 ^8 J- @: Z5 Z! Z% qing frequent erections.- V2 D9 b) ], W1 m5 t; }/ e
Both parents were again questioned about use of6 B# A8 b+ m2 d: y7 a
any ointment/creams that they may have applied to
! J) L) E4 u# m- m2 D% fthe child’s skin. This time the father admitted the* B) v! @0 s) X: u  C4 L& C
Topical Testosterone Exposure / Bhowmick et al 541
6 c# Y9 v; V* a$ h# Q! Wuse of testosterone gel twice daily that he was apply-
5 ?9 {, Z) i2 [: ^* i1 e6 qing over his own shoulders, chest, and back area for
' e8 O3 D- Z, e" ea year. The father also revealed he was embarrassed
: D, z/ g* w6 E; I2 o. Oto disclose that he was using a testosterone gel pre-
5 m8 [/ X" t2 R5 Uscribed by his family physician for decreased libido
8 A! @  d0 u! I# h% x( `, Esecondary to depression.: x  h' y5 `' Y/ t) V( h
The child slept in the same bed with parents.; ~9 \# r, |7 Q
The father would hug the baby and hold him on his
) B. S1 L5 H6 [3 p* q( S( u& Dchest for a considerable period of time, causing sig-. U% S: X5 J, }1 t, K0 ~
nificant bare skin contact between baby and father.; q* n8 V" Y# d  B+ q% I
The father also admitted that after the phone call,, Z. b" U0 P; X" ?1 h9 l9 \+ R
when he learned the testosterone level in the baby; z- w/ G3 J2 o$ \5 l6 G5 U
was high, he then read the product information
: G9 S  k% y( u( J# ^2 Hpacket and concluded that it was most likely the rea-
( C/ h5 e$ }  X- {, {! ~son for the child’s virilization. At that time, they
1 q0 @1 |+ ^. v/ h1 j1 Udecided to put the baby in a separate bed, and the1 v- E3 u/ P' U/ W
father was not hugging him with bare skin and had
' f5 i& l* T9 R4 g3 D2 R( j. }0 _been using protective clothing. A repeat testosterone4 e4 K0 O& z# Z+ T" S& Z0 C
test was ordered, but the family did not go to the% T6 o# J6 l6 P6 t4 n1 F
laboratory to obtain the test.
2 v7 T( i) l+ K2 m3 r3 X1 r/ D! pDiscussion
  m$ a6 O: ~& K% RPrecocious puberty in boys is defined as secondary
- U& j0 S* F- q2 Y3 }2 R4 X9 T3 Y$ gsexual development before 9 years of age.1,4" d: C1 j1 P7 ]; F# k
Precocious puberty is termed as central (true) when
( ?% h: A/ B- Q5 p5 Q$ [9 Git is caused by the premature activation of hypo-, _4 }7 p3 X  ?) b
thalamic pituitary gonadal axis. CPP is more com-
& v5 I- i, e/ c, imon in girls than in boys.1,3 Most boys with CPP0 K; m3 T" R9 N  {
may have a central nervous system lesion that is
0 k0 _- g) x% Qresponsible for the early activation of the hypothal-
. r8 r( S. u! T+ t2 p/ ~$ kamic pituitary gonadal axis.1-3 Thus, greater empha-* }9 Q; }+ G6 m! q! p1 \( H" L
sis has been given to neuroradiologic imaging in
2 [. [( k; \$ n, y* f0 x+ Cboys with precocious puberty. In addition to viril-/ A& Q/ l2 t5 _* [# v" T$ }
ization, the clinical hallmark of CPP is the symmet-2 O, A' z! U9 ~3 ]
rical testicular growth secondary to stimulation by% S9 s! X% t- o
gonadotropins.1,39 K5 [: o* J. Q- `$ C' d
Gonadotropin-independent peripheral preco-0 E$ a, ]6 J3 D* W
cious puberty in boys also results from inappropriate0 Z$ }, F+ x+ ^: t* ~
androgenic stimulation from either endogenous or
: U8 u+ a2 v4 @& ^) nexogenous sources, nonpituitary gonadotropin stim-
: L6 Q# w( @, ?ulation, and rare activating mutations.3 Virilizing: M! b5 E( k7 v; C; B& i- L4 y
congenital adrenal hyperplasia producing excessive& c& Y5 J# v" Q- W2 j* l
adrenal androgens is a common cause of precocious! l5 m3 q  R/ A8 s% h. [
puberty in boys.3,45 N" F2 ?+ d8 O* Q  U
The most common form of congenital adrenal" R  Y$ P, J. K' f; u8 J- [+ p
hyperplasia is the 21-hydroxylase enzyme deficiency.  X7 D# Z! H, s
The 11-β hydroxylase deficiency may also result in
* v# o/ H0 K1 c# H! @5 t7 B  D1 Rexcessive adrenal androgen production, and rarely,
1 h  o0 C: l) H! Xan adrenal tumor may also cause adrenal androgen: M% v/ g* V' X3 N1 @
excess.1,3' E$ ]( n' M& i9 P
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from. G5 P- N7 ~* S3 j& ~' T
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007: z' y, \  Y) N$ U  u/ F$ Z
A unique entity of male-limited gonadotropin-
, J$ i3 e9 K$ X' B  Cindependent precocious puberty, which is also known8 z. ]' x5 T% `/ ~" y, ?
as testotoxicosis, may cause precocious puberty at a9 p1 l* f/ K' d
very young age. The physical findings in these boys! q! Q9 }& W8 r
with this disorder are full pubertal development,
7 t$ }6 B- N- Q. _1 Rincluding bilateral testicular growth, similar to boys$ X. c8 p: g0 e
with CPP. The gonadotropin levels in this disorder
* K1 `, U8 Y/ K: O% r/ t+ g! }are suppressed to prepubertal levels and do not show( M4 X% F) t* g1 Q
pubertal response of gonadotropin after gonadotropin-/ K7 }8 F- F7 W* {* m7 j
releasing hormone stimulation. This is a sex-linked
& H6 q) p4 f) }1 d9 yautosomal dominant disorder that affects only
; ?0 M  K7 ?$ ]+ mmales; therefore, other male members of the family5 s; p  `4 ~/ j( }" F5 g
may have similar precocious puberty.34 G! N# M: _5 [. l6 D5 [# _
In our patient, physical examination was incon-
5 Z  f2 o* w! x7 Psistent with true precocious puberty since his testi-
! z- H0 F2 ?% u5 j6 Dcles were prepubertal in size. However, testotoxicosis6 X; [4 y& ]. {4 q' a; ]
was in the differential diagnosis because his father
# v0 Z3 t4 _2 W7 istarted puberty somewhat early, and occasionally,
- V* s" x, \% F; ^  ~1 Utesticular enlargement is not that evident in the* \+ t1 q: M/ n0 q( f) E+ u
beginning of this process.1 In the absence of a neg-6 o9 m( x! {! Q; e
ative initial history of androgen exposure, our
' c* P9 k( y5 @/ U! `8 r- X2 j5 U) obiggest concern was virilizing adrenal hyperplasia,  ?& O) y( d* z0 p9 C4 T0 N) w. L
either 21-hydroxylase deficiency or 11-β hydroxylase3 j; R) B' }$ e; ?. d5 V
deficiency. Those diagnoses were excluded by find-% d9 Z. X+ ]* |+ W! A. v( k
ing the normal level of adrenal steroids./ N2 S1 C3 C$ t  _
The diagnosis of exogenous androgens was strongly
2 q4 z3 h5 N% @+ W7 S2 Bsuspected in a follow-up visit after 4 months because& x% B+ u/ F" B3 H
the physical examination revealed the complete disap-
) u) G! Q% J7 Lpearance of pubic hair, normal growth velocity, and+ }* \7 ?8 y0 M8 F$ ^; a6 \, d- y5 ?
decreased erections. The father admitted using a testos-8 a5 u, j4 B, p
terone gel, which he concealed at first visit. He was/ ?7 I8 U( T1 ?# R- g( O5 o
using it rather frequently, twice a day. The Physicians’
) x, v4 y4 M$ n, A  t" x$ z% }Desk Reference, or package insert of this product, gel or
) A8 M) s+ G8 V" ycream, cautions about dermal testosterone transfer to
" ]) n! w; j) `unprotected females through direct skin exposure.
- L$ t; f: P- A' z) ~Serum testosterone level was found to be 2 times the8 n# B+ S: T4 ~! G! h
baseline value in those females who were exposed to' ?) [# H$ o( [! r& H$ t
even 15 minutes of direct skin contact with their male
1 ]6 [0 k0 m* epartners.6 However, when a shirt covered the applica-9 @( ~! |( g* C; w$ e
tion site, this testosterone transfer was prevented.
9 o$ S7 c  Z! ~+ }% Z& HOur patient’s testosterone level was 60 ng/mL,
& H# _' H5 B. Y: l; o$ pwhich was clearly high. Some studies suggest that0 K- C  o, t. a5 `4 Z" p9 m3 f' I5 g
dermal conversion of testosterone to dihydrotestos-
& H$ K) ^( R$ n% Z. _4 Kterone, which is a more potent metabolite, is more" ~3 {+ R& B( g. C3 T7 x% F9 m
active in young children exposed to testosterone
, {* F+ H& `2 p! L: D6 oexogenously7; however, we did not measure a dihy-
9 Z! ]% u2 ~9 j5 H) O: bdrotestosterone level in our patient. In addition to
" ?* N+ x# C( l/ q9 v( \' w1 Svirilization, exposure to exogenous testosterone in
6 o% s4 f/ X2 b0 b! echildren results in an increase in growth velocity and
/ d) L- l3 T9 m; ladvanced bone age, as seen in our patient.! G. a! z: t+ ?. K9 L$ B) ~! I
The long-term effect of androgen exposure during) J, W( ^0 j5 q& U- K
early childhood on pubertal development and final
  Y8 e& w, \2 e7 Badult height are not fully known and always remain
% J2 J6 t0 j: P8 H0 fa concern. Children treated with short-term testos-- O) E( U- l! \, Y
terone injection or topical androgen may exhibit some9 J" W  i. e& P% v( k; {+ ]  n
acceleration of the skeletal maturation; however, after
5 o9 e6 e" S4 \8 D/ ycessation of treatment, the rate of bone maturation
& K! ?  r& D6 x, cdecelerates and gradually returns to normal.8,9
6 [: Q! _, H! T$ OThere are conflicting reports and controversy; d9 f+ u( F! i& K
over the effect of early androgen exposure on adult. d, B2 d2 F+ j, \2 F7 k/ ~  \
penile length.10,11 Some reports suggest subnormal. \9 T& R' Q! G+ g8 F
adult penile length, apparently because of downreg-# S- D" z3 w# f/ G) J
ulation of androgen receptor number.10,12 However,
' w4 U) X( v. G: xSutherland et al13 did not find a correlation between
" k/ a1 a9 w8 o: r7 l) pchildhood testosterone exposure and reduced adult
/ R& a+ E6 _+ U  i8 s' U& J1 v* Spenile length in clinical studies.' A4 `. g1 n7 `2 X& k
Nonetheless, we do not believe our patient is* N" {; h' b* S* o# Q
going to experience any of the untoward effects from
0 u* O. }& L; M7 z& M5 w* h) Ytestosterone exposure as mentioned earlier because/ u# A/ e4 h9 _  e+ v" b, U. d
the exposure was not for a prolonged period of time., A( d3 _7 V( L9 z$ Z
Although the bone age was advanced at the time of  u. t& i/ T$ r4 n
diagnosis, the child had a normal growth velocity at7 a# h6 I# p  i
the follow-up visit. It is hoped that his final adult
! s! G3 ~7 \2 t/ g; E* T; Fheight will not be affected.' j, Z: @# g: v  l
Although rarely reported, the widespread avail-
: v2 {- {$ U2 R( `ability of androgen products in our society may
4 m; [9 _5 r& m3 m, X/ n2 V+ [indeed cause more virilization in male or female
' O( B, O% }$ ichildren than one would realize. Exposure to andro-6 i- m0 N) f4 v7 y. G5 {4 m& F
gen products must be considered and specific ques-0 p+ @: N/ K3 _$ D( L3 L+ t
tioning about the use of a testosterone product or
' D3 j, S. d9 jgel should be asked of the family members during, T1 M- F9 k# |8 S9 j1 f  `
the evaluation of any children who present with vir-' M  N' N: w/ j6 F' }' ]' O$ j% D
ilization or peripheral precocious puberty. The diag-
* ~$ s' R4 N9 ~, X9 ynosis can be established by just a few tests and by, |( f7 @0 V& Z9 ]' ?5 u1 ]
appropriate history. The inability to obtain such a1 W) ]  U( o* D! `
history, or failure to ask the specific questions, may0 y4 T+ `2 g6 {! u) O) `
result in extensive, unnecessary, and expensive' B8 B3 z3 [# x. \) l* R& f
investigation. The primary care physician should be
' {! b+ G# H8 i1 j% G, D$ saware of this fact, because most of these children
& X: d( D0 e4 rmay initially present in their practice. The Physicians’! r& k9 W) P6 v- |& W; z8 C' J
Desk Reference and package insert should also put a
4 O5 m0 y  B, t; Twarning about the virilizing effect on a male or' j0 M! A5 H- K  S- K$ m
female child who might come in contact with some-) \8 S# @3 s4 ~- l8 V+ }
one using any of these products.
1 f# y4 R1 ?$ X/ U* FReferences2 E* V2 ^+ J# F, }" Y# U
1. Styne DM. The testes: disorder of sexual differentiation
5 z% D& s+ `: G$ z  X1 U$ G2 Yand puberty in the male. In: Sperling MA, ed. Pediatric- {6 S! z: u, P: W6 _
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
+ U6 b% }- @3 ]% r" O3 N2002: 565-628./ o6 a% \" Z) L( H6 {* K: m3 w' r
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious+ A0 d/ g3 z; [7 N
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old# K9 r& c; m. L0 G2 L& p) _1 c
Boy Induced by Indirect Topical
3 |) H+ i# S% J- r7 x$ \# j4 QExposure to Testosterone
; m# }* }, ?. f* z, f# [, ^Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2' i& g" W0 v( [& L5 ~5 T
and Kenneth R. Rettig, MD12 j6 b% ^! e, O5 D3 T: |
Clinical Pediatrics" @( u4 \% S" Z" U% Y) s
Volume 46 Number 6
( _! R# M" W" G% BJuly 2007 540-543# @. ?* M# Q4 d5 n# d
© 2007 Sage Publications0 I0 x- V& \0 F
10.1177/00099228062966510 x8 z) [) E! A! o  A, v- H$ S
http://clp.sagepub.com
* M/ x6 z+ x6 c8 Q6 l; }6 M/ I/ W+ hhosted at1 g: [) d4 G0 ^
http://online.sagepub.com
! D, `) d+ l/ b- E" ]Precocious puberty in boys, central or peripheral,
" ]) x2 w# {5 r/ Ais a significant concern for physicians. Central
5 J0 b+ t& V4 Q' p% Vprecocious puberty (CPP), which is mediated4 O: [. k: _% G! o9 {( P) @  n
through the hypothalamic pituitary gonadal axis, has6 M+ L- r- Z- O( p
a higher incidence of organic central nervous system
" P1 P& k- }2 ?/ L9 P6 plesions in boys.1,2 Virilization in boys, as manifested
# q0 W3 |! V& Uby enlargement of the penis, development of pubic
! p6 N5 D; x) N1 u: t% C; z; r" i; Ihair, and facial acne without enlargement of testi-3 P+ r" @2 P6 b0 B' U
cles, suggests peripheral or pseudopuberty.1-3 We
' j2 x5 _& N7 ]# Preport a 16-month-old boy who presented with the* x% D. u% ~$ }# ?- K' B
enlargement of the phallus and pubic hair develop-
% U/ a0 ~5 u2 A* T( Y/ P$ {ment without testicular enlargement, which was due
6 Z( _. O! b% J: rto the unintentional exposure to androgen gel used by6 Z9 G* |# m; ~, R! ]
the father. The family initially concealed this infor-
& ~4 _- W7 G( Fmation, resulting in an extensive work-up for this
3 N9 t" V2 v, q* x$ ychild. Given the widespread and easy availability of
. s( E& _' H( x3 ftestosterone gel and cream, we believe this is proba-7 V. i0 M0 t" }* P: s7 I: i! x2 s
bly more common than the rare case report in the& l. O  N+ y( C8 I: [; O# a
literature.4
7 h* A; R8 B8 [/ I6 yPatient Report' i' Y2 X' w! |8 L( S7 N5 \
A 16-month-old white child was referred to the
+ n7 V- ?  u2 T" ]+ @( K( eendocrine clinic by his pediatrician with the concern
6 y5 m1 c. k# I. Dof early sexual development. His mother noticed: X& [. F8 W6 m( G
light colored pubic hair development when he was& s0 d' Y/ \; H/ X+ G
From the 1Division of Pediatric Endocrinology, 2University of
  A% y, Q7 u& b% CSouth Alabama Medical Center, Mobile, Alabama." X) E5 `/ V- }; o+ F; a3 O
Address correspondence to: Samar K. Bhowmick, MD, FACE,; q( w& B; w2 g" \+ }2 }
Professor of Pediatrics, University of South Alabama, College of& K7 t( L+ \: {7 h: {/ Z/ p/ j
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
' D' O2 ^( k; t7 T* P( U/ ge-mail: [email protected].
6 ^" A: l$ }; ]1 I! zabout 6 to 7 months old, which progressively became
4 h+ |7 `) [7 a- k) P% [- @darker. She was also concerned about the enlarge-
) A1 \( C( N: v, gment of his penis and frequent erections. The child2 x5 q: ^" r+ j, b; A- O- q
was the product of a full-term normal delivery, with
1 ^0 V- s8 Q- C8 |a birth weight of 7 lb 14 oz, and birth length of
+ Z9 R6 a2 w! Y- K+ ]20 inches. He was breast-fed throughout the first year
$ S7 S- |1 V& f& b. a9 k4 A5 Kof life and was still receiving breast milk along with
0 Y1 g5 o7 G( s' w& g, Q. Vsolid food. He had no hospitalizations or surgery,
# ]8 Y' |9 h- Q# q0 m& G- ^and his psychosocial and psychomotor development! e3 F1 j6 B. {5 J  c5 R% x
was age appropriate.
! g- n4 [# i" g5 M4 MThe family history was remarkable for the father,
9 J. O2 R4 d% i, F2 M% [& qwho was diagnosed with hypothyroidism at age 16,
9 s2 Z: E$ @  J/ y7 O9 pwhich was treated with thyroxine. The father’s
8 y, P4 A" [. m8 Cheight was 6 feet, and he went through a somewhat
2 M! N, b+ R) O9 ]8 @early puberty and had stopped growing by age 14.* Z+ I8 ]% b5 t0 |9 e
The father denied taking any other medication. The
4 Q# N) J8 v, O; z, \5 R/ Z1 Ychild’s mother was in good health. Her menarche
) s' F7 c8 n: B9 u) y* ?2 |was at 11 years of age, and her height was at 5 feet) i. a" y7 [6 B- @- y( t) ?. y
5 inches. There was no other family history of pre-) d# _9 l& U% X2 L$ V) C! C
cocious sexual development in the first-degree rela-4 x7 ?. H) \+ P5 h2 W
tives. There were no siblings.# H* G4 Z$ |0 w6 Z" H- `2 `
Physical Examination
+ Q' y. E$ `- b  T; BThe physical examination revealed a very active,
' e3 z0 t& O+ X6 Fplayful, and healthy boy. The vital signs documented
8 m+ c. c+ z1 j0 Aa blood pressure of 85/50 mm Hg, his length was
/ f* _+ V# P# ^' z- E90 cm (>97th percentile), and his weight was 14.4 kg
7 I" e3 F5 G! n(also >97th percentile). The observed yearly growth
) u- }, E0 x) ^( F% `8 uvelocity was 30 cm (12 inches). The examination of9 x7 ?8 c/ F3 x. B' l; C, `
the neck revealed no thyroid enlargement.* z' b# v; R; K
The genitourinary examination was remarkable for) n7 K; a: E7 R/ v; L0 T. _+ Y
enlargement of the penis, with a stretched length of) S$ b0 v/ z$ w# T$ S+ T
8 cm and a width of 2 cm. The glans penis was very well" B/ A/ n6 ^) S8 p) o4 r5 P$ r
developed. The pubic hair was Tanner II, mostly around" B2 _# L  |& m) v# X  ^
5405 Q% K$ I; {* ^' c& M1 o
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
) u. K3 r9 x. S" Dthe base of the phallus and was dark and curled. The+ z; ?2 F5 P- l! }9 q
testicular volume was prepubertal at 2 mL each.
. n# ~, G; W% hThe skin was moist and smooth and somewhat
  W- y7 M0 B! r) D8 _oily. No axillary hair was noted. There were no
4 _  I8 h0 t# E; q* }$ wabnormal skin pigmentations or café-au-lait spots.
  L/ T8 ^+ ]; @Neurologic evaluation showed deep tendon reflex 2+" `6 F" D$ s0 {) l  `
bilateral and symmetrical. There was no suggestion
, ^, u) H  @! X& ~) \. _6 i( Jof papilledema./ T5 m" x% C3 W  O8 c
Laboratory Evaluation
- d9 z* `- w; d" y7 GThe bone age was consistent with 28 months by8 J# M8 w+ n- E+ |) C% ]# M
using the standard of Greulich and Pyle at a chrono-
9 J  q* Y0 D2 c& ologic age of 16 months (advanced).5 Chromosomal
% O$ c- X" u( j7 `/ h1 nkaryotype was 46XY. The thyroid function test" f& V) S( b- w& y% T
showed a free T4 of 1.69 ng/dL, and thyroid stimu-9 g; j- n+ O" K& J  f8 r! A
lating hormone level was 1.3 µIU/mL (both normal).
  a) q$ M& A7 `/ z" a- GThe concentrations of serum electrolytes, blood0 k  R$ a. T+ d  s: f* @
urea nitrogen, creatinine, and calcium all were
1 {; G( B  W# _8 w& @within normal range for his age. The concentration" i% B0 p0 c# {1 M; [
of serum 17-hydroxyprogesterone was 16 ng/dL+ y- H7 q! G/ ?8 O0 `
(normal, 3 to 90 ng/dL), androstenedione was 200 p. u. X8 k, t; U: _6 G' p
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
2 D: \9 s' ]5 q- i/ _terone was 38 ng/dL (normal, 50 to 760 ng/dL),2 D8 d8 a3 H8 r+ ?+ g% }2 K/ O
desoxycorticosterone was 4.3 ng/dL (normal, 7 to( @! J  a7 g0 b; J! @( n
49ng/dL), 11-desoxycortisol (specific compound S)! S% Q: {7 V6 N1 M; l( X0 [( P* R
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-! b% X3 e  D1 C* w2 k& L
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total+ f: A5 E# b4 ~8 |
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
1 _. y8 A; M. n: _& eand β-human chorionic gonadotropin was less than
8 F1 H& l. |; B* p" _' ?! I% `* U5 mIU/mL (normal <5 mIU/mL). Serum follicular
5 J! o% a: P2 U% O- Estimulating hormone and leuteinizing hormone; E& m7 E( d0 A. ~1 G
concentrations were less than 0.05 mIU/mL
2 W9 L6 ^& w0 t: n( {- j(prepubertal).
0 e5 |* z% l+ s! E. h! x: F, mThe parents were notified about the laboratory+ V) X6 Y* C5 C" H( j, N
results and were informed that all of the tests were, M8 _- z3 O* f" C8 Q
normal except the testosterone level was high. The, j1 V6 A% q& f# x
follow-up visit was arranged within a few weeks to* U/ s3 s; l: J# s/ E
obtain testicular and abdominal sonograms; how-& y2 O* J6 k8 n) ^
ever, the family did not return for 4 months.
/ q9 l% _# k# b6 k! h; gPhysical examination at this time revealed that the; q0 b% u6 h  a: t* h) p
child had grown 2.5 cm in 4 months and had gained
' G: i( n" Q4 C$ m2 kg of weight. Physical examination remained
7 {( T; v, ^' z9 O4 a$ Eunchanged. Surprisingly, the pubic hair almost com-
& @6 p6 C( ^2 ~8 ]# P4 ~pletely disappeared except for a few vellous hairs at
; t2 N% Q/ p. R; b" gthe base of the phallus. Testicular volume was still 2& P7 ^& _+ ]/ y& h5 o
mL, and the size of the penis remained unchanged.% [: q% E& b4 f
The mother also said that the boy was no longer hav-
8 t( u2 l2 L& T. D" e5 \ing frequent erections.
% H  J1 ^* T; @7 vBoth parents were again questioned about use of6 E9 `- q6 G# a4 U6 m/ P& F
any ointment/creams that they may have applied to4 ~+ x" S' J# Z: v- I, F
the child’s skin. This time the father admitted the, I9 d# X0 B9 \5 i4 {3 l* ]5 k( }" l
Topical Testosterone Exposure / Bhowmick et al 541% O) u- u* D/ z! q) _: ^& s. l
use of testosterone gel twice daily that he was apply-
: J  ?8 r  l1 x6 Z- D, F% Iing over his own shoulders, chest, and back area for2 U' v, R" B, j$ |4 i/ v* _, R
a year. The father also revealed he was embarrassed
( r9 x8 w; C& q+ Nto disclose that he was using a testosterone gel pre-* W3 Z9 d% [  `. A
scribed by his family physician for decreased libido
- g* r% K4 k* d: S+ Xsecondary to depression.# g' ~/ j5 X. \
The child slept in the same bed with parents.
4 C- Y+ A) h" M8 N5 {The father would hug the baby and hold him on his, d, d% Q. [2 G5 Q: c: b
chest for a considerable period of time, causing sig-9 T% i0 c3 |2 U
nificant bare skin contact between baby and father.
' E3 g" ]" a6 K2 w1 W3 v( _# E- vThe father also admitted that after the phone call,
+ g8 J9 R5 {* Q8 z. ]+ M7 awhen he learned the testosterone level in the baby) v; {& Z; _, G) ^# _8 x* E
was high, he then read the product information
* V4 `: K3 {. j: m# wpacket and concluded that it was most likely the rea-
5 w4 f& u4 s+ `0 Rson for the child’s virilization. At that time, they, W0 T9 r) }* f( e7 s; R" G" G& R
decided to put the baby in a separate bed, and the0 v3 ^1 \1 Q5 {0 \) l" o0 r
father was not hugging him with bare skin and had( e1 g! Y3 F! G
been using protective clothing. A repeat testosterone$ A; T2 z  v% o5 S$ b) v0 K: M8 l$ M
test was ordered, but the family did not go to the* E7 m2 }5 Z+ E5 n
laboratory to obtain the test.6 Y. q% w# P5 c+ R; c* n! P5 _
Discussion
4 D  P5 f; X/ vPrecocious puberty in boys is defined as secondary
/ C% o: K) A4 j3 Bsexual development before 9 years of age.1,4( p) F+ V( s& g
Precocious puberty is termed as central (true) when
% H0 \' e% o3 ^6 m- I& B) Cit is caused by the premature activation of hypo-
. C: N# M) Z! G. d1 Ethalamic pituitary gonadal axis. CPP is more com-
* j; \- Y* Y( m; Y+ x4 vmon in girls than in boys.1,3 Most boys with CPP
: Q9 p2 `# o- E/ u$ t! G. Nmay have a central nervous system lesion that is
, p8 ~' ]1 D& U# Eresponsible for the early activation of the hypothal-
, l2 `; s" C* X" z" e3 tamic pituitary gonadal axis.1-3 Thus, greater empha-6 v; L. {9 ?6 P6 S# Z
sis has been given to neuroradiologic imaging in
& p* \9 D- N; N4 n: e: {/ `boys with precocious puberty. In addition to viril-$ G! ?* O! F) s' r8 r
ization, the clinical hallmark of CPP is the symmet-
& a/ m  M8 k+ e$ _' s9 V8 w, k* lrical testicular growth secondary to stimulation by& f9 g& U9 F( p. _; v
gonadotropins.1,3" ]  X3 X% B& ]! B
Gonadotropin-independent peripheral preco-( ]2 A& x- @, c  m( d' ^0 R, m
cious puberty in boys also results from inappropriate
+ I/ |( p3 T8 j3 Oandrogenic stimulation from either endogenous or
3 Z! R; L5 B3 J) B5 Cexogenous sources, nonpituitary gonadotropin stim-# j; y2 q2 q7 D  L
ulation, and rare activating mutations.3 Virilizing: ]; v$ y2 s1 U6 k: {
congenital adrenal hyperplasia producing excessive0 [, l4 D3 z5 c8 C4 `
adrenal androgens is a common cause of precocious4 g" N) W+ V% L6 G+ R; n
puberty in boys.3,48 x7 j/ u, z2 C& q1 x$ a( ]4 q
The most common form of congenital adrenal
7 M, G) f, l. {! s. R( g; O: j1 Xhyperplasia is the 21-hydroxylase enzyme deficiency.
& n- ~: L; j' ]1 ]" }+ pThe 11-β hydroxylase deficiency may also result in* V' ^% r9 b& J! P% {' n
excessive adrenal androgen production, and rarely,
( f! y! F1 k) jan adrenal tumor may also cause adrenal androgen
3 s) ], O# d- fexcess.1,3
" ?, G4 U) M2 c  D4 s7 |* Zat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
" X: k# Q; p% {) @! t+ M% U542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
0 I3 Q, v  m' w3 D# _4 j& [A unique entity of male-limited gonadotropin-
, Y7 \$ \; c  u) P5 Oindependent precocious puberty, which is also known# a% v( ?5 [3 Z3 z- w
as testotoxicosis, may cause precocious puberty at a
6 `) ^: v- C% T1 F4 avery young age. The physical findings in these boys
% L$ [- @4 ~  g$ f, h  B* |with this disorder are full pubertal development,( [  N9 M4 r; B) c
including bilateral testicular growth, similar to boys' x  f6 k  j9 `8 A4 d
with CPP. The gonadotropin levels in this disorder
$ [  [0 _5 u: @" p  p6 g# L  nare suppressed to prepubertal levels and do not show
) m' e+ w5 J- k2 fpubertal response of gonadotropin after gonadotropin-
6 w4 y- p, t: v+ F" greleasing hormone stimulation. This is a sex-linked  |; ]' K# U9 E( M/ c
autosomal dominant disorder that affects only
& z  N5 ]/ c: W6 e9 mmales; therefore, other male members of the family
% X& V2 W, w+ s* \; ^% S$ u( d+ @5 xmay have similar precocious puberty.3
% E5 i8 X: J4 ~' W, DIn our patient, physical examination was incon-5 A: Y% i* `* q: W3 X: u, ]! o
sistent with true precocious puberty since his testi-$ o7 k; V8 |* m( ~! b6 z. V
cles were prepubertal in size. However, testotoxicosis! \" r+ r/ J& r8 y( j8 }0 l
was in the differential diagnosis because his father9 z1 R9 B- O* ?6 U8 x2 Z- {+ n1 Q
started puberty somewhat early, and occasionally,
, _% z- o; l. h. J+ mtesticular enlargement is not that evident in the2 e3 Q. k0 ~$ z7 @8 J4 x' b+ ]* I
beginning of this process.1 In the absence of a neg-2 k' T1 Z8 `$ h0 p
ative initial history of androgen exposure, our" n5 J. }+ w& S/ S* G& y
biggest concern was virilizing adrenal hyperplasia,
# A( q& d4 c0 z; h6 j( p2 Aeither 21-hydroxylase deficiency or 11-β hydroxylase: b) }- l0 p! W' S6 @
deficiency. Those diagnoses were excluded by find-! [" Q. d+ p: {# y( o( h7 C
ing the normal level of adrenal steroids.
0 a  L+ T) g  e5 O( ^. SThe diagnosis of exogenous androgens was strongly
7 n$ u; D- P7 ~  ksuspected in a follow-up visit after 4 months because7 B* \' i0 o$ v! A! L9 T* Z3 p
the physical examination revealed the complete disap-
* D+ S( U5 o3 z! `* M$ wpearance of pubic hair, normal growth velocity, and2 x- _4 u. |2 b
decreased erections. The father admitted using a testos-
; z. U" _+ Y: a& u5 R4 Aterone gel, which he concealed at first visit. He was& c$ e  z2 }9 x- ~0 U) f
using it rather frequently, twice a day. The Physicians’0 i. t! N! ~6 c  _4 V
Desk Reference, or package insert of this product, gel or! z2 S# B/ A. Y1 J; A- j
cream, cautions about dermal testosterone transfer to
3 e# y, `  n6 L8 s" ?unprotected females through direct skin exposure.
8 I6 T- |" o8 X- I; G% v% iSerum testosterone level was found to be 2 times the
7 y% v! E0 t5 B" [baseline value in those females who were exposed to; X) w" `: @' @# z0 w' E
even 15 minutes of direct skin contact with their male
& S- q8 Y- ?) ~  D" A/ k5 `" ppartners.6 However, when a shirt covered the applica-: n* E" _/ [9 Q5 m; ~: p. `: \
tion site, this testosterone transfer was prevented.
# V; I1 p0 E8 e+ m: J3 _Our patient’s testosterone level was 60 ng/mL,- J4 {! h* m) g" f  R
which was clearly high. Some studies suggest that4 ]$ T5 S7 W& _8 w, l
dermal conversion of testosterone to dihydrotestos-7 v. l, j) b, t( J+ T
terone, which is a more potent metabolite, is more
( J4 e- G# f: R7 x5 O! pactive in young children exposed to testosterone1 t5 _# g  W0 l3 B4 t/ W& X+ J5 U+ L
exogenously7; however, we did not measure a dihy-3 T$ a9 u/ A6 _- S* i# @) q9 J
drotestosterone level in our patient. In addition to; p7 ?3 p3 T0 Y( n! q
virilization, exposure to exogenous testosterone in' @) Q& I8 M3 k6 a. w
children results in an increase in growth velocity and) Q% ]. W0 c$ D1 a( O2 u
advanced bone age, as seen in our patient." T0 K7 `8 C; L1 q$ l) S+ n
The long-term effect of androgen exposure during8 p! H8 I. a  R9 e
early childhood on pubertal development and final+ G; k& `2 B3 W
adult height are not fully known and always remain
3 Q3 o8 k8 T' Q# B$ na concern. Children treated with short-term testos-
) k# ]8 G0 k3 j3 Gterone injection or topical androgen may exhibit some
5 l. t$ p" V2 \acceleration of the skeletal maturation; however, after
1 @. S! G, A& w0 I5 ncessation of treatment, the rate of bone maturation; J9 K# U9 f3 n& F# I( p
decelerates and gradually returns to normal.8,9/ c+ R* J* S' \, ?  F  W  n$ r; R
There are conflicting reports and controversy+ K9 Y3 o2 x% M" N1 v; I/ |( l( l
over the effect of early androgen exposure on adult
" S, o9 ?. w4 S- Fpenile length.10,11 Some reports suggest subnormal2 q& S) \8 r0 C, O
adult penile length, apparently because of downreg-* R6 S4 a9 U9 G: K3 }
ulation of androgen receptor number.10,12 However,
, q/ \, w, C8 v& rSutherland et al13 did not find a correlation between! Y8 E' h6 s* K" o" ?+ t
childhood testosterone exposure and reduced adult& e& ~' W" y3 E+ a
penile length in clinical studies.
4 [# L+ M6 \! O/ y- x2 GNonetheless, we do not believe our patient is( p+ |, }8 R; v  N
going to experience any of the untoward effects from
  m9 e9 ^# e8 C$ C' Xtestosterone exposure as mentioned earlier because! r/ }' m' i* W6 V3 H4 F
the exposure was not for a prolonged period of time.
* f) ]( C) K: o. U* E5 O* FAlthough the bone age was advanced at the time of
4 Z+ b/ Z8 f, @! Q5 V; Udiagnosis, the child had a normal growth velocity at
7 r1 L6 \) n' q# z9 Y0 V+ F! Bthe follow-up visit. It is hoped that his final adult) O* d/ K! \' [4 z$ Q0 f
height will not be affected.
1 W$ k! f+ w3 B  U7 {" \" ?8 sAlthough rarely reported, the widespread avail-
5 Z: t; I' j+ ^( ]ability of androgen products in our society may
: I7 Y2 z' g/ P- ]: f& V) hindeed cause more virilization in male or female
: K0 X, y/ w9 ?& G1 c& i8 Q5 g6 r" rchildren than one would realize. Exposure to andro-! o7 P' \/ A$ V+ S0 o6 X1 o% S& Y
gen products must be considered and specific ques-* `  V, K3 d% e7 q2 j
tioning about the use of a testosterone product or  R! w2 }+ H8 l6 `( R$ Y
gel should be asked of the family members during+ g, }+ B/ _  `: A6 I! o# W7 L
the evaluation of any children who present with vir-
6 c0 ]% Y5 y% V; d8 J4 m# Silization or peripheral precocious puberty. The diag-& S7 e/ V9 ~: A4 Z) ?' a, L8 D
nosis can be established by just a few tests and by' K! _; X* w# d5 A6 w" }
appropriate history. The inability to obtain such a/ ]$ p1 C. W5 j- q$ w2 o$ Y+ R9 D- `
history, or failure to ask the specific questions, may: W9 s- A  v9 V+ W7 C
result in extensive, unnecessary, and expensive
0 ]! z, x& O3 l2 Binvestigation. The primary care physician should be6 P! z8 Q* z7 S; ?0 g3 {  L
aware of this fact, because most of these children
. t* j1 X7 c8 P: i  cmay initially present in their practice. The Physicians’
5 [% g; y5 j% L3 k9 oDesk Reference and package insert should also put a7 Q# J5 \$ i) U8 S
warning about the virilizing effect on a male or
0 D" d1 P# B4 {5 \female child who might come in contact with some-- m9 |4 G& S. S; m" M/ u9 E
one using any of these products.
0 U  R- O1 u. T  z9 zReferences# }% O* s/ }  p% s+ ]
1. Styne DM. The testes: disorder of sexual differentiation
6 w  c' w; D$ R. [6 X9 {5 A* h; P/ S# Hand puberty in the male. In: Sperling MA, ed. Pediatric  z( A% ^% P% e* D- d4 i
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;& g0 @1 n4 a0 _/ o, `) ]
2002: 565-628.
$ V6 _! V4 P& j: R2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
  f# R0 }- _$ s, Kpuberty 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
2 l; W1 s/ L/ c8 V) l0 G& x
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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