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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
# z' a8 j, W! [$ V. M* g3 KBoy Induced by Indirect Topical
" |$ k+ @8 v4 a  m( F$ V  Q6 _- tExposure to Testosterone
- f% n. w4 b7 S5 c7 ESamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2' ~$ p! z, S  w& B9 i, y: s) Q/ `
and Kenneth R. Rettig, MD1
0 t0 [" |* P7 O* HClinical Pediatrics
' M$ L& ~) L* N7 `Volume 46 Number 6
5 a$ ?3 N0 D" L; m+ p% p9 AJuly 2007 540-5439 y0 d7 m) |7 g2 T: K
© 2007 Sage Publications
/ _" t. v0 f! i. n- n10.1177/0009922806296651
. t' _8 U: ^$ V+ A; d6 U8 A) j9 \6 Ohttp://clp.sagepub.com& u: B  N5 l3 |$ d2 D
hosted at
: r3 Y* n( G# s& T* zhttp://online.sagepub.com6 h# m0 c3 l/ ^& h
Precocious puberty in boys, central or peripheral,9 C* w9 x# p+ h, B! V0 ?- _
is a significant concern for physicians. Central/ Y0 v6 _6 ]8 Z- u( W! H. X, f
precocious puberty (CPP), which is mediated) L' I. ^/ C7 _  J! t
through the hypothalamic pituitary gonadal axis, has% {& E9 {( g) x' ~1 O. e) a! \3 {
a higher incidence of organic central nervous system( K1 K4 \/ C+ _1 |8 {
lesions in boys.1,2 Virilization in boys, as manifested
, t4 h) ?' @& |5 O- @' Iby enlargement of the penis, development of pubic
" h- M; P# _7 f  ~& Uhair, and facial acne without enlargement of testi-$ y7 Z. x" \% P1 c4 G4 J! s
cles, suggests peripheral or pseudopuberty.1-3 We+ `! a" y3 u( X; V: b8 S
report a 16-month-old boy who presented with the
$ Q. D4 e/ i3 u0 H( x. B" b8 cenlargement of the phallus and pubic hair develop-
4 }2 Q, ~* [2 K2 ?7 I5 Zment without testicular enlargement, which was due+ Y+ j6 g. U1 |0 J
to the unintentional exposure to androgen gel used by0 Y& [) j$ G( O4 J
the father. The family initially concealed this infor-; d) L& I# A* X' v5 _
mation, resulting in an extensive work-up for this' Y+ l8 Y1 e. ]. T6 Y
child. Given the widespread and easy availability of$ ]2 P* p$ a" z
testosterone gel and cream, we believe this is proba-
3 H8 i* n0 F% x$ ~) Xbly more common than the rare case report in the
: U7 Z- i- A# L+ `literature.4
3 I5 H' H$ H+ l* n: R. }" A: R/ EPatient Report' T. `: Z/ h# p. Z5 _7 U7 y
A 16-month-old white child was referred to the
5 Y+ Z( @0 R. ^- s! i) x% Y; Rendocrine clinic by his pediatrician with the concern* e. D; ~- ]: F( l
of early sexual development. His mother noticed6 F# Q% K! c5 T7 v  i( P! ^
light colored pubic hair development when he was
% M5 l4 F( L$ y; `From the 1Division of Pediatric Endocrinology, 2University of
# h2 q, G" e8 A, ]( HSouth Alabama Medical Center, Mobile, Alabama./ J8 x. s- k! `, M; g8 r
Address correspondence to: Samar K. Bhowmick, MD, FACE,- d  i7 j( l2 p5 X8 i9 U0 }
Professor of Pediatrics, University of South Alabama, College of
8 S, g3 B8 I* f; JMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
& ?$ X( R+ i$ e9 I1 L+ Je-mail: [email protected].$ d, m; i, d# E1 e2 n7 `
about 6 to 7 months old, which progressively became8 Z0 Q0 B' G( \; j8 R
darker. She was also concerned about the enlarge-$ z* u" a( s: a5 [3 [* w9 e
ment of his penis and frequent erections. The child3 q$ Y+ W- B4 I, X9 ~. z
was the product of a full-term normal delivery, with8 P+ N4 T  p( e1 \- y* u( E
a birth weight of 7 lb 14 oz, and birth length of$ n: i; j: ]( K# |
20 inches. He was breast-fed throughout the first year! Z2 o1 q- H! R
of life and was still receiving breast milk along with
$ l+ }' K/ f) M' }/ d, L4 ^" \1 esolid food. He had no hospitalizations or surgery,1 z3 e. Z! J8 t7 c! h
and his psychosocial and psychomotor development
1 ]. j' Q7 t7 n: U! Vwas age appropriate.
) V4 q! A- {( H- k& n1 V6 r7 SThe family history was remarkable for the father,, t( z- h9 m& L" y
who was diagnosed with hypothyroidism at age 16,, i4 f- }5 B6 o
which was treated with thyroxine. The father’s% o& l, n6 @3 B
height was 6 feet, and he went through a somewhat, B, J' {- P& W/ ]3 Q
early puberty and had stopped growing by age 14.
7 F  \% k* D" x3 I3 [The father denied taking any other medication. The( ^  i( D% b. Z# ?% \3 N
child’s mother was in good health. Her menarche4 t: s& G9 O- G4 f( b  S* f5 d
was at 11 years of age, and her height was at 5 feet
, o' i0 m: l0 X3 V5 inches. There was no other family history of pre-
; @- ]& M1 T! q0 `  h2 A& K! v& Ncocious sexual development in the first-degree rela-
. v  C  }1 |5 c4 K5 ptives. There were no siblings.% e& r! E' x5 K  N
Physical Examination5 `. r. X; g+ d8 f, ^
The physical examination revealed a very active,5 _- _7 b0 ]9 A$ l3 s$ O1 L* A
playful, and healthy boy. The vital signs documented8 j, n! S) Q7 I$ Y
a blood pressure of 85/50 mm Hg, his length was
7 }8 R! @6 n  C. N$ g+ q90 cm (>97th percentile), and his weight was 14.4 kg! T3 p- b% o$ R5 x8 e" F3 ]
(also >97th percentile). The observed yearly growth
$ L: `% P5 L9 D* E' c. cvelocity was 30 cm (12 inches). The examination of6 [+ j/ H' o1 ^( j- s' [$ g& P
the neck revealed no thyroid enlargement.0 V% @( R# F; E. g( U* F. u/ C
The genitourinary examination was remarkable for& S0 j9 u/ Z3 N! n( J( r+ b/ F
enlargement of the penis, with a stretched length of/ i) ^( [9 U+ U; g
8 cm and a width of 2 cm. The glans penis was very well& c" e" k2 ]" U1 P
developed. The pubic hair was Tanner II, mostly around
. i$ g- z: U' z' _- u4 T, r540
4 b7 z/ |+ R. Eat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
' R, S5 M  k, b: gthe base of the phallus and was dark and curled. The
' E) O0 B0 L5 r3 O) G# }testicular volume was prepubertal at 2 mL each.
! B8 s0 C) Y1 l4 oThe skin was moist and smooth and somewhat
( N! b3 v  g* @, R1 E- ~! L" o1 A1 zoily. No axillary hair was noted. There were no/ v$ Y, q* x9 f' g+ z# t3 B
abnormal skin pigmentations or café-au-lait spots.. Q( k! G9 ~, `9 Y
Neurologic evaluation showed deep tendon reflex 2+
. H* p) m3 e0 r1 Ebilateral and symmetrical. There was no suggestion& C( G; e9 w& }* `. n7 P
of papilledema.- c( s9 s. R- H! J2 R
Laboratory Evaluation
0 \5 N5 K1 ?; p. `' I/ V' QThe bone age was consistent with 28 months by
& {- r  [! {9 \. ?9 u' Tusing the standard of Greulich and Pyle at a chrono-: h4 B+ _* d, U; a0 U* p
logic age of 16 months (advanced).5 Chromosomal
0 G6 m8 `$ r: F& M# Bkaryotype was 46XY. The thyroid function test
( m' o2 o& \& b" o5 Gshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
! z" x1 o1 @, r" qlating hormone level was 1.3 µIU/mL (both normal).
0 M1 Q# L6 N6 x& \The concentrations of serum electrolytes, blood' J% V% ]2 T* o- W
urea nitrogen, creatinine, and calcium all were+ D/ h2 @/ N, Y7 A! u" {9 c
within normal range for his age. The concentration; V- J$ ^+ a$ z2 K1 A* e/ w
of serum 17-hydroxyprogesterone was 16 ng/dL% B/ l4 r  t# K- X8 J( Q' T) a
(normal, 3 to 90 ng/dL), androstenedione was 20. E' F# U3 ^7 Q- N
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-2 @* u2 u' T, w8 t5 L/ S& y5 \
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
/ u  U$ c: }' T: Sdesoxycorticosterone was 4.3 ng/dL (normal, 7 to
0 y; J3 ^& h+ P  M( g49ng/dL), 11-desoxycortisol (specific compound S)
  F( ~) Z) u- Z: ~. T' xwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
: S7 ~+ g3 C# n1 ?/ H2 n3 dtisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total. q2 j4 j# I2 d: P! L* O+ d
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
; d0 m# W. Q1 R1 F' P& uand β-human chorionic gonadotropin was less than5 R9 q2 y- y1 X; ]
5 mIU/mL (normal <5 mIU/mL). Serum follicular
5 Z- O% z3 c3 T6 O; p1 v8 dstimulating hormone and leuteinizing hormone
/ j5 _* Q# p) H; j. pconcentrations were less than 0.05 mIU/mL( Q2 ]) u* G9 H' I( }* h4 x
(prepubertal).
6 p5 r) Q$ D  ?, r, j+ yThe parents were notified about the laboratory
5 g/ \, C# L& l. }results and were informed that all of the tests were* W1 n/ u. v  G+ _' C
normal except the testosterone level was high. The
  K  m% S0 Z" p* Qfollow-up visit was arranged within a few weeks to& v' [' ^3 Q3 v7 _2 q- n
obtain testicular and abdominal sonograms; how-, J7 ?. o+ m' `% Q
ever, the family did not return for 4 months.
. p* J& f' [/ d: [9 cPhysical examination at this time revealed that the$ m) V( F) v2 y" W7 U# ~
child had grown 2.5 cm in 4 months and had gained
, }4 _2 O1 V: d$ Q1 n6 t+ N2 kg of weight. Physical examination remained- A: L" C/ G, n' [* y% r
unchanged. Surprisingly, the pubic hair almost com-
. B. ~+ v& C- F) h( c4 Q6 k" qpletely disappeared except for a few vellous hairs at
4 L9 M2 p+ G+ Y* l' \9 Lthe base of the phallus. Testicular volume was still 2/ u, q$ z- g. M9 }) s$ v2 e
mL, and the size of the penis remained unchanged.
' D. c5 c  i# e/ K2 g# \9 QThe mother also said that the boy was no longer hav-
& @+ c( d- D" t+ n" ~8 xing frequent erections.
3 N. r& p& q- k5 n& TBoth parents were again questioned about use of
( x" m3 L9 r! V) Jany ointment/creams that they may have applied to
" R- M2 r2 j3 c# r9 E! @' D: ethe child’s skin. This time the father admitted the6 [1 z6 E! Z1 s7 w0 y2 i
Topical Testosterone Exposure / Bhowmick et al 541
& v( ?2 z/ [  B4 W# d" x4 Tuse of testosterone gel twice daily that he was apply-  G" o, W: }. m. I2 C  T
ing over his own shoulders, chest, and back area for
) n) D- @( {3 u: v; J* T$ Ca year. The father also revealed he was embarrassed& E6 t/ t1 [( x
to disclose that he was using a testosterone gel pre-: F, R+ ^& I. l
scribed by his family physician for decreased libido
& m. E3 r8 c. y! bsecondary to depression.
. Q, y+ [& ], ]3 ^The child slept in the same bed with parents.' i  p( _- \% a7 P7 E" T
The father would hug the baby and hold him on his. [( Z2 P. V1 L& Y8 ?5 z! @
chest for a considerable period of time, causing sig-
6 ?  l* g* W& F  P% ]; |1 k6 _: h8 Rnificant bare skin contact between baby and father.
7 B9 ?! S" k& B  n& D0 S2 K5 O- [) B% zThe father also admitted that after the phone call,
' g5 a9 C. e, v3 k) Y; owhen he learned the testosterone level in the baby- D/ D5 c9 F" K1 c
was high, he then read the product information
0 b9 L8 S; y! j% ]8 K7 T3 \packet and concluded that it was most likely the rea-) p" _3 |$ e$ B$ u# E5 a
son for the child’s virilization. At that time, they
% Q0 S3 q/ ]) Kdecided to put the baby in a separate bed, and the3 ^( g: P+ |# Y
father was not hugging him with bare skin and had! `; {1 N* F( o/ ]8 v0 Z0 Q  q7 Q
been using protective clothing. A repeat testosterone) m3 W/ V* ~& J* ^( ]0 K0 U
test was ordered, but the family did not go to the  e- [; M. [. h/ F5 i5 O" V
laboratory to obtain the test.) v! O" V9 x4 z. f& C9 g
Discussion0 ?$ |/ `, B. ~- W! f3 q1 m
Precocious puberty in boys is defined as secondary
2 O' e& V  q5 w: S" V2 k3 osexual development before 9 years of age.1,46 j5 D: r! S  H/ I2 C& I" a2 K
Precocious puberty is termed as central (true) when
3 m0 G! Y+ I2 y' V& c3 {" t& ]it is caused by the premature activation of hypo-
/ o' b+ F8 q; `2 N9 ~; i8 V- d6 Mthalamic pituitary gonadal axis. CPP is more com-0 g; b! K5 L4 t" K& ^4 {$ B" V
mon in girls than in boys.1,3 Most boys with CPP* W$ E, X/ F" b3 S
may have a central nervous system lesion that is* v7 p! J  `5 a
responsible for the early activation of the hypothal-" C0 I; W! c5 Y& ?1 m; j2 z) S
amic pituitary gonadal axis.1-3 Thus, greater empha-
8 W! u8 Q* c/ h3 X- X8 h2 e$ D2 qsis has been given to neuroradiologic imaging in
- o/ @) N% [3 k. B$ q7 a6 k, `boys with precocious puberty. In addition to viril-2 K: m' b! o( k; h0 ]& m" L; n/ Z
ization, the clinical hallmark of CPP is the symmet-$ ]7 w) [! a' i- d6 K$ b  A( n8 L- ^
rical testicular growth secondary to stimulation by0 ~7 J' N/ {- V* Q- C
gonadotropins.1,38 ^6 A( A# i4 D; ~$ z/ {6 c! o
Gonadotropin-independent peripheral preco-
# J) d6 M5 Y% m- H1 Bcious puberty in boys also results from inappropriate+ E5 ?- h* n. x6 G" A
androgenic stimulation from either endogenous or
" `# `8 c, T2 ^exogenous sources, nonpituitary gonadotropin stim-
. C% b# c* s+ `$ i, A. y! J+ Z% aulation, and rare activating mutations.3 Virilizing5 B. c- o' G) e' |
congenital adrenal hyperplasia producing excessive* A6 G+ X! l: A) @
adrenal androgens is a common cause of precocious" w( Z4 x+ D; r: w" _( E$ P
puberty in boys.3,49 k1 P( U. Z- o& Q& Y; q$ s6 l
The most common form of congenital adrenal
" F* t! v8 ]& `/ Q7 Q8 u  k. E, N( yhyperplasia is the 21-hydroxylase enzyme deficiency.0 b( [3 y6 Z1 d" X) `8 |* E) d
The 11-β hydroxylase deficiency may also result in
: X- f: t5 h- S. E9 F7 a! Yexcessive adrenal androgen production, and rarely,1 t& h8 S- V3 [% }# V8 J
an adrenal tumor may also cause adrenal androgen
  s. @9 y1 z& w1 [: O  U& v9 E; aexcess.1,3
2 e7 G0 \" k9 O# Iat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
$ \! n3 G8 T4 N! t! x1 m542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
$ I- d' w1 Q: a$ q( HA unique entity of male-limited gonadotropin-* E3 t. m% S4 B
independent precocious puberty, which is also known1 v% l2 I( Z5 f) x7 P' C
as testotoxicosis, may cause precocious puberty at a/ e5 d4 o2 u9 r# C& o" C' h1 q
very young age. The physical findings in these boys/ z0 k1 X2 W6 S! S
with this disorder are full pubertal development,/ G( k' Y+ {5 D9 N0 b
including bilateral testicular growth, similar to boys9 F6 |0 C9 n: W* a) d' l, L
with CPP. The gonadotropin levels in this disorder
- v3 t! Q6 E+ K; t- lare suppressed to prepubertal levels and do not show0 Q( U" T, M; `3 Q
pubertal response of gonadotropin after gonadotropin-
8 F9 K$ X+ B) l: Z+ @& |releasing hormone stimulation. This is a sex-linked) ?. L3 R7 l" M
autosomal dominant disorder that affects only
  l( G$ S  j1 b5 ]2 E& X4 Ymales; therefore, other male members of the family
" j: I, o; T  u1 pmay have similar precocious puberty.31 d1 E, m# m1 f- X% K4 [; G
In our patient, physical examination was incon-
" d0 u: x  s+ T0 R' q. osistent with true precocious puberty since his testi-
9 K* b( U, |; V3 P! P- ~cles were prepubertal in size. However, testotoxicosis
  H2 }8 ]6 e6 Wwas in the differential diagnosis because his father- s1 G' _: |* N6 n4 e" J
started puberty somewhat early, and occasionally,
3 I3 n* ~# g9 i5 ^1 qtesticular enlargement is not that evident in the8 S% |" M  U8 [; t- X4 r  ?# q
beginning of this process.1 In the absence of a neg-
' F& ?  ?& k) ^$ a& pative initial history of androgen exposure, our, f3 m; v, R& R; S0 C6 V: Z
biggest concern was virilizing adrenal hyperplasia,
) M% w; D9 p; W$ l, yeither 21-hydroxylase deficiency or 11-β hydroxylase8 @* O3 j+ s4 x3 R7 Q/ b
deficiency. Those diagnoses were excluded by find-
5 O  R6 ?- w* Q% T" ging the normal level of adrenal steroids.4 Z2 e7 g! w$ c$ ~- K' `
The diagnosis of exogenous androgens was strongly/ [9 T" {, G0 z$ m
suspected in a follow-up visit after 4 months because& B9 K! R! ~) n- X3 p& K) s
the physical examination revealed the complete disap-) R$ s8 S) o8 N# X
pearance of pubic hair, normal growth velocity, and
0 {( M# A' A) C  ^; d2 G" |9 Cdecreased erections. The father admitted using a testos-
- T' k' q! o- F. e& dterone gel, which he concealed at first visit. He was
7 V9 f; X) ?4 u( E3 \* @3 tusing it rather frequently, twice a day. The Physicians’
3 ?% H- ~$ h5 f- c$ E7 xDesk Reference, or package insert of this product, gel or
& F  C; j9 g1 ?0 E* L6 x. z! Acream, cautions about dermal testosterone transfer to
  e7 a$ t7 m+ G# I  O9 [$ iunprotected females through direct skin exposure.
& @7 U( H2 T( x" fSerum testosterone level was found to be 2 times the9 K- f5 m1 I2 Q0 e
baseline value in those females who were exposed to' M6 V6 b" ]  t7 v
even 15 minutes of direct skin contact with their male5 J7 D) r4 b: i5 z$ {2 o
partners.6 However, when a shirt covered the applica-: t" F( S& A8 ?) D3 w+ D% ~
tion site, this testosterone transfer was prevented.+ k5 K4 v" u" Q# D8 c5 u# c& u
Our patient’s testosterone level was 60 ng/mL,% p* D+ G8 r9 y
which was clearly high. Some studies suggest that
4 r$ C1 C2 F, V  h) kdermal conversion of testosterone to dihydrotestos-$ U) j3 G$ `; o2 f8 x
terone, which is a more potent metabolite, is more/ D; s; L7 H8 V9 a  w7 t: i
active in young children exposed to testosterone
& b' a- {1 A% i* Jexogenously7; however, we did not measure a dihy-7 F9 j) v1 G- N' V+ u
drotestosterone level in our patient. In addition to/ V- h! ]$ ]1 r! z, x
virilization, exposure to exogenous testosterone in
: Q* m8 o, O9 C& O: O% D4 |children results in an increase in growth velocity and) o: o* d2 M, e, J
advanced bone age, as seen in our patient.: p: @: `% H7 ]% n
The long-term effect of androgen exposure during
  i9 h$ D  Z- r8 \& Dearly childhood on pubertal development and final, ]  [2 }: u9 f+ |  m  \
adult height are not fully known and always remain
( U: X' V  X2 c% da concern. Children treated with short-term testos-3 ]% A. g7 K7 L$ v: W: H
terone injection or topical androgen may exhibit some
* a" ?- q8 A6 R: H$ ]acceleration of the skeletal maturation; however, after- Z; a+ n( ]3 c' S+ l9 s
cessation of treatment, the rate of bone maturation
  V) m+ y+ C6 ~! Jdecelerates and gradually returns to normal.8,92 `. ]4 ^* R; l% k
There are conflicting reports and controversy
! n. n3 c6 d$ b# N, N, j$ ?( u8 Fover the effect of early androgen exposure on adult
/ Y: R; D) Q1 k! m4 Z) d$ Xpenile length.10,11 Some reports suggest subnormal
) ]- g0 J! u9 a$ W- ]3 e. zadult penile length, apparently because of downreg-* `! e3 u5 U7 E
ulation of androgen receptor number.10,12 However,
; y* {2 G7 u1 i9 p' P" g$ X5 JSutherland et al13 did not find a correlation between( t+ @, T8 A; F5 O/ v% t6 ^
childhood testosterone exposure and reduced adult
* v0 E/ \& s, Y3 npenile length in clinical studies.
- l5 Q0 b8 z0 m& Y0 O0 ?7 mNonetheless, we do not believe our patient is
4 t9 N) x6 j8 Hgoing to experience any of the untoward effects from
  `& _7 Q- T$ ^! y& @; x: D' @! k, stestosterone exposure as mentioned earlier because3 O$ m& H3 I$ H. q  Z6 f% L
the exposure was not for a prolonged period of time.2 h. k9 f2 _; j; }
Although the bone age was advanced at the time of
2 g4 V7 D2 E" Q( ?, H+ s# @& V1 ndiagnosis, the child had a normal growth velocity at
9 v% l9 ^  W; Vthe follow-up visit. It is hoped that his final adult
) G! k& V9 T1 W1 Fheight will not be affected.( @; S& v# P8 X' O2 O4 P4 X
Although rarely reported, the widespread avail-
  C: c7 B6 v6 l; z/ }! kability of androgen products in our society may; G5 O8 k6 W* X% H$ l" R8 b
indeed cause more virilization in male or female' E* a7 N# z2 L3 F4 \5 _" ~
children than one would realize. Exposure to andro-) R# h. [( b; o6 Y
gen products must be considered and specific ques-5 @. h! i# G% W4 s5 b& L
tioning about the use of a testosterone product or: j$ {% |# o( r1 F3 z
gel should be asked of the family members during6 f6 ]+ M0 \- o4 A( a6 Y6 Q
the evaluation of any children who present with vir-8 K1 i6 _: ^$ Z# }
ilization or peripheral precocious puberty. The diag-8 T# g$ ]( G" L( p- [5 Q* t) ]
nosis can be established by just a few tests and by
  D/ A; t2 v7 X4 a* {appropriate history. The inability to obtain such a+ c; U6 k. i- t. A2 Z
history, or failure to ask the specific questions, may2 k' i: g% m* ]
result in extensive, unnecessary, and expensive1 f, K9 q0 s% \( ]$ n1 J
investigation. The primary care physician should be: q0 U& A6 N- k3 e2 H4 U
aware of this fact, because most of these children
: Z% l! L& t) I* e1 D: Bmay initially present in their practice. The Physicians’
3 p: Z, l* ]! d; o" eDesk Reference and package insert should also put a
* u1 V7 F6 w3 ]! @. awarning about the virilizing effect on a male or; _# S& k/ e7 }' ^; m
female child who might come in contact with some-6 p+ l5 g5 }! {8 h9 e" x
one using any of these products.  P7 K1 y! }4 d- ^, L* _
References
3 q* }# n1 p  R, J% f1. Styne DM. The testes: disorder of sexual differentiation
$ O, u' ]9 _" g- \and puberty in the male. In: Sperling MA, ed. Pediatric
" S* q" R" S- E+ DEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;( S8 X: F- l1 }  m2 C) F) X
2002: 565-628.
- H& i4 F! E9 E8 ~. r% ]; ?2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
( }) G7 D# E. H% hpuberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old) X: ?: u+ S; w! B
Boy Induced by Indirect Topical/ a: i' H0 L) |* A9 E; U
Exposure to Testosterone: b# w4 o( c  U' d- o
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
. }' E0 M/ P& uand Kenneth R. Rettig, MD1) }$ R$ \* U3 h4 G+ ?& E
Clinical Pediatrics0 b2 r: D2 C6 y
Volume 46 Number 6  Y8 \. F) Z0 E/ J
July 2007 540-543
% U9 A) U2 U" z( Z, a1 F© 2007 Sage Publications' S: R+ M. R: s
10.1177/0009922806296651
% q; M4 r+ j1 c3 R% ~/ H4 zhttp://clp.sagepub.com! M6 V/ x+ i' S0 f
hosted at
( a  [4 q' |* Xhttp://online.sagepub.com7 ^: v& \% x' G9 I  v( [# A. g2 O5 [
Precocious puberty in boys, central or peripheral,
3 H+ W) Z& J9 C1 C5 Y4 lis a significant concern for physicians. Central
% f9 o( @" n! Vprecocious puberty (CPP), which is mediated# _/ E" ?$ j  L
through the hypothalamic pituitary gonadal axis, has
: F; {5 p3 c3 T. Ka higher incidence of organic central nervous system
2 J6 }/ B* L. N# i5 a  Ylesions in boys.1,2 Virilization in boys, as manifested% d2 o) y% o' ^$ {$ N$ j
by enlargement of the penis, development of pubic6 t7 _$ c" i- E- K
hair, and facial acne without enlargement of testi-; r2 `2 S+ ~% N" O* t3 k* T" c+ ~" G
cles, suggests peripheral or pseudopuberty.1-3 We
0 H' j6 w: ]# `  g9 v: Z& U/ w  M6 Areport a 16-month-old boy who presented with the4 w1 ?' y9 }" g& j
enlargement of the phallus and pubic hair develop-& A; L' f3 V, ]- l+ v9 U/ B
ment without testicular enlargement, which was due1 L1 {$ o# i  [0 D8 M  D8 t
to the unintentional exposure to androgen gel used by$ U: d2 D! D7 R2 N# l, g$ F2 B
the father. The family initially concealed this infor-
2 h. B' u8 v& N# T3 Wmation, resulting in an extensive work-up for this
0 g  l: }3 d1 o. x" xchild. Given the widespread and easy availability of
) m; {6 m* j# P. W- Stestosterone gel and cream, we believe this is proba-$ C5 G9 f  z; t  e8 [1 ^) Q: Z# [
bly more common than the rare case report in the
( a! z8 H2 }  }2 Q9 k8 U+ W0 k" L+ B  Dliterature.4
+ o8 m5 w' J2 g8 ]$ {7 _/ zPatient Report5 ]4 P6 ?, [. M; h0 v
A 16-month-old white child was referred to the
) F8 V. ?, E$ W. q) Vendocrine clinic by his pediatrician with the concern! B0 t/ y; t( N2 N7 K
of early sexual development. His mother noticed- g. X) H* D% _# o! M
light colored pubic hair development when he was
' V6 v  x4 b- `' c3 G! I% JFrom the 1Division of Pediatric Endocrinology, 2University of  ?6 i; n, s& Y) ~+ l" z, _& o- j
South Alabama Medical Center, Mobile, Alabama.- O; p4 k" s9 V* o& g+ v; f
Address correspondence to: Samar K. Bhowmick, MD, FACE,
5 \* F+ }1 P3 q, z, [Professor of Pediatrics, University of South Alabama, College of6 _) |" [7 c1 ^
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;2 B. c. l* ^4 g
e-mail: [email protected].
& S' g$ s+ m4 iabout 6 to 7 months old, which progressively became1 `: ~1 M( a8 z9 z& N) s
darker. She was also concerned about the enlarge-0 [& B/ q% ^5 V: J" P( f* l
ment of his penis and frequent erections. The child
0 ]9 B* J+ D7 a, bwas the product of a full-term normal delivery, with$ p6 G7 B: [9 w
a birth weight of 7 lb 14 oz, and birth length of3 D+ }; H: @/ ^4 Y4 j+ {0 K
20 inches. He was breast-fed throughout the first year! R! O. V! H/ Z+ _) e2 O' G
of life and was still receiving breast milk along with; E! p" ^" j' U- ^5 W
solid food. He had no hospitalizations or surgery,# e0 S( X  L& Z4 l5 r
and his psychosocial and psychomotor development
. G9 k: Z+ J: {- fwas age appropriate.
5 I* J4 i* F; xThe family history was remarkable for the father,# w! l1 z8 Y# O
who was diagnosed with hypothyroidism at age 16,
4 r  c% X2 f! x7 f  ?) swhich was treated with thyroxine. The father’s& _. Y  T8 P) ?+ j2 x$ J0 J+ }' z
height was 6 feet, and he went through a somewhat. V4 H% T+ M) q& x* J5 D
early puberty and had stopped growing by age 14.
$ S' C, f4 L: `2 MThe father denied taking any other medication. The) _7 r" d) P2 Y3 E, U3 ^4 c1 X
child’s mother was in good health. Her menarche+ W5 Q) m) ^5 V" G# b
was at 11 years of age, and her height was at 5 feet
8 X& k$ z" `  a4 h5 inches. There was no other family history of pre-1 S$ q  ]' `8 p! m2 r. t) k: j
cocious sexual development in the first-degree rela-
% i9 d6 v2 L2 y' t& F$ o. {8 itives. There were no siblings.
4 ^+ O4 }* n. k5 @) `2 g; VPhysical Examination; A" O+ i9 {# ]# E; b
The physical examination revealed a very active,: W( G% P9 b( y* Z9 ?" i
playful, and healthy boy. The vital signs documented
% S  \) p" s0 X$ Sa blood pressure of 85/50 mm Hg, his length was
. O& ^8 y! f9 `7 ]7 M6 ~90 cm (>97th percentile), and his weight was 14.4 kg
1 F& l8 g' F0 l* e(also >97th percentile). The observed yearly growth
0 c& I3 d6 F# jvelocity was 30 cm (12 inches). The examination of; Q' G2 p/ ?6 d/ w0 M8 X
the neck revealed no thyroid enlargement.& Q8 X/ H! e; u' t0 G# z: _* `; [
The genitourinary examination was remarkable for* J+ G+ r. r( S* I
enlargement of the penis, with a stretched length of
% `. a5 s* v$ c9 U. @" a) M0 ~8 cm and a width of 2 cm. The glans penis was very well) v! d: W4 B, u+ t9 B8 l9 ~$ U4 L" x
developed. The pubic hair was Tanner II, mostly around
# M  \1 g6 ]4 z1 o+ x5 Z$ a9 k5405 B' ^1 f0 Y4 s, ?6 a" D
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
4 s& i0 E9 G% I: S. gthe base of the phallus and was dark and curled. The4 h* N1 `4 a7 t1 C6 x
testicular volume was prepubertal at 2 mL each.+ R" C( B* ?3 X5 a, u  `
The skin was moist and smooth and somewhat3 u6 c5 O) [: l$ g" s5 Y. t
oily. No axillary hair was noted. There were no8 X( D( z3 y9 Z  [' |9 _
abnormal skin pigmentations or café-au-lait spots.) H1 _7 C  j) i/ i- b" i
Neurologic evaluation showed deep tendon reflex 2+3 _( x2 p, G: K- A/ t
bilateral and symmetrical. There was no suggestion
' ]( R# g* J/ A& o* o" `of papilledema.+ Q/ U# F! \8 z- t  F
Laboratory Evaluation
4 z, y5 G3 N& k2 A1 w/ uThe bone age was consistent with 28 months by$ v5 M" O' c1 H% I- [" {! {' g8 Z
using the standard of Greulich and Pyle at a chrono-0 @2 ]: I# I+ o& Z" c; N8 ]
logic age of 16 months (advanced).5 Chromosomal! `3 X3 w( @. ~8 O* j& l: F: B7 j# z
karyotype was 46XY. The thyroid function test& I! ^$ V3 K6 r/ o1 K, U
showed a free T4 of 1.69 ng/dL, and thyroid stimu-+ k+ h6 h1 `2 z! {# h, T
lating hormone level was 1.3 µIU/mL (both normal).
; U2 _0 u( d+ t7 MThe concentrations of serum electrolytes, blood
$ n3 B- P) h) Furea nitrogen, creatinine, and calcium all were8 i4 [& |; B0 @$ y3 D) m
within normal range for his age. The concentration( s1 {: J) V2 L5 V7 }' R
of serum 17-hydroxyprogesterone was 16 ng/dL
5 v8 f0 ?1 n- d( D' K(normal, 3 to 90 ng/dL), androstenedione was 20# V% X  g4 X6 q- ]/ B# r6 j6 W
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-! E# H2 a2 `0 K+ j  f& g1 W
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
9 n) B! l) K9 w+ ?2 O8 Ldesoxycorticosterone was 4.3 ng/dL (normal, 7 to
) z* I* X* P! `8 c, @+ O49ng/dL), 11-desoxycortisol (specific compound S)
; r& ]& I& X# J4 m9 b( ?was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
* T! w( C/ @# A3 rtisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
% B4 L& q/ \* n! ^; ftestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
) Z' J9 G" l$ @  Nand β-human chorionic gonadotropin was less than; E+ T4 \7 \- c8 _" D
5 mIU/mL (normal <5 mIU/mL). Serum follicular. J# y% \9 L5 R$ g) p0 F
stimulating hormone and leuteinizing hormone' c0 `; {3 v$ I. X; v* W  n1 @
concentrations were less than 0.05 mIU/mL
0 s$ h/ |! S% k(prepubertal).3 g0 [5 z# N9 [) U; Z8 ~, u
The parents were notified about the laboratory
6 O* R4 m' W$ r9 K' L7 vresults and were informed that all of the tests were
& s0 K4 F: M, c: c( Y5 B+ \  gnormal except the testosterone level was high. The
* N( R4 ^* S5 \) Ofollow-up visit was arranged within a few weeks to( }$ e+ Y: @* b# L% |; e$ V8 G; c2 ^! V
obtain testicular and abdominal sonograms; how-
8 p% \4 d( J# z$ k' F4 Z- g4 ]- uever, the family did not return for 4 months.# f* }' E4 S3 l# j( E
Physical examination at this time revealed that the
; b' J9 l2 L4 |* F# q2 V) {child had grown 2.5 cm in 4 months and had gained
: ~( S( r, B, E8 H2 kg of weight. Physical examination remained
- R$ m, Z1 B: f/ _0 k6 Dunchanged. Surprisingly, the pubic hair almost com-
. ?0 E5 W3 q  ?; epletely disappeared except for a few vellous hairs at; W# f. `* S/ r) v
the base of the phallus. Testicular volume was still 2
/ {  P0 z1 y% {' x& v* {! hmL, and the size of the penis remained unchanged.9 c" P- i. z- Q' S: H+ p
The mother also said that the boy was no longer hav-
4 Q2 [0 {* d, q+ w% Ming frequent erections.: M' R; _% S6 c
Both parents were again questioned about use of
/ C1 I; ]* X5 Z! Zany ointment/creams that they may have applied to  Z! F* a" X9 g, f: K! C
the child’s skin. This time the father admitted the
0 z0 J  R- u& `. Q) ?Topical Testosterone Exposure / Bhowmick et al 541
$ [4 X& }+ b" Y! }use of testosterone gel twice daily that he was apply-
' q* q& ^$ p$ g: H- Z0 a% xing over his own shoulders, chest, and back area for
& p" L0 w: {! ?4 A: aa year. The father also revealed he was embarrassed
( f! L4 a# |+ J+ u5 Eto disclose that he was using a testosterone gel pre-4 Y+ A4 v. S5 A8 p* s& ]  ]5 b$ I
scribed by his family physician for decreased libido. D6 h7 ~' o2 e; f7 J
secondary to depression.1 P. S' n. H5 y% G5 ?' y8 W; v% |
The child slept in the same bed with parents.  W8 P" Y8 D. S/ t" r3 Q
The father would hug the baby and hold him on his# s; M2 d; D5 y" C) G
chest for a considerable period of time, causing sig-
8 d* X; e( y% n2 o+ Tnificant bare skin contact between baby and father.# R; Z) Q9 u' G+ q* T# w
The father also admitted that after the phone call,3 v( y$ a/ ~3 c' W+ v( _' D
when he learned the testosterone level in the baby
. h5 f: g/ d% ~was high, he then read the product information) I9 L' E6 V# |; ^
packet and concluded that it was most likely the rea-
  M$ w9 m6 ^( h0 oson for the child’s virilization. At that time, they. ^8 X! u, c* u0 L
decided to put the baby in a separate bed, and the' `+ ~* R: M# Z! a! f8 r8 I$ c
father was not hugging him with bare skin and had
$ g/ n- t- y( j$ A$ v! wbeen using protective clothing. A repeat testosterone
1 T2 A2 M3 q2 k+ v7 y2 Htest was ordered, but the family did not go to the" i" u) Z: R7 c  b/ j
laboratory to obtain the test.4 U' k1 P0 N- u4 c2 z
Discussion
: V9 u/ }$ p/ |4 uPrecocious puberty in boys is defined as secondary
- V' J. @; h+ V1 \2 usexual development before 9 years of age.1,4: r- b7 G8 _  M% }
Precocious puberty is termed as central (true) when0 W# {6 z* K2 N6 r" e/ I( u
it is caused by the premature activation of hypo-
; @  b" [  p! m3 R+ Jthalamic pituitary gonadal axis. CPP is more com-
: M/ ^5 A! y  ~3 g" _mon in girls than in boys.1,3 Most boys with CPP
. K# r- [5 \0 S3 omay have a central nervous system lesion that is
* O/ B, J  F0 k! z' _* S3 Hresponsible for the early activation of the hypothal-( X& h. X7 D3 m4 z, ]
amic pituitary gonadal axis.1-3 Thus, greater empha-6 @* H! h/ j' w/ \: Y: i
sis has been given to neuroradiologic imaging in6 X  P" T( v9 e6 k, s9 }# O
boys with precocious puberty. In addition to viril-: [2 E1 T5 M/ K* R' ^+ E. i8 f
ization, the clinical hallmark of CPP is the symmet-
/ W! ?) |: l! ~5 O( r! {rical testicular growth secondary to stimulation by
- Z( T9 x' x5 Z6 vgonadotropins.1,3
8 K$ J5 _1 o) h' D$ eGonadotropin-independent peripheral preco-& b& A8 v& W9 U
cious puberty in boys also results from inappropriate
8 |% E4 T6 G/ {! Q* gandrogenic stimulation from either endogenous or
& k, A& N1 [$ K' J( D/ uexogenous sources, nonpituitary gonadotropin stim-1 W$ R' M3 A" \
ulation, and rare activating mutations.3 Virilizing
3 I5 _( w8 s) Q) Vcongenital adrenal hyperplasia producing excessive
8 Z2 U4 T  p$ T1 A+ P6 _0 uadrenal androgens is a common cause of precocious
: d8 e+ W6 N+ [) k. E* upuberty in boys.3,48 }$ p6 L8 G0 z" P: ]: Z9 P$ ]3 q3 V
The most common form of congenital adrenal0 Q. P& x* W9 K7 K
hyperplasia is the 21-hydroxylase enzyme deficiency.8 C7 N4 F$ v7 I* x% D/ j  Q
The 11-β hydroxylase deficiency may also result in
4 K* p1 h: |% A4 |# U7 |; c  Lexcessive adrenal androgen production, and rarely,
! C* F8 u. ], h# t" B4 jan adrenal tumor may also cause adrenal androgen' Q- L, f! m% ^) b! J& U) f
excess.1,3% |' S6 n* [7 O1 q1 s
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from& d- d1 P0 L6 ]' i2 w2 O
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007/ ?- b% [) c+ x9 q7 [
A unique entity of male-limited gonadotropin-
( Q  |, _" b+ @; zindependent precocious puberty, which is also known
8 w- }8 g6 f* O$ V' z1 Pas testotoxicosis, may cause precocious puberty at a
8 d8 E3 y* e, W: E7 bvery young age. The physical findings in these boys+ K* r% c8 _* U' }' [; ]5 C8 x$ x
with this disorder are full pubertal development,
: V) _+ P3 n- r3 m  ^( [including bilateral testicular growth, similar to boys
: Z9 G# \& M- v" |. o3 e' nwith CPP. The gonadotropin levels in this disorder% c' m: H8 U9 D1 N$ _9 f
are suppressed to prepubertal levels and do not show" l1 G% o' l4 t# g
pubertal response of gonadotropin after gonadotropin-( W* i, ~, f, X
releasing hormone stimulation. This is a sex-linked
- ]6 K5 K! C7 @3 ^( vautosomal dominant disorder that affects only
, I% I8 o9 k9 V$ v7 G- P& Zmales; therefore, other male members of the family* d5 U  `+ J& |* |1 b0 E4 L
may have similar precocious puberty.35 f) o5 d; g2 D4 Q8 L- j( M* [
In our patient, physical examination was incon-
6 y  O! x9 x, U3 Hsistent with true precocious puberty since his testi-9 S; {# Q2 k) v2 u) ^- G
cles were prepubertal in size. However, testotoxicosis
- h, C7 \+ Z) B6 _" @: Z9 L. Ewas in the differential diagnosis because his father4 O# E4 c9 _6 R" |
started puberty somewhat early, and occasionally,7 m( X$ N, I8 U( m9 E' l
testicular enlargement is not that evident in the
. E7 W: N: M* R- x: Qbeginning of this process.1 In the absence of a neg-: h3 v5 [+ p+ C+ y+ n# k3 \1 v
ative initial history of androgen exposure, our
% d1 @& b8 _& H" ybiggest concern was virilizing adrenal hyperplasia,- v9 D8 p6 b4 A/ c0 V
either 21-hydroxylase deficiency or 11-β hydroxylase. g/ f+ m8 a0 v3 Z
deficiency. Those diagnoses were excluded by find-8 z& p6 L# I% m, h1 b0 Z
ing the normal level of adrenal steroids./ I& q; t; N6 }. X
The diagnosis of exogenous androgens was strongly
' T( s$ I- j/ T) Asuspected in a follow-up visit after 4 months because3 G3 q( C4 k: c- {
the physical examination revealed the complete disap-; p0 S. \; @; d& V% {+ |
pearance of pubic hair, normal growth velocity, and7 j7 s) u0 X7 T; R' @
decreased erections. The father admitted using a testos-0 O+ [3 `" B& J" d8 ]( T
terone gel, which he concealed at first visit. He was
6 `) r* V% @$ l( [) b8 F4 }' ]  pusing it rather frequently, twice a day. The Physicians’* a1 n1 j, ^6 D) X# e
Desk Reference, or package insert of this product, gel or& y6 i0 q9 {/ O% e" n  M8 C; H
cream, cautions about dermal testosterone transfer to2 }: i5 J" p* O
unprotected females through direct skin exposure.
, b) }8 [$ X% pSerum testosterone level was found to be 2 times the
/ A0 I2 t1 _. p; r" w7 P/ abaseline value in those females who were exposed to( r' `  [3 `) j' E2 ^; ^
even 15 minutes of direct skin contact with their male
% c: M. b: R) m2 Opartners.6 However, when a shirt covered the applica-
0 Z8 K$ J7 j6 Gtion site, this testosterone transfer was prevented.
) y0 v( k% t. G9 ^; f6 e4 IOur patient’s testosterone level was 60 ng/mL,
* h3 T8 P) A0 `) _3 H6 Twhich was clearly high. Some studies suggest that! Q2 L4 ^3 ^. E' d5 s
dermal conversion of testosterone to dihydrotestos-3 {8 w/ F0 O) u3 v1 ?( o
terone, which is a more potent metabolite, is more/ g1 @1 A. h5 Q/ ~) n/ I" l( ?
active in young children exposed to testosterone
' v) y4 i. A: {% ~% m0 f6 U$ \exogenously7; however, we did not measure a dihy-
) [8 p$ c, H$ `8 Idrotestosterone level in our patient. In addition to, O9 \; @! b* h, }
virilization, exposure to exogenous testosterone in
/ H5 `4 E* f( p2 n; cchildren results in an increase in growth velocity and$ l0 h6 c+ G8 J( v) O( `
advanced bone age, as seen in our patient.
1 L( v$ l2 w% n6 Z" v# nThe long-term effect of androgen exposure during* J  c6 O( L3 |' I5 m4 G0 ?
early childhood on pubertal development and final
3 o/ L& V9 V% t* V! ^" q% ~adult height are not fully known and always remain. G! ?6 u% c. \* V6 V( K" g
a concern. Children treated with short-term testos-1 E( u" J. K2 j* D9 o9 v
terone injection or topical androgen may exhibit some! n7 T9 Z' E. Z: @- |
acceleration of the skeletal maturation; however, after6 v' ]1 [5 o5 R5 G
cessation of treatment, the rate of bone maturation
2 c' u0 E, N5 }' T8 C" edecelerates and gradually returns to normal.8,9
' w# C+ Q/ S6 q* ?7 A; U& xThere are conflicting reports and controversy' D6 z- J9 R/ c% m
over the effect of early androgen exposure on adult7 H4 Q5 ~/ F) X0 x' G
penile length.10,11 Some reports suggest subnormal
' C4 n: C( j# r/ h" qadult penile length, apparently because of downreg-( ^9 W7 a( B! d* |' F' ]  {" N2 m7 Q! ]
ulation of androgen receptor number.10,12 However,
5 l2 }) J3 H  Q* G5 s5 QSutherland et al13 did not find a correlation between
0 C$ }! K% l) q" Z6 Q  e8 Fchildhood testosterone exposure and reduced adult
" W, F$ d1 e  T+ V: H- G6 bpenile length in clinical studies.
: i! X8 S- r% G- E# |Nonetheless, we do not believe our patient is
4 T+ r. o% ~* Egoing to experience any of the untoward effects from9 y( K) w3 A" H8 z
testosterone exposure as mentioned earlier because* ?5 z6 }* j1 V. s$ z; O7 `+ ^
the exposure was not for a prolonged period of time.
$ z* p1 [; S7 A) M# |) e; jAlthough the bone age was advanced at the time of
% {: \- }0 ]& I  r& n# adiagnosis, the child had a normal growth velocity at
  F0 M4 Z% P; i: }& Z3 Y  x, C$ Bthe follow-up visit. It is hoped that his final adult6 C# X# I8 E. X
height will not be affected.
6 c" a: t  i" |+ Y  Z1 y+ `Although rarely reported, the widespread avail-
+ u+ A' `) ?4 s* q% Qability of androgen products in our society may7 ?6 o+ r9 h3 l/ E" R# h3 @
indeed cause more virilization in male or female4 q& J1 R' P8 |8 ?; ^
children than one would realize. Exposure to andro-
( ^: q$ m+ ^7 Q' d' \8 Agen products must be considered and specific ques-$ D) b6 F6 B- `
tioning about the use of a testosterone product or5 @/ R9 B- I+ h# A# Z+ Y
gel should be asked of the family members during
+ I/ J- w6 n" M$ S) Sthe evaluation of any children who present with vir-; K4 S8 l9 ^5 x& W" X4 D
ilization or peripheral precocious puberty. The diag-
% e3 Y( D0 H" }% enosis can be established by just a few tests and by) R' U0 |1 n) n( B
appropriate history. The inability to obtain such a
# n3 n8 g1 H- }3 a1 p1 shistory, or failure to ask the specific questions, may
3 M8 @& H: F9 [1 U0 @7 I* s1 \! C8 Zresult in extensive, unnecessary, and expensive: ]0 Z+ ~" g7 @& G$ j" b6 _
investigation. The primary care physician should be
& x- n3 M/ d5 b, ~9 C' X: C' P) caware of this fact, because most of these children
/ @# V3 q! P" Y9 S% e$ Lmay initially present in their practice. The Physicians’1 m/ O; V0 T0 W8 a) C/ ?0 e
Desk Reference and package insert should also put a
( c2 c* ]) M  Wwarning about the virilizing effect on a male or
! N+ S( K( |  Z4 J- F9 J# Hfemale child who might come in contact with some-
  w) N* U7 |( ~3 Jone using any of these products.
) @' h" O1 j; D2 o7 k7 g/ Y$ ?( q4 ^2 tReferences( P% }7 f3 H2 a
1. Styne DM. The testes: disorder of sexual differentiation
$ q- i: X/ a/ Z- r* l. T; G6 m4 U( _1 iand puberty in the male. In: Sperling MA, ed. Pediatric
, `' o+ w4 V7 y" i* ?" L$ }Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
5 v5 S* G/ a! o& W1 Q5 ~( N2002: 565-628., k& a# p4 j) \$ G5 p( c9 ]
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious8 v; `# B  l% W9 `
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
. g& q  X8 j7 R' @; y$ `  i4 {1 H, K
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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