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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% B& k. M1 h0 r2 Y" t/ w- v& [
Boy Induced by Indirect Topical5 p. l6 l3 y, E2 L: h1 o
Exposure to Testosterone' m0 O% ^1 [/ {' y- p" L7 ~3 n0 }; a
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
. T/ p4 Y3 S! [% d5 @5 ?0 [7 h2 Yand Kenneth R. Rettig, MD1
0 f- l/ G$ ?$ |( e) JClinical Pediatrics! s! u4 M+ m3 I* u& q3 l8 y
Volume 46 Number 6: b4 b" @. |5 f5 ^8 b
July 2007 540-543
* h% [2 s- l& m+ e© 2007 Sage Publications  V+ @# @( N5 G& m7 U
10.1177/0009922806296651
" F: {/ N* d/ B& Q3 Q. Vhttp://clp.sagepub.com
% v) ?% R$ v; o0 Dhosted at
* s/ k, ]$ k9 }  b- Ohttp://online.sagepub.com7 k9 I0 V* M0 G
Precocious puberty in boys, central or peripheral,/ N. @/ m% l9 x
is a significant concern for physicians. Central( Y/ F) v  ~2 w
precocious puberty (CPP), which is mediated
/ ^+ z: @! {( X# H8 pthrough the hypothalamic pituitary gonadal axis, has5 D! g0 [; ]+ M- J! c/ q0 N
a higher incidence of organic central nervous system0 Y! n4 u- C( E6 V1 R) W
lesions in boys.1,2 Virilization in boys, as manifested, r; r- n+ T. I) ~% B
by enlargement of the penis, development of pubic
! e9 I; k# i4 k( thair, and facial acne without enlargement of testi-3 ]. K1 j3 e5 J2 ]
cles, suggests peripheral or pseudopuberty.1-3 We4 ?0 g# t6 r( X2 s% T& y' |4 j1 ?: o4 K
report a 16-month-old boy who presented with the0 |& e6 ~, K: [3 L6 l
enlargement of the phallus and pubic hair develop-- o( A( A, M5 j) q$ S
ment without testicular enlargement, which was due
! V, W( Y2 \: @7 N6 Uto the unintentional exposure to androgen gel used by0 y) f9 n" x6 w, J+ b1 Y/ ~
the father. The family initially concealed this infor-  S. f9 H9 i- [9 M. b
mation, resulting in an extensive work-up for this/ \) R; Q& j1 M9 a6 H
child. Given the widespread and easy availability of/ a. c. a  r1 i( z5 h
testosterone gel and cream, we believe this is proba-
" Z3 R7 t& Q" i4 u  f8 Bbly more common than the rare case report in the) T; M1 N9 Q" N" T( d2 W
literature.4
" p: q; H/ {% L9 LPatient Report5 ]# `( {  n" K) ]6 ?5 E
A 16-month-old white child was referred to the
" ]; ~+ R0 r% g6 K* H2 Eendocrine clinic by his pediatrician with the concern
6 t, t5 Q) N. _of early sexual development. His mother noticed
% S0 e  X/ w2 Alight colored pubic hair development when he was
5 p) F; X! f  g1 [7 i: e( ?% SFrom the 1Division of Pediatric Endocrinology, 2University of/ m% P- U0 X5 M0 V" D
South Alabama Medical Center, Mobile, Alabama.: U# z  k9 V4 @
Address correspondence to: Samar K. Bhowmick, MD, FACE,2 O$ V+ c9 ^$ K  o8 r; A; e
Professor of Pediatrics, University of South Alabama, College of
7 m* k% I% e. X$ lMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
; k+ k, F8 j- D0 }7 P& We-mail: [email protected].8 }( n3 h# `- T# ?7 [2 k1 E1 @
about 6 to 7 months old, which progressively became
7 P& h1 t) F  mdarker. She was also concerned about the enlarge-4 X. o; W8 U9 o) B% }& b8 T7 O
ment of his penis and frequent erections. The child% O" N: y5 d" K7 q& |+ D, H
was the product of a full-term normal delivery, with
0 y0 T( ~# \$ Qa birth weight of 7 lb 14 oz, and birth length of+ a& ]) H9 Z& T& h1 k
20 inches. He was breast-fed throughout the first year
1 |! o& ?. V- z$ t7 O& T6 `# a6 s* lof life and was still receiving breast milk along with
% E3 O3 g' |, Q4 u) \* Hsolid food. He had no hospitalizations or surgery,
* }' o7 w. x0 ?% ^0 }, Gand his psychosocial and psychomotor development/ Q. f6 A: h& A$ t  q4 A+ d
was age appropriate.1 Z# F# }- @, q" U* n
The family history was remarkable for the father,
) U7 \. h1 O0 o2 }7 w( nwho was diagnosed with hypothyroidism at age 16,- D, O/ g8 b* Z. w2 \) r# o
which was treated with thyroxine. The father’s# |$ m3 b8 |. @: v  i. B0 O+ a
height was 6 feet, and he went through a somewhat% v$ z, Y( d) J$ r1 x
early puberty and had stopped growing by age 14.% ~' |) D" ~( B$ i
The father denied taking any other medication. The
& W1 u# G: H  N. pchild’s mother was in good health. Her menarche
3 x7 U" J8 m) l5 Pwas at 11 years of age, and her height was at 5 feet
) y& g1 A6 n' H; Q$ t0 U' i5 inches. There was no other family history of pre-
: B/ f  x1 k$ M3 G" r" I$ ?cocious sexual development in the first-degree rela-
$ h; F( @7 R, q  E7 L% X5 Ztives. There were no siblings.
+ V, o  d( U9 g" _! g0 y8 ePhysical Examination
: [& U* D4 n% Y6 K; CThe physical examination revealed a very active,+ W5 G  Y* q  s+ t1 ]# O
playful, and healthy boy. The vital signs documented
1 B3 }7 w4 z4 R0 I) O* y. q+ qa blood pressure of 85/50 mm Hg, his length was. h+ C( O/ g6 _5 Y! V- Z
90 cm (>97th percentile), and his weight was 14.4 kg
# o. N5 k6 s  f8 R$ I( j(also >97th percentile). The observed yearly growth
4 Q/ v1 n" Z, z% `velocity was 30 cm (12 inches). The examination of
4 w$ z) |, E0 ^0 f: m" Ethe neck revealed no thyroid enlargement.4 t9 k; e4 e+ @) _
The genitourinary examination was remarkable for- ~# i, N6 B/ A$ E1 d* h1 U' C& ?
enlargement of the penis, with a stretched length of! K/ G( m1 r" J9 P! M1 t
8 cm and a width of 2 cm. The glans penis was very well
1 F& _, J3 @/ k$ k+ e: pdeveloped. The pubic hair was Tanner II, mostly around, {6 j7 }2 Y3 o& h0 \
540% f( [7 ~1 F( e4 ]  C/ ~: q' q) \: @
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
" u( M/ A9 F$ ~8 D. m4 Qthe base of the phallus and was dark and curled. The
/ D6 e3 Z. u5 `  ztesticular volume was prepubertal at 2 mL each.
2 q+ a  T: x8 I1 ?& O) sThe skin was moist and smooth and somewhat
) N0 N$ L+ ^5 K% r9 V" W- g9 toily. No axillary hair was noted. There were no3 O5 A& K) a4 D( K3 O  j% b- ]
abnormal skin pigmentations or café-au-lait spots.
1 `; n. J. n! D( m) j1 ZNeurologic evaluation showed deep tendon reflex 2+5 B0 F' w0 A( a
bilateral and symmetrical. There was no suggestion
# U3 C; h0 L4 @' m5 V1 A* Zof papilledema.; r% _9 d$ _$ m, c5 n' T3 c2 _7 `) v+ G
Laboratory Evaluation
0 F8 W* J3 Y- `8 D) f8 kThe bone age was consistent with 28 months by5 Y2 x" T( [0 c7 B1 @4 v
using the standard of Greulich and Pyle at a chrono-" I* J9 Q" J0 u8 R" a5 Q! ~9 X% B
logic age of 16 months (advanced).5 Chromosomal. K/ _. H& P/ \, k) f/ F
karyotype was 46XY. The thyroid function test
( ~( c! r6 z/ N. n" _& s8 ~showed a free T4 of 1.69 ng/dL, and thyroid stimu-
' J2 c( I  t3 e. |/ t& Klating hormone level was 1.3 µIU/mL (both normal).
7 A" G' X8 @, C: u9 B8 aThe concentrations of serum electrolytes, blood$ C( `' v5 v" U
urea nitrogen, creatinine, and calcium all were( [% O6 h5 o- H
within normal range for his age. The concentration, T) j3 e9 i" a4 \
of serum 17-hydroxyprogesterone was 16 ng/dL
9 _. {. P5 {3 l2 \(normal, 3 to 90 ng/dL), androstenedione was 201 j8 b6 D2 K  z% c( x$ K
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-% ]* k# ~" d* e2 c. r. [
terone was 38 ng/dL (normal, 50 to 760 ng/dL)," q# g9 d3 {& W/ q7 ^4 I
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
, ~* w3 A% F; w6 ?49ng/dL), 11-desoxycortisol (specific compound S)
3 o0 i# S0 _4 O* _; s* ~1 v/ H4 M/ }8 L& ewas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
  F3 V: ]( g* ]; _; gtisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
6 o2 `8 m" {: f- D7 y! l9 x- }4 Rtestosterone was 60 ng/dL (normal <3 to 10 ng/dL),( b7 G. B7 [& \5 V5 e
and β-human chorionic gonadotropin was less than, d- f+ h' f  w' u$ n0 C! v
5 mIU/mL (normal <5 mIU/mL). Serum follicular+ w: H1 N: b7 g& b- ?+ b
stimulating hormone and leuteinizing hormone2 f+ n3 J- o% T! B! V
concentrations were less than 0.05 mIU/mL
/ I$ [1 c; P7 U, L  N(prepubertal).
4 V2 v. w+ ^" B& A/ ]$ P7 ?The parents were notified about the laboratory, l6 B4 B0 Z* ^  z) E. O
results and were informed that all of the tests were
" [1 M: M+ ~5 @normal except the testosterone level was high. The- M9 o3 f* b* v; D
follow-up visit was arranged within a few weeks to, ], {* R7 C& W
obtain testicular and abdominal sonograms; how-2 x' Y! x5 l; N& Y' O
ever, the family did not return for 4 months.
, w) }. S: c7 S1 y6 Z: x( y2 S0 x$ k/ oPhysical examination at this time revealed that the8 a, e. f8 C5 L5 Q  e5 ~' i7 p; c
child had grown 2.5 cm in 4 months and had gained9 D9 h; a. m: \- ]* z
2 kg of weight. Physical examination remained
( \- E% K+ v9 n0 Hunchanged. Surprisingly, the pubic hair almost com-
9 O, ~  W( m* [/ i% [% _pletely disappeared except for a few vellous hairs at
) H+ T- W8 F3 n  Q0 x: xthe base of the phallus. Testicular volume was still 2
4 j7 z/ t- q1 y. d0 `: `mL, and the size of the penis remained unchanged.# \) g5 d+ c) s4 {  U7 s, @
The mother also said that the boy was no longer hav-* Z# L$ c4 _- R- k+ f) O  Y& i
ing frequent erections.
$ q6 C$ `9 k% N1 z/ }$ M% H. u+ @Both parents were again questioned about use of
! Y9 `" ]9 g; P% T1 }any ointment/creams that they may have applied to3 j* W: i; k* t" K- l# q9 ]
the child’s skin. This time the father admitted the2 D+ M4 w1 H* F- u
Topical Testosterone Exposure / Bhowmick et al 541
8 a% F0 y" [/ [' yuse of testosterone gel twice daily that he was apply-7 x2 F, w# F; n( n/ u( a0 O' }& X
ing over his own shoulders, chest, and back area for1 c6 }) E, N0 H, r* ~0 z$ N% J4 Y
a year. The father also revealed he was embarrassed' y8 {$ @5 u. ~8 J0 ~/ X
to disclose that he was using a testosterone gel pre-
( @9 U& e1 v3 nscribed by his family physician for decreased libido- y; S) Z+ d$ ~* l' F' k) R
secondary to depression.! X. D! @8 p" x( m6 F  v! J
The child slept in the same bed with parents.7 I8 ]& p6 M4 p1 `5 G
The father would hug the baby and hold him on his
9 s3 c" f8 j7 q* Schest for a considerable period of time, causing sig-
! E0 S! Z, ^0 \7 Q- I) H. W& nnificant bare skin contact between baby and father.
  Z+ c5 ~* J4 ^7 oThe father also admitted that after the phone call,: h2 l6 g, O1 t& F' ?0 f! t
when he learned the testosterone level in the baby
( N5 o% u8 Z! B6 {was high, he then read the product information
" a2 T' C$ {: h0 Ppacket and concluded that it was most likely the rea-
2 b) L( e9 h8 ]7 R- [; A* N: Cson for the child’s virilization. At that time, they9 }( h8 k8 f) I* H$ i" ^4 L
decided to put the baby in a separate bed, and the
( R! \. x$ `7 b/ yfather was not hugging him with bare skin and had$ p. v( z. p7 T( R( F( C
been using protective clothing. A repeat testosterone; F7 P( V% S+ w- `" H2 [
test was ordered, but the family did not go to the" d4 Y9 q. v, y& ~
laboratory to obtain the test.8 C) j* f  z! [* l
Discussion
4 j3 h/ @. ?. p2 }7 _/ m' hPrecocious puberty in boys is defined as secondary
- @& I% t) h( V# l1 k) A9 b1 U7 G3 osexual development before 9 years of age.1,4
( V2 a9 B8 F% @Precocious puberty is termed as central (true) when- a  a/ p  t% X2 Z! s7 j/ g/ p
it is caused by the premature activation of hypo-8 c# S' t8 r8 H
thalamic pituitary gonadal axis. CPP is more com-9 T6 [: u  }* q4 j# d9 l/ [2 I8 I
mon in girls than in boys.1,3 Most boys with CPP
8 o1 i+ E2 j7 X. ?# |- Omay have a central nervous system lesion that is
' @+ c5 F' |# |! g' jresponsible for the early activation of the hypothal-8 E' D/ z3 B4 l6 c
amic pituitary gonadal axis.1-3 Thus, greater empha-1 j$ p  o$ G5 A7 l: L% Z( ?: k' t6 }
sis has been given to neuroradiologic imaging in
" w9 d3 f$ z8 aboys with precocious puberty. In addition to viril-( U% I; x% ^3 W- ~6 P
ization, the clinical hallmark of CPP is the symmet-
4 q/ a* G% X( f8 `- Qrical testicular growth secondary to stimulation by( r% v! Y7 M% L0 h3 q
gonadotropins.1,31 O4 a5 N% d) J) @7 K9 s
Gonadotropin-independent peripheral preco-
! `& Y9 t& x  Q( V- Ccious puberty in boys also results from inappropriate
0 ]7 C6 B3 a; c5 U) L7 g5 vandrogenic stimulation from either endogenous or
  U1 J  E, ?: Oexogenous sources, nonpituitary gonadotropin stim-# P  ~1 T' x: F/ a
ulation, and rare activating mutations.3 Virilizing
" n4 H* W0 n* N2 s! Rcongenital adrenal hyperplasia producing excessive
5 p, G6 ]0 T7 Q  q- M: |3 gadrenal androgens is a common cause of precocious
" R* {8 r$ g7 k) r, k6 H7 apuberty in boys.3,47 t- x+ }' X5 f$ B7 ?2 P
The most common form of congenital adrenal
5 S% D" y' H8 s0 b' ~8 Hhyperplasia is the 21-hydroxylase enzyme deficiency.
4 @. f8 O" f, U- rThe 11-β hydroxylase deficiency may also result in2 @- i6 G9 k% w* h
excessive adrenal androgen production, and rarely,
- c0 j3 t' L, han adrenal tumor may also cause adrenal androgen
7 M4 Z$ `, s: V$ Q, _" o* Iexcess.1,3. B& c% J# p  _! K
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
4 A. t2 I' V" o- e( f542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
+ _3 M8 y. d# ~+ G7 u+ eA unique entity of male-limited gonadotropin-$ g% `# o$ x$ |# {+ a# q. `6 c9 K
independent precocious puberty, which is also known9 C+ ?3 N  }/ E* j
as testotoxicosis, may cause precocious puberty at a# ^" m* P# @6 M  e' @0 P- l
very young age. The physical findings in these boys
. m! k2 |  _3 A3 k% wwith this disorder are full pubertal development,
8 J: ]$ l! E1 b8 }" J+ vincluding bilateral testicular growth, similar to boys
( I) {/ b! q" X, x% G0 I9 ]with CPP. The gonadotropin levels in this disorder
2 r) J- ^5 }: eare suppressed to prepubertal levels and do not show- g7 Z2 Y2 s" e
pubertal response of gonadotropin after gonadotropin-2 ]& y& g' g. n* u1 w0 d
releasing hormone stimulation. This is a sex-linked% X! r  i. r: i: |9 V
autosomal dominant disorder that affects only
4 X" ]) e. D( i( Z% Y$ B, Jmales; therefore, other male members of the family
4 Z5 t' A& Z; ymay have similar precocious puberty.34 o" f8 w5 Y; }; h: D! N
In our patient, physical examination was incon-
1 H! m# h$ B/ @  psistent with true precocious puberty since his testi-
: g' c' V+ }* S2 [+ {. \cles were prepubertal in size. However, testotoxicosis
2 W* x0 X) e# T1 fwas in the differential diagnosis because his father
% O2 j6 M1 A2 Z1 U1 {9 D/ ystarted puberty somewhat early, and occasionally,
+ k- M- K: W) A$ j4 Ltesticular enlargement is not that evident in the
: Y5 }; H7 l  W, ]% ?beginning of this process.1 In the absence of a neg-
! `# @1 |+ B- p+ P6 i+ [ative initial history of androgen exposure, our" }' D6 e  S' L8 P
biggest concern was virilizing adrenal hyperplasia,, I0 j! _; Z5 [! A0 v/ Y/ N  d
either 21-hydroxylase deficiency or 11-β hydroxylase4 v9 r1 [- M1 ?5 J( `! n; F! p
deficiency. Those diagnoses were excluded by find-
7 a8 G( o9 Z- v$ ~! T$ Q: b2 }! D! Eing the normal level of adrenal steroids.
: H6 R& {% W$ C, S; vThe diagnosis of exogenous androgens was strongly
' {$ G6 N  P% S% @* o  W( Ssuspected in a follow-up visit after 4 months because
" B7 r$ F6 G+ L9 t& c, M5 s, Dthe physical examination revealed the complete disap-- F) R+ ]1 ]1 e- N; m
pearance of pubic hair, normal growth velocity, and
8 f& l- g+ p5 s( E4 {, O9 O4 ?decreased erections. The father admitted using a testos-
% o7 A$ n7 c  ?& Q. P) mterone gel, which he concealed at first visit. He was- U/ [7 V8 B/ J7 W+ r
using it rather frequently, twice a day. The Physicians’! ^/ a/ T' n; Q$ K$ O
Desk Reference, or package insert of this product, gel or
3 n. K( G0 u* ?; ?- q; u0 mcream, cautions about dermal testosterone transfer to0 t$ `/ |' m# D" ]$ `1 h0 m1 s
unprotected females through direct skin exposure.
  c, _6 r6 y; q" O+ J' SSerum testosterone level was found to be 2 times the
  \- D. A) i9 F& Q6 nbaseline value in those females who were exposed to
9 W$ h0 n" M$ @7 Reven 15 minutes of direct skin contact with their male( [3 z  e! i. @* P0 B
partners.6 However, when a shirt covered the applica-* E1 C% e1 @2 m  ~
tion site, this testosterone transfer was prevented.0 a$ h% j* w: G4 d8 ?
Our patient’s testosterone level was 60 ng/mL,
% m2 J! z) Q2 twhich was clearly high. Some studies suggest that
4 O) R1 v' L7 S! u' O( Pdermal conversion of testosterone to dihydrotestos-, M. s. L( Z8 t0 c2 c9 ?
terone, which is a more potent metabolite, is more
+ j9 d* \/ l; f2 sactive in young children exposed to testosterone8 F6 U0 q. I* G+ G5 L
exogenously7; however, we did not measure a dihy-
  n- f! X' n8 W3 gdrotestosterone level in our patient. In addition to
) U. e( c# B  R9 a2 F$ nvirilization, exposure to exogenous testosterone in
0 [$ _9 n: ]. k; p$ ?children results in an increase in growth velocity and
% `; F' ]! J1 R+ w; ^, l9 K1 p7 zadvanced bone age, as seen in our patient.4 c; Q$ p6 C7 q
The long-term effect of androgen exposure during5 p/ l0 h- @( ?- o# k/ n, `
early childhood on pubertal development and final
5 Z) h& s- p1 f. Q6 z6 E& `adult height are not fully known and always remain
# ]- m) d3 J0 Ja concern. Children treated with short-term testos-  k) h/ I8 f7 t0 F6 ]0 t/ W
terone injection or topical androgen may exhibit some! T0 X! s9 _( n0 x9 I2 r
acceleration of the skeletal maturation; however, after
) }, l( F. X! Hcessation of treatment, the rate of bone maturation
/ |( o3 ^' ^. Ddecelerates and gradually returns to normal.8,92 f2 y/ ]$ @, ^, v+ g
There are conflicting reports and controversy
9 `+ i' M$ T, j; q: oover the effect of early androgen exposure on adult  O5 z' i' e* ~  U. V
penile length.10,11 Some reports suggest subnormal
3 z% l# a8 [, z' G* P3 Xadult penile length, apparently because of downreg-7 G& l9 k. C4 i/ o$ J
ulation of androgen receptor number.10,12 However,
3 P  }; T+ A$ k5 cSutherland et al13 did not find a correlation between( W1 O9 v9 ?7 F* Z) a9 `
childhood testosterone exposure and reduced adult2 W9 I8 W1 V5 x7 L  j: ]6 S2 L
penile length in clinical studies.
" w* s) `# U% S7 M, S: qNonetheless, we do not believe our patient is
$ I, B5 I/ o# m2 c1 egoing to experience any of the untoward effects from/ Y" _" E; ?: ^3 o
testosterone exposure as mentioned earlier because, n3 ^) G2 b' F4 r# q
the exposure was not for a prolonged period of time.6 s  s" S+ {) D( [" }5 N
Although the bone age was advanced at the time of3 v2 o- O; v$ A
diagnosis, the child had a normal growth velocity at  j9 b- e( `  S3 _1 o
the follow-up visit. It is hoped that his final adult
5 N+ @0 g  A% T9 y9 ~height will not be affected.$ p" y4 I# g. q" D
Although rarely reported, the widespread avail-
0 e7 Q. u, F; Iability of androgen products in our society may/ k( Y& i8 `( L
indeed cause more virilization in male or female
( T. [- Z* n0 I# a0 }children than one would realize. Exposure to andro-
  a3 O5 v2 q2 Z0 Jgen products must be considered and specific ques-
2 ^4 H" ?3 a# A8 Q3 g4 G+ z3 ftioning about the use of a testosterone product or
+ E" @4 O) j: Ggel should be asked of the family members during$ X0 S: Z; Q+ f+ S* y; k4 D$ Y7 L' Y' o+ b
the evaluation of any children who present with vir-
: E* ?, O+ E" w% o4 s0 oilization or peripheral precocious puberty. The diag-% \  I; r7 b% F. ~& n+ c6 O6 m3 _
nosis can be established by just a few tests and by. N" L8 c9 K* G+ u- o
appropriate history. The inability to obtain such a" C, @" e% B! ?$ A  x3 P! t
history, or failure to ask the specific questions, may' H/ X0 [2 m" X& k; |) k
result in extensive, unnecessary, and expensive6 c, J: S2 Z- q: _: ?
investigation. The primary care physician should be' u9 F+ i% s# u8 X
aware of this fact, because most of these children6 {$ t3 P& S8 w) o' Z* K
may initially present in their practice. The Physicians’: H9 P1 ^7 y: J" F
Desk Reference and package insert should also put a& w, F; g) v3 C4 y& [, L
warning about the virilizing effect on a male or
- J* D; F# l& x# F; v) ~- Ffemale child who might come in contact with some-& b# x+ `# M: t& ~( o! \. O$ m
one using any of these products.: L5 Q) V/ K! c* h  v
References
6 t3 L: q7 i* ^- Y! X* L1. Styne DM. The testes: disorder of sexual differentiation7 K# n& i* P, A. t/ D! n1 b9 d' g
and puberty in the male. In: Sperling MA, ed. Pediatric# L# C. c" L( e  N
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
- F- K. P0 _) g, \. B$ D2002: 565-628.$ \0 J! a9 G3 p9 X9 `
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious* D) u* O/ A% c
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
6 e3 U. i; Z# o+ N2 D; mBoy Induced by Indirect Topical4 X+ u" e3 |& Y2 N1 W- v7 I
Exposure to Testosterone
# {& D' `; v# h- q# G/ }$ n0 Q8 w) FSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2: k) p" x& I. c5 `. M. l- Z
and Kenneth R. Rettig, MD1
  X9 Y8 ~: ~: v" r9 X$ ?6 oClinical Pediatrics* @( u7 b) Z. Q0 z9 z7 g
Volume 46 Number 6. E  o. J8 ], E/ s$ r$ \) }8 |
July 2007 540-543
: z9 C  k  V! z" X: E9 }© 2007 Sage Publications0 M1 o( Y/ C5 G, @" B6 g' Z; C
10.1177/0009922806296651
  B$ f4 O4 I( vhttp://clp.sagepub.com
+ \* H# t; g' P0 d' U* P. `hosted at
& v1 B& `+ i/ whttp://online.sagepub.com0 V8 f8 U* Z9 }) s( f) F
Precocious puberty in boys, central or peripheral,& G# d% J2 }& H3 a$ h- S
is a significant concern for physicians. Central
* N9 C; _  x/ m; P+ ?( S9 u  @precocious puberty (CPP), which is mediated
  i$ a! Q. M3 Z2 N; Ithrough the hypothalamic pituitary gonadal axis, has& H1 u$ G! w7 m
a higher incidence of organic central nervous system
4 L; s) U4 ?7 k) J! E4 b0 }6 `lesions in boys.1,2 Virilization in boys, as manifested
" t' z$ ^" {) {+ Z, A, ?8 Nby enlargement of the penis, development of pubic: o3 W2 c/ v1 Z' Z
hair, and facial acne without enlargement of testi-. X0 _; c: w4 o
cles, suggests peripheral or pseudopuberty.1-3 We
& d! x, A/ ~! y' s% p8 wreport a 16-month-old boy who presented with the- ^) Z9 Z7 c% r, a# P" h3 r
enlargement of the phallus and pubic hair develop-
3 o6 H) T5 A" k+ C- u* mment without testicular enlargement, which was due- x9 R; g5 L: Z' H& W& j
to the unintentional exposure to androgen gel used by# r2 |3 s1 u6 w: n( t! `7 x6 j2 _3 ^
the father. The family initially concealed this infor-
5 H, n& ~9 E% c1 a) K. \5 {1 B* Xmation, resulting in an extensive work-up for this
; p8 o: Z( P& O6 S! N4 ?* o- Z: Y8 Echild. Given the widespread and easy availability of' b5 Z2 L4 i0 `
testosterone gel and cream, we believe this is proba-3 t$ |/ a4 [& v+ f
bly more common than the rare case report in the
0 I9 c  Q; ~8 ~' w# U1 ]literature.4. y: M6 F" F1 r3 V
Patient Report! Q' r9 y# T* c, Y% L
A 16-month-old white child was referred to the
/ `, f8 j9 r( F. A; Iendocrine clinic by his pediatrician with the concern
6 f+ T' [! w) B$ \' a2 D0 pof early sexual development. His mother noticed) P' K) l0 T* e$ V
light colored pubic hair development when he was
/ A# ]: }, A2 I9 B8 {From the 1Division of Pediatric Endocrinology, 2University of: X, g- j+ y# M2 T7 \6 w
South Alabama Medical Center, Mobile, Alabama.
# t1 l5 N5 K3 d7 o+ o% B. @6 [Address correspondence to: Samar K. Bhowmick, MD, FACE,
  B6 g" y8 z6 d; G( A3 ZProfessor of Pediatrics, University of South Alabama, College of
) g3 S& x. D5 x+ ]6 jMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
2 T4 u! ?4 d4 @( y6 B1 ]e-mail: [email protected].  C7 v  x* L, h/ L% q& A) S# l6 d
about 6 to 7 months old, which progressively became3 Y6 m# C- e, r' ~& Y; u
darker. She was also concerned about the enlarge-
  ?$ j) J) `4 V! V% r$ ~  J, }ment of his penis and frequent erections. The child2 l* A6 z! S' \# c9 m
was the product of a full-term normal delivery, with+ v( o' k9 Z3 {/ G2 ~
a birth weight of 7 lb 14 oz, and birth length of
9 x1 B! P& @0 L0 }) O; H# [20 inches. He was breast-fed throughout the first year
7 G4 ^# {' R* M' g, ~of life and was still receiving breast milk along with
7 E( J( C; L" |: {/ B: w# x, Psolid food. He had no hospitalizations or surgery,# L8 H2 g3 U/ A, u$ j
and his psychosocial and psychomotor development+ q! Y& d9 ?- }
was age appropriate.3 c, [! t/ w6 y5 t
The family history was remarkable for the father,
9 B/ G7 E* L" E' G4 O! @; _who was diagnosed with hypothyroidism at age 16,
) D& e* m# Y3 @8 W/ m$ pwhich was treated with thyroxine. The father’s
8 Z2 c! ^' t+ I( `" R, u. uheight was 6 feet, and he went through a somewhat
( z8 b% p& t7 u& X2 d" v# V8 Oearly puberty and had stopped growing by age 14.$ C! h- x( t* g
The father denied taking any other medication. The( T, r+ l- U7 j- ]& B3 a% g
child’s mother was in good health. Her menarche, r# i  R2 l) g5 F
was at 11 years of age, and her height was at 5 feet' N- B% `) q1 g: \' l4 p
5 inches. There was no other family history of pre-3 W  Q: ?6 b$ @# _) z/ S/ d0 W" t
cocious sexual development in the first-degree rela-
% L; ]. h) s% ?/ b3 c9 e  C4 mtives. There were no siblings.
! ~9 U# t% W2 [; u. NPhysical Examination. k( u3 ]4 P3 ]* }3 v9 [' C
The physical examination revealed a very active,
  c! M: y' _7 ^playful, and healthy boy. The vital signs documented, j8 M/ D: w7 G
a blood pressure of 85/50 mm Hg, his length was
' D6 I- d0 f9 _! @90 cm (>97th percentile), and his weight was 14.4 kg( n, x! M2 i# }+ p8 N
(also >97th percentile). The observed yearly growth
7 ]. t8 i' Z+ u0 s3 Rvelocity was 30 cm (12 inches). The examination of; q3 |" q+ M2 @
the neck revealed no thyroid enlargement.$ m" I/ s8 Z0 c+ I" }9 ]( s3 a
The genitourinary examination was remarkable for3 S: {) ]3 N. q; g5 {4 r& J
enlargement of the penis, with a stretched length of
) M: j, ?" A# B/ s2 S( s  \! @% _8 cm and a width of 2 cm. The glans penis was very well
4 V$ h6 r: [7 S4 r! pdeveloped. The pubic hair was Tanner II, mostly around7 C' w* H1 I! i0 `( o1 Y
540
- G% q1 C5 d% |7 O; j; \5 Nat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from' }4 {- E0 t8 U! o6 C; ~2 c2 V
the base of the phallus and was dark and curled. The
% U" D5 T; M; h' f, y4 a% ttesticular volume was prepubertal at 2 mL each.0 t: G) t" ^9 ^5 W) R6 T
The skin was moist and smooth and somewhat! Q6 E7 `. E. @; w
oily. No axillary hair was noted. There were no
. D$ H1 O4 o! Iabnormal skin pigmentations or café-au-lait spots.
( H9 l! L# f7 \  {9 `- k  r/ KNeurologic evaluation showed deep tendon reflex 2+8 ~, Z% G) B  }$ ~2 c% k5 ]
bilateral and symmetrical. There was no suggestion. e+ [, x+ k5 v# @. K( p$ Z# Q
of papilledema.
1 x4 p+ i4 R" L6 G% a# XLaboratory Evaluation
1 ~$ x9 f9 {$ a, x: WThe bone age was consistent with 28 months by
$ w0 v) z. o+ a. E' w" Busing the standard of Greulich and Pyle at a chrono-
$ O9 H2 \: i, I8 b1 ^logic age of 16 months (advanced).5 Chromosomal8 E  r. Q5 v7 _: t$ ?/ Y
karyotype was 46XY. The thyroid function test
) ?, u0 I1 e0 l( z9 [, Zshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
$ r8 c% ~5 Y. K* }, ^lating hormone level was 1.3 µIU/mL (both normal)." t: e. b% i3 }' }; J9 ]
The concentrations of serum electrolytes, blood3 b5 v6 \6 k4 q/ w8 m
urea nitrogen, creatinine, and calcium all were, q% G& o, l0 C3 s: I& B; ~& L
within normal range for his age. The concentration7 G' u3 D1 y# |
of serum 17-hydroxyprogesterone was 16 ng/dL* U  S4 `. H9 W5 y
(normal, 3 to 90 ng/dL), androstenedione was 20$ ?' {8 U$ V* _/ E( P
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
. u# V2 s& C8 q( l0 R( fterone was 38 ng/dL (normal, 50 to 760 ng/dL),7 X* R/ |* @5 k  l0 }4 _
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
8 U, M; C$ z8 K) w" _2 z49ng/dL), 11-desoxycortisol (specific compound S)" d5 D, T* O* ]2 P- r
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-- g5 H2 J( d- S% P
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total* r" Q; O( J2 w: M' m$ r# s# I
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
* [$ H* S" {" K. `. D6 Yand β-human chorionic gonadotropin was less than
2 O$ ?) ~+ Q' x5 @* f8 j5 mIU/mL (normal <5 mIU/mL). Serum follicular2 [' U  \- k! \2 {5 L
stimulating hormone and leuteinizing hormone3 Z' ?5 b6 W' T  X/ ]
concentrations were less than 0.05 mIU/mL
' {8 P4 m# u& t' y% y$ L(prepubertal).
, H" y9 p* d, [2 }# qThe parents were notified about the laboratory
8 o+ O' G6 U0 i9 v" Oresults and were informed that all of the tests were
! C: f* _5 ]( C$ |normal except the testosterone level was high. The
; |# a$ x8 u/ I, D) z( |' ifollow-up visit was arranged within a few weeks to
" N0 \; i2 J3 W$ ?; Cobtain testicular and abdominal sonograms; how-
) \8 V3 ]2 Q5 Q) b3 r! G! R) sever, the family did not return for 4 months.
: ~+ F7 R# Z1 y" C: D- m' @Physical examination at this time revealed that the
% F* ^. i* A4 b9 g# |0 ]$ H" v7 u+ ~child had grown 2.5 cm in 4 months and had gained0 Y# x' X0 {, I
2 kg of weight. Physical examination remained
  T# {8 W3 x( H# t' gunchanged. Surprisingly, the pubic hair almost com-
9 ~7 X  ^1 G4 ^/ y* R6 L& s% Hpletely disappeared except for a few vellous hairs at
. `1 ]0 ~% D8 u8 w' Uthe base of the phallus. Testicular volume was still 2
2 E: l) D* S9 D# D* Z9 v  UmL, and the size of the penis remained unchanged.
$ _% d* V. f1 v+ P, |3 H. iThe mother also said that the boy was no longer hav-
1 }: t5 _4 U& P9 c7 B) a& P. ping frequent erections.3 {4 f  R! B& M& p3 j$ F7 A& L
Both parents were again questioned about use of: Q/ b, q2 N, R( C- ~. U
any ointment/creams that they may have applied to& M. A9 ~" f, {" A. q; I4 S( N
the child’s skin. This time the father admitted the
- g: u  J* n+ [4 \/ k& h, Q6 PTopical Testosterone Exposure / Bhowmick et al 5418 M/ z0 c& M- _' J. Q
use of testosterone gel twice daily that he was apply-5 j* f! N1 U( b  q' ]7 U' o% k& x
ing over his own shoulders, chest, and back area for  H- F8 k3 r/ m+ y+ A
a year. The father also revealed he was embarrassed/ M3 |" G8 T2 S5 r( y2 i
to disclose that he was using a testosterone gel pre-  V1 J( X& ~% g9 m$ M' q, e
scribed by his family physician for decreased libido
4 e* S0 ]: m, U2 Q, X4 W6 u$ {# Psecondary to depression.
/ z( L* a# u3 m  n7 @The child slept in the same bed with parents.0 x, w: W, R3 U
The father would hug the baby and hold him on his
" B/ W, U, J; G$ M0 ?9 I: uchest for a considerable period of time, causing sig-
) V- s# z. v% J* snificant bare skin contact between baby and father.1 t$ Z! L8 [) |" N: B) P8 K5 Y
The father also admitted that after the phone call,
  D+ k. N! J% R2 E; G, Y9 }3 y! H2 Awhen he learned the testosterone level in the baby$ P7 {; S2 e* A# ]$ U" X+ f/ [
was high, he then read the product information) r. M8 u! B% \* H
packet and concluded that it was most likely the rea-
& A- G% B: c" I  Wson for the child’s virilization. At that time, they
# `8 F7 A+ v& ]- ~) U  y" idecided to put the baby in a separate bed, and the
& c+ z2 T1 J1 K) X0 lfather was not hugging him with bare skin and had) M+ g. p: N# A* w* C; t
been using protective clothing. A repeat testosterone
5 I3 s) N: ?$ Wtest was ordered, but the family did not go to the
' b# C% d! W4 u. @laboratory to obtain the test.- [. [7 J% X$ E  H0 }& ?
Discussion
3 x; ]! r0 w1 @3 D1 qPrecocious puberty in boys is defined as secondary
8 B4 X0 _2 }2 ~. _8 ^& Vsexual development before 9 years of age.1,4
6 t; d1 ^6 x$ p3 Q' r/ y, |7 X, XPrecocious puberty is termed as central (true) when4 _* m6 G$ |$ ^$ `
it is caused by the premature activation of hypo-
- I& I+ a' B3 k6 K, j' dthalamic pituitary gonadal axis. CPP is more com-
  H% T5 m; L# w% Qmon in girls than in boys.1,3 Most boys with CPP# Q$ |! W$ K( S- s; C
may have a central nervous system lesion that is1 n' s+ A( o5 U6 @- V# P0 }
responsible for the early activation of the hypothal-
# X% m9 R( w- {1 c' d  A. hamic pituitary gonadal axis.1-3 Thus, greater empha-& S- P3 z% F8 ?3 I! Z
sis has been given to neuroradiologic imaging in& Z& {$ f5 Y8 U1 _( u5 L6 E' |
boys with precocious puberty. In addition to viril-
# Q9 P/ F0 F0 Q4 B0 ~# Tization, the clinical hallmark of CPP is the symmet-6 L; E2 B  n( \4 g8 [
rical testicular growth secondary to stimulation by+ V% X4 {, M+ j: Z, U
gonadotropins.1,3
# p/ [' o0 |  c8 v4 w  ]Gonadotropin-independent peripheral preco-+ j& }* B' C+ O( i
cious puberty in boys also results from inappropriate- B: y5 t& Z: M' x' w- B
androgenic stimulation from either endogenous or
/ Q* s' \, V. I0 J. k$ `exogenous sources, nonpituitary gonadotropin stim-; Z( w, x* t- {
ulation, and rare activating mutations.3 Virilizing
; K0 @: d) \$ l0 a& _3 hcongenital adrenal hyperplasia producing excessive" [) N' F' `* z+ E1 `$ l9 z3 o0 V
adrenal androgens is a common cause of precocious' B3 G' k% r7 X' E) T6 y% I
puberty in boys.3,4/ s4 F2 Z+ a$ y$ C  g( }
The most common form of congenital adrenal# T+ z  l+ H! C3 g& p, m8 D
hyperplasia is the 21-hydroxylase enzyme deficiency.  N. ?4 _2 ^2 H/ i7 p
The 11-β hydroxylase deficiency may also result in/ R* x( H( n0 S, Y# d
excessive adrenal androgen production, and rarely,( c! U; @5 ~5 ?, r1 W7 S. b
an adrenal tumor may also cause adrenal androgen
8 z! D, z2 Q+ D' D( k' bexcess.1,3
( i, u7 E; W  Aat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from- v8 E5 D7 |2 H3 o) w. C
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
! @  U- D8 x2 T, VA unique entity of male-limited gonadotropin-
8 [: e0 K4 [- _: z; \independent precocious puberty, which is also known8 y9 J8 l$ ~; e
as testotoxicosis, may cause precocious puberty at a
2 y+ Q# Y. I0 U+ B! Dvery young age. The physical findings in these boys0 b' ~3 G- w2 x+ c0 b
with this disorder are full pubertal development,
2 i; ~7 t3 v  bincluding bilateral testicular growth, similar to boys3 n2 S5 `6 e9 |/ x$ }
with CPP. The gonadotropin levels in this disorder
8 ^% X: t! [9 I& Lare suppressed to prepubertal levels and do not show2 p6 O5 v. @  V
pubertal response of gonadotropin after gonadotropin-
% I( D* p2 @- ^! ]+ t6 ^9 v+ B9 Areleasing hormone stimulation. This is a sex-linked1 A. {0 }( J$ Z& Q! f8 P9 [
autosomal dominant disorder that affects only$ G) J  k' m. H4 \
males; therefore, other male members of the family8 ^% }/ E9 @% L0 B& P7 @2 \& o
may have similar precocious puberty.3
# Y  D+ R7 Y% ^0 d1 vIn our patient, physical examination was incon-
( z0 }6 R2 T* _' y1 msistent with true precocious puberty since his testi-
7 a. J/ n6 ?9 |3 m4 B; Zcles were prepubertal in size. However, testotoxicosis- K6 Q& K1 t8 m) [, a3 q$ a7 x
was in the differential diagnosis because his father
6 a. n6 V: e: |2 }started puberty somewhat early, and occasionally,. [7 h2 }) o# n# S1 S; x/ y
testicular enlargement is not that evident in the/ b  ~$ V; K. n% U- S; A3 U2 Y
beginning of this process.1 In the absence of a neg-, R) i# J: Z6 [  d' c  D
ative initial history of androgen exposure, our
2 O* H& x$ j3 F9 qbiggest concern was virilizing adrenal hyperplasia,/ |) u; `# _" c1 o! F+ Y* W
either 21-hydroxylase deficiency or 11-β hydroxylase- M$ S' _" u% r/ Z# I/ k' B4 C* X
deficiency. Those diagnoses were excluded by find-% Y9 _4 d$ H3 r8 P
ing the normal level of adrenal steroids.; B8 m4 v5 A: c# E( S
The diagnosis of exogenous androgens was strongly5 s! E2 o8 D3 m' ~
suspected in a follow-up visit after 4 months because/ V3 C$ ~+ O$ [3 u7 l' s% D
the physical examination revealed the complete disap-
3 r$ s6 q& V. h4 j- O5 Q, S1 x1 D  J. kpearance of pubic hair, normal growth velocity, and# ?, V0 t0 ?9 M  {4 V( X
decreased erections. The father admitted using a testos-, W+ R! G- [0 H; u) p: p" x
terone gel, which he concealed at first visit. He was6 W6 c; W4 W+ N- a1 l
using it rather frequently, twice a day. The Physicians’
- Q( Y( C: x! }- l; [/ b1 ~Desk Reference, or package insert of this product, gel or
5 d5 X- u+ s) W9 Q; Xcream, cautions about dermal testosterone transfer to
9 O9 K6 k' c% a. Z  i+ k( q- lunprotected females through direct skin exposure.
9 F1 j% t9 ~) ~3 qSerum testosterone level was found to be 2 times the0 v: L5 M/ [* g5 [' f, a) z# E
baseline value in those females who were exposed to' U  w$ K) ~) h6 O. _% G+ n
even 15 minutes of direct skin contact with their male
' Y$ B6 E0 B, V; ~& wpartners.6 However, when a shirt covered the applica-
/ W2 K8 g# P5 {; o8 stion site, this testosterone transfer was prevented.) Z6 P) t4 U( h/ f1 a) P) @
Our patient’s testosterone level was 60 ng/mL,
: x# @4 @' i# E, a) A/ B$ A" Lwhich was clearly high. Some studies suggest that
# ?- v8 G8 m1 v' l% k9 F9 r' hdermal conversion of testosterone to dihydrotestos-
, D5 m5 l5 `4 Y5 e4 q6 c4 p4 Q! T" Eterone, which is a more potent metabolite, is more
5 v9 ~5 ~1 c1 V* v7 b; r% J, H6 Yactive in young children exposed to testosterone
- _3 V% R9 q. b! @% t0 Y+ Vexogenously7; however, we did not measure a dihy-! c" Y0 N) l3 k
drotestosterone level in our patient. In addition to
( A2 J; B8 o. i2 M1 {& b8 J5 Z1 N. Tvirilization, exposure to exogenous testosterone in
1 t8 O( p, \2 u" ^- G0 T$ k! h" |children results in an increase in growth velocity and
6 y) H+ N" a; d7 o2 T7 F% P8 gadvanced bone age, as seen in our patient.
0 e* J# d5 ~9 @, j1 AThe long-term effect of androgen exposure during1 H1 g/ m7 n. [* x+ h# c
early childhood on pubertal development and final! S& F4 G. W9 f' Q0 a  G
adult height are not fully known and always remain9 F. e1 |3 j6 @, O2 x
a concern. Children treated with short-term testos-8 Y; Q, d$ W& ?: G7 e: A! W
terone injection or topical androgen may exhibit some" {+ U+ B; i2 W
acceleration of the skeletal maturation; however, after
8 e% P+ k! C  [) Q2 o* U: Jcessation of treatment, the rate of bone maturation
- r6 _% |7 P6 Udecelerates and gradually returns to normal.8,95 i8 z0 c% @% z
There are conflicting reports and controversy
* w% H& [% H; Iover the effect of early androgen exposure on adult
# ^  _! C0 @0 T* g3 hpenile length.10,11 Some reports suggest subnormal' `. U% g: t8 H2 A7 m
adult penile length, apparently because of downreg-
8 Q0 ?& Z5 s# \) z8 Kulation of androgen receptor number.10,12 However,8 [1 ~- m  \, m% O
Sutherland et al13 did not find a correlation between
7 ^' i6 j( R; m( o) Ychildhood testosterone exposure and reduced adult
( |/ A, ]" W4 B  x; V6 Epenile length in clinical studies.& s+ \# e4 j% i: E7 i. W
Nonetheless, we do not believe our patient is: e3 R8 l2 F( X0 g6 C" Y
going to experience any of the untoward effects from+ O  Z' F7 C& @) O* F
testosterone exposure as mentioned earlier because/ D0 _7 P2 |4 }8 t5 y' V3 `
the exposure was not for a prolonged period of time.
3 u. X, D- |* s  [; w7 }2 cAlthough the bone age was advanced at the time of
# v! ]% P3 ^5 m2 |$ kdiagnosis, the child had a normal growth velocity at
2 ]0 _0 T0 o: y& x2 ethe follow-up visit. It is hoped that his final adult
* ~% [/ @& Q: s5 kheight will not be affected.: K! ~( S$ F$ O" i2 A/ l
Although rarely reported, the widespread avail-3 i) I! }9 p- j4 Q7 v, }! u
ability of androgen products in our society may
9 F7 Q- P2 ~: D' F3 Jindeed cause more virilization in male or female
9 m0 ]+ M4 i& _0 x8 P$ x8 Bchildren than one would realize. Exposure to andro-4 `7 Y$ C5 r% w' ]5 b2 B) f
gen products must be considered and specific ques-$ [# k9 \1 _! D6 h  n- ~4 n
tioning about the use of a testosterone product or
. L4 L" |+ H, |) b9 F! kgel should be asked of the family members during
& t3 Q$ k' s6 ?) fthe evaluation of any children who present with vir-
" B2 X. V( Z0 L4 J6 Bilization or peripheral precocious puberty. The diag-
4 `9 r9 N1 m6 E) W" ~nosis can be established by just a few tests and by8 t+ O8 i5 p* T# M$ E
appropriate history. The inability to obtain such a& `& ?2 p$ V$ }; o0 N
history, or failure to ask the specific questions, may5 E6 m. z. P0 g5 x6 _
result in extensive, unnecessary, and expensive  J6 X0 H+ U9 w
investigation. The primary care physician should be4 H! h2 Y' A# ~) s1 h
aware of this fact, because most of these children
* l$ w7 t7 R" \6 [  t0 Q8 Fmay initially present in their practice. The Physicians’
8 a7 _& ]! m8 x3 WDesk Reference and package insert should also put a, F' m# p2 e% D5 T& I
warning about the virilizing effect on a male or
  H! ~! [6 Q! Q" k9 ~' ofemale child who might come in contact with some-
; |6 S# y" o* D8 D' e( r) O% Q; c1 Uone using any of these products.
( v+ r' ?7 I* G# H" b, KReferences
/ U! R4 Q' R7 ?+ H( C, _1. Styne DM. The testes: disorder of sexual differentiation
, {; [' L0 C  C- @4 z; [% c; ~0 |and puberty in the male. In: Sperling MA, ed. Pediatric
$ r# W6 O+ r2 a* _/ uEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
% K8 e6 Z$ G6 C2002: 565-628.1 k5 \. Q. Q& y' p
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
" S9 o3 v  t1 h" y  m" lpuberty 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
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4个什么样的?
發表於 2025-1-19 02:41:05 | 顯示全部樓層

: F+ F6 N- S/ B5 |" `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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