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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
3 M/ B0 c( n7 o! }; L' R; tBoy Induced by Indirect Topical! |: f' [: `2 g: Y/ k* X
Exposure to Testosterone
. p9 X; |9 V. [5 C9 mSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,21 I6 G7 W7 u8 u# n9 @% q
and Kenneth R. Rettig, MD1
) U) s, r1 }  }4 tClinical Pediatrics
+ o! l5 S; x& W  u6 C- Q  B2 d& P' G+ ]Volume 46 Number 6
5 @2 p- E% O$ A, c9 K# YJuly 2007 540-543
5 V+ d0 u) k; w/ i1 c7 F6 u* e; R© 2007 Sage Publications% f% n) P) x$ G7 x: E0 u( P& i0 t- L
10.1177/00099228062966514 K/ Y/ Z/ X) @' Y; [
http://clp.sagepub.com
( ^4 z1 k3 q7 Z; [+ J# Ahosted at
! s! ?5 x  [0 j9 E* k: thttp://online.sagepub.com* q( W- g. ?# }. O5 i
Precocious puberty in boys, central or peripheral,
; P# \9 f0 W9 ]* o0 Zis a significant concern for physicians. Central# V" R. D4 a4 g. b6 ^
precocious puberty (CPP), which is mediated& T' R- u2 w0 f( n0 [4 T
through the hypothalamic pituitary gonadal axis, has
" P8 R  w& a* G9 aa higher incidence of organic central nervous system6 ~8 K  L. l5 ]' K$ k- K3 x( g, Q
lesions in boys.1,2 Virilization in boys, as manifested: ]# A! w: c0 y7 A1 X) T; @- f; S
by enlargement of the penis, development of pubic
( L! Y! Q9 w7 U# c2 [hair, and facial acne without enlargement of testi-
; j4 V2 U6 N/ q4 gcles, suggests peripheral or pseudopuberty.1-3 We
  c. V- M! G$ ]report a 16-month-old boy who presented with the; B7 v& ?& S& i6 Z7 S% ~
enlargement of the phallus and pubic hair develop-( U* _: M! e  y; R, {0 `
ment without testicular enlargement, which was due
; c" p  q/ G4 K, U  hto the unintentional exposure to androgen gel used by
5 r, [* H4 }3 J: j( O5 z0 E8 Z+ s2 Gthe father. The family initially concealed this infor-
. a4 ^  {( G- qmation, resulting in an extensive work-up for this6 h. F/ I0 I3 h6 Z, w
child. Given the widespread and easy availability of
+ E% W9 G9 _# G  Ltestosterone gel and cream, we believe this is proba-' z% n1 g* B" b6 I( \# N- `5 c
bly more common than the rare case report in the- A6 Q5 r; ]3 b+ _) ?& l
literature.4; ]  S- S+ U+ q: v
Patient Report2 j5 a$ n; f9 M. k! V3 k( |
A 16-month-old white child was referred to the
8 o8 R0 |6 }" q3 c9 `6 Dendocrine clinic by his pediatrician with the concern
2 P, E' z; s% r: A# H. k$ Dof early sexual development. His mother noticed9 ?. l, C8 n# m. @- [, ^/ K$ Q
light colored pubic hair development when he was
1 I1 ]6 L8 X. n2 k: U  _From the 1Division of Pediatric Endocrinology, 2University of
3 `8 a0 h8 Z, p9 rSouth Alabama Medical Center, Mobile, Alabama.; A" s& s9 V7 \" u
Address correspondence to: Samar K. Bhowmick, MD, FACE,0 X% [2 Y+ `+ V4 Y
Professor of Pediatrics, University of South Alabama, College of1 R0 f$ \/ P8 B" o" M% Z
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;" m7 Q: z% \$ n7 k( D) c+ t
e-mail: [email protected].% h! w" ~; l* S3 P- |3 w6 t
about 6 to 7 months old, which progressively became; V0 w3 j: C* t- R
darker. She was also concerned about the enlarge-; \5 e& q  n! r
ment of his penis and frequent erections. The child
( g5 e: W- W5 g$ w+ ?( _6 G5 mwas the product of a full-term normal delivery, with
, z* \% F* h* Q- g9 Y7 ~a birth weight of 7 lb 14 oz, and birth length of; f+ {" v+ s; e' l+ t5 \
20 inches. He was breast-fed throughout the first year
3 p* y7 x' D! h" H, l* Mof life and was still receiving breast milk along with( A( C) b9 X$ }( c" p$ v8 {; Y, _
solid food. He had no hospitalizations or surgery,' I) V$ n( {, I4 ~1 l7 t' X
and his psychosocial and psychomotor development, q0 S+ B9 W+ y
was age appropriate.
: B6 J6 B- w; k  k4 u, h" g1 OThe family history was remarkable for the father," o; n& t; j, {( E- V- F! _1 A3 B
who was diagnosed with hypothyroidism at age 16,
: u9 v  D9 y: u. z& L' ewhich was treated with thyroxine. The father’s
7 G" I# M  ?6 p, H" bheight was 6 feet, and he went through a somewhat
# V6 B+ A5 o0 m, e1 J2 Q5 W7 Rearly puberty and had stopped growing by age 14.
$ k2 z2 E0 [" v1 r* A  b9 LThe father denied taking any other medication. The
4 l# k& |' @6 J1 b+ @child’s mother was in good health. Her menarche
0 C" w8 T6 ~7 m7 m: y/ d5 Jwas at 11 years of age, and her height was at 5 feet: p3 L* U+ s- L7 T9 J
5 inches. There was no other family history of pre-
. G- U% D$ w" u( T7 ccocious sexual development in the first-degree rela-
; q5 d; M+ ]- Z6 K* i0 {tives. There were no siblings.  u& A) H$ v( p. v
Physical Examination0 Y8 U$ C0 `8 @1 T4 ^2 t
The physical examination revealed a very active,: m9 d3 M8 [. ?" t( @7 p
playful, and healthy boy. The vital signs documented' u) y( r; D2 {
a blood pressure of 85/50 mm Hg, his length was% h+ A5 Z" s4 v/ _4 M
90 cm (>97th percentile), and his weight was 14.4 kg
# W+ v% T) S$ T* l& L7 b(also >97th percentile). The observed yearly growth% a9 w! `1 I0 ^' B' h5 @3 t% b2 e
velocity was 30 cm (12 inches). The examination of: o3 Z  `' e9 _; K
the neck revealed no thyroid enlargement.. P. B- s+ {* R2 }/ q! F  E9 |- _4 |! a
The genitourinary examination was remarkable for
( o) s6 r0 a, J1 Lenlargement of the penis, with a stretched length of
$ i) C/ ^, }- p( j8 O0 g1 O9 V8 cm and a width of 2 cm. The glans penis was very well
4 S* _  R# G+ ?9 G) r: U" ddeveloped. The pubic hair was Tanner II, mostly around
: `4 |( u, O. m3 Y# j! Y$ e540+ i, Y* c0 ]1 t2 P" v( r$ q  m
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from  w5 g$ r8 \( e, o0 l. [
the base of the phallus and was dark and curled. The
9 S# O: b7 L; f: g) s( stesticular volume was prepubertal at 2 mL each.
9 }9 m% b" \  U, u% R% iThe skin was moist and smooth and somewhat
4 C0 F% s- \9 o8 `1 Poily. No axillary hair was noted. There were no6 m6 c" y& l) f" Q
abnormal skin pigmentations or café-au-lait spots.1 l) ?3 b, J' F- g2 i% E! ?
Neurologic evaluation showed deep tendon reflex 2+
7 ^: {% @# _# l6 Ybilateral and symmetrical. There was no suggestion5 _3 ^9 m2 I1 Q8 S
of papilledema.
$ h  w2 F. L1 d  `Laboratory Evaluation
' U( \3 c; k; G3 L% F) eThe bone age was consistent with 28 months by& }) ~! h- N# S0 b* E5 p5 P
using the standard of Greulich and Pyle at a chrono-
! s; Q" V$ g+ s2 z. z6 Ologic age of 16 months (advanced).5 Chromosomal
8 J! ]4 a2 p6 s) i: ?* qkaryotype was 46XY. The thyroid function test
$ g, d! Z  _2 L% u8 jshowed a free T4 of 1.69 ng/dL, and thyroid stimu-. ]( `. v# J& v+ E# a0 _/ s
lating hormone level was 1.3 µIU/mL (both normal).
* B% x& R3 ]+ wThe concentrations of serum electrolytes, blood
1 p: ?5 F: T! a' wurea nitrogen, creatinine, and calcium all were
# `3 H+ ~5 L$ {4 J% wwithin normal range for his age. The concentration
3 l3 c4 T! M' m5 aof serum 17-hydroxyprogesterone was 16 ng/dL
; ], i% ^: u5 S$ u$ M(normal, 3 to 90 ng/dL), androstenedione was 20
+ {% d( ~* W' vng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
7 N2 p0 T% _+ c* [8 x+ w# Gterone was 38 ng/dL (normal, 50 to 760 ng/dL),
: ]8 H$ d5 V* b: v; n( sdesoxycorticosterone was 4.3 ng/dL (normal, 7 to
  I1 b2 i( y8 q! _49ng/dL), 11-desoxycortisol (specific compound S)
# r2 U4 @( g0 w4 [5 uwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
$ c. O9 A3 P1 i% o5 ftisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
" ^5 T. r- L! S6 B9 mtestosterone was 60 ng/dL (normal <3 to 10 ng/dL),9 U( X$ _0 R2 }% F( }& D$ a2 Q
and β-human chorionic gonadotropin was less than
% B1 Y# m& }9 B3 [4 h8 u7 ?5 mIU/mL (normal <5 mIU/mL). Serum follicular) k; C8 L. d: |- r6 \' P
stimulating hormone and leuteinizing hormone0 H; m; B& U7 N) C; G. e
concentrations were less than 0.05 mIU/mL! M6 V! x) {$ E6 ?2 Y: j5 k2 G
(prepubertal).
9 X% R0 f' p2 C* }3 `The parents were notified about the laboratory
5 o$ J( ^1 W& y6 |' g! l& [& Bresults and were informed that all of the tests were
' @% d2 m3 i; m( A1 U8 p) ?/ ~normal except the testosterone level was high. The' v  o9 e0 L* ?  @* D' U/ e. L
follow-up visit was arranged within a few weeks to' [0 ~: p5 ]0 C) }6 f. M* i9 a
obtain testicular and abdominal sonograms; how-" ]2 V9 `3 d! \& ^: l. ]  D6 S
ever, the family did not return for 4 months.
* y9 Y4 ^: b  V* H8 Z; m+ ?4 IPhysical examination at this time revealed that the6 V' ^' T8 ~# r+ N- ]: G
child had grown 2.5 cm in 4 months and had gained: W4 G5 s! m: J& B9 q5 e2 |# ]& R: _
2 kg of weight. Physical examination remained
4 ^/ h  c2 v9 k, ?* zunchanged. Surprisingly, the pubic hair almost com-7 [- M6 B8 O% z: I
pletely disappeared except for a few vellous hairs at# _' J8 ^2 U  Y4 j
the base of the phallus. Testicular volume was still 2+ `* F* H3 P2 J
mL, and the size of the penis remained unchanged.3 _* W: J  t: p& Y- Q
The mother also said that the boy was no longer hav-$ @( }" o/ Y, \* U$ u& w
ing frequent erections.
5 V9 U% {" @" Y" O5 B) j9 n7 A' [Both parents were again questioned about use of; I  _; m+ x5 d) e+ V$ ~
any ointment/creams that they may have applied to4 c- a; ~; O# K2 \: M
the child’s skin. This time the father admitted the
$ o% |8 R- X3 H7 \9 NTopical Testosterone Exposure / Bhowmick et al 541: x3 u+ e; Q  A
use of testosterone gel twice daily that he was apply-" ?7 G, Y) Y  P
ing over his own shoulders, chest, and back area for
( i# w: ]4 I% z% p0 F/ ]9 O/ Aa year. The father also revealed he was embarrassed* g- y" s8 ?2 L) J" J% D6 ^2 [0 j: C
to disclose that he was using a testosterone gel pre-9 h6 }: Q9 w6 K9 ^
scribed by his family physician for decreased libido8 I* n. J" }$ \3 K
secondary to depression.
# t& X6 [; y& Q+ ^' \6 @6 {The child slept in the same bed with parents.& G: p" z+ ^4 U7 u# }7 `
The father would hug the baby and hold him on his" S7 v3 T. R4 E4 R. N% u
chest for a considerable period of time, causing sig-# ~0 g) H0 Z- ]( ~5 q8 i
nificant bare skin contact between baby and father.8 d6 V8 A  l4 [. v+ r
The father also admitted that after the phone call,
" ^8 c3 c9 w; a* b/ L& h& uwhen he learned the testosterone level in the baby
; t* v! T# s) ]3 `" zwas high, he then read the product information
0 p8 J: g, y# xpacket and concluded that it was most likely the rea-
& ^% T) k; r3 g; z% g9 y) Cson for the child’s virilization. At that time, they2 ?' g' v$ i4 N. h
decided to put the baby in a separate bed, and the% j( ]4 S! N" C- T
father was not hugging him with bare skin and had8 q# x) Z3 T1 f* z
been using protective clothing. A repeat testosterone
" a5 u" F8 x  D. Ttest was ordered, but the family did not go to the- O  r9 H, y/ E( j/ U
laboratory to obtain the test.
/ K8 g" D4 z7 ]7 }5 W& F2 }& T& rDiscussion
) d4 Z1 W3 C5 R- W8 RPrecocious puberty in boys is defined as secondary
, q; S" i) N8 Q8 c" L( qsexual development before 9 years of age.1,4/ g' n) l! N0 n
Precocious puberty is termed as central (true) when/ ~. d) \/ X& {" |4 l! v. x' O
it is caused by the premature activation of hypo-& h) H6 \, x% u7 Q# {, ]
thalamic pituitary gonadal axis. CPP is more com-
3 |/ t/ W% D5 [5 D" K6 T3 z' Umon in girls than in boys.1,3 Most boys with CPP
5 T) g; c5 j5 K7 Q0 Omay have a central nervous system lesion that is+ I  ?7 Y4 w, i
responsible for the early activation of the hypothal-4 j$ i% D2 i4 n" u9 |8 ]4 _
amic pituitary gonadal axis.1-3 Thus, greater empha-# L# _# G0 s( j0 t3 u
sis has been given to neuroradiologic imaging in
2 r9 w0 i8 A9 C" t& eboys with precocious puberty. In addition to viril-
/ k/ |$ p9 u8 D. {. }" }ization, the clinical hallmark of CPP is the symmet-
6 F% b% Y3 V5 g! \. N/ ^' ~- |rical testicular growth secondary to stimulation by) f8 E/ S2 r5 z6 n
gonadotropins.1,3
/ L6 V8 y# A3 M1 a8 {Gonadotropin-independent peripheral preco-/ a6 M9 j. y5 u. y0 h$ V
cious puberty in boys also results from inappropriate
- h7 n- D! ?; wandrogenic stimulation from either endogenous or3 s: Q1 N; ^; l1 F' f! [2 y
exogenous sources, nonpituitary gonadotropin stim-
1 F" o: z9 V; {9 A* Xulation, and rare activating mutations.3 Virilizing2 P/ w) _( g, A* ~, B* C
congenital adrenal hyperplasia producing excessive
& O. [8 a' }) L6 d* Yadrenal androgens is a common cause of precocious
3 b6 v2 g7 E1 Z/ Vpuberty in boys.3,4
+ t6 k' \$ c0 R' k5 ^- Z3 i* PThe most common form of congenital adrenal- c( ]! b. S0 b3 D$ d" j
hyperplasia is the 21-hydroxylase enzyme deficiency.
: ~, e; \% o* lThe 11-β hydroxylase deficiency may also result in
! U+ u$ u2 _; e9 D2 B7 Gexcessive adrenal androgen production, and rarely,
0 T" O  n3 }8 }1 Gan adrenal tumor may also cause adrenal androgen
0 x+ ^. b! U2 ?2 w2 m! zexcess.1,3+ ^9 I5 _2 h) [/ W, M6 d/ {" y6 c
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from) N- J2 [: d9 Z! X6 |
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007- l8 N- A# G" R4 E
A unique entity of male-limited gonadotropin-
! O/ s4 A1 s. v/ `- ^) Jindependent precocious puberty, which is also known
4 U' r+ G3 b1 e: W1 \" m$ p/ _as testotoxicosis, may cause precocious puberty at a
) r/ V' g5 Z' y6 ]; Y9 Hvery young age. The physical findings in these boys
, S# D4 o. q5 y( E  a% a+ x6 Vwith this disorder are full pubertal development,
$ F6 h9 y' @) M' n( }- Kincluding bilateral testicular growth, similar to boys8 u! w8 F5 I! n
with CPP. The gonadotropin levels in this disorder
' S3 K' Z! n; p4 |3 n% f5 care suppressed to prepubertal levels and do not show
! Q* r8 K& N- P4 R1 l1 F+ X9 t0 Dpubertal response of gonadotropin after gonadotropin-
0 L" E3 ]" T3 z3 jreleasing hormone stimulation. This is a sex-linked+ h/ E, P% c$ I% L0 m( e7 w
autosomal dominant disorder that affects only; j* ~( O& r& ?
males; therefore, other male members of the family2 F. r$ c+ \: g
may have similar precocious puberty.3
2 ^7 t( P; R2 ~6 ]5 _6 _In our patient, physical examination was incon-
, T' E6 y4 D. T5 @: Dsistent with true precocious puberty since his testi-
. M# X, C  @* m, Ocles were prepubertal in size. However, testotoxicosis
9 ^" k7 Q$ {  S) ?8 c$ Wwas in the differential diagnosis because his father3 G  k4 G% ]) B
started puberty somewhat early, and occasionally,
" }$ [# w5 U2 J0 ?; Otesticular enlargement is not that evident in the; j( j2 P3 Q1 X) a
beginning of this process.1 In the absence of a neg-5 l/ s' ?# ~8 ]' L
ative initial history of androgen exposure, our
8 ?0 {7 E$ q$ ?2 Jbiggest concern was virilizing adrenal hyperplasia,
  J$ F$ T3 X' u6 `either 21-hydroxylase deficiency or 11-β hydroxylase
. c0 y- }3 M& l; Rdeficiency. Those diagnoses were excluded by find-
0 k2 G( b3 W( ~; D& F! c, [ing the normal level of adrenal steroids.0 s* H/ p- T* ^% p
The diagnosis of exogenous androgens was strongly6 m7 R0 H0 v! Q/ x. b' k6 i& E
suspected in a follow-up visit after 4 months because  m' R1 K! \4 x0 ^
the physical examination revealed the complete disap-
4 L3 C/ N" G2 N8 Tpearance of pubic hair, normal growth velocity, and
6 F7 W4 X& F" y2 |: Wdecreased erections. The father admitted using a testos-* b/ U( F2 A. w4 c
terone gel, which he concealed at first visit. He was% `( O" T( w# H- a( N
using it rather frequently, twice a day. The Physicians’5 W/ ~' H7 k9 p
Desk Reference, or package insert of this product, gel or
9 b! {# w! ^% a$ B3 @& }4 S' {cream, cautions about dermal testosterone transfer to% L4 M$ _( v3 t0 A. U$ g
unprotected females through direct skin exposure.
( J. ?- N1 g  `. H; v; _+ JSerum testosterone level was found to be 2 times the
: O. `# d1 k" e. Mbaseline value in those females who were exposed to
  h1 @; I5 m# b. i) M8 b, Oeven 15 minutes of direct skin contact with their male
% J6 y( ~7 d4 k: Y0 T/ b" |! kpartners.6 However, when a shirt covered the applica-. O# s  Y8 Y6 Z0 h4 f
tion site, this testosterone transfer was prevented.- n) m, h% C# x  D9 J% ]7 Z6 ]
Our patient’s testosterone level was 60 ng/mL,9 F6 n1 ?  I$ M
which was clearly high. Some studies suggest that1 W$ C- f( D( {$ f9 l8 b$ ?
dermal conversion of testosterone to dihydrotestos-
' z" B  }( v$ U0 F( q; Vterone, which is a more potent metabolite, is more, L( R% U) p, G% t& B8 S! g! q2 }
active in young children exposed to testosterone
% V2 v+ R, q$ `" D4 \exogenously7; however, we did not measure a dihy-. Q- }9 x4 Y% J  v$ `. |
drotestosterone level in our patient. In addition to. N& ^( u5 O) u/ F/ V- L* D7 ^' [0 F
virilization, exposure to exogenous testosterone in
8 U5 x9 y& q7 B; M6 D: Hchildren results in an increase in growth velocity and$ P; a8 r0 n) B- O8 S
advanced bone age, as seen in our patient.
1 C5 Z  E5 V7 C+ V& k9 z) jThe long-term effect of androgen exposure during
! I) p2 W+ H) A6 f' O- k, Searly childhood on pubertal development and final
7 R) _6 A1 d1 g( |+ s% O% p- Uadult height are not fully known and always remain* p+ j8 i5 w' @# N) s5 L) K1 c
a concern. Children treated with short-term testos-( f( T6 U& {+ b, I
terone injection or topical androgen may exhibit some
$ }$ f9 x1 J( V2 v- j; Q: `acceleration of the skeletal maturation; however, after
2 e7 P5 g( B$ H' Z) ?, Vcessation of treatment, the rate of bone maturation
( Z6 O' F" `7 S7 y, C3 S9 ~- Cdecelerates and gradually returns to normal.8,9
# @5 \' O  k$ {' XThere are conflicting reports and controversy- U  Q" ~9 r7 E
over the effect of early androgen exposure on adult3 ?+ m/ {; S4 v
penile length.10,11 Some reports suggest subnormal
' Q" t1 w1 s" H6 o8 Q9 o3 o& Badult penile length, apparently because of downreg-- F7 K+ |; V' I% e0 R0 O
ulation of androgen receptor number.10,12 However,
4 j& R. V; g' aSutherland et al13 did not find a correlation between7 s9 o) V( v+ U, K% m
childhood testosterone exposure and reduced adult
1 N! y3 p! G' F. F: m2 Kpenile length in clinical studies.
& u% v  T1 t0 R: ^+ hNonetheless, we do not believe our patient is. y: G0 b* G- j
going to experience any of the untoward effects from% j  ^  d9 P7 k8 g) J0 a0 Y
testosterone exposure as mentioned earlier because+ Z5 f. x6 t0 ^7 c
the exposure was not for a prolonged period of time.9 T* F6 s0 ?$ y; C' L/ V
Although the bone age was advanced at the time of, t8 c) N* g  k% E% m( y
diagnosis, the child had a normal growth velocity at
" [  A( e+ T7 N0 M2 a: i* a) fthe follow-up visit. It is hoped that his final adult- w4 a9 T( `9 U+ a9 H
height will not be affected.6 K) C, f5 e3 p, U
Although rarely reported, the widespread avail-+ f0 w3 k' m7 \3 H6 |2 P
ability of androgen products in our society may
  X9 h& `, E+ e. B7 w6 D* uindeed cause more virilization in male or female% P/ m! ]4 e- ^! U* @# \1 w" M
children than one would realize. Exposure to andro-$ q$ e8 S. W& r6 u
gen products must be considered and specific ques-- I) ~0 l- L3 D/ u$ Z! ]0 m) n: @
tioning about the use of a testosterone product or
, M' x& H) g) L" O+ H) U" Y8 pgel should be asked of the family members during+ H8 s  O7 `# B
the evaluation of any children who present with vir-5 d( m# e( K) B
ilization or peripheral precocious puberty. The diag-
! M2 j/ J7 r) ]$ ^) c! E2 c( Ynosis can be established by just a few tests and by# L. \5 M1 p5 y  G- Q
appropriate history. The inability to obtain such a' @  U$ {0 R* m  O2 i
history, or failure to ask the specific questions, may
# E  j/ k4 q0 m; n; _result in extensive, unnecessary, and expensive
/ |- m, G/ @$ D; O$ b3 B  ainvestigation. The primary care physician should be
( b9 Q  ~4 d. N8 k8 E1 faware of this fact, because most of these children
0 R% y) R! E4 m+ I. }1 M0 Pmay initially present in their practice. The Physicians’
: }" B! n2 x. V) E) eDesk Reference and package insert should also put a' u4 |7 H4 ^+ K  G6 I2 u: ]4 |" H
warning about the virilizing effect on a male or& y. {0 V/ C& N( ^
female child who might come in contact with some-1 `. T0 \  T+ m# p
one using any of these products.* `" \3 @) M1 a5 p$ O
References/ N4 ~, F5 U" I! N. L
1. Styne DM. The testes: disorder of sexual differentiation
) A$ I6 W+ z1 _) i* P$ band puberty in the male. In: Sperling MA, ed. Pediatric
7 l& h- h! R5 O" q( i. f5 uEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
- I# {* i# N! O, }: z4 j9 \2002: 565-628.' v, ~* j" R# ~8 o
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious: b- C* M) o6 X/ B. r7 Y
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
( a$ |  V3 x- O( b+ {Boy Induced by Indirect Topical
7 G0 G2 M5 C9 T6 X- oExposure to Testosterone
$ l# e2 J8 {: r* cSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2" G9 D0 @1 U8 d4 b8 Z: P2 u
and Kenneth R. Rettig, MD1
1 w  G$ M6 Y6 C3 QClinical Pediatrics
# j6 k0 v- n1 DVolume 46 Number 6; R) Q. O2 ]% v3 o# g
July 2007 540-5439 q2 X& `( i2 s1 o
© 2007 Sage Publications& G0 g& k  _- d  c! \2 s
10.1177/0009922806296651
4 j4 D3 m( ], lhttp://clp.sagepub.com
/ x4 V4 l5 H8 ?, S9 n4 ~2 Ahosted at0 C  X! s: q) j% r3 X1 I
http://online.sagepub.com
+ y0 E9 j9 s+ V) ^* E9 RPrecocious puberty in boys, central or peripheral,
& x4 E! [, W# m9 t6 n; `is a significant concern for physicians. Central* h# E% g& V8 P1 M1 T5 R9 C. K2 a- i
precocious puberty (CPP), which is mediated
5 B. F  m: p% ]7 V4 |through the hypothalamic pituitary gonadal axis, has
) x& P& w$ A) ^a higher incidence of organic central nervous system
- v8 P1 f: W1 n% M+ F1 r7 olesions in boys.1,2 Virilization in boys, as manifested6 v+ R4 n0 @6 u0 l$ j
by enlargement of the penis, development of pubic" ]3 s- B% [5 f" k" ]" t% G
hair, and facial acne without enlargement of testi-
2 m% l0 h1 Z3 m6 scles, suggests peripheral or pseudopuberty.1-3 We
* c% R6 V' J7 \6 `report a 16-month-old boy who presented with the( v; B  d- K, A# b# E1 G; H$ h
enlargement of the phallus and pubic hair develop-
' k) D% }3 @) h' P, ~ment without testicular enlargement, which was due6 |4 t1 K! Y$ D2 o; Q# b
to the unintentional exposure to androgen gel used by( ^/ M2 R/ r3 e$ |2 ~
the father. The family initially concealed this infor-
. E( N0 H4 H/ W; \, ^mation, resulting in an extensive work-up for this1 ^" ~; L- E; G  ~
child. Given the widespread and easy availability of8 ^/ h/ ?& G4 Y$ A( i) J3 W& q
testosterone gel and cream, we believe this is proba-
- s8 S2 R, w) H) [7 k% J" Cbly more common than the rare case report in the
8 m; T0 {* F' Z+ W$ `; @, U6 Mliterature.4
3 V& a' f7 t- ?3 b8 `% @. u/ uPatient Report1 a* \- s; |9 c1 S) [* v
A 16-month-old white child was referred to the2 D2 T" V7 x9 N" r1 F( ^7 C  }8 e: O
endocrine clinic by his pediatrician with the concern* t# V1 R9 x& z. L9 M' R9 B
of early sexual development. His mother noticed
. ?7 o; i, F& h* P) Klight colored pubic hair development when he was7 Q2 u% h: H1 O, v2 V
From the 1Division of Pediatric Endocrinology, 2University of5 Z) S" V' ~8 E( T/ ^+ |: M' J/ v
South Alabama Medical Center, Mobile, Alabama.
- y# z6 ^- W$ kAddress correspondence to: Samar K. Bhowmick, MD, FACE,
  Z. a+ d  |2 R4 g; MProfessor of Pediatrics, University of South Alabama, College of
& {2 g4 U) H5 e( a- ^( d& VMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
7 C! A5 c" \! t! |$ ee-mail: [email protected].
1 r$ ]4 e3 H2 u; @! l7 sabout 6 to 7 months old, which progressively became' I, `. p: D$ R8 M' h9 ]! L) J- V
darker. She was also concerned about the enlarge-
. K0 [9 O; @3 H4 N% l3 lment of his penis and frequent erections. The child' Z$ ^( C( m) M3 P
was the product of a full-term normal delivery, with
3 ^! B- s7 X9 |# I8 e( O0 ia birth weight of 7 lb 14 oz, and birth length of: W5 O, ^7 Q* g6 l7 t/ V2 _
20 inches. He was breast-fed throughout the first year
' T# @4 r) f" {  `$ S% tof life and was still receiving breast milk along with
' ]3 M+ j) A8 ]9 Rsolid food. He had no hospitalizations or surgery,- y/ Q4 z0 ]' e) c6 M3 Q' ]8 q
and his psychosocial and psychomotor development
. ~6 P# \9 T6 L2 p/ h/ wwas age appropriate.2 [7 O/ G/ a3 H+ E! u( B) Q
The family history was remarkable for the father,% o1 B3 c1 T4 S# \" s6 M
who was diagnosed with hypothyroidism at age 16,
" m+ }7 C7 j4 `% Twhich was treated with thyroxine. The father’s
3 {. _  ~8 B  P. \height was 6 feet, and he went through a somewhat; m+ ~& \7 ?! |- F2 Z5 ?
early puberty and had stopped growing by age 14.
) l6 _/ C! J9 O1 {/ U7 W) YThe father denied taking any other medication. The  a# z% H" X' c7 a4 n9 y
child’s mother was in good health. Her menarche; L8 r+ A  `% c
was at 11 years of age, and her height was at 5 feet% v' S3 s, B9 E: s' X6 V. c2 v
5 inches. There was no other family history of pre-' z' L# x6 X. S4 e
cocious sexual development in the first-degree rela-
# Y/ I/ f" D/ G9 C0 s% ]$ J+ ?tives. There were no siblings.
% N" H" x0 |' \5 T) p; n8 o8 RPhysical Examination
. u4 Q$ d. D! w9 \6 T0 H" ~/ zThe physical examination revealed a very active,# n1 P( ~0 u0 |( H9 f& c+ n
playful, and healthy boy. The vital signs documented
0 o4 k' w4 ^. J# `a blood pressure of 85/50 mm Hg, his length was& _5 L( C1 L! Y" U
90 cm (>97th percentile), and his weight was 14.4 kg$ \+ W  s0 a' r5 z# \, c
(also >97th percentile). The observed yearly growth3 K/ b9 {. W. f1 _5 \2 y
velocity was 30 cm (12 inches). The examination of6 p# s; X" G, w/ x# ?
the neck revealed no thyroid enlargement.0 r5 B' B1 w/ i6 S7 R3 x2 d7 V6 _) B
The genitourinary examination was remarkable for
. H; B5 d+ O- S2 @3 T0 X9 ]* }- [enlargement of the penis, with a stretched length of
. A* l& ^% n& O0 _; R3 ]8 cm and a width of 2 cm. The glans penis was very well% s/ J8 a& y0 Z: E# Y5 ?. R2 M7 f
developed. The pubic hair was Tanner II, mostly around
# [+ V0 Z. I1 d  i. F% o540
- ]& B" M! Y# O- t/ }at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
4 j. ]7 S0 G& F" y6 n- S5 e5 zthe base of the phallus and was dark and curled. The5 u; q" v# `9 k3 i# n$ c4 \( r7 C
testicular volume was prepubertal at 2 mL each.
1 j2 n4 I- U6 A) ^' ]7 qThe skin was moist and smooth and somewhat
, k. ^" w" f' x. ]1 ^4 {( Yoily. No axillary hair was noted. There were no
# L2 v5 R1 b9 |1 a3 q% xabnormal skin pigmentations or café-au-lait spots.$ Q% \" l& E# ?, ?$ u
Neurologic evaluation showed deep tendon reflex 2+! I! W) m2 L+ I, S
bilateral and symmetrical. There was no suggestion
% x1 {2 m1 q" Eof papilledema.4 L6 l( z8 s: v" H1 {% \! n9 A
Laboratory Evaluation3 p, H* A2 `7 f% @. S
The bone age was consistent with 28 months by
. A1 u0 ]8 c$ h2 J8 C! C1 gusing the standard of Greulich and Pyle at a chrono-/ K+ j4 p/ \; i8 _# Q1 u5 O. O
logic age of 16 months (advanced).5 Chromosomal4 o+ z/ v1 e% r+ Y2 T% A! K
karyotype was 46XY. The thyroid function test
2 [8 t* v: d+ V: w, rshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
" y$ m$ e$ J+ zlating hormone level was 1.3 µIU/mL (both normal).
$ ~2 B+ Z: @2 Z7 ^The concentrations of serum electrolytes, blood
3 e$ H: I9 R+ N+ S/ j% Zurea nitrogen, creatinine, and calcium all were
# @0 E; l; ?8 n& Y" Jwithin normal range for his age. The concentration
: y6 ~2 d; W/ v, v: qof serum 17-hydroxyprogesterone was 16 ng/dL
/ U1 i/ R1 G" }5 z4 g0 W2 `(normal, 3 to 90 ng/dL), androstenedione was 20
9 p5 j1 N6 d* U3 j- v8 i; cng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-7 g) S! ^6 _  V" O) b0 t4 I
terone was 38 ng/dL (normal, 50 to 760 ng/dL),$ v! k5 u- B  X5 [8 e3 u8 g6 K
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
! h/ Q$ S( H5 N. b1 c49ng/dL), 11-desoxycortisol (specific compound S)" Z' z$ @* v3 \! \( L
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
5 r/ p1 T9 Q& z8 y8 d" p& c6 xtisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total4 N2 b- w6 z- |/ j, [9 ?
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
* r6 z- n; `# J$ G: g+ ?and β-human chorionic gonadotropin was less than
1 Q; R/ T0 ^% B: I, T5 mIU/mL (normal <5 mIU/mL). Serum follicular
" ]4 X4 O7 k3 v6 z) jstimulating hormone and leuteinizing hormone
0 i7 n6 F& u, M( X& Q( |concentrations were less than 0.05 mIU/mL: n8 ]$ v( y$ q4 r$ m% R$ t
(prepubertal).
0 V% j0 B( u! P& BThe parents were notified about the laboratory
# Z) N. i3 ^) Y& O. u7 y4 Cresults and were informed that all of the tests were
3 f; }  D  p( }' v' Y! j8 fnormal except the testosterone level was high. The7 c7 o, r/ H) Q: H2 ?
follow-up visit was arranged within a few weeks to
- E$ o" \3 M% f" n7 tobtain testicular and abdominal sonograms; how-
" H. W$ }& G  F5 L7 j% F* L8 Gever, the family did not return for 4 months.
! ]. a% F; H% }$ jPhysical examination at this time revealed that the
8 R+ c+ \) H6 \+ Uchild had grown 2.5 cm in 4 months and had gained
9 b' s. `* {1 n3 i1 e2 kg of weight. Physical examination remained! w' W" c. R; K5 ^# L% C( E7 a
unchanged. Surprisingly, the pubic hair almost com-4 T, z. \2 Y  V9 v  F6 F2 u0 x
pletely disappeared except for a few vellous hairs at
/ p2 E/ W; P( @* q' k$ kthe base of the phallus. Testicular volume was still 2
1 B& s2 l+ E7 i' J+ Y5 nmL, and the size of the penis remained unchanged.0 ?4 C3 [# A/ j3 @
The mother also said that the boy was no longer hav-( O7 o' l) C7 i
ing frequent erections.
; p4 |3 {, m5 b. aBoth parents were again questioned about use of2 _: z( [- e8 x+ S
any ointment/creams that they may have applied to
! s9 T9 d  y) Q( A! k* f; Vthe child’s skin. This time the father admitted the+ q/ ~4 Z1 J& j" {+ d6 y4 L
Topical Testosterone Exposure / Bhowmick et al 541
1 l& g! h* u/ m8 xuse of testosterone gel twice daily that he was apply-$ z0 I% k8 ]1 K, v" K
ing over his own shoulders, chest, and back area for
/ i. V( S9 }& Ea year. The father also revealed he was embarrassed0 u, Y' E- k% A5 u. ]
to disclose that he was using a testosterone gel pre-/ }" `+ C+ I/ f* d+ R3 {
scribed by his family physician for decreased libido& S' @) y8 H$ M7 k
secondary to depression.3 J" d, s- s2 q6 e  K. z4 O
The child slept in the same bed with parents.6 Q# N! M1 s9 |  j
The father would hug the baby and hold him on his% h- A5 u# I6 t- w3 Q
chest for a considerable period of time, causing sig-! C- @7 a! q" o9 x# I6 L, |
nificant bare skin contact between baby and father.% y2 C5 |7 e* p. T
The father also admitted that after the phone call,
' c/ {$ j9 P- o2 h% s( r" Fwhen he learned the testosterone level in the baby8 r5 s, _) v4 f$ d. X; S' Y
was high, he then read the product information+ R. D7 M1 a) n: @4 ]# d, A. @
packet and concluded that it was most likely the rea-
7 b) ~0 v2 A: Q1 bson for the child’s virilization. At that time, they
7 i' l, G/ a7 }: pdecided to put the baby in a separate bed, and the
  o- n, R' Q6 c' B  a' c- Cfather was not hugging him with bare skin and had
' P2 I9 O" f  Q6 T4 Ubeen using protective clothing. A repeat testosterone: W9 f2 d, X8 r
test was ordered, but the family did not go to the
7 _5 e7 U9 b& q/ C* P0 ^laboratory to obtain the test.
( ?: U, h0 [9 R+ L( c1 \3 q' KDiscussion% [) O5 j& w) K) q& ^- {' H4 B% o
Precocious puberty in boys is defined as secondary
* }; B2 @2 a) ^' I3 I; U# x0 p$ a9 [4 F) ]sexual development before 9 years of age.1,46 O5 _/ t8 s+ d; n8 V- H. b: P
Precocious puberty is termed as central (true) when
' F4 t9 u0 [+ O5 Vit is caused by the premature activation of hypo-6 i( w/ h% D/ Y. u/ N
thalamic pituitary gonadal axis. CPP is more com-
* L" Y3 j9 a% P7 [mon in girls than in boys.1,3 Most boys with CPP
: V3 l( @$ E7 r% D# f" vmay have a central nervous system lesion that is
: x6 ~# ?7 t! V7 Presponsible for the early activation of the hypothal-* V7 }# R- i( p7 d9 A6 f* G
amic pituitary gonadal axis.1-3 Thus, greater empha-" E, {$ w% k6 E3 E$ n' m. V2 V+ {
sis has been given to neuroradiologic imaging in0 J8 b  c" D( {3 D9 k
boys with precocious puberty. In addition to viril-
0 Z0 F% t( ?+ |% Y5 r0 Vization, the clinical hallmark of CPP is the symmet-* r6 z' _/ E  \$ g; m, j) a9 H
rical testicular growth secondary to stimulation by
: M% x' o8 t  S, @6 p0 {, Igonadotropins.1,3
$ h* f" G* d5 {# O; J$ u+ N* pGonadotropin-independent peripheral preco-; e9 j1 w! n4 l4 N: h+ _
cious puberty in boys also results from inappropriate
. L: b( c( \0 `+ b! d8 c6 K3 Pandrogenic stimulation from either endogenous or9 G! R. b, W8 L
exogenous sources, nonpituitary gonadotropin stim-* k# T4 P' r6 e, d
ulation, and rare activating mutations.3 Virilizing
* m$ F8 \- i- d# {congenital adrenal hyperplasia producing excessive
# n  @) \7 W& M0 C2 r/ Kadrenal androgens is a common cause of precocious; u2 M6 w: c" O( L- B# p; K5 y& v
puberty in boys.3,4
  Q, R* z* c) K, r. yThe most common form of congenital adrenal
# ~4 g6 Z7 p( j4 l, n1 u6 p1 x2 Jhyperplasia is the 21-hydroxylase enzyme deficiency./ o+ M" `3 g: A) |; _! [+ h( Z
The 11-β hydroxylase deficiency may also result in
* I8 j" ?4 g" g& T1 ]! I% f+ k; gexcessive adrenal androgen production, and rarely,
/ h" z+ M; w' j6 Xan adrenal tumor may also cause adrenal androgen
: [- o7 m- O, Wexcess.1,3; h% w$ v1 B/ I. @; _1 q# G) l9 @
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
% `1 q7 T, j/ d' X542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
& V1 p+ m- x5 d5 O" ~# A' y7 UA unique entity of male-limited gonadotropin-
4 i* s3 H$ |5 j7 F4 P; q* uindependent precocious puberty, which is also known5 E8 G0 u* K2 M/ }7 l
as testotoxicosis, may cause precocious puberty at a7 }# P9 K) O( l; a! b  Q& ?" {7 {
very young age. The physical findings in these boys* |. y9 b' q3 ^/ ~/ z: w, @7 H
with this disorder are full pubertal development,- ?/ y" M; X4 e- E+ C. {
including bilateral testicular growth, similar to boys
, k+ {7 \/ t& T& Hwith CPP. The gonadotropin levels in this disorder; L" f. t! O) w3 x* D& R
are suppressed to prepubertal levels and do not show& V2 k5 G# z8 H" y, v
pubertal response of gonadotropin after gonadotropin-
$ V2 r& E9 d0 s5 Oreleasing hormone stimulation. This is a sex-linked9 l% W9 C  X% _5 C+ d
autosomal dominant disorder that affects only
7 [) ]0 i3 J8 f( L5 I* o6 }' omales; therefore, other male members of the family; j0 Q* T0 N) z2 F5 ?. S+ g
may have similar precocious puberty.3/ Q/ i5 m# n, x8 @
In our patient, physical examination was incon-" H. S$ {+ N4 e2 P. f9 K) G' w
sistent with true precocious puberty since his testi-
9 f7 k( ?* B  ~$ Vcles were prepubertal in size. However, testotoxicosis" ?$ ^7 P, w3 |+ I$ I
was in the differential diagnosis because his father) a1 c5 M$ S6 s6 c5 w1 p) A
started puberty somewhat early, and occasionally,: W, X$ X, n7 _4 q
testicular enlargement is not that evident in the
  F* u" N2 B1 w, ibeginning of this process.1 In the absence of a neg-
) ]# r( U0 N" p8 o6 x; Yative initial history of androgen exposure, our  W$ L9 L1 O0 e; m
biggest concern was virilizing adrenal hyperplasia,9 i; a6 {. O: ~1 B, c5 k4 x
either 21-hydroxylase deficiency or 11-β hydroxylase) s& _1 J7 X: g& P
deficiency. Those diagnoses were excluded by find-' O* G# \( x, C. i3 @" u5 H
ing the normal level of adrenal steroids.5 a  z7 N' [2 b1 [! |9 Q
The diagnosis of exogenous androgens was strongly
7 G+ B' \+ i, n) m4 d1 N, Gsuspected in a follow-up visit after 4 months because
; o" ]7 G( ?% y2 Nthe physical examination revealed the complete disap-
7 e6 k2 J9 [3 [# _pearance of pubic hair, normal growth velocity, and
! t, Z/ B; B9 W) Hdecreased erections. The father admitted using a testos-
  v' A. O6 ]/ G3 W# e) m( ]  {terone gel, which he concealed at first visit. He was
& V5 |# A5 W) }$ V* f1 C4 F* vusing it rather frequently, twice a day. The Physicians’% \, d5 P; F2 u+ p2 k
Desk Reference, or package insert of this product, gel or
. r" v; Z  P! Bcream, cautions about dermal testosterone transfer to" r, X' n1 y* }6 [" t$ a: r! C5 f
unprotected females through direct skin exposure.
' ?% |$ a8 E7 [+ K& F( ^1 oSerum testosterone level was found to be 2 times the2 d' X, {! }, C, u' ^
baseline value in those females who were exposed to
2 q& L3 C. u) b' `5 f; Geven 15 minutes of direct skin contact with their male
& n. @& L8 t4 L5 h7 n" ~1 `partners.6 However, when a shirt covered the applica-5 `1 x! E+ Q: W) ?3 V& ~; u
tion site, this testosterone transfer was prevented.
- F6 b  R* }9 k, w0 x: JOur patient’s testosterone level was 60 ng/mL,
# {5 l- ]2 i/ ?& _3 e9 l  ?which was clearly high. Some studies suggest that2 u  t1 h3 R" s5 h) g5 m% z
dermal conversion of testosterone to dihydrotestos-( e7 R, I5 U7 |; `) }# p
terone, which is a more potent metabolite, is more
, _4 W* W1 N4 u, R- E! Wactive in young children exposed to testosterone% W+ H# k8 ~: v9 v5 j
exogenously7; however, we did not measure a dihy-$ `1 B9 x3 a" U, u
drotestosterone level in our patient. In addition to
8 Q7 K  _) ^" a7 t+ p' O; |virilization, exposure to exogenous testosterone in. E" c. b  }0 k9 J
children results in an increase in growth velocity and1 \/ K6 o& T- P; m% C4 l
advanced bone age, as seen in our patient.
% ^, F0 u4 F. F  J4 tThe long-term effect of androgen exposure during
$ o5 C9 [0 Q+ `1 w0 I. ^8 W) pearly childhood on pubertal development and final$ I2 Z* @3 M8 L& f4 Q
adult height are not fully known and always remain
- _8 S4 B9 {+ G) k  {  \a concern. Children treated with short-term testos-& ?% u  z4 r# Y4 r
terone injection or topical androgen may exhibit some8 R: A9 k  B) A; X
acceleration of the skeletal maturation; however, after
$ n# T, S: }0 N1 l7 S8 E- Zcessation of treatment, the rate of bone maturation
* G9 ^* \2 U; f/ r$ ddecelerates and gradually returns to normal.8,9
: h+ n" x" L. w7 k; mThere are conflicting reports and controversy
9 g0 ]/ K5 v5 D& e- U  n* Nover the effect of early androgen exposure on adult
8 I" T& e# B4 ypenile length.10,11 Some reports suggest subnormal
- |! X' {* i6 aadult penile length, apparently because of downreg-
  _/ d2 s. O! b' ?1 H8 p7 w# Julation of androgen receptor number.10,12 However,
* U8 w( _0 `; g! JSutherland et al13 did not find a correlation between
# A* o0 }# `0 d3 Lchildhood testosterone exposure and reduced adult
: v" X5 E# T, s2 Z  Y) ?$ f# Npenile length in clinical studies.
3 W6 c9 C0 g: {& W7 [Nonetheless, we do not believe our patient is7 K& s# F, u( ~5 ~7 w" m- G2 P
going to experience any of the untoward effects from
; {$ H, @; @1 O# i4 F( gtestosterone exposure as mentioned earlier because, V, Q6 a2 F( j
the exposure was not for a prolonged period of time.
7 d& A% B6 r) s8 m8 c% [Although the bone age was advanced at the time of/ i/ C! \7 M% l4 L$ d4 U
diagnosis, the child had a normal growth velocity at
, r( d+ U' Z0 ?) ], a7 y) Wthe follow-up visit. It is hoped that his final adult6 l2 d* J( c5 X' {
height will not be affected.
- Q) j. W( q! X$ c* \Although rarely reported, the widespread avail-
( p* }7 v# T1 z7 _1 u: V2 fability of androgen products in our society may0 }% I8 X' H! d9 }& n8 q& r) l
indeed cause more virilization in male or female. R; y0 j2 d% [3 t! u) j$ R
children than one would realize. Exposure to andro-7 A' C4 M' o: a% B: ~% h
gen products must be considered and specific ques-9 v4 G% Q- o- J
tioning about the use of a testosterone product or
4 X' Q" k) Y6 m/ A( Egel should be asked of the family members during# o2 m6 ?1 s2 R  N  M* C  M! @
the evaluation of any children who present with vir-9 {! Q  W1 w0 U/ Y
ilization or peripheral precocious puberty. The diag-  }* m2 r- t8 w5 Q3 z
nosis can be established by just a few tests and by9 G$ A+ C3 C. F1 Q
appropriate history. The inability to obtain such a
' Y& c7 C: u) `9 q3 ^) zhistory, or failure to ask the specific questions, may
0 Q* T5 c5 X6 u$ ~result in extensive, unnecessary, and expensive
) A0 Z! e. `$ t' ~! A' F3 Hinvestigation. The primary care physician should be
9 L7 P/ C3 U7 \* q* u8 L" o1 e' v( Paware of this fact, because most of these children
0 b# z, \) m* k0 P) omay initially present in their practice. The Physicians’2 a7 `; y% Z! n" R9 ]8 k
Desk Reference and package insert should also put a- h% F% e6 C4 c
warning about the virilizing effect on a male or
& x7 l. R  l8 f$ Lfemale child who might come in contact with some-
4 L# `! d* v- Fone using any of these products.
1 |! M& M8 X& {, r" U; X1 t4 EReferences+ r0 T6 h" l# T! R4 t7 Q7 C
1. Styne DM. The testes: disorder of sexual differentiation& T! T7 c- U- s
and puberty in the male. In: Sperling MA, ed. Pediatric* L% u: O2 b' @* U5 B
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;" V. Y2 h" u( ?" M& H4 W1 o1 d/ W6 N
2002: 565-628.+ H2 A" g* \  S9 \
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
8 F6 K9 Q! ~( i. F, apuberty 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
! S8 n: b# x" K- }! c) q, d% f8 P+ C
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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