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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% ]2 Q4 @3 o& }' J
Boy Induced by Indirect Topical
# t8 A& ]) \- ^! ~; w/ Q3 CExposure to Testosterone# N7 j1 |: Z9 |( q" m: I
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,29 b% B- A4 G  G, |0 X
and Kenneth R. Rettig, MD1# Q8 w* P% C, p
Clinical Pediatrics; ~8 Y  y0 {" v; R& K$ Z8 i1 h8 Q  f
Volume 46 Number 6; z! ~, `/ `% ^4 d8 I5 Y6 [* h
July 2007 540-543& b% A+ _' k0 f( G( r# f
© 2007 Sage Publications  b. I2 K+ p$ y! _! i0 z. @
10.1177/0009922806296651
+ G7 r! `, B( A3 ^% {6 ~8 Bhttp://clp.sagepub.com
3 l% m4 s3 Y0 a% {hosted at9 d( G, M3 L- C
http://online.sagepub.com; L1 |. k/ C. l
Precocious puberty in boys, central or peripheral,
% c5 [" ]. L0 i( ris a significant concern for physicians. Central% l3 e& u. n! n0 y
precocious puberty (CPP), which is mediated
  H3 J: z+ L0 g/ [7 ^, @/ e9 U; Pthrough the hypothalamic pituitary gonadal axis, has
% {/ Y* S9 p( q) xa higher incidence of organic central nervous system
  L/ ]8 e; S' F$ u5 C4 s+ klesions in boys.1,2 Virilization in boys, as manifested
2 q! N' ]9 H. ~8 V& lby enlargement of the penis, development of pubic' a! u$ D+ N- o+ E8 Y
hair, and facial acne without enlargement of testi-/ b( J4 ~- b3 B0 t+ `5 g3 t
cles, suggests peripheral or pseudopuberty.1-3 We
3 U& ?! L) N; V0 W7 w& l$ Preport a 16-month-old boy who presented with the
" Q) ^& C( C2 t* J+ j/ yenlargement of the phallus and pubic hair develop-6 W" Z( A2 y0 t$ H! o2 R$ p
ment without testicular enlargement, which was due
2 f! D% g" f9 ^3 e& Q% s1 w  Eto the unintentional exposure to androgen gel used by5 x. q0 u; n7 e9 L) ~+ l9 ~
the father. The family initially concealed this infor-3 s1 e# b+ s' g, ^3 R) s" k
mation, resulting in an extensive work-up for this
: N0 _. h/ V- O$ L3 {" ichild. Given the widespread and easy availability of
1 t, t5 C% r9 ?! ltestosterone gel and cream, we believe this is proba-; R1 I' c6 Z4 a6 {# c& b5 w; L
bly more common than the rare case report in the  [. }( u7 @  D4 a0 N: z7 n
literature.4
9 @4 Z. q2 D5 @8 _- kPatient Report
: g" {0 y" ]* YA 16-month-old white child was referred to the
; H2 Z+ e" m0 `! m9 h- {( jendocrine clinic by his pediatrician with the concern8 M- E  L$ F( x  a
of early sexual development. His mother noticed
. ]# d6 W9 i, Dlight colored pubic hair development when he was/ V  w8 _8 T* V% B8 p7 y
From the 1Division of Pediatric Endocrinology, 2University of- ]9 o# m( U* k- h2 k6 g
South Alabama Medical Center, Mobile, Alabama.+ V' T: q- E8 h% y6 }
Address correspondence to: Samar K. Bhowmick, MD, FACE,9 W$ T1 ~9 Q: _
Professor of Pediatrics, University of South Alabama, College of' B, \# m& O9 }1 s; T  h
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
, F3 G; F6 f4 X/ P$ I+ We-mail: [email protected].4 _/ J0 ~4 s- C+ D( N& s
about 6 to 7 months old, which progressively became
( K$ a: e5 b5 jdarker. She was also concerned about the enlarge-# P# P) e6 \$ C4 m) b, L# A
ment of his penis and frequent erections. The child" Y/ o+ R4 C1 j
was the product of a full-term normal delivery, with0 l  F2 @& r( A. L+ J
a birth weight of 7 lb 14 oz, and birth length of9 q7 J) ~1 f; P0 ~7 B
20 inches. He was breast-fed throughout the first year6 w* }. V7 o" K0 o
of life and was still receiving breast milk along with9 A& Z% A! e( a9 B: w) y
solid food. He had no hospitalizations or surgery,. v5 s: T5 H; Q! ?' j* A; a
and his psychosocial and psychomotor development
7 a+ r9 }5 r0 ?was age appropriate.) q8 X$ d! ?% L/ r& g/ R- o
The family history was remarkable for the father,4 J6 V' d, E" g, K0 a3 i5 q
who was diagnosed with hypothyroidism at age 16,
4 q$ p3 v1 K2 U3 ]; Ewhich was treated with thyroxine. The father’s  ]5 S7 k8 _; R6 J& |$ t. D3 @
height was 6 feet, and he went through a somewhat
+ Z, g1 w* m' \. Searly puberty and had stopped growing by age 14.
: [) l/ C& F: VThe father denied taking any other medication. The
; y( J7 Z% e2 N, z. pchild’s mother was in good health. Her menarche; F/ A) m) f9 u! T2 r
was at 11 years of age, and her height was at 5 feet
3 Q) m2 \& I6 H/ P: d% d5 inches. There was no other family history of pre-
% \9 ?6 _$ w: h. q: @7 D, _/ Pcocious sexual development in the first-degree rela-
* L% C/ q0 C$ ~tives. There were no siblings.
! V# n4 K7 I( ^, ?+ DPhysical Examination' E" ]& t+ _, m9 g' a8 K+ ^
The physical examination revealed a very active,2 W* x$ X$ m+ g4 e8 b. \
playful, and healthy boy. The vital signs documented
; H4 T1 y* K* I7 ?  ea blood pressure of 85/50 mm Hg, his length was
; O( M" P2 d, T7 s- \% Y. ^90 cm (>97th percentile), and his weight was 14.4 kg
. _6 y( k9 U9 D  L+ d2 X$ ~* K3 `) W(also >97th percentile). The observed yearly growth
: D# F' V$ l+ w1 g6 [velocity was 30 cm (12 inches). The examination of1 B8 b! x! K. y  `
the neck revealed no thyroid enlargement.
" Y( c* W5 \' `. {The genitourinary examination was remarkable for9 ^5 R4 `6 y! D
enlargement of the penis, with a stretched length of- U" s5 O3 p8 ~3 k5 N) ]  v4 m" H
8 cm and a width of 2 cm. The glans penis was very well( d6 L* S5 F  D8 I3 i' r$ a  T
developed. The pubic hair was Tanner II, mostly around  S. C9 U" t8 c
540
. \9 b6 V. e) J7 ~- k/ G' ~/ nat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
6 k- b# o3 _) r9 S; w& I9 }the base of the phallus and was dark and curled. The# [5 m3 z3 {; X3 V3 x- P) ?
testicular volume was prepubertal at 2 mL each.
1 J* G9 u( ?2 O$ F, }3 yThe skin was moist and smooth and somewhat* Y' A  O5 E7 y% E9 m4 {
oily. No axillary hair was noted. There were no) H3 M1 n: t: @7 {- V
abnormal skin pigmentations or café-au-lait spots.3 T- _; m  p' p. r/ K
Neurologic evaluation showed deep tendon reflex 2+
* l% r4 l6 r6 N+ l( _2 B* Jbilateral and symmetrical. There was no suggestion
# R% @- i* j9 G" d  \of papilledema.
- \4 l4 J% {* |Laboratory Evaluation, ~( U) x; ]/ j/ u0 l* W7 B
The bone age was consistent with 28 months by
8 G& F8 ^/ X: F- x; y4 \: f. eusing the standard of Greulich and Pyle at a chrono-
' M2 q' w: r4 Q  C7 M; G0 y( slogic age of 16 months (advanced).5 Chromosomal
) W) L! U: [0 g# w2 J4 d( d! Xkaryotype was 46XY. The thyroid function test
4 n: v/ T9 B7 t  ?showed a free T4 of 1.69 ng/dL, and thyroid stimu-
: h' G6 @7 \3 S. Hlating hormone level was 1.3 µIU/mL (both normal).
$ F8 V1 V8 |) S* E0 HThe concentrations of serum electrolytes, blood
# K8 Q7 R$ P* W; r) o" wurea nitrogen, creatinine, and calcium all were. r) R- P, {+ a0 B3 h- J# R
within normal range for his age. The concentration% Q. u4 X: [6 S0 K3 ]. _3 H3 F
of serum 17-hydroxyprogesterone was 16 ng/dL: ]6 u& I4 o/ Y, j4 N0 \" e3 I& G
(normal, 3 to 90 ng/dL), androstenedione was 20
8 r$ F! a% E+ T: K( m  wng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-  C( Z& X# o0 e1 G
terone was 38 ng/dL (normal, 50 to 760 ng/dL),* I  }9 h- u& k
desoxycorticosterone was 4.3 ng/dL (normal, 7 to: I5 q& w3 `; R0 _/ u  n4 [
49ng/dL), 11-desoxycortisol (specific compound S)' o' r: ~. Q( z5 j
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-/ V- Q5 e! m& ]
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total) p) V% g8 X& l" p% N8 B. y
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),* \9 _, L! d7 ?& D3 T3 ?" d, A
and β-human chorionic gonadotropin was less than
& Z  r2 y- i, P4 l2 ^7 X5 mIU/mL (normal <5 mIU/mL). Serum follicular
0 d1 \4 i. y% a/ J) ystimulating hormone and leuteinizing hormone
4 _; |; e$ h5 e/ o; q$ m& u. {& {* C0 Jconcentrations were less than 0.05 mIU/mL
% c9 c- W5 k8 m(prepubertal).
, {1 ]* e7 f6 I# n; F7 qThe parents were notified about the laboratory& u4 v5 A) @/ F0 Y* r
results and were informed that all of the tests were$ b; s$ {3 E% l, V( K
normal except the testosterone level was high. The0 P; M( H# ~7 @% e4 v# G6 r) x! c
follow-up visit was arranged within a few weeks to) [  R* _4 v1 c' m4 A
obtain testicular and abdominal sonograms; how-& Q5 ^7 e; f7 ^' M
ever, the family did not return for 4 months.
- W9 t! q' V" [$ MPhysical examination at this time revealed that the6 h. u3 N$ O1 e
child had grown 2.5 cm in 4 months and had gained
  v4 ~9 a3 X9 w: R+ t2 kg of weight. Physical examination remained
  y+ c& k0 U& C+ v$ I. ?unchanged. Surprisingly, the pubic hair almost com-
$ o, P( \  S1 t* {! |. Y) `pletely disappeared except for a few vellous hairs at/ M; B9 r5 Q- e2 U# M, S
the base of the phallus. Testicular volume was still 2
  f1 Z, i' C& h: J! |5 ~/ \4 [9 b, WmL, and the size of the penis remained unchanged.' B1 p2 y$ C$ W% d& Q. v( E; w- v
The mother also said that the boy was no longer hav-
0 y1 W- A* {; m+ Q' Ging frequent erections.
9 ]! E/ K' J! |% \Both parents were again questioned about use of
  z. d; f# ?/ X$ V- J' iany ointment/creams that they may have applied to
9 W# J; U! e6 v& W/ m" I4 Pthe child’s skin. This time the father admitted the, _2 l* R: [7 u( _/ ?: }
Topical Testosterone Exposure / Bhowmick et al 541
  ~: K4 b( s  {& a4 suse of testosterone gel twice daily that he was apply-6 _  B7 ^5 d, H: Q/ G7 R: ?
ing over his own shoulders, chest, and back area for2 M: |' _  P& m/ r( L7 h9 D
a year. The father also revealed he was embarrassed& M4 G& N: D4 h; c; e2 d, g
to disclose that he was using a testosterone gel pre-
2 h; Y% e. n  _scribed by his family physician for decreased libido: r/ f$ I% O6 c' z% e
secondary to depression., M0 k9 S5 \- B: u1 l2 K. x' u
The child slept in the same bed with parents.
" C- ]( n& f; ?$ ^, gThe father would hug the baby and hold him on his
9 F8 Q9 b. O3 `; U- b5 `chest for a considerable period of time, causing sig-
$ P3 }0 g2 w1 A2 R  A5 X9 A3 jnificant bare skin contact between baby and father.
: R2 H8 j- ?" S! M7 K6 vThe father also admitted that after the phone call,4 ]! p3 j. b4 M# O2 O# _* V
when he learned the testosterone level in the baby
7 i2 p& m( Y0 R' Nwas high, he then read the product information
3 u! i$ O$ s4 i/ Apacket and concluded that it was most likely the rea-
' n# O6 C6 h8 G3 Tson for the child’s virilization. At that time, they
) ~6 U1 `( r8 ?6 v  x) hdecided to put the baby in a separate bed, and the) R4 h, H) R0 d
father was not hugging him with bare skin and had' \6 p$ k# Y/ H, L9 [' g
been using protective clothing. A repeat testosterone. c+ K" w/ l8 c3 ?  k' g% @
test was ordered, but the family did not go to the
& R- e; t8 ]+ y; F" [laboratory to obtain the test.; t$ r7 H7 o* c9 k1 e& ]' ~- {& F
Discussion$ d+ N7 Z- ^: I" l7 M
Precocious puberty in boys is defined as secondary
# L. P  L: ]) g: Y& `$ S5 q! Fsexual development before 9 years of age.1,4
' {/ j* E, \# s% I$ C# tPrecocious puberty is termed as central (true) when) l8 }$ T. U  n8 j# @$ N. |
it is caused by the premature activation of hypo-
, v5 H7 M2 i1 C/ F6 p( @% F2 Fthalamic pituitary gonadal axis. CPP is more com-5 d5 s0 H' x+ U1 E5 B6 C
mon in girls than in boys.1,3 Most boys with CPP( A% ~  o' C9 v3 P( ~* t- Z% P
may have a central nervous system lesion that is/ s7 [1 r  u9 x5 F
responsible for the early activation of the hypothal-/ A  V/ ~, p. p0 ^2 h5 s
amic pituitary gonadal axis.1-3 Thus, greater empha-
* j- T" t- v& I% H# Osis has been given to neuroradiologic imaging in* e6 f+ z3 C% ?8 y+ p3 z4 o
boys with precocious puberty. In addition to viril-$ ~0 h" \( G+ h  ~# \3 Z5 l
ization, the clinical hallmark of CPP is the symmet-: B: h/ b' n* t9 v1 z
rical testicular growth secondary to stimulation by
0 r8 G- K, J8 ?gonadotropins.1,37 ?5 B3 ?9 Y' q/ q) L
Gonadotropin-independent peripheral preco-/ _# ^* G% U  P# g
cious puberty in boys also results from inappropriate
( g1 C; l! T3 r, |: A" D& i0 Pandrogenic stimulation from either endogenous or# }* G, v& U& a5 m( x: f3 g& L
exogenous sources, nonpituitary gonadotropin stim-
' v, h8 {( B+ o( N2 bulation, and rare activating mutations.3 Virilizing
' f: C* C- E4 j" v( Rcongenital adrenal hyperplasia producing excessive) a* Z2 {' g! `0 W9 U2 h
adrenal androgens is a common cause of precocious
1 \# I. ^: q! Z, Opuberty in boys.3,4
1 X9 R, [3 K* t- o! q) |" CThe most common form of congenital adrenal
1 T  p" D4 M1 khyperplasia is the 21-hydroxylase enzyme deficiency.
/ X; D9 e; L: {  ?& ]" Z" R0 iThe 11-β hydroxylase deficiency may also result in
. Y9 Z" T( m/ j! ?5 \, ~excessive adrenal androgen production, and rarely,
; p7 F3 J2 u- k8 ~7 D! V4 Ean adrenal tumor may also cause adrenal androgen
% R5 j6 c4 X  sexcess.1,3; {$ [. K5 {; I. {% r  r: f' p+ O+ q
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
4 y: b2 f6 }( t542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
( F1 V( h! o" X$ cA unique entity of male-limited gonadotropin-. H2 D2 b+ F2 H* M3 A+ \! f
independent precocious puberty, which is also known2 C) P3 J; I- \& C
as testotoxicosis, may cause precocious puberty at a$ t- |% F. ~, W
very young age. The physical findings in these boys
2 f; @# E- v3 y$ m6 q' g7 lwith this disorder are full pubertal development,
* q1 y8 @+ e2 Hincluding bilateral testicular growth, similar to boys& f. t& a5 j5 o/ P5 O" w. `* f; D' X
with CPP. The gonadotropin levels in this disorder3 n# o- e4 a- {4 V. a. Z
are suppressed to prepubertal levels and do not show  r* c" g' x9 t% |+ w
pubertal response of gonadotropin after gonadotropin-
+ s" Y8 s; N% wreleasing hormone stimulation. This is a sex-linked& n$ f% w, y, F6 }, b
autosomal dominant disorder that affects only  T- g) A6 g0 D
males; therefore, other male members of the family
2 w% |# q+ |2 p( [: |, P' ?1 Pmay have similar precocious puberty.3* E/ S" H; f. }! V( }: y
In our patient, physical examination was incon-
$ X0 p' X0 f( O) `- bsistent with true precocious puberty since his testi-- ~: [' J- N9 _, U1 I
cles were prepubertal in size. However, testotoxicosis. _9 S9 N. m- \1 ]; _9 Z, T. F
was in the differential diagnosis because his father
3 q6 u: b2 j: H( ]started puberty somewhat early, and occasionally,
" l  q- {9 x$ W6 N2 ~, wtesticular enlargement is not that evident in the/ A8 n  S: q5 r& u
beginning of this process.1 In the absence of a neg-
& o% Y' c" s3 t/ m% y/ s* Rative initial history of androgen exposure, our9 P' G4 v1 N) P8 e
biggest concern was virilizing adrenal hyperplasia,
4 v8 P: J% G/ r7 z' i1 Z5 d* `either 21-hydroxylase deficiency or 11-β hydroxylase4 r: ^# C) ]+ ^( b9 v, B
deficiency. Those diagnoses were excluded by find-
4 B5 @; w1 n0 C5 w/ Y3 {ing the normal level of adrenal steroids.
0 r: f* E! A0 dThe diagnosis of exogenous androgens was strongly8 R2 w. D2 \0 l% Z- |2 D
suspected in a follow-up visit after 4 months because' @  X9 I% m/ H% \, ^# s3 }
the physical examination revealed the complete disap-: X7 i, W& D* i) a" N* n# E
pearance of pubic hair, normal growth velocity, and1 D/ x7 [8 v. V/ K% Z
decreased erections. The father admitted using a testos-
+ B3 N6 O. x5 Dterone gel, which he concealed at first visit. He was
5 k+ C. Z& ?5 q1 Q8 a4 `$ Ausing it rather frequently, twice a day. The Physicians’; ^; k3 ~" Q4 Q/ o+ f
Desk Reference, or package insert of this product, gel or
+ w) q& Y" N1 r  @cream, cautions about dermal testosterone transfer to
& T' D6 R" Q6 V8 Zunprotected females through direct skin exposure.
3 C; e  P" a5 s" t  fSerum testosterone level was found to be 2 times the  f* X' a( N9 c- N+ y$ ]0 C
baseline value in those females who were exposed to  y) p" g4 t1 A7 H- y6 i' j& B2 N
even 15 minutes of direct skin contact with their male. X6 g% v8 n0 @6 x9 N+ X9 h8 ]
partners.6 However, when a shirt covered the applica-
* P! P7 w7 D& ~8 y- t* r$ U5 g2 Etion site, this testosterone transfer was prevented.' m4 G, G: p! ^3 x6 W5 l7 p/ i/ R
Our patient’s testosterone level was 60 ng/mL,$ q1 n, }+ h1 E( w( f
which was clearly high. Some studies suggest that
4 N8 h+ L; _' x6 hdermal conversion of testosterone to dihydrotestos-+ z" w2 P- z) F9 d4 `7 S
terone, which is a more potent metabolite, is more
7 z* b$ @0 r2 {8 d8 Kactive in young children exposed to testosterone/ d2 d: ?2 p4 o; U9 r+ p
exogenously7; however, we did not measure a dihy-( U/ D+ a5 @6 o& c8 J; ]# y. j. N! E
drotestosterone level in our patient. In addition to
6 K' Q, T, j9 i; }8 jvirilization, exposure to exogenous testosterone in
1 Y. H$ J; [' X& y% qchildren results in an increase in growth velocity and
6 M3 \" A. ]# z  qadvanced bone age, as seen in our patient.
: A% S) e7 F' o+ ]' lThe long-term effect of androgen exposure during4 |3 `3 Y% z. h
early childhood on pubertal development and final
5 ^0 n$ p# O7 b2 M$ n; nadult height are not fully known and always remain( L9 }- v& K: T8 n1 _) I* H
a concern. Children treated with short-term testos-# G% p. o2 K7 j; z4 U  ]% L$ a
terone injection or topical androgen may exhibit some
& z  e$ U1 {( @' P9 N2 jacceleration of the skeletal maturation; however, after% f1 _: e: q$ T) J( ]2 C, S4 R5 l
cessation of treatment, the rate of bone maturation
: z1 \6 z, J, I6 D" `decelerates and gradually returns to normal.8,9
4 i) l8 b, I; l3 ]! J. NThere are conflicting reports and controversy
* J  M0 k5 Y; V0 r7 O4 ^. {over the effect of early androgen exposure on adult" t7 {  P! w: d9 [; @
penile length.10,11 Some reports suggest subnormal8 ?' I9 J9 N. a
adult penile length, apparently because of downreg-
0 R  l/ s/ z4 w* B5 b  H$ L( @ulation of androgen receptor number.10,12 However,
& }+ m4 e& Y9 E4 D( s) i+ MSutherland et al13 did not find a correlation between
2 r+ h+ Q8 y4 T( j: ?childhood testosterone exposure and reduced adult
: J% s, }4 l# Z* ^penile length in clinical studies.
5 l' F# }& ~7 k; L! H+ h& cNonetheless, we do not believe our patient is# k3 S- P: W6 r& x  o: S
going to experience any of the untoward effects from6 ]2 ^$ m0 a. p& U
testosterone exposure as mentioned earlier because' v  w. w  ?6 ]
the exposure was not for a prolonged period of time.% v4 L, }/ s2 k
Although the bone age was advanced at the time of
5 t) J. |( ]7 v/ f1 Gdiagnosis, the child had a normal growth velocity at
9 u. _/ [3 |4 Z+ n0 v3 Qthe follow-up visit. It is hoped that his final adult5 d" A, |+ S! z8 D
height will not be affected.8 `5 Y- i3 u* u4 l8 |% F8 o
Although rarely reported, the widespread avail-
3 E! S+ w2 e* ~! C" wability of androgen products in our society may* A& T9 K3 D8 t2 h% C' ~( v
indeed cause more virilization in male or female
8 y* I' s( `! ^" ]& H( U2 _8 `children than one would realize. Exposure to andro-1 [3 t8 z0 P/ ?. c3 Y1 x& Y5 `
gen products must be considered and specific ques-
5 p7 ~( h0 M+ Y/ i' F7 Ctioning about the use of a testosterone product or
. K4 A) q) ?3 M7 g. r( kgel should be asked of the family members during3 ^4 H% |4 I0 j$ `* J! F
the evaluation of any children who present with vir-% D) z0 ~, s* o2 r$ B: C
ilization or peripheral precocious puberty. The diag-. L4 `2 r: C/ ~% w
nosis can be established by just a few tests and by1 M) o6 K& u3 T* p  o2 @. D
appropriate history. The inability to obtain such a( X+ H) l5 l1 a& N
history, or failure to ask the specific questions, may
$ w, o# W; |  _5 s' nresult in extensive, unnecessary, and expensive4 \# ]& B; w# ^! k" v5 {
investigation. The primary care physician should be& G7 {. h" s6 ]) J
aware of this fact, because most of these children
( \  c( U% J: j# F* A2 x9 @may initially present in their practice. The Physicians’
$ |. u! H$ I4 l5 u( V/ [2 [) YDesk Reference and package insert should also put a- d$ z$ S0 O6 Z+ X) C% p
warning about the virilizing effect on a male or
/ l# V4 o) C: s# T1 Jfemale child who might come in contact with some-5 g/ o3 s% x, b+ H& w
one using any of these products.
- I+ f) t1 o; u' gReferences% `: G8 K2 F# h$ T9 F
1. Styne DM. The testes: disorder of sexual differentiation# D! t1 o1 }! z
and puberty in the male. In: Sperling MA, ed. Pediatric0 P; R; j1 F( I) I  {+ \
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
: a8 M, A. B& T( G2002: 565-628.
7 _1 _3 f9 s% o2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious; ?+ C" f" P* O; F# G/ }" n3 X
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old* z( O% T: |0 A
Boy Induced by Indirect Topical; [( C! U5 z2 X: p0 @  ?+ ]
Exposure to Testosterone# ^  t/ |$ B4 E8 o
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
7 o/ P4 o4 D7 ]1 r5 u& pand Kenneth R. Rettig, MD1! O% ], U6 q  N2 W! n# u
Clinical Pediatrics  \& k1 F2 m' X6 `' j" c: G
Volume 46 Number 6
+ x2 p" a7 d5 `! U7 v; G( hJuly 2007 540-543% i9 Q6 d& a' |4 ^5 [+ N0 P) ^
© 2007 Sage Publications
' s+ s8 v* y( y' X* b7 g0 t10.1177/0009922806296651/ f+ t1 I4 m' D
http://clp.sagepub.com, X* i' T: `8 h
hosted at
; m3 o3 w+ _/ e$ M7 Ihttp://online.sagepub.com: w/ L2 S( Z) Y. h1 _* r% n2 n9 }" s* p
Precocious puberty in boys, central or peripheral,
) `9 N* ^9 j: G* @( h  z0 Ris a significant concern for physicians. Central
4 b6 o4 @! S6 J5 ^/ P% h& x+ Kprecocious puberty (CPP), which is mediated' b) B5 T" {6 Y' J0 Y, f% E( E
through the hypothalamic pituitary gonadal axis, has
% U1 D" [  l& U2 m$ }2 sa higher incidence of organic central nervous system
9 C) B0 N. u' G5 q3 o/ Y# |* Mlesions in boys.1,2 Virilization in boys, as manifested
5 Z2 y5 F8 y8 Q/ B- k7 D: r9 kby enlargement of the penis, development of pubic) D- F# B/ b( D$ f5 W
hair, and facial acne without enlargement of testi-
4 y8 w5 q5 s2 J% x4 p$ jcles, suggests peripheral or pseudopuberty.1-3 We/ b4 @" M" G: \8 R' B9 Q1 m% Y* J
report a 16-month-old boy who presented with the
) x/ y9 x0 n% Q4 a* N* Aenlargement of the phallus and pubic hair develop-3 C, @2 K# \5 V: x7 f
ment without testicular enlargement, which was due6 j& _' C$ M$ A  g# [+ \9 l
to the unintentional exposure to androgen gel used by8 q3 |! _0 @4 P6 k- n! g$ H
the father. The family initially concealed this infor-, u4 s5 O) ?* d( c; j
mation, resulting in an extensive work-up for this% J. E; m% ?$ B0 H4 O+ |4 ?3 {; ~) m
child. Given the widespread and easy availability of9 P' O) n- J8 e8 o6 W
testosterone gel and cream, we believe this is proba-
7 m' ~5 |* K/ g( {9 v/ a# Gbly more common than the rare case report in the0 Q: s! v& Y# F2 S+ F
literature.4* ~6 @, P6 W5 n( j4 ]3 [$ @4 c
Patient Report
+ D* G/ P1 p; K7 l6 rA 16-month-old white child was referred to the& c. O6 j. \' d- ~5 v+ b# @7 q
endocrine clinic by his pediatrician with the concern* T. g8 p$ c: m0 v4 L6 A/ h
of early sexual development. His mother noticed5 e! {* p. X) V$ o# D# ~6 p
light colored pubic hair development when he was
8 g2 a! t) [2 w+ w( j/ oFrom the 1Division of Pediatric Endocrinology, 2University of
( f- B4 f! X( h$ a( }South Alabama Medical Center, Mobile, Alabama.
9 S0 c4 z, x0 ^0 FAddress correspondence to: Samar K. Bhowmick, MD, FACE,
& m7 [6 p9 c5 H, N; _Professor of Pediatrics, University of South Alabama, College of7 j: e8 _$ O. g+ P  n# V# \
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;% u+ y+ A+ M+ ]: Z  p# X
e-mail: [email protected].% z# c$ Y1 s, M3 o  p
about 6 to 7 months old, which progressively became6 X" }7 w; c3 w$ V$ c2 e! I1 z
darker. She was also concerned about the enlarge-
* K( J# A% h  G& I2 Y' Kment of his penis and frequent erections. The child1 }) \! a3 q2 J4 M
was the product of a full-term normal delivery, with9 _) P+ g' b$ ^
a birth weight of 7 lb 14 oz, and birth length of
( P: ^0 O8 [4 S8 `. ?& u9 h20 inches. He was breast-fed throughout the first year
# _' w) L1 l8 uof life and was still receiving breast milk along with& T" D4 [5 ?. W! G
solid food. He had no hospitalizations or surgery,0 }4 t  K; t# x. t7 c2 y
and his psychosocial and psychomotor development
7 R5 U4 I, Q- {" {0 @1 X3 ~- p3 }0 p7 ewas age appropriate.3 K$ L7 Y% X* ^" k# p7 M0 H5 Y0 n7 V# M
The family history was remarkable for the father,
, w8 {  O+ q; i. Owho was diagnosed with hypothyroidism at age 16,4 ]! |# L+ H+ c. }4 J3 D6 ]! ?$ u
which was treated with thyroxine. The father’s7 l# `8 i2 [+ y; T: f( G6 {$ Z3 @
height was 6 feet, and he went through a somewhat
3 N3 K. X: L. M1 Mearly puberty and had stopped growing by age 14.
' {- c# |. N+ Z/ A& X0 wThe father denied taking any other medication. The
7 n* ]  |4 E. c7 echild’s mother was in good health. Her menarche+ j& K3 b. {6 k6 C" o
was at 11 years of age, and her height was at 5 feet
- `/ y) U! W3 G8 ~! F5 inches. There was no other family history of pre-
! `8 i/ B* ^% h$ vcocious sexual development in the first-degree rela-
" w5 \' x( f4 F4 [tives. There were no siblings." P. n( N2 x5 U
Physical Examination6 W8 o5 z9 O% |# s0 l
The physical examination revealed a very active,+ z7 H* K4 |* b% Y2 {9 ?
playful, and healthy boy. The vital signs documented
% x* e% h) G# k# N, o6 d1 qa blood pressure of 85/50 mm Hg, his length was" v3 {/ p& q3 a/ X% c, l
90 cm (>97th percentile), and his weight was 14.4 kg" p  r2 R; J6 a+ b& o" ]6 Z
(also >97th percentile). The observed yearly growth+ C' Y6 L$ r, z* l/ @/ o, N
velocity was 30 cm (12 inches). The examination of
7 X  E6 @  X- n9 `' Lthe neck revealed no thyroid enlargement.7 z% j+ m% x9 ]$ D5 I' J
The genitourinary examination was remarkable for
9 v2 k3 p. p2 P2 @  L* Denlargement of the penis, with a stretched length of
! u; |, b: T; d( g. w0 {2 B8 cm and a width of 2 cm. The glans penis was very well
3 U4 I3 S' d+ }! R' u' g. Gdeveloped. The pubic hair was Tanner II, mostly around
0 E+ Q: S* K% h' x5 r540
. o9 g/ C0 X, Y( C' Mat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from0 _. ?3 i7 ]. T  z
the base of the phallus and was dark and curled. The# F- u% Y5 d: ~( U6 t5 A# X2 y* q
testicular volume was prepubertal at 2 mL each.
$ H. {% M4 u3 ~+ z5 l) KThe skin was moist and smooth and somewhat8 l4 a$ D% y4 t5 K" Z- `$ _
oily. No axillary hair was noted. There were no
; q+ V' @5 {: ~, q$ |abnormal skin pigmentations or café-au-lait spots.
% q# a" Y* U: b9 F; R# ^' UNeurologic evaluation showed deep tendon reflex 2+
$ l  D/ U: A$ b0 `bilateral and symmetrical. There was no suggestion
' H* v0 p! i8 E% I' k% xof papilledema.
" t2 e6 M4 n- _1 hLaboratory Evaluation
# j/ C0 a. S" G2 j( B  k* GThe bone age was consistent with 28 months by( u0 G4 i7 F) z& r- v
using the standard of Greulich and Pyle at a chrono-) q" i0 d% r' S3 }/ T; O4 s) |8 A
logic age of 16 months (advanced).5 Chromosomal/ ^8 A* l) ]+ i
karyotype was 46XY. The thyroid function test
/ C% C# Q4 O# U8 Y! Vshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
. F3 {. M* h% p2 K& G  Qlating hormone level was 1.3 µIU/mL (both normal).
& c* T; Q8 ^8 E" F" N8 `# SThe concentrations of serum electrolytes, blood
/ C- E( W* |8 vurea nitrogen, creatinine, and calcium all were( d  ]; t3 I3 @9 x; F# r
within normal range for his age. The concentration" ?. x4 ^5 H) r7 x( |6 ]+ R' g
of serum 17-hydroxyprogesterone was 16 ng/dL
, [. F* B8 I! A+ F: r8 N9 |9 A1 a(normal, 3 to 90 ng/dL), androstenedione was 204 k& Q7 d/ a% x. x
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
* K6 \1 x( B. `, K0 H9 `5 pterone was 38 ng/dL (normal, 50 to 760 ng/dL),
6 ^$ ]3 m: B  `desoxycorticosterone was 4.3 ng/dL (normal, 7 to) i. u8 n: M" L: i7 Y" {* v  T
49ng/dL), 11-desoxycortisol (specific compound S)  F9 B2 i# J1 J2 P# O2 P
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-( F/ w( }# M" o  ^" e. t
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
, S: H* O5 m( Y0 H' i5 Mtestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
$ _: h% M' D/ _. B5 @+ E" r+ ^and β-human chorionic gonadotropin was less than
3 ^) R6 q$ s+ t5 {& Z0 S5 mIU/mL (normal <5 mIU/mL). Serum follicular6 `: t3 \8 e- I" c$ m: |. s
stimulating hormone and leuteinizing hormone
1 O( i& k* r/ o. [, B. D4 n; V7 @concentrations were less than 0.05 mIU/mL9 d# O/ H& x7 ?/ V
(prepubertal)., k$ X- z1 Q# }+ X) P
The parents were notified about the laboratory; ^; x1 |4 E% l# C9 A
results and were informed that all of the tests were- k! f: E- W3 T
normal except the testosterone level was high. The# Y. x; m; d9 h7 K+ C
follow-up visit was arranged within a few weeks to# c; Y, ^& _, g. S
obtain testicular and abdominal sonograms; how-
8 {! V2 `( [6 ], F! _& Hever, the family did not return for 4 months.
0 G* g9 S9 p. s5 NPhysical examination at this time revealed that the5 l. K2 G( @2 p6 \. y
child had grown 2.5 cm in 4 months and had gained
6 J5 t6 B) ^3 R2 ^2 kg of weight. Physical examination remained
( h8 S8 a, }* r% ^* W5 S+ kunchanged. Surprisingly, the pubic hair almost com-' u" |* H0 F9 a5 k& j5 \
pletely disappeared except for a few vellous hairs at+ k( _' O% z* _  D
the base of the phallus. Testicular volume was still 2) Y: i; m! B1 W% l
mL, and the size of the penis remained unchanged.2 [* B% @$ A5 o: m8 [0 t' c4 c
The mother also said that the boy was no longer hav-9 [" E& n5 g/ X; G
ing frequent erections.) M6 B, ~! y# g. k5 U/ V
Both parents were again questioned about use of
5 e* t/ V1 R8 D) }. F: b0 x# lany ointment/creams that they may have applied to9 X; `) Z, T3 i* M1 I1 x$ L
the child’s skin. This time the father admitted the6 `* [+ O5 U6 y+ _$ o2 T
Topical Testosterone Exposure / Bhowmick et al 541* y( F% H3 o! s2 v: b
use of testosterone gel twice daily that he was apply-
/ G8 {: b* Y- h' L9 h4 qing over his own shoulders, chest, and back area for
8 H" T$ A& B  }" f* wa year. The father also revealed he was embarrassed" R$ F) ?# l1 A( ?
to disclose that he was using a testosterone gel pre-
2 I7 w; ^9 q- \9 }" ]scribed by his family physician for decreased libido' @$ Y% r6 Z1 C4 v9 S- \+ L
secondary to depression.6 G5 e) o% m. {* n9 x* o5 n$ J
The child slept in the same bed with parents.
" e  _% v- T5 w0 W" {; K! W8 wThe father would hug the baby and hold him on his
8 u( B7 ?/ j3 {- B9 jchest for a considerable period of time, causing sig-/ e' R' q: X3 q3 M, Z
nificant bare skin contact between baby and father.; ?+ ^; [) V' ?+ v
The father also admitted that after the phone call," `: U+ r, S6 E$ K
when he learned the testosterone level in the baby6 N& C3 V$ m% n7 s6 U; l
was high, he then read the product information1 `+ K" k1 ~4 x% n; L! G
packet and concluded that it was most likely the rea-
1 M% }  o: _7 K3 B  n1 n5 Z9 {son for the child’s virilization. At that time, they
- T3 b3 A; Y* g. @7 j0 ~decided to put the baby in a separate bed, and the
5 k0 ^9 \0 b; T- h( b5 C7 D9 hfather was not hugging him with bare skin and had
1 T9 M) F$ L: T: kbeen using protective clothing. A repeat testosterone
4 J' Y5 m! y0 I- i4 l* ltest was ordered, but the family did not go to the
, i& V; O; x2 U  ylaboratory to obtain the test.; a3 e$ H  {# Z( @) n0 |
Discussion, k; Z9 Z& e3 P. w
Precocious puberty in boys is defined as secondary
: n- O9 z6 D. h# L: msexual development before 9 years of age.1,4: u  o( ~3 i7 K7 Z0 ~
Precocious puberty is termed as central (true) when
- H2 ?" _: p" X  ^. H/ |; L7 Y) N# oit is caused by the premature activation of hypo-! z2 p6 S; A8 x6 v; n8 f5 Q9 E
thalamic pituitary gonadal axis. CPP is more com-4 Q( t' r/ {( T9 R, }$ c) }7 d
mon in girls than in boys.1,3 Most boys with CPP
) \% @. B" P9 t& U# y4 D- Vmay have a central nervous system lesion that is
# T9 r$ H) o' ]  n7 F6 vresponsible for the early activation of the hypothal-
, M$ e$ \7 v( S* G! Oamic pituitary gonadal axis.1-3 Thus, greater empha-
3 R0 S3 U2 c& m  q' t$ Isis has been given to neuroradiologic imaging in7 Y! F; q8 W- v1 ]$ z
boys with precocious puberty. In addition to viril-% \5 b$ s# O8 U% h" y
ization, the clinical hallmark of CPP is the symmet-
2 z' a" N! O6 G, H8 V% n* J3 F$ zrical testicular growth secondary to stimulation by
. A+ w$ R0 z1 Y# j) ygonadotropins.1,3
- f( S. _; I- @1 L3 P: I5 fGonadotropin-independent peripheral preco-
6 P+ k; {$ o9 lcious puberty in boys also results from inappropriate
: W; f6 v4 ?* X& L: {/ C2 }+ k* dandrogenic stimulation from either endogenous or; N, t$ M  q, h( K1 R
exogenous sources, nonpituitary gonadotropin stim-
  p: o2 ?6 f9 R5 U6 J) Z1 C  ]7 rulation, and rare activating mutations.3 Virilizing$ X! k" Z3 y+ Y' i9 b( o# B* Y  I
congenital adrenal hyperplasia producing excessive
/ f9 C+ T" ?7 P- }# I* f2 tadrenal androgens is a common cause of precocious5 j/ `9 [$ U: o+ N3 y
puberty in boys.3,4
$ l$ {/ Q) Z6 Z6 ~( I0 H8 oThe most common form of congenital adrenal
) _5 d7 B  `) mhyperplasia is the 21-hydroxylase enzyme deficiency.3 k$ q5 i% q/ g4 d6 j4 F
The 11-β hydroxylase deficiency may also result in* r- J' b. m$ m5 v
excessive adrenal androgen production, and rarely,4 Q$ c9 P6 }, n% D: o8 @; v$ N
an adrenal tumor may also cause adrenal androgen
' q6 s6 ?6 E" e" S, N! F$ D9 {$ ?excess.1,30 w  }/ t7 w  {$ n( f3 `
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from/ j6 s2 V! e: i
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
+ D4 W; d9 g, }  p, g- nA unique entity of male-limited gonadotropin-
7 m. x7 ~8 X# c6 M% ~+ P& Nindependent precocious puberty, which is also known
5 a/ ?5 l. o. ?; H) ~1 Ias testotoxicosis, may cause precocious puberty at a4 U( D  ~9 f- v# h; o! C
very young age. The physical findings in these boys: j$ |) t) e7 ^$ K, K. @2 w
with this disorder are full pubertal development,
. i* q) y0 R/ f" k& E% Zincluding bilateral testicular growth, similar to boys# J7 v$ u, C2 k2 @
with CPP. The gonadotropin levels in this disorder
$ ]3 i9 z' I0 x/ S! }/ L3 jare suppressed to prepubertal levels and do not show5 [& M' g, y3 e  [! }- Q: Q8 B
pubertal response of gonadotropin after gonadotropin-  T0 N& _' \5 ~6 b: r
releasing hormone stimulation. This is a sex-linked
1 x4 @' o) u- q% O0 Zautosomal dominant disorder that affects only" }$ L7 B6 t. r- I: {# @
males; therefore, other male members of the family" t. T8 X- z1 ]1 Z# X# s# _
may have similar precocious puberty.3
2 O- A& U1 ^" C* VIn our patient, physical examination was incon-& M+ f4 \0 x2 ?4 |' X
sistent with true precocious puberty since his testi-' F+ x0 k+ E# [& C. l/ m
cles were prepubertal in size. However, testotoxicosis& t& Y' A! q( \
was in the differential diagnosis because his father1 }0 S8 S- P: M3 u! D6 z
started puberty somewhat early, and occasionally,: Y. [0 ~, a0 W
testicular enlargement is not that evident in the
5 O6 R# w# T7 s9 \beginning of this process.1 In the absence of a neg-
) ~" }: V6 d; J5 Y5 `1 O: Eative initial history of androgen exposure, our$ I) G! |! s9 e8 o' J" l
biggest concern was virilizing adrenal hyperplasia,, Y& |' k  F+ _& H" ~2 f0 g/ Y
either 21-hydroxylase deficiency or 11-β hydroxylase& p% |8 O3 @% `" Y  I. b
deficiency. Those diagnoses were excluded by find-7 G& \0 @' }4 f4 G+ c$ m5 [
ing the normal level of adrenal steroids.: C7 I! Z- K/ M" Q
The diagnosis of exogenous androgens was strongly
' `7 E4 }$ C& y+ Gsuspected in a follow-up visit after 4 months because3 |  T3 e7 j$ K, x0 U
the physical examination revealed the complete disap-
, y6 e$ N# C' {; Q* t2 ]pearance of pubic hair, normal growth velocity, and: ?1 c+ c6 [, X4 O5 J
decreased erections. The father admitted using a testos-
' B. j0 f; Z4 v* y6 z" uterone gel, which he concealed at first visit. He was
5 L3 a2 {1 z3 D* q/ Y4 Susing it rather frequently, twice a day. The Physicians’
5 D2 p# j) ]8 A# _- `Desk Reference, or package insert of this product, gel or
/ f6 l5 S/ Q% M9 W  L- Y! wcream, cautions about dermal testosterone transfer to* i4 Y8 m* Q/ y' M  J3 O. z
unprotected females through direct skin exposure.
& l5 X2 R' f5 E! q7 q! ASerum testosterone level was found to be 2 times the
6 r2 J' U- s- q$ n9 u; B0 y6 sbaseline value in those females who were exposed to
. K2 L  S+ @2 W1 K: Aeven 15 minutes of direct skin contact with their male. D+ d! n/ I  }* @5 K& z, p% ^
partners.6 However, when a shirt covered the applica-
! j5 |8 U- J# {; D/ M2 w* htion site, this testosterone transfer was prevented.5 i' H1 e+ A' @9 Z4 V. W, o
Our patient’s testosterone level was 60 ng/mL,+ S$ {; K" P* {0 @3 T
which was clearly high. Some studies suggest that
" W( W! o9 r& t( q0 f2 g$ ldermal conversion of testosterone to dihydrotestos-
1 a& d: f- X1 o# E" M6 v5 Bterone, which is a more potent metabolite, is more
6 u8 E2 w( L. |. `# ]8 Yactive in young children exposed to testosterone# C$ l1 X7 \+ E- Z. S- K; z* t
exogenously7; however, we did not measure a dihy-& ^4 Z( v9 _% Q! ?0 r5 @
drotestosterone level in our patient. In addition to6 p. }! I7 f% f$ H) g& U
virilization, exposure to exogenous testosterone in7 I$ S3 O1 n, I# ~* d, \
children results in an increase in growth velocity and/ M* ]# m# `& _, R0 J% X2 y# b* N" q
advanced bone age, as seen in our patient.
' T0 A  \; x/ I: nThe long-term effect of androgen exposure during2 r# R! d7 {, ^* E9 s
early childhood on pubertal development and final
4 A6 H: [6 W5 A( {! @& |adult height are not fully known and always remain: x! r: k& y2 [
a concern. Children treated with short-term testos-
3 f, v7 N  x/ D& `( yterone injection or topical androgen may exhibit some) D& ~2 s+ T* m7 g' d
acceleration of the skeletal maturation; however, after
% x; U8 R& @8 j1 p8 gcessation of treatment, the rate of bone maturation
6 L6 B1 t, b, M' N( Bdecelerates and gradually returns to normal.8,9  m( s7 K- P3 c5 v0 L; u. p8 h2 o
There are conflicting reports and controversy
6 ^7 `( D9 |+ g& T2 l9 ~1 v1 Yover the effect of early androgen exposure on adult$ `: G) H# I+ ~1 @6 r2 _5 C
penile length.10,11 Some reports suggest subnormal
2 M6 c! C7 x+ ?3 |: {- S" \adult penile length, apparently because of downreg-4 H8 \3 Y( I) |7 W- R" \1 j) N
ulation of androgen receptor number.10,12 However,
5 }) y4 W4 _/ c% K9 }! f' s0 M) `. GSutherland et al13 did not find a correlation between
: Z1 D# L$ {4 @/ b: r' uchildhood testosterone exposure and reduced adult
, ]  s7 A; m( `3 spenile length in clinical studies.0 x( L8 `  ^3 W% X8 s" w
Nonetheless, we do not believe our patient is: p! v: A: l% e% e5 t( V4 m3 k$ ^
going to experience any of the untoward effects from
" V5 Y* P6 H1 f# r; E1 r% Ctestosterone exposure as mentioned earlier because
! m( W/ y  q, D, M- Y) U4 Tthe exposure was not for a prolonged period of time.
' ]. w2 b! Q, H6 b& H  fAlthough the bone age was advanced at the time of
5 ^6 r( [3 P, {8 D+ c) [diagnosis, the child had a normal growth velocity at) N  o' W' |, C3 z" b) Z
the follow-up visit. It is hoped that his final adult
6 F# E5 j7 k+ d. z) `height will not be affected.( I& q" L9 r( p5 v! N# R
Although rarely reported, the widespread avail-2 c. K# @' _+ D) S
ability of androgen products in our society may
' c! u) U1 C2 {/ w% |' g1 Oindeed cause more virilization in male or female
5 W; W6 w" u# `, o6 B, cchildren than one would realize. Exposure to andro-
; r' Q8 L% `3 c& t7 v' Z4 D6 tgen products must be considered and specific ques-
, S( v. v+ s6 c4 |, ationing about the use of a testosterone product or9 K1 c  [6 F3 e! d4 G
gel should be asked of the family members during+ o8 o8 F  x; `  X, \% C9 K
the evaluation of any children who present with vir-( s+ K: ]9 P7 a- D
ilization or peripheral precocious puberty. The diag-' e8 K4 P0 ?( [4 Y; P
nosis can be established by just a few tests and by, B8 I4 v7 H( S
appropriate history. The inability to obtain such a
7 p/ H" v( z6 x9 fhistory, or failure to ask the specific questions, may
8 E( l; G3 a% o: |7 C0 Jresult in extensive, unnecessary, and expensive& c3 U& g* A" M! L
investigation. The primary care physician should be! Z1 L9 U& f- p) v$ ~# G! g
aware of this fact, because most of these children( ]1 H: E: z3 K" e9 `7 r
may initially present in their practice. The Physicians’* c# L, F- D6 ~: g, Y
Desk Reference and package insert should also put a; U& a/ v6 R" i1 P2 V( C- S- G
warning about the virilizing effect on a male or8 [$ p0 [& ?. i; [
female child who might come in contact with some-
6 c. Y8 q% Q& ^' Lone using any of these products.
9 k3 L" P: L5 A5 A3 W) NReferences
+ L* Q* {8 b* {. U3 T1. Styne DM. The testes: disorder of sexual differentiation
2 e" G) L3 {+ I3 S! Z, I8 Dand puberty in the male. In: Sperling MA, ed. Pediatric# ?9 D5 D& z7 I6 \
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;, f7 p, W. L! E: F/ m/ q1 u( ]
2002: 565-628.0 v. I7 S7 R' s7 ?3 e5 f2 f+ K
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
7 @& O; `$ w2 f4 lpuberty in children with tumours of the suprasellar pineal
發表於 2025-1-7 21:59:43 | 顯示全部樓層
這個我收藏了!謝謝分享!WK的資源越來越豐富,這少不了大大的辛勞!
發表於 2025-1-10 10:43:39 | 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
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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

$ c; H- [3 i- D# o* I' B9 h, q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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