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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
8 J9 c/ u+ N, X' }$ OBoy Induced by Indirect Topical
1 y. K2 |6 F3 ?4 I5 A$ |Exposure to Testosterone8 a+ D- a/ Q3 v1 E7 k3 W( A
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
; M+ F% m$ M. A9 nand Kenneth R. Rettig, MD1$ L; Y) j, U1 l  ^( `
Clinical Pediatrics
. Q2 |$ ~2 \9 X0 B8 pVolume 46 Number 65 g; Q. |0 T' u" O7 U
July 2007 540-543( L* o  D# L5 v; d
© 2007 Sage Publications1 K5 U! [, K9 U# {* z
10.1177/0009922806296651% z0 j: j$ L& i2 P5 {# Z
http://clp.sagepub.com
  R; [' [# a8 t1 {) `1 H' Zhosted at
! h, r: q' X0 E+ V; U  xhttp://online.sagepub.com/ G2 H3 l- o5 @* ?
Precocious puberty in boys, central or peripheral,8 K, z" g/ G! Z$ P4 S
is a significant concern for physicians. Central
, ~6 D1 @. s' p8 E) D8 }precocious puberty (CPP), which is mediated: A3 `4 {8 {5 a( H7 f' U+ s
through the hypothalamic pituitary gonadal axis, has
# ~+ l2 I. F0 ]2 ]: R5 Wa higher incidence of organic central nervous system4 {+ l5 g- @, d* J0 I! F
lesions in boys.1,2 Virilization in boys, as manifested
6 Y+ x; F; M9 |+ K- [+ w5 Aby enlargement of the penis, development of pubic. V+ Z. Y4 \" h. D8 A, f8 X
hair, and facial acne without enlargement of testi-
. B: ?5 B* m! o1 b, X4 }0 `- ?cles, suggests peripheral or pseudopuberty.1-3 We
/ v( a. x' u' [report a 16-month-old boy who presented with the
! x; m! X5 ?' |5 n+ `6 `% O  `enlargement of the phallus and pubic hair develop-2 ?! r# I( s3 [" Y$ B
ment without testicular enlargement, which was due0 K. k; E6 R- r; o7 n/ S) q
to the unintentional exposure to androgen gel used by  p# Z1 ]1 W9 Y) l5 J# P' T
the father. The family initially concealed this infor-
, t2 U' n7 r! l' X! k- b6 hmation, resulting in an extensive work-up for this" N" V0 g+ _: p+ H, N
child. Given the widespread and easy availability of
- j1 l7 \! A+ b* C. jtestosterone gel and cream, we believe this is proba-
7 V4 g, F9 n$ J/ rbly more common than the rare case report in the
, g: n2 t5 {' I* v+ p- |literature.4
% ?# A" p& f& a; n8 |Patient Report- u$ V% t; C5 Q9 W5 R0 t( G" v
A 16-month-old white child was referred to the
2 K9 p& x* @+ Fendocrine clinic by his pediatrician with the concern
$ @0 y9 u$ }, S' v$ M# Uof early sexual development. His mother noticed
" x" m9 m7 N' q* I9 h6 d! }light colored pubic hair development when he was
# J% x$ c* l* U, D  q3 Y3 K) tFrom the 1Division of Pediatric Endocrinology, 2University of5 c5 e3 k  C% }, p8 J# Y
South Alabama Medical Center, Mobile, Alabama.8 Z6 R) z! s0 D3 O) @' B$ `. y
Address correspondence to: Samar K. Bhowmick, MD, FACE,
: c* M' j3 R, i7 w/ }* v% H- UProfessor of Pediatrics, University of South Alabama, College of' t, [' V: s  z* ?
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;" P0 Z9 M! Z5 s8 P
e-mail: [email protected].1 T* H" X' [' U+ k; S9 B
about 6 to 7 months old, which progressively became) D* |2 W7 G# e6 B5 l" ^  z
darker. She was also concerned about the enlarge-
: t6 r$ J* T8 w  c/ a- y4 m+ Qment of his penis and frequent erections. The child( G: l4 L% o4 u
was the product of a full-term normal delivery, with# w. D+ J2 u* Q6 y6 N5 ?. i9 P
a birth weight of 7 lb 14 oz, and birth length of5 k+ L8 ^, @( T
20 inches. He was breast-fed throughout the first year
4 }9 P, w+ g  ^& }! Uof life and was still receiving breast milk along with: W9 T4 I. C* U+ q# y# ]# y
solid food. He had no hospitalizations or surgery,4 k. `/ H5 Y9 K7 G# m, R6 j
and his psychosocial and psychomotor development4 R* x/ ~& H$ [* x
was age appropriate.4 d) }* A" H' F# @
The family history was remarkable for the father,, y/ v& `! O# I" O
who was diagnosed with hypothyroidism at age 16,
: L, R9 [$ h7 p: b  T- B/ ?0 }which was treated with thyroxine. The father’s
; }% g. o8 [' Q3 K$ n1 Lheight was 6 feet, and he went through a somewhat1 }0 r& N* X  p8 X% i1 X, P
early puberty and had stopped growing by age 14.5 g# p" }0 K7 W
The father denied taking any other medication. The
. X  ~1 w" Q! e  T$ _2 [* vchild’s mother was in good health. Her menarche# b4 s1 ^& j! y; e6 Q
was at 11 years of age, and her height was at 5 feet, c$ Q+ G2 `: N3 X
5 inches. There was no other family history of pre-3 O- z, F+ V/ D, W: q5 a& Q
cocious sexual development in the first-degree rela-
& R0 g& a- ~% t' n9 B- Btives. There were no siblings.9 y% e; t+ F" B4 K
Physical Examination
8 |0 S+ i1 d1 p& e3 V. LThe physical examination revealed a very active,3 P, Y! H0 V9 a# e3 `
playful, and healthy boy. The vital signs documented
6 x$ e: O( U. z0 Fa blood pressure of 85/50 mm Hg, his length was
) R' e$ m: Y9 W+ k! G6 Z) z90 cm (>97th percentile), and his weight was 14.4 kg
# }2 C! _# D/ P+ r* e(also >97th percentile). The observed yearly growth' |# e0 K( B. b8 J0 |7 D9 ]! m
velocity was 30 cm (12 inches). The examination of
- |5 U/ \; X- j9 @5 }( k, Jthe neck revealed no thyroid enlargement.
2 Y5 O* b; U- ]+ OThe genitourinary examination was remarkable for
! a! e5 ?  X8 T* \$ a$ v6 ]1 menlargement of the penis, with a stretched length of" y8 w7 Z- v, T  t
8 cm and a width of 2 cm. The glans penis was very well
. C* ^3 A; F* e6 ~+ Edeveloped. The pubic hair was Tanner II, mostly around
7 h5 Z5 _* g, N% T1 Z( J' I5402 n! U+ T( P) c6 E% u
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
0 V# w% u: O7 |9 fthe base of the phallus and was dark and curled. The& b& ]2 G; J6 a5 o9 @' R
testicular volume was prepubertal at 2 mL each.* n' f4 I+ Y. @9 c( E. A
The skin was moist and smooth and somewhat" c( n4 `+ t" z+ T% j
oily. No axillary hair was noted. There were no
7 [! n, a* H) j0 u, Eabnormal skin pigmentations or café-au-lait spots.
8 h2 J" k/ T# D8 e" K$ D7 B% ^# |Neurologic evaluation showed deep tendon reflex 2+) ~4 |7 w  u( a
bilateral and symmetrical. There was no suggestion5 w7 f) y" P. h- P
of papilledema.
6 T- H2 t1 K- A+ ULaboratory Evaluation
; A1 L8 G1 e8 n5 O  B/ o- w# OThe bone age was consistent with 28 months by$ Y0 o( b, A2 {  R7 F. p8 F) `* U
using the standard of Greulich and Pyle at a chrono-
0 f! R3 I( o6 Plogic age of 16 months (advanced).5 Chromosomal
. s1 o/ E* s' H7 w5 }' U; w5 akaryotype was 46XY. The thyroid function test& R7 S& J% ?, _3 K4 a" c8 I
showed a free T4 of 1.69 ng/dL, and thyroid stimu-' s1 ~4 b6 m) f0 ~
lating hormone level was 1.3 µIU/mL (both normal).
' Z0 [2 B4 i( K& G! X# PThe concentrations of serum electrolytes, blood
  d: n+ M- |% P* h( Surea nitrogen, creatinine, and calcium all were
: W6 O3 @6 y/ y9 |" ~within normal range for his age. The concentration
: u% ]+ y2 p# T. Aof serum 17-hydroxyprogesterone was 16 ng/dL
5 f  S3 L' M9 C(normal, 3 to 90 ng/dL), androstenedione was 20
/ e7 u' D% ^- [' g5 vng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-) u; O  E# G! }& a/ w! B8 l1 H# ]
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
/ [0 w2 [3 I8 K: ~( J& i6 Ydesoxycorticosterone was 4.3 ng/dL (normal, 7 to, W) P& Y7 A  Y. R6 t" E
49ng/dL), 11-desoxycortisol (specific compound S)6 `6 s* G- X6 R
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
+ A4 e! P4 g8 O$ Utisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
' e4 g) a6 q, V# o( X: P/ Mtestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
, b) [- O9 F' T* s& ~and β-human chorionic gonadotropin was less than% V- p4 S. o+ N: D5 J. x0 p9 _4 Q
5 mIU/mL (normal <5 mIU/mL). Serum follicular/ j1 ^- f& q6 E, E
stimulating hormone and leuteinizing hormone( ^* U" s+ ?, j/ e% Q+ G
concentrations were less than 0.05 mIU/mL  r3 F2 B+ U) [, p+ b
(prepubertal).0 q3 z5 I( D2 A1 o4 W
The parents were notified about the laboratory
, B# d8 t5 I+ q; M" {results and were informed that all of the tests were0 w7 d; p+ V3 n, ]& Z/ }
normal except the testosterone level was high. The
1 a# b4 z- w7 j: f+ r$ d2 u7 sfollow-up visit was arranged within a few weeks to8 W' w" m2 |2 b( ]! \1 Y: _
obtain testicular and abdominal sonograms; how-
! k/ W' O. }& _. }( |& mever, the family did not return for 4 months.$ ^3 q! B* L! R. `; A/ c+ b
Physical examination at this time revealed that the3 \, S/ m* c# c/ e
child had grown 2.5 cm in 4 months and had gained
6 {: G. F) J. C8 `# E  c2 kg of weight. Physical examination remained
2 E3 p# L- f$ e- m8 Ounchanged. Surprisingly, the pubic hair almost com-
5 a. l1 Z- q% v2 }pletely disappeared except for a few vellous hairs at
5 ?: ?& {8 _1 |; _4 P6 b% y  y8 E* ythe base of the phallus. Testicular volume was still 2
( {* b9 U' R  X; S4 o/ HmL, and the size of the penis remained unchanged.
, I5 r% T% e( Q1 ^& k) H0 V$ KThe mother also said that the boy was no longer hav-
# T* ]/ ~% v! i- g/ s6 _2 W( fing frequent erections.- ?2 T. O; F& S& E
Both parents were again questioned about use of
& b8 P% Z, @; S' l. @0 e2 Aany ointment/creams that they may have applied to
% l, h/ [, U8 X7 n* t9 S, dthe child’s skin. This time the father admitted the
0 N- Y( w) m4 Q, @Topical Testosterone Exposure / Bhowmick et al 541$ D1 ~5 C+ k& G; E! f
use of testosterone gel twice daily that he was apply-
) a* Q; m- x  V$ u! B; ~ing over his own shoulders, chest, and back area for) O- C! R3 ~, s3 ?# ~& H  c  t7 ^
a year. The father also revealed he was embarrassed  {6 B2 x2 U3 w/ i
to disclose that he was using a testosterone gel pre-
4 M& I' ?  _: i" P  O- @scribed by his family physician for decreased libido
! P8 Z# V2 B$ S3 x# M6 D, jsecondary to depression.
* |5 F. E' d# o2 j, t- n2 xThe child slept in the same bed with parents.
0 @$ `- Z" [, M. L' f6 L4 X' G( cThe father would hug the baby and hold him on his
4 D/ r+ O4 Z. q' Q( jchest for a considerable period of time, causing sig-
, D3 m. u" D; V5 R* Jnificant bare skin contact between baby and father.
' }: o$ ^/ k! \The father also admitted that after the phone call,
0 \8 s6 f- Q3 q/ w4 awhen he learned the testosterone level in the baby
: t1 L1 Z( V; R% c- I, k' Mwas high, he then read the product information7 v- N: t0 K. o7 S
packet and concluded that it was most likely the rea-+ G2 v% ^) T0 I; J+ Q+ R
son for the child’s virilization. At that time, they
( x& P- M9 C+ x" sdecided to put the baby in a separate bed, and the0 J- R0 C' ~; L
father was not hugging him with bare skin and had
4 R+ F: F6 K) Q7 ]1 Rbeen using protective clothing. A repeat testosterone
+ N4 X3 ?3 S7 \test was ordered, but the family did not go to the
; I& n. A% X  a' T6 blaboratory to obtain the test.
. o: |8 ~( Y+ c% H, NDiscussion. h! B$ t0 u5 p; h3 [0 f/ h
Precocious puberty in boys is defined as secondary9 o/ w$ K1 N" Z1 j: z
sexual development before 9 years of age.1,4* G# e5 X6 L) m
Precocious puberty is termed as central (true) when7 s$ n/ c  i) e# _- Q
it is caused by the premature activation of hypo-& ~1 o( q9 i, E# ?. ]; ~
thalamic pituitary gonadal axis. CPP is more com-
1 J& m) A0 ^/ Y' x) k8 W/ x1 [2 |& a) Tmon in girls than in boys.1,3 Most boys with CPP1 p9 O: r- E* x" m
may have a central nervous system lesion that is
: O0 s. T- W/ b( |& p' X7 ], nresponsible for the early activation of the hypothal-
+ r3 C; C' h# w; j9 N1 Tamic pituitary gonadal axis.1-3 Thus, greater empha-' j: O. I6 ]& ]1 y/ X5 n3 C
sis has been given to neuroradiologic imaging in
# Y: Y/ A* ?6 aboys with precocious puberty. In addition to viril-
% B2 K* p' @& Q! y; eization, the clinical hallmark of CPP is the symmet-3 \6 C" T; D$ L* C( N
rical testicular growth secondary to stimulation by
; X; R( Y" ?" k- f9 ?6 Rgonadotropins.1,3' w' j7 H! G/ h3 R
Gonadotropin-independent peripheral preco-
' c) H; W& E7 @! G% ~cious puberty in boys also results from inappropriate0 o. K( q  o( `8 y& k
androgenic stimulation from either endogenous or
! h- B3 b# N3 O, L7 [+ Vexogenous sources, nonpituitary gonadotropin stim-6 I/ s& P# o! ]2 f; [
ulation, and rare activating mutations.3 Virilizing
( `) r1 Y  W8 b3 A, ]. l9 ycongenital adrenal hyperplasia producing excessive! A+ ?, n# y" @$ A7 {) j# u1 m% M
adrenal androgens is a common cause of precocious4 [* \7 K( u' a0 H% b
puberty in boys.3,4
# `9 i* M  u. }- K3 w* [4 rThe most common form of congenital adrenal  e$ C; A  m8 Y) K" ?/ C3 t, ~% \
hyperplasia is the 21-hydroxylase enzyme deficiency.6 J: k4 M1 C. \. n( u
The 11-β hydroxylase deficiency may also result in) b% ]9 Y. J$ R$ C' y
excessive adrenal androgen production, and rarely,0 G, M* T9 y/ `( Q
an adrenal tumor may also cause adrenal androgen
7 n$ i, A. m) ~% W  C3 T2 C; mexcess.1,32 {: |6 a+ s% C3 M/ N3 a3 W
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
" G( r! w; l( V542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
3 u' `, ]0 p5 g: u+ k& Z4 j; m  lA unique entity of male-limited gonadotropin-8 j5 Z$ A0 d8 Q( v7 B8 Z7 L6 k! U
independent precocious puberty, which is also known8 X! E2 e2 r3 d) `4 ]2 S
as testotoxicosis, may cause precocious puberty at a# z. \4 n- @3 P- n5 [" D* C* a) O
very young age. The physical findings in these boys
% [8 G8 r. N. V# b* s( p3 f" wwith this disorder are full pubertal development,, i9 k, R1 W% Y3 W0 ?* E1 U, e
including bilateral testicular growth, similar to boys+ N. y. j3 `+ r: m# V8 Z7 ~
with CPP. The gonadotropin levels in this disorder
0 _- m+ }) f5 Uare suppressed to prepubertal levels and do not show' W! k- e8 K7 s7 X& @
pubertal response of gonadotropin after gonadotropin-2 }2 ?/ q' I1 F% c8 k' z. Q% s
releasing hormone stimulation. This is a sex-linked0 T! c4 W; [- d) r
autosomal dominant disorder that affects only
& Y) g. e8 i+ }. Y( Y! n( [males; therefore, other male members of the family
6 @  [7 E7 t/ O8 \: e% ?: e8 umay have similar precocious puberty.3
4 d  q5 J! P' ^, P8 b! q7 aIn our patient, physical examination was incon-
0 Y3 z4 u4 w, T0 n/ R! Gsistent with true precocious puberty since his testi-- Y) ~. c2 k4 T: J0 Z8 n; z. S; C- X* K
cles were prepubertal in size. However, testotoxicosis
- f7 |- C0 ?) q  @* U  D/ awas in the differential diagnosis because his father5 A0 k: e1 N( N4 o# o+ L1 J& e8 |
started puberty somewhat early, and occasionally,: N, Y2 h0 t% I
testicular enlargement is not that evident in the1 ~8 T) o% @/ o) [7 |
beginning of this process.1 In the absence of a neg-+ \4 ^; e& w3 e% b; D: [# [
ative initial history of androgen exposure, our/ A+ P9 K3 c5 g5 M$ m
biggest concern was virilizing adrenal hyperplasia,
/ I* w- }2 F+ F3 j! qeither 21-hydroxylase deficiency or 11-β hydroxylase
0 X8 K( ~4 c4 n) s1 k; ~deficiency. Those diagnoses were excluded by find-$ _: ]# a7 ]" x. N* r, b
ing the normal level of adrenal steroids.  j: }+ u4 D+ \, I4 n
The diagnosis of exogenous androgens was strongly5 u8 ]7 ~; L. L
suspected in a follow-up visit after 4 months because5 Q6 T4 n6 t* c8 n- l! F' `1 G
the physical examination revealed the complete disap-- O  n  [  A4 z6 x9 a
pearance of pubic hair, normal growth velocity, and; o1 U% O# k: j- ~1 U6 k' A# F% ?
decreased erections. The father admitted using a testos-
7 ^( j0 ^4 ^; m3 }terone gel, which he concealed at first visit. He was$ n4 X% f: C( e4 k: _6 j  _! b! ^' B
using it rather frequently, twice a day. The Physicians’
' ~% u4 W7 _+ y0 v' BDesk Reference, or package insert of this product, gel or2 O3 t. G- J. G- `/ k) K
cream, cautions about dermal testosterone transfer to$ [0 k5 E3 ~& f
unprotected females through direct skin exposure.
$ |) _9 q) i+ c6 `6 c( n9 i1 rSerum testosterone level was found to be 2 times the
; @1 l5 z, v) Z$ h; nbaseline value in those females who were exposed to
( a) i. L% M4 Y6 E2 reven 15 minutes of direct skin contact with their male
$ A! Q* d& z6 M* o+ g$ {' Dpartners.6 However, when a shirt covered the applica-
) o8 }  L, Y! R  ption site, this testosterone transfer was prevented.- y. Y$ Y  j" c* B+ E/ V
Our patient’s testosterone level was 60 ng/mL,# q$ J) `: q/ A# [
which was clearly high. Some studies suggest that
( R: D$ n, Y$ u/ Y( r% k0 U1 mdermal conversion of testosterone to dihydrotestos-
+ v/ C' b0 k9 J( U4 l$ n: fterone, which is a more potent metabolite, is more
9 k1 n% T# t- y( f% i9 \$ tactive in young children exposed to testosterone7 ~4 N: e% f' b0 e. x2 h2 M
exogenously7; however, we did not measure a dihy-
0 K5 ^) Q  t- h2 L  _$ Bdrotestosterone level in our patient. In addition to
* I, j( [3 d( o+ K- Zvirilization, exposure to exogenous testosterone in" n& l$ B6 K- e, Y
children results in an increase in growth velocity and
' E7 V) U" q6 q- Zadvanced bone age, as seen in our patient.& o& @* l' g1 w" c; q& E9 i
The long-term effect of androgen exposure during
- B# W3 y, I7 [; [2 c9 ?early childhood on pubertal development and final$ D7 j$ M. T$ |, a. ]
adult height are not fully known and always remain6 N6 _+ g7 n, S9 X+ ?/ O
a concern. Children treated with short-term testos-9 r9 s+ g5 _( k$ ~
terone injection or topical androgen may exhibit some
+ V" y6 B- C. d7 V1 B4 ^acceleration of the skeletal maturation; however, after
' r8 W$ Q, L! h  f) Fcessation of treatment, the rate of bone maturation/ W, n$ Y& Y, `
decelerates and gradually returns to normal.8,9
& J! h6 r# p% }6 v6 M1 B: c' a3 fThere are conflicting reports and controversy2 Z' \0 k( @& _
over the effect of early androgen exposure on adult, w; R6 c1 |3 ^3 C  J6 U4 @
penile length.10,11 Some reports suggest subnormal" D3 a1 Z2 H9 r+ n9 X
adult penile length, apparently because of downreg-
4 w8 ]2 D# b: B; u, n/ bulation of androgen receptor number.10,12 However,; d* }+ P9 s( ^+ B* m! [) A
Sutherland et al13 did not find a correlation between
2 O+ A7 w8 M, [/ q" {childhood testosterone exposure and reduced adult. l% ?5 I0 i. {) y  s- o1 ^6 ?
penile length in clinical studies.
+ X5 J* g3 r, D/ WNonetheless, we do not believe our patient is! D8 L" {  e( b
going to experience any of the untoward effects from( p$ M) H7 X2 k$ N3 U
testosterone exposure as mentioned earlier because
" k" o" v- p1 A' B' Dthe exposure was not for a prolonged period of time.
8 R' ^, ~9 q+ A% RAlthough the bone age was advanced at the time of
6 M  i- V4 d- X+ x' Mdiagnosis, the child had a normal growth velocity at3 B- p) z# T# R" a, S; o: L4 S( D
the follow-up visit. It is hoped that his final adult$ R3 C2 t; C' [7 }/ t* @
height will not be affected.
( c8 X  B6 ]$ SAlthough rarely reported, the widespread avail-
. S1 v& I0 o* n5 W1 z' Cability of androgen products in our society may) U' t5 Z1 t% \9 s- n7 ~
indeed cause more virilization in male or female
% c3 F. `6 m2 S3 j: D, M" fchildren than one would realize. Exposure to andro-) x0 U% z4 j" r) R
gen products must be considered and specific ques-2 D% `/ ]2 J( b* x; _1 n- P2 v
tioning about the use of a testosterone product or
& ?+ w4 E! R3 o* Z# X" z) qgel should be asked of the family members during/ P& Z$ l6 O4 }- S) w9 V. p0 e
the evaluation of any children who present with vir-
6 k) x1 z' y% r7 silization or peripheral precocious puberty. The diag-) `  ^0 q( Z7 W- R5 o
nosis can be established by just a few tests and by: Y' v, z! k4 Z+ w$ k* E$ M
appropriate history. The inability to obtain such a
7 }5 W: a( Y! C; |2 Uhistory, or failure to ask the specific questions, may5 h7 k8 J( ?- A
result in extensive, unnecessary, and expensive
8 C$ `9 B  G' x# |. dinvestigation. The primary care physician should be
2 j% O' t" t  |' haware of this fact, because most of these children6 Y' k. F4 a8 b+ Q6 F& H- Q: K
may initially present in their practice. The Physicians’1 e" u- F  |; b# q
Desk Reference and package insert should also put a2 }5 D1 z7 |; K, K
warning about the virilizing effect on a male or
* M  L' f' c; Q- e3 mfemale child who might come in contact with some-: L6 \5 m# a( \3 Y. e% {2 q  `
one using any of these products.3 d$ A9 [& V8 w6 {- ?# \* s
References
$ \0 f! }9 A. q( C5 w1. Styne DM. The testes: disorder of sexual differentiation
) Q3 ?4 N: t" b( M0 K+ zand puberty in the male. In: Sperling MA, ed. Pediatric! C- `0 ^' o' L8 L" a# F
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
% J7 ]- D# H- e2002: 565-628.. {% V' e/ `! w; X6 c6 Y
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious6 N, R' g" `, H$ k6 s# E# Z
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
* x/ K! N6 }0 xBoy Induced by Indirect Topical
  w* y5 {0 l& e3 h/ p+ bExposure to Testosterone
; q9 |+ w# i" Z5 y0 ?Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2. {1 r3 i; O" n4 ], P/ [
and Kenneth R. Rettig, MD1$ [! ~3 N+ K% B! U5 g% D/ a
Clinical Pediatrics! i5 y) }) L7 H( J% c
Volume 46 Number 6
9 N% r' f% `( Q+ kJuly 2007 540-543
3 z2 M+ o7 N5 F8 `3 ~© 2007 Sage Publications
8 j: q* B3 @1 O8 ^- a10.1177/0009922806296651
4 \: M! \+ V  C3 Y5 O/ @http://clp.sagepub.com" U4 e( a4 v& a3 t
hosted at/ a: N0 e6 u3 P
http://online.sagepub.com
  r" W. Z) ~* g6 FPrecocious puberty in boys, central or peripheral,- K1 e$ j" J& G+ \7 V: f/ @: j+ H
is a significant concern for physicians. Central, F7 s" m6 G  Q* b4 C1 `- A
precocious puberty (CPP), which is mediated
8 f1 o1 t/ |' E- Jthrough the hypothalamic pituitary gonadal axis, has# y+ L8 |* b# A& e. L- \9 D
a higher incidence of organic central nervous system5 n8 P1 F+ z0 R! a" N# G+ l- S
lesions in boys.1,2 Virilization in boys, as manifested+ ^( \5 B" k2 X5 w4 t4 ]
by enlargement of the penis, development of pubic* a1 G0 a" c9 l7 |4 p8 q0 @
hair, and facial acne without enlargement of testi-! U; e8 F, e" \* J" ^
cles, suggests peripheral or pseudopuberty.1-3 We' h* [" K! K! E# x! a! f( I
report a 16-month-old boy who presented with the4 V' G4 E2 h: J& E
enlargement of the phallus and pubic hair develop-
& F. T" x6 `/ Q- q  i8 ement without testicular enlargement, which was due
$ M& u. @& T3 E0 X) ]" ]4 rto the unintentional exposure to androgen gel used by% O* K& l3 E, p5 L, C
the father. The family initially concealed this infor-& [- Z; z+ V6 N* Q- J4 J1 y* q- V
mation, resulting in an extensive work-up for this
2 z, L: t6 O5 z* y" vchild. Given the widespread and easy availability of
5 z. {* O$ j6 A. K" ytestosterone gel and cream, we believe this is proba-' M. n3 M# p. g5 P4 s
bly more common than the rare case report in the# u( W5 K/ x1 |! {, F* j1 A- P
literature.43 _4 W* ^4 S8 X) ]
Patient Report
- S) u+ B$ i/ v! |A 16-month-old white child was referred to the
* X& U/ J% H4 y* A( Y( Pendocrine clinic by his pediatrician with the concern; [8 L: p/ A( b& a% V% X3 R
of early sexual development. His mother noticed4 {2 z4 ~0 g0 x3 t
light colored pubic hair development when he was
+ \. D& ^0 W& j1 cFrom the 1Division of Pediatric Endocrinology, 2University of
8 x' v: N! `1 N- p' D& PSouth Alabama Medical Center, Mobile, Alabama.
. W( K+ E/ a. P( m' o& _Address correspondence to: Samar K. Bhowmick, MD, FACE,
2 P" \* S, m; zProfessor of Pediatrics, University of South Alabama, College of
& |5 J3 D% B3 V' x+ \# H/ y) WMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;. m  X' A% c4 {4 M6 L
e-mail: [email protected].
8 C5 L3 \9 d3 `7 yabout 6 to 7 months old, which progressively became$ V9 _& ?' b  V5 H) I
darker. She was also concerned about the enlarge-9 x  \+ V2 t. n6 `  ~
ment of his penis and frequent erections. The child; M1 _; {# p( k: o, ^
was the product of a full-term normal delivery, with
/ J- m7 @( E! E; U+ ?3 j6 Qa birth weight of 7 lb 14 oz, and birth length of
9 m. z$ E, M. j$ I2 ~0 P20 inches. He was breast-fed throughout the first year. H6 s3 P2 g. @; Z% V  F4 G) K2 A
of life and was still receiving breast milk along with% R+ g, S0 P& f' ~2 ^+ u
solid food. He had no hospitalizations or surgery,! l3 c: j4 R7 k1 B! }
and his psychosocial and psychomotor development
4 [  f1 ^) u3 {' B% a8 M4 h3 R' Owas age appropriate.) Y* d9 `& z" w- G0 S6 y
The family history was remarkable for the father,2 F" D; P' M1 k' m- A1 g
who was diagnosed with hypothyroidism at age 16,* z/ m" M8 S9 c
which was treated with thyroxine. The father’s
& U* I  [; n3 B: bheight was 6 feet, and he went through a somewhat- P+ E6 r# f# E; P. s5 s
early puberty and had stopped growing by age 14.' x7 ^( m( p% A/ S- Y
The father denied taking any other medication. The
* l2 E& d% I+ o! @6 ochild’s mother was in good health. Her menarche2 y9 X& K' u) ~1 D! E
was at 11 years of age, and her height was at 5 feet
( {  A  z  \0 Z5 inches. There was no other family history of pre-( r5 `* N- o0 `2 j( J
cocious sexual development in the first-degree rela-
- F2 W% T5 {8 J" c+ htives. There were no siblings.' E# Y% @7 \: w0 a; e, I
Physical Examination
1 |+ K9 P3 o+ N$ X' d# h% V( E" t/ UThe physical examination revealed a very active,
+ y: b- u9 ~* i& [& Y/ L5 O9 Uplayful, and healthy boy. The vital signs documented
# g. m( {( f' U( G) Z6 t. Ta blood pressure of 85/50 mm Hg, his length was  E6 i% L% p  `) P0 @( |- a$ s' D% `) h8 a
90 cm (>97th percentile), and his weight was 14.4 kg
0 H' c+ H6 q" x, L; Z" {  w(also >97th percentile). The observed yearly growth3 V; T+ C/ d4 {# S. |, `' R
velocity was 30 cm (12 inches). The examination of& ]2 v' v. `( W( Y3 J/ ?, X6 C' b1 a
the neck revealed no thyroid enlargement.5 O) a8 r% [) H# x6 Q! [- b) m
The genitourinary examination was remarkable for
0 s0 b, D2 `% N, v9 tenlargement of the penis, with a stretched length of
1 ?6 r, O+ U% j! B5 X1 L) E7 }; D8 cm and a width of 2 cm. The glans penis was very well2 ^. \! `# d  v! {" w+ z* p2 z+ {+ f
developed. The pubic hair was Tanner II, mostly around
( p2 R$ S# A1 t2 K- z8 e540+ |" n" q3 L* H6 |5 D, f
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
" i9 p  n: m. D: y- r" S0 J+ athe base of the phallus and was dark and curled. The0 x6 N+ c% o3 O, S0 {1 d
testicular volume was prepubertal at 2 mL each.
7 X9 O/ J  ^5 L. ~  C7 g% ?- _0 NThe skin was moist and smooth and somewhat
, g2 M$ ]) f  o* S% {4 q: Eoily. No axillary hair was noted. There were no2 U% }3 y" Z" m% Q: G2 E& v
abnormal skin pigmentations or café-au-lait spots.
* |1 D, f* [2 y8 k& \( o( XNeurologic evaluation showed deep tendon reflex 2+
, \3 s5 w; Y5 E$ \bilateral and symmetrical. There was no suggestion* {7 a; u' S* |- L, q
of papilledema.* }8 d. w, Z1 z( @* K% ^7 C4 ~
Laboratory Evaluation
! D& |7 A" n# L1 n0 n( S/ p) CThe bone age was consistent with 28 months by! Q0 k4 [9 d+ s( c; o2 [0 p2 G% e" a, c
using the standard of Greulich and Pyle at a chrono-
& c# ^9 Y2 ^' y) C/ W' llogic age of 16 months (advanced).5 Chromosomal
5 w8 p7 B) e. j% g3 c+ N' Jkaryotype was 46XY. The thyroid function test
/ Q+ U* M, X8 b( rshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
8 O; t- m+ l3 q4 |. ~lating hormone level was 1.3 µIU/mL (both normal).
( f/ s' A& x9 [0 W! t  h; {9 I: nThe concentrations of serum electrolytes, blood5 }) U2 l8 c& B  C) m7 }7 H
urea nitrogen, creatinine, and calcium all were
$ T; ?! B( r9 H4 e/ I, K* H# swithin normal range for his age. The concentration0 t; y* s# n- a7 X/ v# X
of serum 17-hydroxyprogesterone was 16 ng/dL
6 i6 t0 ^$ `, S9 W. H5 _/ v4 O# }(normal, 3 to 90 ng/dL), androstenedione was 20
. z) }* N' Y; N6 Y* q" Z  B1 S! Vng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
5 ]" x7 U/ _7 r% c- qterone was 38 ng/dL (normal, 50 to 760 ng/dL),& F0 g! i. y& S5 q1 g8 A5 m
desoxycorticosterone was 4.3 ng/dL (normal, 7 to- Z! T$ S1 v  \" j, q: L6 u1 X
49ng/dL), 11-desoxycortisol (specific compound S)
6 x5 O; L! D1 e, g5 `was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
, t/ d' V. n( S. R' Ktisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total8 g/ J1 G4 s* {  c% x* F3 u; {
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
" N, s" t. Z& z7 a3 uand β-human chorionic gonadotropin was less than6 ~. I% W+ L4 L/ S# E
5 mIU/mL (normal <5 mIU/mL). Serum follicular
- L/ X2 J9 U# p" qstimulating hormone and leuteinizing hormone& h  B6 l2 H0 }& p8 g5 w
concentrations were less than 0.05 mIU/mL: F! E3 \3 I$ |- Z
(prepubertal).2 S8 K5 M- J& q& a+ z
The parents were notified about the laboratory
  l. I/ N8 ~0 B% }3 y/ K* S# Jresults and were informed that all of the tests were( I8 \+ K; Q% O, h
normal except the testosterone level was high. The
6 a8 W1 l. Z( N% ]follow-up visit was arranged within a few weeks to1 m4 T& R- v% a2 q6 N
obtain testicular and abdominal sonograms; how-4 ?/ w1 U; O, x3 \  Q
ever, the family did not return for 4 months.% j/ l- n# Z5 x1 V- c3 h
Physical examination at this time revealed that the
: t; |1 U6 c. {0 v' j0 \& Vchild had grown 2.5 cm in 4 months and had gained% j" s7 e3 m5 e# s. p4 `2 M5 ]
2 kg of weight. Physical examination remained
/ H0 b! K/ B. b3 t% }5 }unchanged. Surprisingly, the pubic hair almost com-  X& K, D' @# D5 d  b5 f% L8 u
pletely disappeared except for a few vellous hairs at2 i0 D! p: ~  c3 E. W
the base of the phallus. Testicular volume was still 2
4 E: E- o/ f9 p  u, w; B  @mL, and the size of the penis remained unchanged., D- F0 }" b- ?, C, {
The mother also said that the boy was no longer hav-. v: r% m+ z' m# m2 @
ing frequent erections.& a4 u2 f  ]2 p" u$ e) A( k5 J$ l% j
Both parents were again questioned about use of6 u3 o- O; d% Q; Y% r$ Z+ N
any ointment/creams that they may have applied to
1 x7 c: X' N$ ]! ^the child’s skin. This time the father admitted the
; \4 G1 \) c4 t$ uTopical Testosterone Exposure / Bhowmick et al 5413 z1 @; \& b& H
use of testosterone gel twice daily that he was apply-
4 H; W! u/ W0 q) Z' v8 R/ X1 qing over his own shoulders, chest, and back area for
$ u) f. l' G1 c* c; Qa year. The father also revealed he was embarrassed( g  N/ g( n+ V7 b* s
to disclose that he was using a testosterone gel pre-( G. m4 j; |2 P* M0 [
scribed by his family physician for decreased libido3 E6 X, ^5 x- @$ K3 e# l% ^
secondary to depression.8 C* V/ J- v* `* v
The child slept in the same bed with parents.$ p2 W: \7 ~4 C* R- M
The father would hug the baby and hold him on his) t/ A% d! q5 Y% g0 T  d* g6 r9 ]
chest for a considerable period of time, causing sig-& J5 A7 q5 g; u* ~9 L! E! L5 |
nificant bare skin contact between baby and father.
; G7 H+ S1 M/ y0 ]The father also admitted that after the phone call,8 `  d( i( Q+ C! ~# w8 }
when he learned the testosterone level in the baby
" Q. O6 [8 X2 D; r6 H+ [was high, he then read the product information2 [# d: ~1 s, i6 S8 ^- o7 k( v
packet and concluded that it was most likely the rea-7 p3 ]; ~, a$ j/ o& a( c7 N
son for the child’s virilization. At that time, they
% T9 u" e+ y" D- ~% ^decided to put the baby in a separate bed, and the& z8 n9 ^3 c" V& l+ A: Y
father was not hugging him with bare skin and had
" [: B( `' l2 h) Q8 C% nbeen using protective clothing. A repeat testosterone
  ^7 N( D9 H& {5 I+ rtest was ordered, but the family did not go to the# W% p1 N' S) e# t' Q
laboratory to obtain the test.
8 I4 D- x; o9 \( Z9 JDiscussion( m1 t! B0 F7 j/ F  N: {
Precocious puberty in boys is defined as secondary; W; P. u+ X& E4 Z5 `$ ^
sexual development before 9 years of age.1,4. t# X" C1 u9 o$ D" q% A
Precocious puberty is termed as central (true) when
0 R1 D% G4 `6 ~% z# Z  Uit is caused by the premature activation of hypo-
7 Y) R# y: a3 U7 c8 N5 `* E% |thalamic pituitary gonadal axis. CPP is more com-' t& z6 F2 E  W
mon in girls than in boys.1,3 Most boys with CPP" x( O7 k. m+ [! S3 p# c/ r
may have a central nervous system lesion that is
- f% R8 t: X- b" _0 eresponsible for the early activation of the hypothal-8 F0 V% N. \- Z5 l' Z+ {
amic pituitary gonadal axis.1-3 Thus, greater empha-5 H" p4 G8 ^* h9 o" R9 L
sis has been given to neuroradiologic imaging in
  D4 n0 ]% r5 {% z# Fboys with precocious puberty. In addition to viril-
+ U8 H, [$ l/ ~" \4 U- nization, the clinical hallmark of CPP is the symmet-
7 ^' G9 l2 b( \# Lrical testicular growth secondary to stimulation by" ~. a" L) _! c# Y" B6 A
gonadotropins.1,3
- }* F' `$ A" M3 [& Z. l0 ~* QGonadotropin-independent peripheral preco-
: c4 ?/ K! E+ H% \" w# Pcious puberty in boys also results from inappropriate, H/ V, \; |. m7 L
androgenic stimulation from either endogenous or# |2 o1 |9 ?0 @  e1 H
exogenous sources, nonpituitary gonadotropin stim-
& i3 ~, f3 I( w2 ]3 ^1 w9 }ulation, and rare activating mutations.3 Virilizing$ D% y( q7 s* J& \- C
congenital adrenal hyperplasia producing excessive" f6 y+ t, A" \) |8 D, A
adrenal androgens is a common cause of precocious3 U. C! ]% z& Q; g/ F
puberty in boys.3,4
2 {/ o" P% v$ [% B; aThe most common form of congenital adrenal; z, S4 c" ?+ @! }' {
hyperplasia is the 21-hydroxylase enzyme deficiency.
+ |$ A  t8 Z' KThe 11-β hydroxylase deficiency may also result in
; i# V9 p; I; r- T5 mexcessive adrenal androgen production, and rarely,
# Z( P" T; d( X) aan adrenal tumor may also cause adrenal androgen& Y% d  i/ P& v1 d( q6 D9 x' v! s7 M
excess.1,3
+ e" r, `9 Y- iat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from+ C& Y) d4 O6 ?. u, O0 O. S
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007. @0 }  U" z) b& D
A unique entity of male-limited gonadotropin-
" n0 }6 {( f% g; l, Z3 u; qindependent precocious puberty, which is also known
9 d3 I& A0 O4 R6 z: n  kas testotoxicosis, may cause precocious puberty at a& Z6 C+ }- H( C6 L9 U6 L( }9 o/ q
very young age. The physical findings in these boys7 Y9 u( ~8 H( j( e2 G4 t
with this disorder are full pubertal development,
9 v/ t7 e# t5 `3 _8 F( dincluding bilateral testicular growth, similar to boys1 r( Z8 u0 H8 h+ P
with CPP. The gonadotropin levels in this disorder
: Z/ j$ p: {/ d: Z3 kare suppressed to prepubertal levels and do not show+ O6 S* U6 i" y0 ?+ f" O, w
pubertal response of gonadotropin after gonadotropin-- ^+ |, B! }: q, I+ ~+ R, q: J* C
releasing hormone stimulation. This is a sex-linked# g* ~+ N0 G( L( ~6 P
autosomal dominant disorder that affects only* |7 s7 D/ c, l( W4 n2 H! F: n" c+ B
males; therefore, other male members of the family, H7 [  I+ k0 Z
may have similar precocious puberty.3* |6 W& X; T& \. f  q0 n, @! Y
In our patient, physical examination was incon-0 b2 ^# q  x* V. X3 ]( y1 C
sistent with true precocious puberty since his testi-
2 j: |7 Y% o% X5 O& U3 ucles were prepubertal in size. However, testotoxicosis, C! M0 }. i  M8 C; s2 l) A
was in the differential diagnosis because his father$ f; P+ j3 g0 X9 a# N% n. b% E
started puberty somewhat early, and occasionally,
- M3 @7 u; U- h: p' T( w" ktesticular enlargement is not that evident in the
! O- v; ?* S/ R0 C% O( l+ _beginning of this process.1 In the absence of a neg-
' v# f( C9 G2 F- o0 z/ J3 Eative initial history of androgen exposure, our6 ]+ U* {$ ?& t. Q; E
biggest concern was virilizing adrenal hyperplasia,
) y# |6 F; D/ l3 T( Neither 21-hydroxylase deficiency or 11-β hydroxylase
2 U+ p9 Y) H( Q! m( hdeficiency. Those diagnoses were excluded by find-
7 U+ U# ~2 \7 R# ]; b8 i6 A* ding the normal level of adrenal steroids.
0 {0 f; ^5 Z6 s% @% ~, s* e. Z0 GThe diagnosis of exogenous androgens was strongly1 d5 H" K* F4 n" t! }2 i
suspected in a follow-up visit after 4 months because# Q4 w4 U, |9 G: n
the physical examination revealed the complete disap-; u8 l( D  U7 [+ k. H
pearance of pubic hair, normal growth velocity, and
0 C9 Z2 h5 k# e" F6 Ydecreased erections. The father admitted using a testos-
- s4 ]5 H% W* Zterone gel, which he concealed at first visit. He was7 {: A( p! c7 w# f- C
using it rather frequently, twice a day. The Physicians’
* r( g6 B1 S0 W5 w) lDesk Reference, or package insert of this product, gel or, |6 y6 d5 \& T4 O3 \
cream, cautions about dermal testosterone transfer to
0 N  \4 N$ u5 x3 Xunprotected females through direct skin exposure., H* j6 W: {" G$ B/ r( j
Serum testosterone level was found to be 2 times the
* K$ s' _; d: v  E6 y7 E8 Z+ o9 Kbaseline value in those females who were exposed to* K* J! U; O, h8 C: N
even 15 minutes of direct skin contact with their male; D/ b. v" P/ i6 e
partners.6 However, when a shirt covered the applica-3 l$ v; y4 C; Q) \, F  m
tion site, this testosterone transfer was prevented.
8 o6 Q( i0 x- m! oOur patient’s testosterone level was 60 ng/mL,( b6 C( R! y0 o* z  y8 f* ^# N3 }
which was clearly high. Some studies suggest that
: D( K$ ~' t" z" `* l* wdermal conversion of testosterone to dihydrotestos-
$ ?% \( d: g- Y; r+ {7 y% |& uterone, which is a more potent metabolite, is more! N! q! F: h3 o
active in young children exposed to testosterone0 E4 r/ i( Y+ f0 b5 s
exogenously7; however, we did not measure a dihy-' `' W' j  S* a' S8 Y
drotestosterone level in our patient. In addition to. X5 Y& u& V% V3 _0 \9 X: W
virilization, exposure to exogenous testosterone in, j+ z5 j4 W) X. p2 e# n4 Z) E
children results in an increase in growth velocity and
1 o3 S0 L& ~* W. ~* Yadvanced bone age, as seen in our patient.
  x) C: p2 H  y+ EThe long-term effect of androgen exposure during
( M/ k, b# R  g* [1 y, C' dearly childhood on pubertal development and final
% J: q$ l  h# X3 Dadult height are not fully known and always remain
( T5 W/ |% i7 ia concern. Children treated with short-term testos-" j' Q0 H9 `/ o$ G' b) t$ l/ j
terone injection or topical androgen may exhibit some# ~! X  c; i) t
acceleration of the skeletal maturation; however, after
! u; A3 k# I& O+ m+ T: f6 `$ K) v; Tcessation of treatment, the rate of bone maturation$ V" m6 v* V5 R, w" q
decelerates and gradually returns to normal.8,9
& J7 _3 J2 c* bThere are conflicting reports and controversy
# V4 i/ {) g3 J8 ^  [; q- @" [% \  Xover the effect of early androgen exposure on adult3 J1 S$ i5 X6 p. L1 B+ d8 t
penile length.10,11 Some reports suggest subnormal
5 e0 H# ?8 S3 L* a: a. X2 eadult penile length, apparently because of downreg-
8 y) |) A8 ?1 H) k3 N" ^ulation of androgen receptor number.10,12 However,
8 g' z3 ]6 ?9 E9 N# l$ w1 L' a5 ZSutherland et al13 did not find a correlation between
5 D* C3 Z- X/ J% I) A& K, ]( i2 Qchildhood testosterone exposure and reduced adult% x) ~1 @  k. b3 q' A! z. Z0 v( [
penile length in clinical studies.7 e# a0 U7 a. ]& f
Nonetheless, we do not believe our patient is
! Z# k, C* {$ P  ^going to experience any of the untoward effects from
: W' b0 u1 ~+ l( C( G/ ktestosterone exposure as mentioned earlier because
2 y) A$ ~$ i1 T+ z$ P5 |the exposure was not for a prolonged period of time.
+ Y& ~- q& Z" T# VAlthough the bone age was advanced at the time of
7 Y8 l$ _/ g3 w* R, a- P  ]- Udiagnosis, the child had a normal growth velocity at
- L  t( f' i2 u' V5 {' uthe follow-up visit. It is hoped that his final adult/ ?8 Q$ C" A3 u7 G0 t, R. v0 K" v
height will not be affected.
( Z2 c: T/ _4 dAlthough rarely reported, the widespread avail-. I7 g& N; w$ X( H
ability of androgen products in our society may
" c; l' y5 F' L' l3 lindeed cause more virilization in male or female
' [* Y& k+ f" ^8 n$ Cchildren than one would realize. Exposure to andro-
7 E; j! a; f0 m7 C1 Q2 r1 y' g) n' z* bgen products must be considered and specific ques-% p: {2 B. Y" L$ m
tioning about the use of a testosterone product or( U% n3 y+ a$ A
gel should be asked of the family members during
; N) y+ @; {+ ?& F, l" i3 F7 Pthe evaluation of any children who present with vir-
; X$ J* T, H$ U( r! s0 H! Wilization or peripheral precocious puberty. The diag-
. i# N# _) C" H0 g& Onosis can be established by just a few tests and by9 v* Z# s6 o: ]& a  R( q5 I, X3 k
appropriate history. The inability to obtain such a
0 \* w6 O  P! u9 v0 Zhistory, or failure to ask the specific questions, may$ c3 F! D; m% P9 ^
result in extensive, unnecessary, and expensive
: U* Z; v# }! ^) S/ qinvestigation. The primary care physician should be  Z2 O3 C8 H" J, H9 `- _2 i' u* N
aware of this fact, because most of these children9 O5 Q# N' h$ S- ~* B$ Z1 w
may initially present in their practice. The Physicians’
' x" }9 m) K6 m" j# ^% P  J* fDesk Reference and package insert should also put a
# s- |/ Z( j8 G& v: e2 f& lwarning about the virilizing effect on a male or
  f/ q% a, v7 g: Y/ efemale child who might come in contact with some-: M( K! e# S! w1 |9 s
one using any of these products.
# w, I* G3 L3 L6 J& M: k7 @- ~References
+ b& V4 G1 m8 q  w1 i1 @1. Styne DM. The testes: disorder of sexual differentiation
" g' T+ ]1 ?/ |! x1 ^: V! {and puberty in the male. In: Sperling MA, ed. Pediatric  k' J7 e, r# y& B. f
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
- W0 i' j" t: L2002: 565-628.
2 ]( }0 h8 d, i4 Y) L* O6 R" X2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious  M5 _) }9 f0 v( i; F
puberty 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
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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

* S. ^9 I+ e7 k1 z  [1 Q; w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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