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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 @, f1 I( E; G' C' p+ `# i. ABoy Induced by Indirect Topical- q) _6 [0 b1 _/ o
Exposure to Testosterone
  y$ s$ C$ R8 k/ c2 Z0 }Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
4 \) h2 z/ B+ vand Kenneth R. Rettig, MD1, \# i; d5 u* N# q; v6 S, |
Clinical Pediatrics- \* y. o& q6 n  ~
Volume 46 Number 6" d3 E2 T/ X. O9 d3 D* j# ~
July 2007 540-543- \& Y% f! R, u& W" O6 D, W; U
© 2007 Sage Publications" s  E6 x9 W% M% D
10.1177/0009922806296651
; V( K! j8 i9 x. jhttp://clp.sagepub.com* n4 J& Q1 Y9 e
hosted at
3 o% W- x" {. Thttp://online.sagepub.com8 |# B: M$ B" q" [2 q3 S  s# S
Precocious puberty in boys, central or peripheral,- H' X2 K  f, o$ S3 e
is a significant concern for physicians. Central
& G5 E- }" f, P* X: ?precocious puberty (CPP), which is mediated( i, k: _6 m+ a
through the hypothalamic pituitary gonadal axis, has
- K$ |5 d9 l6 R$ b) H$ ga higher incidence of organic central nervous system
- l5 I; t$ M+ Q* S7 K) B, s# ?lesions in boys.1,2 Virilization in boys, as manifested
3 E4 k; y0 p% q; F1 L, ~by enlargement of the penis, development of pubic
0 {8 I& L2 w$ Shair, and facial acne without enlargement of testi-
. V2 |2 u( [( C9 Q; e5 Ucles, suggests peripheral or pseudopuberty.1-3 We, P1 G3 Z, e+ O/ N1 l6 a! ~
report a 16-month-old boy who presented with the# |5 [0 k$ l1 G  |: o2 E
enlargement of the phallus and pubic hair develop-/ n) @) g8 f2 T3 A3 y1 w
ment without testicular enlargement, which was due
; V! H! H9 B, Zto the unintentional exposure to androgen gel used by
3 ?% B4 n6 |2 d, Ithe father. The family initially concealed this infor-9 w$ u4 J! }2 p- h9 @' k+ p
mation, resulting in an extensive work-up for this- r4 |8 S* c9 v; O0 X! A
child. Given the widespread and easy availability of
+ L* r; W: R8 H$ ~4 ~testosterone gel and cream, we believe this is proba-
+ L& h# J4 a0 ebly more common than the rare case report in the
/ k0 a3 X4 b3 D( D! |literature.43 w3 T$ a9 b% \% T3 H% Y) }0 N
Patient Report& M1 U4 c& p( ]0 [6 |+ d! q2 F
A 16-month-old white child was referred to the' w% a# Y4 j7 h0 Y
endocrine clinic by his pediatrician with the concern
" ]' P  m) {* e8 R( c" S5 ?of early sexual development. His mother noticed
) _( L" |' L* `: F/ i  n, Mlight colored pubic hair development when he was
5 [0 D" ^/ z5 T) V6 {! xFrom the 1Division of Pediatric Endocrinology, 2University of
- v( ~( B9 C) j/ YSouth Alabama Medical Center, Mobile, Alabama.
7 }# Y/ N! \+ ^5 D6 W7 mAddress correspondence to: Samar K. Bhowmick, MD, FACE,% k' F# G2 v; ^# q( `& \$ i
Professor of Pediatrics, University of South Alabama, College of2 B9 U8 t( E: C/ h) q) A! d
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
  g' \* k% |7 le-mail: [email protected].
( C0 C# K7 _% \1 j# Yabout 6 to 7 months old, which progressively became! ~0 V5 ^( [! V$ B
darker. She was also concerned about the enlarge-, t- e( p4 a/ F; Z
ment of his penis and frequent erections. The child
+ A. d/ m2 A; v  Vwas the product of a full-term normal delivery, with- {% e) B5 R* x
a birth weight of 7 lb 14 oz, and birth length of$ T* U4 o" P9 l  W7 y% b9 o
20 inches. He was breast-fed throughout the first year) E6 m# [% u2 `" e. F/ `3 c' b
of life and was still receiving breast milk along with. h! ~3 [. Z) F  ]. T
solid food. He had no hospitalizations or surgery,, _& J; c% J  `+ L6 ~: q3 f" j
and his psychosocial and psychomotor development+ |5 B: u2 @* d/ s$ w
was age appropriate.
, f. k5 c, X* @3 M% wThe family history was remarkable for the father,' P5 H& E( R  t2 s1 U9 S6 i3 O
who was diagnosed with hypothyroidism at age 16,
- D  y2 [8 m  i# L6 k3 [3 Rwhich was treated with thyroxine. The father’s, h* s/ Q# c/ ~1 P9 ^/ g
height was 6 feet, and he went through a somewhat
$ s9 H. N6 A; h! E6 s- U6 Learly puberty and had stopped growing by age 14.
0 Q- _. W2 d0 [$ \The father denied taking any other medication. The
3 @$ X, U# j. O, Pchild’s mother was in good health. Her menarche! d- S6 B" t% F' J4 A, z6 A
was at 11 years of age, and her height was at 5 feet, P* i( P- W0 {8 f2 {
5 inches. There was no other family history of pre-! A* r6 G* b; M3 N) q4 _8 O
cocious sexual development in the first-degree rela-
- b: s. |4 J) I# C8 g6 Ytives. There were no siblings.
  E1 ?& e1 ~1 M; y, }# SPhysical Examination0 B* W: Z; S* x/ P- z
The physical examination revealed a very active,
6 N+ w* q  h# Z& h# }playful, and healthy boy. The vital signs documented# o/ b7 X$ o( z! O" g5 y
a blood pressure of 85/50 mm Hg, his length was6 \. b5 j$ F- S( J
90 cm (>97th percentile), and his weight was 14.4 kg! R  s& i9 T/ U- m) v, }  ^
(also >97th percentile). The observed yearly growth
: J7 ]' h" h. @  Z+ I9 _velocity was 30 cm (12 inches). The examination of
6 R9 |2 W# t- I7 q0 p% q: ]the neck revealed no thyroid enlargement.0 r5 |# J  D. A# S" c* q5 _
The genitourinary examination was remarkable for0 z; R. }: z) o
enlargement of the penis, with a stretched length of
. e' P1 l4 Q$ W( q% l2 S) c3 ^/ [8 cm and a width of 2 cm. The glans penis was very well
9 R* B. s2 w  Edeveloped. The pubic hair was Tanner II, mostly around8 ^/ Z4 k3 i# X
5408 m# N( ]- @' O; d* x2 ^# t
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
) B4 D$ t0 v1 `' u, sthe base of the phallus and was dark and curled. The
7 o. J/ n' U$ x5 mtesticular volume was prepubertal at 2 mL each.
, l3 C7 m1 t& L! DThe skin was moist and smooth and somewhat
* K0 t  q6 _$ L2 joily. No axillary hair was noted. There were no
: Q7 ]8 q3 r3 @# |abnormal skin pigmentations or café-au-lait spots.% V" o4 t1 D# \; W2 p. N( m# @
Neurologic evaluation showed deep tendon reflex 2+
& |8 D4 q# V6 xbilateral and symmetrical. There was no suggestion
5 `) G8 g4 J, {of papilledema.
2 F3 e1 _% m  b6 M% T1 w7 @0 fLaboratory Evaluation
1 r3 r$ ?, M# k9 @& [The bone age was consistent with 28 months by+ @* Y+ V( T9 ~2 q% v' @, s
using the standard of Greulich and Pyle at a chrono-& D) {& ^5 s0 U7 ^4 A! Z7 d/ x
logic age of 16 months (advanced).5 Chromosomal/ x: P  G/ I5 `' V5 M6 A' `
karyotype was 46XY. The thyroid function test
5 M, o& H* A6 o1 M* R# R- l0 R8 Mshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
4 ^+ U6 ^% A6 h+ \  C9 t. blating hormone level was 1.3 µIU/mL (both normal).2 C7 h$ g6 Y9 N4 |; f* B& O
The concentrations of serum electrolytes, blood' m  E: J: D1 c+ |& e/ o
urea nitrogen, creatinine, and calcium all were
2 V7 k1 L2 J/ m2 z+ u+ Uwithin normal range for his age. The concentration0 h5 `7 \  A5 _. W0 l6 M3 U4 r
of serum 17-hydroxyprogesterone was 16 ng/dL) y  W1 |! W7 E; u
(normal, 3 to 90 ng/dL), androstenedione was 20
9 T; w& D) v) p6 o. Eng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
4 q1 S7 f# V  A# `0 h2 |" O% o( ^terone was 38 ng/dL (normal, 50 to 760 ng/dL),
8 I8 k) @6 Q4 @/ N+ d# bdesoxycorticosterone was 4.3 ng/dL (normal, 7 to
  p# {, y! d8 J( @* y49ng/dL), 11-desoxycortisol (specific compound S)
2 C8 O0 _, T3 n; A% owas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-* d: B+ Y9 f' f0 N. {
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
# J$ ]) @3 \) t+ f: ?: n: g) ttestosterone was 60 ng/dL (normal <3 to 10 ng/dL),# E7 ]" D/ q7 p* r( X
and β-human chorionic gonadotropin was less than
- d" x3 t& J, S: N5 mIU/mL (normal <5 mIU/mL). Serum follicular
5 C3 t& r( f' U2 T# S1 l& N+ Nstimulating hormone and leuteinizing hormone, q; q+ K6 ^7 D
concentrations were less than 0.05 mIU/mL
' n3 p* F  a# b/ M( P( d' Q(prepubertal).! g2 T7 Y( V+ n/ C# n0 D. N
The parents were notified about the laboratory
% X, \, r* V" T# Y  O' rresults and were informed that all of the tests were+ M. R- r6 ?7 {
normal except the testosterone level was high. The# B6 P5 K8 s/ d/ W6 j
follow-up visit was arranged within a few weeks to
/ f# O* F; F" V- T  f! aobtain testicular and abdominal sonograms; how-- u9 b* R. o+ n+ o. g" r$ ]
ever, the family did not return for 4 months.
9 H9 n, q9 z+ V  m/ W( v' WPhysical examination at this time revealed that the
  L6 X% N( s' z' f7 M8 k5 V0 K5 Schild had grown 2.5 cm in 4 months and had gained( H6 k& U7 a: y- \! S2 H
2 kg of weight. Physical examination remained# p% r) M7 g! i
unchanged. Surprisingly, the pubic hair almost com-
+ s1 ~! c8 Y2 [* ]: j2 ]( Upletely disappeared except for a few vellous hairs at
1 n; z2 R' e4 H. {1 uthe base of the phallus. Testicular volume was still 2
- X; S' Z  A& C, ?  NmL, and the size of the penis remained unchanged.$ a$ ?# t  c, E/ M
The mother also said that the boy was no longer hav-* ?& l6 A! A% b0 Y! d
ing frequent erections.
- g7 R6 n1 T7 h( J3 M5 l% rBoth parents were again questioned about use of+ k4 q. V  q8 @$ [9 w. Q% F# F
any ointment/creams that they may have applied to; \1 _2 k6 g2 X' L- s8 }
the child’s skin. This time the father admitted the
) Y, @  r1 h+ X5 wTopical Testosterone Exposure / Bhowmick et al 5416 l/ y. S% q: U: d
use of testosterone gel twice daily that he was apply-
% m& x. b* `' N( h- {& d2 |' j" aing over his own shoulders, chest, and back area for) l' n( {: F! w. Y/ K  O
a year. The father also revealed he was embarrassed
- f; E: X9 s" yto disclose that he was using a testosterone gel pre-. Q! u- Y5 ^* g3 M
scribed by his family physician for decreased libido+ S1 J5 |5 Q& o& L% v* j/ P
secondary to depression.
6 i* {9 t$ n3 @5 ^The child slept in the same bed with parents.: }' s7 k; _! M7 O7 q" \6 }
The father would hug the baby and hold him on his
! h+ U: {; |0 w* X6 I, F, Wchest for a considerable period of time, causing sig-9 W+ \0 I/ I) s9 O& p- j* c
nificant bare skin contact between baby and father.3 X: `0 h9 q) z5 l, X5 t
The father also admitted that after the phone call,
5 Y  A5 n% O* l# Ywhen he learned the testosterone level in the baby
0 y. X; n3 A8 V% I" @. Qwas high, he then read the product information
/ c5 \6 L) ~% n4 K2 zpacket and concluded that it was most likely the rea-
' J# e8 c0 w4 o2 n( R, L: m) dson for the child’s virilization. At that time, they5 `! l: Q1 }7 i% n
decided to put the baby in a separate bed, and the( t& i) L* [' h: r$ P
father was not hugging him with bare skin and had' S" g- R+ w8 J, B& H7 @) N
been using protective clothing. A repeat testosterone4 Y1 i$ Q' t, }$ |) H# ?
test was ordered, but the family did not go to the
2 @% K9 Z* m* ]+ V$ g' Q0 E) Ulaboratory to obtain the test.( \8 Q9 p6 i: p9 ^% u! {, H
Discussion8 o* J$ Y8 @" ?- Y
Precocious puberty in boys is defined as secondary
- R& i9 L  \1 v4 d7 A- q0 v. f6 Hsexual development before 9 years of age.1,4
3 P$ M+ l5 ^1 Z* v6 {9 o! _+ mPrecocious puberty is termed as central (true) when
( `" T* T) m9 P( A  ]- d: f3 i. q7 Pit is caused by the premature activation of hypo-5 b% ~( d) f4 G( ?/ V: u/ C
thalamic pituitary gonadal axis. CPP is more com-
, Z" O* C+ Q9 n' `( l6 B" Smon in girls than in boys.1,3 Most boys with CPP; [, E: O# g. l2 d
may have a central nervous system lesion that is
6 j8 b; |# t- H0 i6 `+ t3 Eresponsible for the early activation of the hypothal-* i# q4 ]* o- M5 @: `! W3 V0 x! ^
amic pituitary gonadal axis.1-3 Thus, greater empha-
- V* V4 ~8 X( t$ C( e0 ^3 e2 Zsis has been given to neuroradiologic imaging in
- ^# A0 Z9 B4 M  xboys with precocious puberty. In addition to viril-
1 j8 [, E) J. s7 d) n7 H# L* rization, the clinical hallmark of CPP is the symmet-6 [; y. _# u: e4 z( s
rical testicular growth secondary to stimulation by
8 q, B2 x, g1 F/ U' p* u; U5 Egonadotropins.1,3
& C0 P% k' M/ zGonadotropin-independent peripheral preco-
1 |5 E9 J/ E( x* s. z4 Acious puberty in boys also results from inappropriate. D9 C! w; K7 Z% M& @  B
androgenic stimulation from either endogenous or2 ]% x0 ~% {" }, w+ R1 L; z
exogenous sources, nonpituitary gonadotropin stim-2 F8 x+ t$ ]5 s% ~+ x( f
ulation, and rare activating mutations.3 Virilizing
5 c2 I6 P% A, \congenital adrenal hyperplasia producing excessive
' F+ S! h) d$ V+ M7 H6 H0 |" aadrenal androgens is a common cause of precocious
; s' @, B) i! }6 ]3 E+ Hpuberty in boys.3,4
4 J2 X# |% x- Z/ I1 ~The most common form of congenital adrenal& s5 d# f. W  _3 X  p4 K& h- d0 u
hyperplasia is the 21-hydroxylase enzyme deficiency.
/ ]' v' W* l0 a3 j/ R: g" p$ zThe 11-β hydroxylase deficiency may also result in
6 d$ g: I, h9 [' P$ Hexcessive adrenal androgen production, and rarely,
; X; K% _6 x6 Z6 m- kan adrenal tumor may also cause adrenal androgen
" I; S. @2 ?, x: Z9 p) yexcess.1,35 k" Y* i$ j4 W
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from% R; C3 m' @# r  S& n
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
! d  Y5 f. `1 L" y& g8 F( EA unique entity of male-limited gonadotropin-
4 Z9 _3 o% i" [  t1 d7 T6 z$ ]7 _independent precocious puberty, which is also known
3 g' i& _! s4 l  T0 r9 Ias testotoxicosis, may cause precocious puberty at a& n9 z5 Q! B  P. _8 r* V
very young age. The physical findings in these boys
- i# Y4 h3 a" s9 P  _- _with this disorder are full pubertal development,
  E& Z: g! A" Tincluding bilateral testicular growth, similar to boys
! L2 g7 T8 F; uwith CPP. The gonadotropin levels in this disorder% \3 w" Q+ W/ W
are suppressed to prepubertal levels and do not show
0 ^" X' Z0 ]9 M! [/ epubertal response of gonadotropin after gonadotropin-
# E0 ~5 G; N  H4 [releasing hormone stimulation. This is a sex-linked4 |; d' ^5 R$ u9 H
autosomal dominant disorder that affects only. R1 j  ]( j, J4 t
males; therefore, other male members of the family
8 r# d& V3 a# [% jmay have similar precocious puberty.3
$ i, n: u+ z- I! {! q  YIn our patient, physical examination was incon-3 l7 G0 Q8 T: G. k- a; f" w
sistent with true precocious puberty since his testi-* z9 v) S3 i+ n7 H# `* }
cles were prepubertal in size. However, testotoxicosis
% z6 G) L) v2 S& t% u, M: C* Qwas in the differential diagnosis because his father) U' D0 X. X/ y% o
started puberty somewhat early, and occasionally,. Z9 b6 @3 h, g) C) a, u- v% T" k( l
testicular enlargement is not that evident in the
* C' B8 E8 J4 x0 U- f/ Y( `beginning of this process.1 In the absence of a neg-
7 b! A. j3 }0 C- B4 ^; Q- n' I! C( i; [ative initial history of androgen exposure, our
) |$ A$ W6 @! o& j3 @0 R) [0 _# _) ?biggest concern was virilizing adrenal hyperplasia,
& y8 Y2 u7 H6 c) M# D% @either 21-hydroxylase deficiency or 11-β hydroxylase
! F1 K$ I, w  c9 Zdeficiency. Those diagnoses were excluded by find-
7 x& v. d; Z5 Cing the normal level of adrenal steroids.
  i4 |  D; i2 JThe diagnosis of exogenous androgens was strongly: j+ v! s% h; Y- M+ m6 g: w, U
suspected in a follow-up visit after 4 months because
; d" |; Y, i5 Q% I* zthe physical examination revealed the complete disap-/ e  Q9 O8 m: k, v0 M: O, W5 T
pearance of pubic hair, normal growth velocity, and
0 I% d" R( i& w- ?' N. wdecreased erections. The father admitted using a testos-& J* N1 _9 G: F* r4 ?! L9 G
terone gel, which he concealed at first visit. He was
7 T- k& j& z2 O7 ?using it rather frequently, twice a day. The Physicians’4 u4 Q, ^7 x% V+ J* D4 j# f
Desk Reference, or package insert of this product, gel or7 E2 m6 y% k5 ]7 F  b5 j; {
cream, cautions about dermal testosterone transfer to
  n+ v7 O8 g$ L' h( ^" Kunprotected females through direct skin exposure.9 G1 i! [. t7 {5 C/ w
Serum testosterone level was found to be 2 times the
- X5 P5 M) s5 T( b4 w, [$ S! }+ qbaseline value in those females who were exposed to, d6 N1 V+ L1 G) Q$ R
even 15 minutes of direct skin contact with their male) y! W# D8 j; V7 d& R: B* k
partners.6 However, when a shirt covered the applica-. @- Z3 [" o9 W- G0 c" Z
tion site, this testosterone transfer was prevented.
8 \5 V- }9 d! \, v4 y0 xOur patient’s testosterone level was 60 ng/mL,
% a8 p- t: G* [; b7 }which was clearly high. Some studies suggest that  f5 X5 g( ~8 }# f9 w
dermal conversion of testosterone to dihydrotestos-+ j- I: @" r5 U
terone, which is a more potent metabolite, is more
6 |' U& h/ e0 M- h# ?9 z" ]active in young children exposed to testosterone
: J: t+ _2 C6 ^9 q9 Nexogenously7; however, we did not measure a dihy-. C9 Y; Z& J! m3 M
drotestosterone level in our patient. In addition to4 s( }$ C. G/ N* ?
virilization, exposure to exogenous testosterone in- t  j! p1 {. k) J6 M7 l( P
children results in an increase in growth velocity and
' \5 p: h, y3 A# Yadvanced bone age, as seen in our patient.( E' {/ x' Y5 x! x+ ]1 y0 I4 Z
The long-term effect of androgen exposure during
& u( H1 l- m; ?! _" q3 Dearly childhood on pubertal development and final
! j0 S# [% x* [; A3 z1 Wadult height are not fully known and always remain
, r# o" ?' A% x6 La concern. Children treated with short-term testos-! u2 }- v: a8 b$ {: J: ^
terone injection or topical androgen may exhibit some. ^5 S( `) _8 q" Q8 Q
acceleration of the skeletal maturation; however, after
4 j. X8 [0 V% q6 J$ k8 pcessation of treatment, the rate of bone maturation2 F; ~4 b  N2 W
decelerates and gradually returns to normal.8,9
( ]3 ^( v; H0 NThere are conflicting reports and controversy' o) |2 h1 Q# W  R5 A5 J
over the effect of early androgen exposure on adult% c/ S' a. f6 e1 ]6 R/ {  F5 t
penile length.10,11 Some reports suggest subnormal' X. D9 Z. @0 W
adult penile length, apparently because of downreg-
  V  e7 X8 h& D3 o/ c" Z- G7 B( Fulation of androgen receptor number.10,12 However," ?9 ]5 Q7 w- }: R0 ~: Y9 B8 `
Sutherland et al13 did not find a correlation between" v9 F+ o4 F  C: t& W
childhood testosterone exposure and reduced adult! ]' M0 s6 |$ A0 s
penile length in clinical studies.* S6 F! z, E2 A5 x! ~
Nonetheless, we do not believe our patient is$ ^4 e6 ?/ i3 t( W
going to experience any of the untoward effects from
+ f. M' A/ U; v& Mtestosterone exposure as mentioned earlier because- m6 x2 |, ^( e+ i. i) ]6 {
the exposure was not for a prolonged period of time.) G8 s0 ?; ]/ l
Although the bone age was advanced at the time of/ w- d0 P* q% D4 G! U
diagnosis, the child had a normal growth velocity at' t7 u$ F; y, D" Z$ I( p
the follow-up visit. It is hoped that his final adult
: O6 E3 R/ \: y1 fheight will not be affected.
: ?5 M8 V5 F* a! V6 \Although rarely reported, the widespread avail-
* K2 O; K9 k! O7 R4 B, p  h* Vability of androgen products in our society may/ M7 Q) y4 [0 N: q7 j
indeed cause more virilization in male or female
6 x$ U5 g, w' t+ ]/ n. V# w! Cchildren than one would realize. Exposure to andro-) Q# _/ a* Z: M: T
gen products must be considered and specific ques-6 g, ?) G; A' E
tioning about the use of a testosterone product or0 ~8 a4 I3 F5 R1 o) ]+ M( x
gel should be asked of the family members during6 H; [/ e5 ]; M9 f4 {  @6 ]7 \2 W# S6 ~
the evaluation of any children who present with vir-
- s' g3 m# H) X  ]1 gilization or peripheral precocious puberty. The diag-- P6 e- @' @% Q! R; n+ O
nosis can be established by just a few tests and by& X5 g) x. W: t! U7 H# E) G
appropriate history. The inability to obtain such a
; f# ?% \9 r9 M3 Y: ?2 ~2 Ohistory, or failure to ask the specific questions, may
' h" _( ~$ v  h5 O7 [2 r$ mresult in extensive, unnecessary, and expensive6 J8 Z1 b+ D) q& I5 B: d5 T
investigation. The primary care physician should be, Y, r4 R! _0 D# o: i
aware of this fact, because most of these children
" g7 G1 E7 Z$ _% M* u' y* Amay initially present in their practice. The Physicians’
1 {2 w% @6 C' z6 y: LDesk Reference and package insert should also put a
9 c7 j% x, O. G3 M. H2 Vwarning about the virilizing effect on a male or
. j- t) I/ @; B% m/ \9 sfemale child who might come in contact with some-
/ [3 d3 z# E& aone using any of these products.9 z# x3 |+ n* u, b* ^8 z' |1 v
References
7 w; E8 P7 a3 s( z5 t. s9 t) b1 f1. Styne DM. The testes: disorder of sexual differentiation
, f* P5 R* I3 R0 D0 N0 pand puberty in the male. In: Sperling MA, ed. Pediatric& B" e$ h$ k% G% m
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
& |/ z) f) H' d& r* y/ n2002: 565-628.
# L8 Q# z& O6 I  k  Z2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious! b9 w' {3 N) `* n' ]) t8 T9 F
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old" {9 o( A% z! I
Boy Induced by Indirect Topical
- E  y3 x, A3 j6 K* n/ I$ rExposure to Testosterone8 W, L" m) b6 Y% Z/ N. b; y9 |
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2+ K5 |/ N. X# {. @1 z
and Kenneth R. Rettig, MD1
2 @' ?& {( b  n9 v1 FClinical Pediatrics7 e# H# Z' {: t& c
Volume 46 Number 6
7 E* v$ z0 l. b* hJuly 2007 540-543% I* h; @5 P' S
© 2007 Sage Publications
' T. w7 H! y; k, i7 f1 Q10.1177/00099228062966512 A( c: C% I# K$ I- s5 S0 D  E5 G
http://clp.sagepub.com# i0 A% m3 E$ J$ j
hosted at/ r- G9 h6 x7 T4 ~6 X1 k
http://online.sagepub.com
. O& |% U* S3 f+ kPrecocious puberty in boys, central or peripheral,
: C1 w- [6 ^' U' z$ Wis a significant concern for physicians. Central3 ]7 v+ M- T, }, A/ W: B8 Y
precocious puberty (CPP), which is mediated, K( U! V  ^2 s' D/ A/ r5 L
through the hypothalamic pituitary gonadal axis, has6 Y: Y2 c2 [6 \1 T. R# a/ n, e4 N
a higher incidence of organic central nervous system$ Y2 N1 N) C% L! W# O6 h* B$ f' R5 a
lesions in boys.1,2 Virilization in boys, as manifested
) l% q& i! J, L! Y/ `+ Vby enlargement of the penis, development of pubic% T6 k! H$ Y0 `3 U0 j
hair, and facial acne without enlargement of testi-
" x, W6 j8 `" I/ jcles, suggests peripheral or pseudopuberty.1-3 We5 R' Y1 J6 j/ }' v
report a 16-month-old boy who presented with the
3 m* W3 [0 q& s' w  A" a6 x" ~/ @enlargement of the phallus and pubic hair develop-+ v  w: z* z. w; C' Q
ment without testicular enlargement, which was due$ L0 s0 K! P5 C1 h
to the unintentional exposure to androgen gel used by
5 M% v, k" R* W2 y! Q$ S: @the father. The family initially concealed this infor-: Y) h" k9 j9 ]- i* V
mation, resulting in an extensive work-up for this) G+ z# d$ d& Z( h9 h7 ]
child. Given the widespread and easy availability of
' n7 X: _% V( r1 H; Jtestosterone gel and cream, we believe this is proba-
, r" {( P! o' h" |" E5 fbly more common than the rare case report in the7 j* y+ a: C( x3 O1 V
literature.4# J& t) ]' A9 e; ~( r$ X7 |
Patient Report. |0 b& d# ~( m* |: c
A 16-month-old white child was referred to the
4 ~. o2 l3 F& Z! M$ Sendocrine clinic by his pediatrician with the concern7 ^9 \2 C1 H( w; n3 X
of early sexual development. His mother noticed
; }" D6 [& d, |& H5 Ylight colored pubic hair development when he was
) I$ L) K, o5 {1 Q5 d" QFrom the 1Division of Pediatric Endocrinology, 2University of- u* C! U& [* W0 s* d, Q
South Alabama Medical Center, Mobile, Alabama.
! z8 f9 k) {. X9 F# o9 `& tAddress correspondence to: Samar K. Bhowmick, MD, FACE,5 q7 z4 K! u, D$ O% y
Professor of Pediatrics, University of South Alabama, College of, j. B5 g5 |. q( N
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;2 y% l% N9 e: i
e-mail: [email protected].
% Z$ C' ^: A3 d/ h; Rabout 6 to 7 months old, which progressively became
. t. M; b. i! F+ p, @" d$ Cdarker. She was also concerned about the enlarge-" \) l; S: @& a3 ^9 p4 y% T
ment of his penis and frequent erections. The child
. P2 w  P( y( W: y7 g  P5 q: ?+ e1 lwas the product of a full-term normal delivery, with
( q! X5 w0 |5 x* m# D' X4 Ra birth weight of 7 lb 14 oz, and birth length of: H5 Y$ G" M) \# P6 ?1 Z
20 inches. He was breast-fed throughout the first year
/ h2 c, f6 ~$ i0 tof life and was still receiving breast milk along with9 Q6 K! s" j6 I. G
solid food. He had no hospitalizations or surgery,, ?/ m7 R0 S$ }% A8 v) Q0 L  `, o
and his psychosocial and psychomotor development7 u9 j( v* G7 |2 M2 ^
was age appropriate.7 k2 @2 K0 A( U5 W/ r' h
The family history was remarkable for the father,8 n( Q+ a. h" b7 s
who was diagnosed with hypothyroidism at age 16,
  @- M) i% I& u- U- e8 hwhich was treated with thyroxine. The father’s, n( v- X* u6 L) z/ E- @
height was 6 feet, and he went through a somewhat( D) s. R7 N$ a2 f0 z
early puberty and had stopped growing by age 14.2 D1 ^3 ]$ h5 U' V8 G0 o
The father denied taking any other medication. The
% o5 M, P- ]9 G7 I9 n# V1 L) Xchild’s mother was in good health. Her menarche
' M1 R& C  v+ r" ^0 v1 l0 Bwas at 11 years of age, and her height was at 5 feet+ @: X' ^8 J7 q
5 inches. There was no other family history of pre-
; r5 _: o: l$ p) k* E/ U5 X! `cocious sexual development in the first-degree rela-' e+ D; t% H  I* \1 s
tives. There were no siblings.+ s; s; n0 f5 q: z
Physical Examination' m: k7 P, R% }5 h! H( `% }
The physical examination revealed a very active,
, q9 u2 W, C; h3 P& rplayful, and healthy boy. The vital signs documented' A& l. D4 l1 z8 X9 r
a blood pressure of 85/50 mm Hg, his length was( E; u& N& D4 C' H" J: ?. C% K' |
90 cm (>97th percentile), and his weight was 14.4 kg
) Q* |% D: o* b( V4 m(also >97th percentile). The observed yearly growth
3 g) o2 a5 x+ X7 c5 cvelocity was 30 cm (12 inches). The examination of7 z( e# G/ Q' H5 Q
the neck revealed no thyroid enlargement.+ K0 P. ~* _1 }) Y6 l
The genitourinary examination was remarkable for5 s' w& @$ u& M/ `2 J# \8 I; g, l
enlargement of the penis, with a stretched length of9 |0 T& z% G+ J9 G+ ~! r8 W
8 cm and a width of 2 cm. The glans penis was very well# R. A3 O: g0 ]7 V
developed. The pubic hair was Tanner II, mostly around1 o  U* Q2 l4 i4 V# r/ h' r
540
  c$ a" r) ^+ Y! @6 `at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from$ D5 [# k+ c7 }. |" s; U
the base of the phallus and was dark and curled. The
; z% L: i7 {1 z! F- A6 Btesticular volume was prepubertal at 2 mL each.
1 g' ?& k8 C: [  e: O! nThe skin was moist and smooth and somewhat& G. [- [1 P" K  G9 T! o
oily. No axillary hair was noted. There were no
' v  z  p3 a! U5 y5 c) T  pabnormal skin pigmentations or café-au-lait spots.+ y$ K3 }- }# x" D5 T( }* E
Neurologic evaluation showed deep tendon reflex 2+
& u" V  A+ H% z+ a5 jbilateral and symmetrical. There was no suggestion5 D* H) u+ I) j+ P- \% P! v
of papilledema.
# k9 n$ `4 s0 [  ~! L- JLaboratory Evaluation
4 H. w$ e  s) J  s' ZThe bone age was consistent with 28 months by# V1 Q" R( c+ P4 {) _! ^
using the standard of Greulich and Pyle at a chrono-
! S( \* w1 {* G: a. N2 llogic age of 16 months (advanced).5 Chromosomal0 J% K* [! }+ a: A, s! h7 q8 t; i/ k
karyotype was 46XY. The thyroid function test
1 L* e$ S# b) O7 ?& j" wshowed a free T4 of 1.69 ng/dL, and thyroid stimu-( B* f4 S, u) j1 a* u
lating hormone level was 1.3 µIU/mL (both normal).
  u; x8 t4 M( Q2 ^The concentrations of serum electrolytes, blood
( n* L) ^- g5 ]urea nitrogen, creatinine, and calcium all were
. Z$ o8 ~3 ?1 s* c: Lwithin normal range for his age. The concentration4 Y8 z& h, z2 _: e. J: s
of serum 17-hydroxyprogesterone was 16 ng/dL
" ~# \' o  t: q(normal, 3 to 90 ng/dL), androstenedione was 20! Q% c" Q/ |4 {. z/ r& O. x
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
2 W6 v" P. o0 [5 j! Oterone was 38 ng/dL (normal, 50 to 760 ng/dL),
3 b0 \1 c2 r1 }1 w( X% {* bdesoxycorticosterone was 4.3 ng/dL (normal, 7 to
2 i9 q! a0 D) ?4 H& R) I49ng/dL), 11-desoxycortisol (specific compound S). n! p, h- }( v& t, C% k0 J
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-, ~7 r" X& d6 {8 V' c
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
/ F. m* e% v: K% @2 P& P6 e, N+ e. K+ Otestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
  {" s7 d+ v9 ^8 p$ Xand β-human chorionic gonadotropin was less than
) r8 m6 V3 K0 {5 mIU/mL (normal <5 mIU/mL). Serum follicular9 o1 ^, D2 R, ^9 p% T: `$ D  @
stimulating hormone and leuteinizing hormone
0 I, N! |' f3 m9 l9 ]concentrations were less than 0.05 mIU/mL
1 G  q4 w9 k' i2 ]0 p% f6 m9 I(prepubertal).
7 g4 e$ I" p' x, O. k8 [The parents were notified about the laboratory
/ S$ B, T/ u; m& ?2 ?0 bresults and were informed that all of the tests were
! o: C4 N0 m8 e) ?0 f5 Cnormal except the testosterone level was high. The$ x  T# |1 ]% L& m& O5 ?
follow-up visit was arranged within a few weeks to
' V5 M3 O1 V( Y5 ^* A. w' `% K1 fobtain testicular and abdominal sonograms; how-
! I( I# g6 h; p. Fever, the family did not return for 4 months.
2 g- p( H1 z' _2 A7 U* hPhysical examination at this time revealed that the. q" Q: v8 W# q0 y
child had grown 2.5 cm in 4 months and had gained
1 K2 ]5 Z" o8 K& I; {* i7 `2 kg of weight. Physical examination remained. E: @: c, o, [+ U
unchanged. Surprisingly, the pubic hair almost com-
2 X4 H- g6 K/ zpletely disappeared except for a few vellous hairs at8 a! j$ r6 ]1 s9 U7 t* w$ U( L. _
the base of the phallus. Testicular volume was still 2$ }# P! v6 j' `' U, s0 {
mL, and the size of the penis remained unchanged.( C2 J. @: @( B) ~( c& r4 n
The mother also said that the boy was no longer hav-
0 t+ y' D5 M, g; wing frequent erections.+ f! V$ ^& w" |1 [7 ^" h
Both parents were again questioned about use of
1 {: r6 s& d  t- I/ P0 qany ointment/creams that they may have applied to5 K- F8 T2 ?! O- d4 f5 v
the child’s skin. This time the father admitted the. U# j# W4 b6 g' a' ~
Topical Testosterone Exposure / Bhowmick et al 541+ w- ^+ V" q- ?7 d
use of testosterone gel twice daily that he was apply-
. e# g! ]% T% T2 A. u  d3 [* a* Qing over his own shoulders, chest, and back area for( b* D' c. b% _. t0 k# _
a year. The father also revealed he was embarrassed
6 A4 S. J0 ]2 \3 Z+ v9 Kto disclose that he was using a testosterone gel pre-$ H$ l( i7 n( Y. a" N7 W! e
scribed by his family physician for decreased libido
, n! ^; K2 I. W# K$ E5 s' d1 Ysecondary to depression.
. u# ?1 _% |  d, ^3 _1 [The child slept in the same bed with parents.) P) l, w, e/ |! R+ S1 g* k5 N  }
The father would hug the baby and hold him on his9 f' `: }# p# C  J7 f7 D) }
chest for a considerable period of time, causing sig-
- n4 b7 ]5 n# C4 E7 ]( w+ onificant bare skin contact between baby and father., i2 q7 Z  w6 G4 c  \. c$ ?8 W
The father also admitted that after the phone call,. b6 `* }5 b3 ?! R  ~
when he learned the testosterone level in the baby: g) u4 V$ z" Z3 H* Z1 Y! @) a
was high, he then read the product information
) L! o) D* }6 n$ v( Cpacket and concluded that it was most likely the rea-
+ N9 E4 E: }/ gson for the child’s virilization. At that time, they
% \7 h/ Q4 X$ c( Ddecided to put the baby in a separate bed, and the
  g, p/ i4 ?5 n- T- Vfather was not hugging him with bare skin and had
" z5 R0 N7 @: o. T0 i$ V6 a' `been using protective clothing. A repeat testosterone. v' e' r5 f0 S! {3 r
test was ordered, but the family did not go to the; s  f+ Y7 e& P2 n+ ^/ l4 t
laboratory to obtain the test.4 r1 X( {0 u* O
Discussion/ D# G! L+ E4 N# [. [" V( P
Precocious puberty in boys is defined as secondary
6 a* u; Z1 E' I; _sexual development before 9 years of age.1,4
* P  F/ a3 {) X; g* s/ xPrecocious puberty is termed as central (true) when) j3 K6 V  h: ]- N9 a3 o
it is caused by the premature activation of hypo-8 M% z, ?1 H6 Z7 r
thalamic pituitary gonadal axis. CPP is more com-
$ J! ]8 M" Z: Rmon in girls than in boys.1,3 Most boys with CPP
* F4 s) A% \, w3 V) u/ {  @may have a central nervous system lesion that is! P8 w2 A0 q+ c9 t2 B5 {
responsible for the early activation of the hypothal-
1 @" O  e2 U+ B: [; l1 lamic pituitary gonadal axis.1-3 Thus, greater empha-- ?! ^0 N$ S0 n  C; _
sis has been given to neuroradiologic imaging in" n+ w; T2 \1 q: ~# P
boys with precocious puberty. In addition to viril-" w: \1 f% F9 l5 B7 T
ization, the clinical hallmark of CPP is the symmet-
; G0 \9 x8 r4 T3 w3 j& o! Brical testicular growth secondary to stimulation by
) `. w2 W& a, i" Agonadotropins.1,3
" x; z. z8 n3 l6 |7 T2 HGonadotropin-independent peripheral preco-' R' Z; B4 k7 Q6 w' l
cious puberty in boys also results from inappropriate- N, e# C2 Y# \/ S* N* h0 z& S
androgenic stimulation from either endogenous or, y8 a& r: Q4 t
exogenous sources, nonpituitary gonadotropin stim-. r' J* I( e( E* T. ]% P! O
ulation, and rare activating mutations.3 Virilizing
/ n. F1 W/ W' f9 O4 Xcongenital adrenal hyperplasia producing excessive
( S& j# n7 S. Z- Jadrenal androgens is a common cause of precocious3 F: h# @( v3 g* C: T; @3 M; k
puberty in boys.3,49 \+ d1 k9 u$ @, [" ]+ u. d
The most common form of congenital adrenal
3 U" H5 x* V+ k3 v: t; fhyperplasia is the 21-hydroxylase enzyme deficiency.
6 O  s( A& M1 S. x* X$ y+ TThe 11-β hydroxylase deficiency may also result in) M- Y, S2 U$ g6 h: n9 K1 _; o
excessive adrenal androgen production, and rarely,3 S) g/ S% h& ]" r! o
an adrenal tumor may also cause adrenal androgen: A4 e' j7 y# \8 N9 U( l" n) F
excess.1,3* n6 L+ L3 H+ T, T4 z
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from7 k/ l3 A" _( _
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
: V. C7 y# L1 z8 N2 `2 G# sA unique entity of male-limited gonadotropin-$ l, P9 \) }* `& o
independent precocious puberty, which is also known$ B4 v2 {* N! N" A1 o# o1 w1 i* H
as testotoxicosis, may cause precocious puberty at a
5 Y3 d! `) K, E( s: r5 c! y* O4 Z! \very young age. The physical findings in these boys4 D% J% }. z4 U5 N7 f$ N
with this disorder are full pubertal development,+ ~$ N0 Q  }& ?" ]5 I, X- w
including bilateral testicular growth, similar to boys4 N6 g1 [+ V9 t  u* w  m8 R
with CPP. The gonadotropin levels in this disorder
1 V; p8 M& P; z- z+ R, r& Iare suppressed to prepubertal levels and do not show
8 J/ A, Q$ z& d4 ~pubertal response of gonadotropin after gonadotropin-" Z7 V% l% s7 y& x: ~: {+ P9 r+ u5 T
releasing hormone stimulation. This is a sex-linked- h- P4 {: K  _% n2 E8 X
autosomal dominant disorder that affects only
% ^; M, U& J3 w1 a. P- O- smales; therefore, other male members of the family
7 Y! @2 _  L, L3 dmay have similar precocious puberty.3
5 c" g' k, \3 K0 i9 GIn our patient, physical examination was incon-
: ]& p3 |5 w$ \/ [, v7 f9 Hsistent with true precocious puberty since his testi-# Q9 n% N: y+ c# h% t! ?
cles were prepubertal in size. However, testotoxicosis; Q  _% [# a, `' V/ F
was in the differential diagnosis because his father& h1 ?" h$ U% @3 S2 ~) ]
started puberty somewhat early, and occasionally,
0 F! v; z& P# C$ f( Gtesticular enlargement is not that evident in the1 M( h( v# N/ v( _: V# D$ [
beginning of this process.1 In the absence of a neg-; x* ?, n4 O" V$ k" l6 T' R7 H
ative initial history of androgen exposure, our
0 R6 y5 V0 h! R1 Pbiggest concern was virilizing adrenal hyperplasia,
1 m1 f) R, I: ^5 X5 s! |either 21-hydroxylase deficiency or 11-β hydroxylase
2 Y  a0 ?4 a, M% `; y. Y: {& udeficiency. Those diagnoses were excluded by find-+ E7 F' ]! a- }$ K6 k
ing the normal level of adrenal steroids.; n1 D- g/ S+ E. g
The diagnosis of exogenous androgens was strongly; y$ T9 O% J% c0 l
suspected in a follow-up visit after 4 months because2 y% y! H) f3 ~( X# r  Z+ d
the physical examination revealed the complete disap-
2 C6 h' _. J' Z7 wpearance of pubic hair, normal growth velocity, and% C. D3 w: y7 B* r" i
decreased erections. The father admitted using a testos-$ R3 A' x, [5 C4 u  G, C" s
terone gel, which he concealed at first visit. He was/ o9 e$ f; q+ I7 B+ Q
using it rather frequently, twice a day. The Physicians’
2 R# @# t8 a0 V8 k  ^5 [5 lDesk Reference, or package insert of this product, gel or6 ~. P& D% c: D/ X- z
cream, cautions about dermal testosterone transfer to
. `- P. F! w2 i0 g6 W; H3 D$ |* H: Runprotected females through direct skin exposure.
! F2 g% _+ ]4 W. KSerum testosterone level was found to be 2 times the& r0 m% t% e0 h& R4 P' J
baseline value in those females who were exposed to
) j6 E# d% s/ W: Z' Y; Veven 15 minutes of direct skin contact with their male
4 q1 Q5 J0 R) Xpartners.6 However, when a shirt covered the applica-% L, N9 K1 y# U* D& }# L& h+ Y
tion site, this testosterone transfer was prevented.& o1 X/ k; g/ M9 S* N$ g* b  ^+ @! G
Our patient’s testosterone level was 60 ng/mL," ]. d& ?) X) q! h
which was clearly high. Some studies suggest that
# a' T" _8 }: u% Edermal conversion of testosterone to dihydrotestos-
& ]$ F4 Z+ S' u! k5 }' Zterone, which is a more potent metabolite, is more
$ E4 s7 |3 h$ I4 Dactive in young children exposed to testosterone
7 }  m$ D" j1 T  H9 |5 }exogenously7; however, we did not measure a dihy-4 D: R3 v- `1 K0 T: s8 e
drotestosterone level in our patient. In addition to
1 s7 {  s  F0 `9 t% [" jvirilization, exposure to exogenous testosterone in
0 n* m: l" j2 w" kchildren results in an increase in growth velocity and- E1 x4 m0 n9 S& s4 V; ]! l
advanced bone age, as seen in our patient.
  b* e+ [! [1 o+ HThe long-term effect of androgen exposure during
9 D7 ]+ G7 f/ yearly childhood on pubertal development and final
* \9 ~; X* b* z3 d' D1 L8 nadult height are not fully known and always remain7 c$ t: W, I5 I* O; Z' ?6 P
a concern. Children treated with short-term testos-
7 Z  ?% M: r" M2 Aterone injection or topical androgen may exhibit some
" Z1 A3 [% N% P6 O( [7 B3 U& Kacceleration of the skeletal maturation; however, after' W  N) ?4 T6 v7 d" Q- d1 a7 {- W, \
cessation of treatment, the rate of bone maturation
1 j& X9 G; A0 a5 [3 T1 O! Jdecelerates and gradually returns to normal.8,9# G6 h$ m  S# y# D
There are conflicting reports and controversy
; g/ T. k; H: W( y: k+ U' a5 oover the effect of early androgen exposure on adult4 O* k, ?) z+ B+ T
penile length.10,11 Some reports suggest subnormal# c9 S. k; |$ C% n; u
adult penile length, apparently because of downreg-
+ F' C/ L; _) d- C( @% h. dulation of androgen receptor number.10,12 However,' L1 r6 R  b) W0 S
Sutherland et al13 did not find a correlation between& A6 U4 N' a; s5 j* M/ G4 y
childhood testosterone exposure and reduced adult
; P1 y, ~; U, C) Ipenile length in clinical studies.9 W. r# j/ }& L, Z
Nonetheless, we do not believe our patient is
/ I! `) r) S$ f; _* zgoing to experience any of the untoward effects from1 k: L& s7 [4 |3 o# G: ]+ E" q! m
testosterone exposure as mentioned earlier because" g( w" x7 P. F% \4 ^
the exposure was not for a prolonged period of time.
% d( R) P7 ~/ V- zAlthough the bone age was advanced at the time of
6 k3 `; N+ A3 Y6 w* g5 x! Qdiagnosis, the child had a normal growth velocity at) Q0 M- A3 D7 k; |1 z
the follow-up visit. It is hoped that his final adult
" C# ?+ f. g; `5 s+ v6 lheight will not be affected.
0 `- w! i: p1 _Although rarely reported, the widespread avail-! ]8 @0 k- |- O
ability of androgen products in our society may
" a- s8 y$ K5 U, d% r6 `indeed cause more virilization in male or female
4 Y4 \& D  N2 r9 w+ Pchildren than one would realize. Exposure to andro-
8 `: j# Y  m! r/ [) \6 ~& y, }9 Jgen products must be considered and specific ques-5 A# m" a) J, [
tioning about the use of a testosterone product or
! v$ _! w& K# J& R" F0 t+ _gel should be asked of the family members during
  R# A: P3 B1 E0 R1 \" ^' R: @( Kthe evaluation of any children who present with vir-
2 D) l6 v. R) R! g0 O6 Uilization or peripheral precocious puberty. The diag-
' g: s0 |  u* _4 ?3 S* A  Unosis can be established by just a few tests and by
' Q/ ~9 [! O7 ]% \appropriate history. The inability to obtain such a8 t  f' b0 C: l) [! C
history, or failure to ask the specific questions, may% s) g8 G9 t. s/ P
result in extensive, unnecessary, and expensive
( w# c3 Z* g1 {: Vinvestigation. The primary care physician should be
! p3 p  M) [. b6 a# x- e4 Laware of this fact, because most of these children& s  c  X2 E1 K0 f6 h
may initially present in their practice. The Physicians’5 L& q7 @6 t0 m' g8 q8 h$ W
Desk Reference and package insert should also put a+ j( h2 I+ a% i8 x; C# C
warning about the virilizing effect on a male or! l% d' r( ^9 {3 E% c
female child who might come in contact with some-
6 _. W" a, ?' P  _  |one using any of these products.$ b" T. p& m: F0 G5 G2 e' d
References4 u' S- P; g" x: _  p
1. Styne DM. The testes: disorder of sexual differentiation9 l+ {) C$ z& m& g) f2 q7 E8 z* T
and puberty in the male. In: Sperling MA, ed. Pediatric5 v! g  l! e' I' x3 ^5 {, O% Y
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;: g$ G* {" ]6 B9 q
2002: 565-628.1 U8 s7 r3 w! J4 d+ q% ?7 R
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious0 F5 }" W. P7 F  h) r& b* Y. J
puberty in children with tumours of the suprasellar pineal
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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

4 C" J, x& A/ j8 S4 y7 ~9 A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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