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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
$ t' B  F0 H+ @4 y+ o6 p2 m' E3 FBoy Induced by Indirect Topical
, O3 N. z$ U% AExposure to Testosterone
5 Z$ y- }6 f& I5 H3 |+ L' M4 \Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2. x1 P- ~' P# C( i1 ~4 ^
and Kenneth R. Rettig, MD18 }! D& r! |7 v3 `4 g$ I) C
Clinical Pediatrics  S* v7 h( }2 r6 e/ T2 v6 e
Volume 46 Number 6
2 I$ d4 y5 f! B+ O, UJuly 2007 540-543
, s- K6 }5 A! W8 e$ T8 ~" M© 2007 Sage Publications1 p7 _& J& ?) ?' y
10.1177/0009922806296651" ~0 j" R9 A0 b1 l3 }! V+ ]0 L
http://clp.sagepub.com: f8 ~) w1 U# T8 F+ K
hosted at1 N/ q9 C, R4 z' u; m: ?0 o
http://online.sagepub.com
9 J; n. Z3 L' Q6 v. C" Y1 mPrecocious puberty in boys, central or peripheral,
0 s- u; q+ [6 L5 Xis a significant concern for physicians. Central7 }  N' d$ s4 x
precocious puberty (CPP), which is mediated9 ~; C, m2 P: h; c' m& g
through the hypothalamic pituitary gonadal axis, has
+ A3 t. S0 t1 y; A) Za higher incidence of organic central nervous system3 b+ a& p- a7 `4 q$ J; D1 i' z* s
lesions in boys.1,2 Virilization in boys, as manifested$ F# ^6 m9 U! ~) `; q1 f
by enlargement of the penis, development of pubic
' v% I1 u. B  l" qhair, and facial acne without enlargement of testi-! I. M/ l2 _# v4 C/ ^& k
cles, suggests peripheral or pseudopuberty.1-3 We  @0 v' Z" j. [6 r
report a 16-month-old boy who presented with the
8 @% e; O. W) V) kenlargement of the phallus and pubic hair develop-! e" c; v/ `1 i2 e
ment without testicular enlargement, which was due
3 L  L; ]! E( G  @7 x4 T$ Cto the unintentional exposure to androgen gel used by/ |6 J7 l/ ?$ P7 A1 y4 D: j
the father. The family initially concealed this infor-2 e# m* u& t% x. U+ ?
mation, resulting in an extensive work-up for this- }" N0 s& ]1 P6 g% E+ h9 e, E  m
child. Given the widespread and easy availability of2 V6 e. W- |9 \
testosterone gel and cream, we believe this is proba-
2 s" Z$ a4 X* U4 T' `4 fbly more common than the rare case report in the+ Q( ^* y- H" [4 h& M3 N- P1 z
literature.4% ~+ D5 T+ t: b! Y
Patient Report
! E; m- r, o) sA 16-month-old white child was referred to the8 B5 z* @: i5 ^% J" n* Y" h. Y& Z% H3 G
endocrine clinic by his pediatrician with the concern
6 n  N: n" b5 p( ^* S' {of early sexual development. His mother noticed# [1 w+ G; j. d* v0 c
light colored pubic hair development when he was
1 ?% W% l; K$ y. n. Y& uFrom the 1Division of Pediatric Endocrinology, 2University of
: p7 |  y' a+ M9 b" RSouth Alabama Medical Center, Mobile, Alabama.4 X  s& w. [0 J6 u  L  D+ q) n
Address correspondence to: Samar K. Bhowmick, MD, FACE,, m$ o9 M  ]- V( b7 ?1 M
Professor of Pediatrics, University of South Alabama, College of
, M( V, V1 |# b8 t& TMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;3 V! D, b0 x! K2 V  u0 h" y  g
e-mail: [email protected].
4 G1 K' }/ z, E9 i6 G" k$ Oabout 6 to 7 months old, which progressively became
$ m$ E+ j/ b7 d. y* Xdarker. She was also concerned about the enlarge-! i) P! `" p$ O, k6 T7 {: m7 H
ment of his penis and frequent erections. The child
- O, f2 O% T9 l+ Vwas the product of a full-term normal delivery, with8 H0 F/ `! z5 x6 c2 Y' d$ R- v1 e
a birth weight of 7 lb 14 oz, and birth length of
0 Q2 r5 i$ J* u3 f( A$ Q, u20 inches. He was breast-fed throughout the first year
+ ^; i, N- \  S7 Rof life and was still receiving breast milk along with
% [  T% v. a" |+ H- O' |solid food. He had no hospitalizations or surgery,
6 w' H1 _) k' |4 J' g. a6 v2 w# w. Oand his psychosocial and psychomotor development) N, c) j( W3 j! e$ B, ^
was age appropriate.7 I6 l. L/ A' i0 \8 n) E2 A
The family history was remarkable for the father,
% j& ]% K3 B8 J7 {who was diagnosed with hypothyroidism at age 16,
( ^% A" N9 H! x7 h7 Swhich was treated with thyroxine. The father’s) t5 H) y2 e# {* j* P1 \8 u: j+ T
height was 6 feet, and he went through a somewhat+ z9 ]3 Y  a5 F0 m: h7 ?
early puberty and had stopped growing by age 14.
+ T: u, c7 e- H2 `% l& HThe father denied taking any other medication. The
3 z7 y4 o4 V4 G" hchild’s mother was in good health. Her menarche
9 C$ L. d5 y  Q2 k9 J/ E+ wwas at 11 years of age, and her height was at 5 feet
2 B" F( @; E2 K" M. ^( W9 Z5 inches. There was no other family history of pre-3 y4 _% v2 i! u. W* j$ U
cocious sexual development in the first-degree rela-
7 |  c* j% T! T7 \tives. There were no siblings.
: }+ p! n- O' {; `$ PPhysical Examination
+ f( a7 n3 ]! i. [4 EThe physical examination revealed a very active,9 V9 P& ~' {. ^7 n& O" {
playful, and healthy boy. The vital signs documented/ ]& p: Y2 p3 O1 V' x+ Q
a blood pressure of 85/50 mm Hg, his length was; Y; G% F' x/ @5 c+ _" b
90 cm (>97th percentile), and his weight was 14.4 kg
  o: w  k- d9 T2 b  B# a) v% ?(also >97th percentile). The observed yearly growth
9 Y7 Z* w7 g/ a# T6 ]; G" x, Vvelocity was 30 cm (12 inches). The examination of, v) o0 p. U( w2 x- Y7 }3 _
the neck revealed no thyroid enlargement.$ r- z3 N  Q/ X
The genitourinary examination was remarkable for
' w1 P  C) B8 t( g6 Q8 X1 u8 E( eenlargement of the penis, with a stretched length of; l7 g0 L8 O5 u) r0 `' x
8 cm and a width of 2 cm. The glans penis was very well
" O  }3 \: i# `& ndeveloped. The pubic hair was Tanner II, mostly around
- a9 Y1 t$ F8 h$ B" W540# O# l9 L( e5 l( D0 a- a6 d
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
6 s% N( o* a2 w/ i& H. L7 ^the base of the phallus and was dark and curled. The- q) U* g' H6 u( c
testicular volume was prepubertal at 2 mL each.: P1 d7 B9 ?3 ?# ^: T+ L! I
The skin was moist and smooth and somewhat' X' n8 V) `, T3 w
oily. No axillary hair was noted. There were no0 A& q' W) k* w5 \4 a! s9 _1 x( I. h
abnormal skin pigmentations or café-au-lait spots.
% T. q& t; S! A) xNeurologic evaluation showed deep tendon reflex 2+8 K6 V1 b$ @8 L
bilateral and symmetrical. There was no suggestion( ~9 g" g6 S. o
of papilledema.
) G, K9 {& W2 }7 O3 C* kLaboratory Evaluation
6 Q( Y& I8 S* A+ ?2 cThe bone age was consistent with 28 months by5 }" @* q% }7 N" {+ D1 N
using the standard of Greulich and Pyle at a chrono-7 \; Z0 N/ a8 v% X( ^( P6 s
logic age of 16 months (advanced).5 Chromosomal
, P* ?3 ?6 ?0 A- a4 Y) o* c0 vkaryotype was 46XY. The thyroid function test
: O* f* |* K  ]& Gshowed a free T4 of 1.69 ng/dL, and thyroid stimu-  o* D/ `& f, C
lating hormone level was 1.3 µIU/mL (both normal).; m0 X. Q0 w4 f. M' J) U8 ~
The concentrations of serum electrolytes, blood0 n* z) l7 W: r; n$ V: f3 {& L/ \
urea nitrogen, creatinine, and calcium all were4 |1 `4 e) P# z, E& Q
within normal range for his age. The concentration) I2 @  i2 c; u* S
of serum 17-hydroxyprogesterone was 16 ng/dL
1 U) X! H: U: y4 f, W(normal, 3 to 90 ng/dL), androstenedione was 20  \5 r# U" }! s0 q* D' t
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-; ?9 h8 h8 K" Z; Y$ S
terone was 38 ng/dL (normal, 50 to 760 ng/dL),1 k. M# d* m5 H0 |
desoxycorticosterone was 4.3 ng/dL (normal, 7 to; J& P2 k5 a; {
49ng/dL), 11-desoxycortisol (specific compound S)
* J7 U5 C8 f/ M5 u4 @+ m; o+ o5 E  mwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-% e; p. S2 ?) Z2 s  U
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total, d8 y9 B. V. x, |4 y
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
( q: r+ X6 L9 p$ I& F) ]% iand β-human chorionic gonadotropin was less than# B! N6 h5 w. p% j
5 mIU/mL (normal <5 mIU/mL). Serum follicular" }: h. m' s' C  }
stimulating hormone and leuteinizing hormone
2 U+ r0 k; K4 p3 O* m  e$ x7 Gconcentrations were less than 0.05 mIU/mL+ E+ N" @$ z" R* A$ n
(prepubertal).
- n- K+ A% B; y2 W, l3 a5 VThe parents were notified about the laboratory
* w+ X3 N# v9 M, a" P: N8 R! cresults and were informed that all of the tests were; E; L2 f# m: P. A2 v
normal except the testosterone level was high. The
) Q# j$ B1 c3 rfollow-up visit was arranged within a few weeks to; b" R, X, K3 ^1 k
obtain testicular and abdominal sonograms; how-
$ h1 C' \; G# `# @ever, the family did not return for 4 months.& q0 B+ N" E( x* I& Q* b
Physical examination at this time revealed that the' I3 s9 ~0 I( }
child had grown 2.5 cm in 4 months and had gained
: [$ d: L: J# o) g2 kg of weight. Physical examination remained+ A$ d' y! Y, x% W$ X( l5 A5 `
unchanged. Surprisingly, the pubic hair almost com-) l8 w+ D: A; {, ]8 g
pletely disappeared except for a few vellous hairs at$ O) S$ b5 @/ k5 ?
the base of the phallus. Testicular volume was still 2
8 K1 w3 H/ C: ]& x. |mL, and the size of the penis remained unchanged.9 v. h7 ~2 _3 Q* f" }
The mother also said that the boy was no longer hav-
" m3 s8 g$ e  H# Zing frequent erections.+ m4 |) x: K# V4 e0 F
Both parents were again questioned about use of& K# }/ w" N  @$ Y0 m0 U
any ointment/creams that they may have applied to
  B. Q! l  y: I, T2 l- a2 x1 Nthe child’s skin. This time the father admitted the& q) j! d) O: Y$ c# t  L  w
Topical Testosterone Exposure / Bhowmick et al 5419 [+ D$ d. w# b: J
use of testosterone gel twice daily that he was apply-
& M4 F* j5 Q: R% ?" C# q$ i2 Oing over his own shoulders, chest, and back area for
2 w: A) S7 @: Z# \3 Ba year. The father also revealed he was embarrassed
" |9 Z& _, e2 p; F/ e1 p# P1 ]to disclose that he was using a testosterone gel pre-) I  F# J) {; m: P9 U3 s  D$ o  s/ K
scribed by his family physician for decreased libido
$ }' x( Y1 A5 osecondary to depression.
4 C" X8 F% M0 DThe child slept in the same bed with parents.
/ O# a9 K. X. H- J+ d  nThe father would hug the baby and hold him on his' V: H/ j" c& ~
chest for a considerable period of time, causing sig-$ x! q" F- [' ^
nificant bare skin contact between baby and father.$ W- M& g: W3 k
The father also admitted that after the phone call,7 u) h4 H5 @! _5 P' J$ c! t6 j
when he learned the testosterone level in the baby1 W5 `* f6 Q! {3 ~# L7 {
was high, he then read the product information& Q" W9 G* P0 A; \" j$ B
packet and concluded that it was most likely the rea-
0 ]$ C' t+ N" ^# ]0 M" Hson for the child’s virilization. At that time, they
; y4 F& o  D- Ydecided to put the baby in a separate bed, and the
! H$ l/ p# A- q7 L8 j$ V% vfather was not hugging him with bare skin and had
  D, M" Q% ?* {; t, B8 H# ~been using protective clothing. A repeat testosterone
9 q" v2 f6 I5 w% ~: V- q, W/ i' Ztest was ordered, but the family did not go to the; \8 A  }3 ~4 _1 o
laboratory to obtain the test.
8 x- r1 X& f" Y* NDiscussion; u' S' Z3 U: D! ^0 W5 R
Precocious puberty in boys is defined as secondary8 Z4 C* g2 g' N1 t0 t# B' d
sexual development before 9 years of age.1,4; ^( A5 C5 d" P
Precocious puberty is termed as central (true) when
; k+ Y# t" Q: Q: z6 l+ e" Lit is caused by the premature activation of hypo-! l6 H. @! X6 {. Q0 X( L
thalamic pituitary gonadal axis. CPP is more com-7 h4 Q( R# K* J
mon in girls than in boys.1,3 Most boys with CPP+ B- d6 \" x0 V$ a3 _
may have a central nervous system lesion that is: z! }6 O% P/ X, J" ]( K
responsible for the early activation of the hypothal-/ S9 B+ k) h/ F) v
amic pituitary gonadal axis.1-3 Thus, greater empha-' x" e7 e" B1 L- S  `
sis has been given to neuroradiologic imaging in% C% [" f! _9 b) P& o$ F3 p
boys with precocious puberty. In addition to viril-
& s# O' s6 G4 ^+ C" oization, the clinical hallmark of CPP is the symmet-
% e3 |3 r) {( y/ h% ?, H% ^- Irical testicular growth secondary to stimulation by* n: q7 U0 j. I* D
gonadotropins.1,3, [2 V0 n7 ^- b; I4 {3 E+ w
Gonadotropin-independent peripheral preco-' u& c1 v$ B% _6 Q' i; s  A
cious puberty in boys also results from inappropriate
* w* {& a, L% K: i: L4 U5 q6 H, bandrogenic stimulation from either endogenous or& x  q* s  H! Z3 g' ~. v
exogenous sources, nonpituitary gonadotropin stim-
; n+ G6 n8 [( ]ulation, and rare activating mutations.3 Virilizing% M$ {0 _. @+ G! [
congenital adrenal hyperplasia producing excessive
6 W4 Y* L2 P$ ^7 aadrenal androgens is a common cause of precocious
4 _" q; `* n# o$ ]puberty in boys.3,47 x% Z9 S+ z) B/ e9 }9 r
The most common form of congenital adrenal
" x7 t4 U3 r% c* A. @" _, shyperplasia is the 21-hydroxylase enzyme deficiency.
* C8 H, }8 V, h! P3 PThe 11-β hydroxylase deficiency may also result in7 @& L0 ^5 }+ R( {' Y
excessive adrenal androgen production, and rarely,
: J9 r% e( k; H- J' z% t8 Ban adrenal tumor may also cause adrenal androgen
  u6 l3 S: B. r" Q. [' {& aexcess.1,30 q9 S: w& M' J: ^8 `
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from, I( t' k7 r% ?
542 Clinical Pediatrics / Vol. 46, No. 6, July 20077 M9 r: `: b! L4 Y9 i6 }
A unique entity of male-limited gonadotropin-
" B( c( S# p5 j8 |independent precocious puberty, which is also known
0 A: U0 p( o! V8 c/ N1 K4 A( ?as testotoxicosis, may cause precocious puberty at a
6 ^, a, V  s0 c9 [' d+ }6 Y. n' Overy young age. The physical findings in these boys
) Y) s' |6 ^) M# ^: U* Xwith this disorder are full pubertal development,
3 d) c. U; s0 E& i$ j% zincluding bilateral testicular growth, similar to boys
  [3 h* }# N* @+ g8 |with CPP. The gonadotropin levels in this disorder
& V0 N' r/ ]- Q8 K! T; kare suppressed to prepubertal levels and do not show
: z+ b7 k4 Y: ypubertal response of gonadotropin after gonadotropin-! i# k" y2 s: ^* P: y4 d4 ~& a
releasing hormone stimulation. This is a sex-linked: b6 [; [. |& D+ @
autosomal dominant disorder that affects only
6 a4 G0 _3 M) Kmales; therefore, other male members of the family; @+ V5 E+ I5 Q4 l/ Q
may have similar precocious puberty.39 k5 b  s) {# a
In our patient, physical examination was incon-2 w0 A! l8 ~9 b, `& }' I) _
sistent with true precocious puberty since his testi-
- E5 d, o8 v) L+ |" o+ _; bcles were prepubertal in size. However, testotoxicosis  [. x" l2 M) V; I" D* N+ `3 C& q" I/ \  E/ h
was in the differential diagnosis because his father
5 Y  H: z' G5 v9 v. g. r$ F$ a1 xstarted puberty somewhat early, and occasionally,
; n2 A# X- D/ ]6 y+ g& v% }4 Vtesticular enlargement is not that evident in the
/ t) O% {% Y3 \% a! b. dbeginning of this process.1 In the absence of a neg-& l7 ]. r2 i8 N! Q. Y# `
ative initial history of androgen exposure, our
8 Q  f7 z+ |8 P, z& a+ Zbiggest concern was virilizing adrenal hyperplasia,
3 P/ u& u  P+ Z/ ^5 J$ Meither 21-hydroxylase deficiency or 11-β hydroxylase3 [. c5 |9 \9 X2 y. H
deficiency. Those diagnoses were excluded by find-
+ u1 O" \/ X7 R- K' q5 \/ |ing the normal level of adrenal steroids.
/ ^$ Q8 k$ J, G; I( b( f8 EThe diagnosis of exogenous androgens was strongly! Y. v4 {# U4 J/ {! H5 l6 C
suspected in a follow-up visit after 4 months because( J* ^3 ?% `, ~- I& o0 T
the physical examination revealed the complete disap-
* D4 \0 W6 o! i3 R8 l7 }9 p' ?pearance of pubic hair, normal growth velocity, and
0 t/ w( B9 X6 p! d* hdecreased erections. The father admitted using a testos-: g' o5 J5 H' I4 e% G- a" @
terone gel, which he concealed at first visit. He was
' t8 P: ^1 r5 f$ v0 L* gusing it rather frequently, twice a day. The Physicians’+ N5 \( r, t, y" b1 y! B
Desk Reference, or package insert of this product, gel or( l9 U7 I& T* s0 D
cream, cautions about dermal testosterone transfer to7 J" E4 L6 A0 \6 b. l
unprotected females through direct skin exposure.
0 @% ?6 g/ s; z  ?% {2 HSerum testosterone level was found to be 2 times the) \3 I( o, X6 |5 E
baseline value in those females who were exposed to) f& \4 h/ ^0 ~; [" N! H
even 15 minutes of direct skin contact with their male, H% V4 _* l, \
partners.6 However, when a shirt covered the applica-( Y- u3 a  M6 ^' N3 D4 u! q
tion site, this testosterone transfer was prevented.
+ r( D0 n# n9 B( j& V1 x# MOur patient’s testosterone level was 60 ng/mL,! \* c, A$ ?2 _  ~# T
which was clearly high. Some studies suggest that
1 p" C7 Q+ o: I/ Ddermal conversion of testosterone to dihydrotestos-
$ a9 L( ?+ `' \% }" R# N+ @terone, which is a more potent metabolite, is more3 \4 t1 {2 _1 t0 k0 G
active in young children exposed to testosterone
' T# t, L0 V5 |: F  Jexogenously7; however, we did not measure a dihy-! H1 h4 w; R0 J6 u5 j
drotestosterone level in our patient. In addition to
" I( x) V9 `! d2 z7 M' c- ~0 zvirilization, exposure to exogenous testosterone in, Q$ R4 `: R7 J
children results in an increase in growth velocity and
4 D, i( I9 x* B, O# C2 H0 [/ w  u& Kadvanced bone age, as seen in our patient.
* C; d* v# A. g3 m" `* EThe long-term effect of androgen exposure during
5 C& `( M: y% b4 S+ z: M- H% P4 Vearly childhood on pubertal development and final3 p" s6 f! p8 D  u; t" D( U
adult height are not fully known and always remain
# R: m1 l' Q7 ra concern. Children treated with short-term testos-
# {9 T2 x0 l6 z* l; ?# [7 nterone injection or topical androgen may exhibit some: F% L) R. j% [! `. ?8 G
acceleration of the skeletal maturation; however, after/ k* E  [# x4 H9 n: |
cessation of treatment, the rate of bone maturation
6 X* }4 `8 G- J! |# zdecelerates and gradually returns to normal.8,9
" [. s. E& V" z9 fThere are conflicting reports and controversy
( u" l. C* j% Z5 k2 Sover the effect of early androgen exposure on adult
; y2 u7 c. T6 r, r8 Q" rpenile length.10,11 Some reports suggest subnormal. {% n3 v: s5 }( G! b; X5 i- E
adult penile length, apparently because of downreg-
; y/ r3 j- f/ @: j4 s" F/ A$ Eulation of androgen receptor number.10,12 However,7 v) Z# t1 v) w, f
Sutherland et al13 did not find a correlation between. o1 `6 ~4 `/ P2 _& @! d7 E; _* ?
childhood testosterone exposure and reduced adult4 V2 g& d+ }6 o) s
penile length in clinical studies.0 O# n) o& s1 a7 t: C
Nonetheless, we do not believe our patient is* H( H8 E* `' F+ O! H
going to experience any of the untoward effects from1 a5 s& U& b% l# Q, `
testosterone exposure as mentioned earlier because
% I4 J+ L" b- L9 Ythe exposure was not for a prolonged period of time.
: r2 Z  y& `' e( O. XAlthough the bone age was advanced at the time of  M+ |' z# `. U2 s
diagnosis, the child had a normal growth velocity at; Q. U; J$ b1 ?  p# f2 l. q
the follow-up visit. It is hoped that his final adult! ^1 r* c9 e  G/ ], q5 @. L
height will not be affected.
( X- a5 ?8 y2 a5 BAlthough rarely reported, the widespread avail-; C! `" F5 s- W: D6 r
ability of androgen products in our society may
4 C) \2 Z1 o% K9 _/ u* {- c) c; d4 M1 Yindeed cause more virilization in male or female
# w7 e3 u* s% Ochildren than one would realize. Exposure to andro-
2 Z' n: z; G  ]9 rgen products must be considered and specific ques-# z' P  j8 h% j+ n
tioning about the use of a testosterone product or
0 K8 J, V7 U/ T+ T( X) [0 Bgel should be asked of the family members during- _3 C" c& Q6 g5 t( s8 e
the evaluation of any children who present with vir-' x1 o  ^0 [& C4 f" e
ilization or peripheral precocious puberty. The diag-
5 H( ]/ Z3 E7 t3 V5 V5 Znosis can be established by just a few tests and by
9 g2 ?* t1 T2 h% C' M0 V; `3 Happropriate history. The inability to obtain such a) x" S* E( l4 g4 i
history, or failure to ask the specific questions, may
8 P, Z4 e2 C' T. W' Iresult in extensive, unnecessary, and expensive& d' k) A/ m( o( A  {/ M
investigation. The primary care physician should be
# n( C3 L9 s1 S1 }. Taware of this fact, because most of these children
9 l6 g3 L. s$ @% f/ h1 |! Jmay initially present in their practice. The Physicians’
5 S/ g! t* c! M  _$ t0 n9 gDesk Reference and package insert should also put a
( x2 v$ S: }. w# c3 Iwarning about the virilizing effect on a male or
% d+ q" x4 H; b$ Nfemale child who might come in contact with some-
- l; a$ ~* `- E0 Y2 e* H" E) @% _* pone using any of these products.
, v0 E3 S$ t" L* [- F+ Y7 {" bReferences
& a, g( J; M0 Q+ e1 K2 F1. Styne DM. The testes: disorder of sexual differentiation
) k1 i# w! V. R& g: ?and puberty in the male. In: Sperling MA, ed. Pediatric
' z4 X0 O$ q6 @6 F" c9 J5 j3 ?# h5 J. rEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
; G0 V1 w( D2 y# f' b2002: 565-628.  g' T& K9 v3 P
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious: A- x: u+ V4 O  G8 _5 e
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old% H- F, q2 ?' Z# C
Boy Induced by Indirect Topical
- u2 s+ ]0 g) o2 ^  H6 TExposure to Testosterone
# |( G0 k/ u: H7 r  I  z, ]Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
& g  m( _& S5 p1 P/ B8 f- wand Kenneth R. Rettig, MD1& p/ H; _! h$ b* f) O$ [- g
Clinical Pediatrics
2 p. }. X- l/ Z* a1 K9 U7 ZVolume 46 Number 67 v* e5 ]0 G( J$ H" d% f; n
July 2007 540-543) R  `" B( G  X
© 2007 Sage Publications6 {% m8 u1 f6 w* P" Y7 W
10.1177/0009922806296651( {8 _1 ^! r; h/ o5 i; i
http://clp.sagepub.com
3 I, ]6 U5 n% m0 f5 R4 uhosted at
) u1 s! i4 S7 Y2 ?http://online.sagepub.com
$ @9 w1 Z# h$ J" G" U3 b' B) `Precocious puberty in boys, central or peripheral,' }! ~. D, h; W% \0 b  G; N
is a significant concern for physicians. Central
5 }9 p' f, j. @) M2 eprecocious puberty (CPP), which is mediated+ }" n0 Y; S( R# n' k
through the hypothalamic pituitary gonadal axis, has- S6 D  R, u, }
a higher incidence of organic central nervous system
: I. Z7 }- {% K! Tlesions in boys.1,2 Virilization in boys, as manifested
5 J' I  Q, A. k/ W. `by enlargement of the penis, development of pubic
9 j' k5 [2 d! h; A# Y0 Bhair, and facial acne without enlargement of testi-
; d' q1 p. C! X) g2 Gcles, suggests peripheral or pseudopuberty.1-3 We
4 D) B! C- F4 z; [0 h( e$ creport a 16-month-old boy who presented with the) k2 y5 X: P6 A- k* I
enlargement of the phallus and pubic hair develop-* a+ N1 ]# a7 c
ment without testicular enlargement, which was due
0 k  ~+ h2 ?% y1 t2 ito the unintentional exposure to androgen gel used by
, y; v3 E1 o% y( s- }! Qthe father. The family initially concealed this infor-/ ?/ G3 F7 V0 [0 l" j& }0 R& g
mation, resulting in an extensive work-up for this
1 b- D4 v) o, q( q+ p' M/ j; e/ r3 Echild. Given the widespread and easy availability of# q# X9 Y$ n- z# b( P0 S
testosterone gel and cream, we believe this is proba-
1 y' A7 P4 M0 B+ l# {bly more common than the rare case report in the
5 v" O' o$ o+ V0 Y8 Z; _. Sliterature.4( Y+ N: H$ y7 i% b( J+ I5 C
Patient Report$ E) x9 ]7 q4 s; j: X9 e  `
A 16-month-old white child was referred to the
7 j+ b, R5 m0 ?2 n# X) Lendocrine clinic by his pediatrician with the concern0 e' a  W# P# X1 t6 P! C1 t
of early sexual development. His mother noticed
" B/ O7 f0 O' A! h3 k8 i, g% A# ~light colored pubic hair development when he was6 m5 g# j4 V1 k
From the 1Division of Pediatric Endocrinology, 2University of" ~/ {% y& ^4 T; z* c; {7 t' Y
South Alabama Medical Center, Mobile, Alabama.8 `. z3 D) b- f2 Z  X1 o
Address correspondence to: Samar K. Bhowmick, MD, FACE,' Z$ O# j4 B, g8 }* M5 d, ~. X
Professor of Pediatrics, University of South Alabama, College of
$ P% @4 N# o# e/ o8 HMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;1 N2 X* P+ V2 h4 f  e
e-mail: [email protected].5 H& Z4 u4 w3 s0 @7 U2 W
about 6 to 7 months old, which progressively became/ d' ]# c1 g  N& F0 @) Z8 G( G
darker. She was also concerned about the enlarge-% [' e# C* C3 [. Z+ j( l9 b& v5 V
ment of his penis and frequent erections. The child3 e' ]0 G/ W$ \8 m" `, i
was the product of a full-term normal delivery, with
6 \& Z* |8 _2 ?, I$ X) v3 U9 T! x0 ja birth weight of 7 lb 14 oz, and birth length of
$ B! x  T" V. o, v  j20 inches. He was breast-fed throughout the first year
5 w1 T$ M) u9 Tof life and was still receiving breast milk along with
( j2 T; C8 ~8 U; `% }7 Zsolid food. He had no hospitalizations or surgery,! [% [. T- I9 C. _1 z8 Y, r
and his psychosocial and psychomotor development7 g6 {4 v. W) V. o
was age appropriate.* j( J$ i' L5 Q
The family history was remarkable for the father,$ t# K- K3 F9 g, u3 P# E: e5 a
who was diagnosed with hypothyroidism at age 16,
; a5 I* I: I" Z( Pwhich was treated with thyroxine. The father’s
. A8 e. _8 X3 I; w5 q/ I: pheight was 6 feet, and he went through a somewhat
6 s$ i" ~: k5 m1 W7 f) p3 I) aearly puberty and had stopped growing by age 14.
8 _& E& s4 N; m, ?0 rThe father denied taking any other medication. The
2 k/ X% v( q2 {3 y: m* Cchild’s mother was in good health. Her menarche
) D4 O/ c8 b$ B# o0 Jwas at 11 years of age, and her height was at 5 feet
2 f1 M7 o6 a6 y! h, m! q5 inches. There was no other family history of pre-& C9 Q0 O; r1 {0 d5 \
cocious sexual development in the first-degree rela-
4 g  i( P8 l* J* w8 e/ Jtives. There were no siblings.# B" `7 C% V, R5 t! F
Physical Examination- K' C) d, ~* W6 n6 y
The physical examination revealed a very active,6 J- z3 v  H4 p5 a7 C. w6 J/ G
playful, and healthy boy. The vital signs documented
9 L3 j$ W' `" Z8 va blood pressure of 85/50 mm Hg, his length was
9 |  t: c$ d% H4 n4 e: C90 cm (>97th percentile), and his weight was 14.4 kg+ ?+ G( K: W% t9 v
(also >97th percentile). The observed yearly growth
) e% @2 g5 K: j. F# svelocity was 30 cm (12 inches). The examination of, [6 b. f' {6 i  g! X
the neck revealed no thyroid enlargement.
/ E3 o9 d/ U  Y/ }% EThe genitourinary examination was remarkable for% j. U. w/ J; U* s
enlargement of the penis, with a stretched length of7 p2 k6 i( T# G6 ?, z
8 cm and a width of 2 cm. The glans penis was very well
3 o2 ?# e3 t' z& ~developed. The pubic hair was Tanner II, mostly around
! r: ]7 _6 z8 l  l0 J; L5403 h3 }6 `2 t* U
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from: B% x* M7 c  V7 [
the base of the phallus and was dark and curled. The, x* m7 b0 @( F
testicular volume was prepubertal at 2 mL each.
5 @$ n, C: N5 B/ P8 |The skin was moist and smooth and somewhat
' L6 j( ?# I$ _: }oily. No axillary hair was noted. There were no3 W2 \- x8 X- r8 c
abnormal skin pigmentations or café-au-lait spots.
- t6 o$ w' t# R) N- J1 o( o) |Neurologic evaluation showed deep tendon reflex 2+
! p2 B, F% m4 ?+ X7 D" ebilateral and symmetrical. There was no suggestion& F1 _0 j( i; U
of papilledema.$ }: ]/ @5 d/ F& ^4 C
Laboratory Evaluation
. N. I3 y# x; v' ^: XThe bone age was consistent with 28 months by
& \& a/ ]6 {9 iusing the standard of Greulich and Pyle at a chrono-, M2 z# b8 l+ ?+ L, a5 a
logic age of 16 months (advanced).5 Chromosomal6 t2 P' \4 @+ i% V3 @6 f
karyotype was 46XY. The thyroid function test
2 N) Y' }" \1 \; t7 Nshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
! }0 `4 E4 P. j: g! N0 E5 X1 R% Mlating hormone level was 1.3 µIU/mL (both normal).
9 B' ~+ w5 {" l2 U6 |) iThe concentrations of serum electrolytes, blood0 j0 w8 [/ L8 C6 R' X
urea nitrogen, creatinine, and calcium all were9 ^9 G' A" T) j# f2 g* }
within normal range for his age. The concentration
- G! r, {1 d: ~3 Eof serum 17-hydroxyprogesterone was 16 ng/dL9 `+ r+ e# N0 L( B$ a
(normal, 3 to 90 ng/dL), androstenedione was 205 {* N0 m+ U% g2 @
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
' [5 Y8 q* j0 R1 K4 |terone was 38 ng/dL (normal, 50 to 760 ng/dL),( O  Z; i0 c7 b( x- @3 s' i
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
$ T# k  i$ i7 P* w; w5 @- H; h49ng/dL), 11-desoxycortisol (specific compound S)
2 ^4 d& _( h: F4 A" e6 Swas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
8 A/ q. _$ `* F0 i  Ctisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total2 k4 k, R1 g  a: F+ ?* L( r+ @
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),5 r1 g8 Y, j; v! T5 H2 s
and β-human chorionic gonadotropin was less than* K+ p# O3 x: ~/ ^" x
5 mIU/mL (normal <5 mIU/mL). Serum follicular; p" @6 }9 d0 T, X
stimulating hormone and leuteinizing hormone
) p, X7 Y* y4 z  x8 G7 Zconcentrations were less than 0.05 mIU/mL2 m9 o/ [" F7 f2 [& O" a2 E- ]  U
(prepubertal).
8 ~2 t3 L0 F5 D' q1 iThe parents were notified about the laboratory
8 ]! ^9 o9 A8 s: F2 eresults and were informed that all of the tests were+ l! v6 o5 o. H2 I' G" Z
normal except the testosterone level was high. The
/ k  b8 T. _; t/ J* p2 w' _' ifollow-up visit was arranged within a few weeks to7 s) o3 L! i, J% ]$ Q
obtain testicular and abdominal sonograms; how-( b$ X9 r4 u& b* _
ever, the family did not return for 4 months.
2 h7 O: r  a& n2 C  b7 }Physical examination at this time revealed that the
5 I5 Q1 @4 w' l  g1 nchild had grown 2.5 cm in 4 months and had gained+ L% G' V' n6 i' b1 ?
2 kg of weight. Physical examination remained
) U& b) j2 H' M% zunchanged. Surprisingly, the pubic hair almost com-1 E2 w- @  v9 p' q
pletely disappeared except for a few vellous hairs at
6 I$ e3 f( O; P1 Fthe base of the phallus. Testicular volume was still 2* K, V+ B$ F6 x0 r( {* X
mL, and the size of the penis remained unchanged.
$ W( {: s3 C7 q. z! R% w  a  v+ FThe mother also said that the boy was no longer hav-
8 P2 h4 f1 J; H+ a+ g: Aing frequent erections.6 o* n; {: w, x6 Z. h" v
Both parents were again questioned about use of! A# q# J: E/ j3 R- y
any ointment/creams that they may have applied to
& l. K8 x) D% r- E1 m2 Ethe child’s skin. This time the father admitted the& U; X. f1 _1 `! Z+ e4 t
Topical Testosterone Exposure / Bhowmick et al 541+ X7 ]+ [0 k8 l; E* N3 l1 n3 E$ D, {. ]
use of testosterone gel twice daily that he was apply-
: C+ s9 P( a) u2 r9 U/ Aing over his own shoulders, chest, and back area for
8 |9 X- S  X) ]. O+ }% \a year. The father also revealed he was embarrassed* }$ J8 A# M  \; V' |
to disclose that he was using a testosterone gel pre-
# J3 z% D8 T9 _* A& zscribed by his family physician for decreased libido' X( ?0 C/ f+ ^% E% d, M' x8 H/ ]
secondary to depression.& \% h+ f3 F; W
The child slept in the same bed with parents.
/ _8 b+ K( x7 H$ tThe father would hug the baby and hold him on his; w$ _1 N/ u  c& J& B( o
chest for a considerable period of time, causing sig-
* O1 g) H4 U$ U( l( D* Rnificant bare skin contact between baby and father.
1 Q5 V/ f7 i" ^0 g9 S& k3 @The father also admitted that after the phone call,
. g$ q  @9 x' j$ n! Y5 Ewhen he learned the testosterone level in the baby2 _8 E' g0 X  j+ i7 Y5 I
was high, he then read the product information
* ~! d3 v4 K; G+ P+ i1 [& k% Tpacket and concluded that it was most likely the rea-
$ j1 W5 h' Q* }0 F/ pson for the child’s virilization. At that time, they
% b/ ^5 I& \; k6 Q0 N+ Q  zdecided to put the baby in a separate bed, and the
$ D: W: i8 Z* Cfather was not hugging him with bare skin and had
) o. `  I8 [7 hbeen using protective clothing. A repeat testosterone
' W2 x4 P* j9 `/ N# I! Q; Qtest was ordered, but the family did not go to the
3 ?& H1 ?# E$ j0 Z' llaboratory to obtain the test.
) V2 ^7 Q1 F% d! O2 _% G) ^5 qDiscussion
' g8 n( f: o8 l! lPrecocious puberty in boys is defined as secondary
5 K7 m1 {1 _  s/ _sexual development before 9 years of age.1,4
) n& m7 s  p4 X3 h! d! uPrecocious puberty is termed as central (true) when/ c3 j" K2 R; [$ _5 h# ?6 A# b
it is caused by the premature activation of hypo-
7 a  h/ n, J$ e  d, h1 Lthalamic pituitary gonadal axis. CPP is more com-
) b9 X( N& D; P' z( q( d# Nmon in girls than in boys.1,3 Most boys with CPP, B$ e- t% U  Y1 n
may have a central nervous system lesion that is
" Y  D, P+ w3 M& n- Hresponsible for the early activation of the hypothal-" z# m- u; F; G2 m. K4 h
amic pituitary gonadal axis.1-3 Thus, greater empha-2 ~" j( S4 Z8 g& d: T8 C7 n
sis has been given to neuroradiologic imaging in
: T+ d# z) T& B; ]# {- \( q6 Oboys with precocious puberty. In addition to viril-/ y( U% C1 c2 Y5 W$ G
ization, the clinical hallmark of CPP is the symmet-
. S  a3 ^* N' \" a! Z8 ~6 J/ A% [rical testicular growth secondary to stimulation by
9 `/ L- e; a& H1 W  _+ Sgonadotropins.1,3
4 o  i! z& Y* ?! K& e7 lGonadotropin-independent peripheral preco-+ W7 j& P, x, Z8 o+ r# D
cious puberty in boys also results from inappropriate
( D9 f% @5 F5 n7 _% F! iandrogenic stimulation from either endogenous or
0 ^) q+ J- a, w" i9 f& V+ \exogenous sources, nonpituitary gonadotropin stim-+ b# i0 d* e$ ]1 R( P1 N9 `
ulation, and rare activating mutations.3 Virilizing
2 e8 f6 v. E" n3 X: V4 g: n0 scongenital adrenal hyperplasia producing excessive* C; F* I' h' z: W! z7 x9 d0 `4 N
adrenal androgens is a common cause of precocious
' J" H! t5 q9 X; ~( c7 T7 Upuberty in boys.3,4
5 E  n: @" E) e5 a, BThe most common form of congenital adrenal
' l9 y' G2 ^# v4 l6 n- r9 ~hyperplasia is the 21-hydroxylase enzyme deficiency.
- U: e2 M. ?- x$ x4 [) hThe 11-β hydroxylase deficiency may also result in
' U1 `2 @9 ^5 Z0 u4 `excessive adrenal androgen production, and rarely," V0 I1 R" _8 w
an adrenal tumor may also cause adrenal androgen
! S2 y9 s8 Y) K0 y5 _% l; Sexcess.1,3- m# V& T$ U+ U0 p) l
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
! }  ?; L1 o3 O* k  {542 Clinical Pediatrics / Vol. 46, No. 6, July 2007$ u/ Z- G' h- c9 s; N/ o" u1 p; O
A unique entity of male-limited gonadotropin-
; ~, n, |1 W6 R3 Q6 `. Windependent precocious puberty, which is also known7 \& L6 |$ E2 C0 p. v/ ?; H; `" j
as testotoxicosis, may cause precocious puberty at a& n8 }' x+ L  G$ L8 W5 h
very young age. The physical findings in these boys# |! U1 f  `) n0 n
with this disorder are full pubertal development,
/ G7 J* _4 P$ Y  p: d$ ?; E4 k; _( m0 Kincluding bilateral testicular growth, similar to boys
7 B, S: O' A4 M+ }$ i( V6 ywith CPP. The gonadotropin levels in this disorder" d0 i3 w+ H5 q2 _+ a
are suppressed to prepubertal levels and do not show- ]2 q, |& Q* M  j
pubertal response of gonadotropin after gonadotropin-# k+ H( T' \+ V% o0 A( M  G5 N  m% v% ^
releasing hormone stimulation. This is a sex-linked4 G/ ]6 G0 q5 ^7 {5 y
autosomal dominant disorder that affects only+ k* H  N+ G0 {8 Y- K6 {
males; therefore, other male members of the family0 K' Q9 [- |- f0 E
may have similar precocious puberty.35 L1 P5 H/ z. E. h; R3 X
In our patient, physical examination was incon-5 y5 H& f* F8 V& E. ~
sistent with true precocious puberty since his testi-
, S/ F; p# B4 N( \6 w- T$ `cles were prepubertal in size. However, testotoxicosis- T6 Q5 R6 p. M
was in the differential diagnosis because his father
2 m0 _# L. Q, Wstarted puberty somewhat early, and occasionally,- @2 A+ e3 V3 I8 A0 D
testicular enlargement is not that evident in the# `/ X  N0 R$ P: U3 ]* v# U
beginning of this process.1 In the absence of a neg-% k$ @4 U7 w; ^% V) F
ative initial history of androgen exposure, our
8 h3 b" v1 v+ w9 L, r6 Q9 Vbiggest concern was virilizing adrenal hyperplasia,
# N! @& r/ u0 l3 [2 ceither 21-hydroxylase deficiency or 11-β hydroxylase
* n4 |! }2 e& ddeficiency. Those diagnoses were excluded by find-$ @' j, ^5 s' T/ F
ing the normal level of adrenal steroids.
( N; Q' S+ Y0 B9 Y/ f* I) |3 XThe diagnosis of exogenous androgens was strongly
9 }6 L- j4 ]) ^" ^3 M( n( Zsuspected in a follow-up visit after 4 months because$ z$ g5 F$ S/ v: J! [
the physical examination revealed the complete disap-
4 [" x. i1 ?9 ?) P, s6 e+ K  e% `6 vpearance of pubic hair, normal growth velocity, and
9 k/ P; f- e" n2 Gdecreased erections. The father admitted using a testos-
7 x3 q+ @2 L! M; aterone gel, which he concealed at first visit. He was
# D  ?4 E# Y! V7 l4 t, Xusing it rather frequently, twice a day. The Physicians’
) r: |3 u* f/ o; l% ]Desk Reference, or package insert of this product, gel or
* T) @! u% _* S$ Qcream, cautions about dermal testosterone transfer to/ g( V- g- Q! j3 I0 U9 K( I
unprotected females through direct skin exposure.
) N0 Q% F1 T$ \+ {* v3 VSerum testosterone level was found to be 2 times the
+ |3 `; l- t& W: H& l. ?5 l: ybaseline value in those females who were exposed to
0 _9 a) Z8 k6 m2 e  deven 15 minutes of direct skin contact with their male
, K9 ~; n$ p1 F' X- `  q$ Ppartners.6 However, when a shirt covered the applica-
1 p* n; |- t( a) h7 Q, Rtion site, this testosterone transfer was prevented.
7 R: Y$ z' i% b* bOur patient’s testosterone level was 60 ng/mL,
3 z: ^& r! |& H, L1 vwhich was clearly high. Some studies suggest that: i: f3 k' u  K4 _4 E) [2 b, L
dermal conversion of testosterone to dihydrotestos-2 c- f: T4 b0 k, A! F
terone, which is a more potent metabolite, is more
  e6 l2 H; l1 _) x4 p( z( Factive in young children exposed to testosterone
+ i( ^6 K7 P5 o9 hexogenously7; however, we did not measure a dihy-
" S) v( B9 Q6 n) jdrotestosterone level in our patient. In addition to
( n# r" f7 I  a) s4 r8 l# d: uvirilization, exposure to exogenous testosterone in
9 {8 O7 P$ p: Z3 J! Uchildren results in an increase in growth velocity and
5 i& P8 X$ x8 z& _advanced bone age, as seen in our patient.; j3 ?9 \: g$ S1 ~  e; J! j
The long-term effect of androgen exposure during  ~8 V# l, D- E0 {) b
early childhood on pubertal development and final) o! Q, P. l2 B8 \4 n; \
adult height are not fully known and always remain
2 y7 p# F9 A! _) ^: Fa concern. Children treated with short-term testos-, s) E3 D$ q# D2 Q6 y: R
terone injection or topical androgen may exhibit some
: B8 S% w) O0 A0 z0 q$ Cacceleration of the skeletal maturation; however, after
0 N* o8 |. J& \  s, Ncessation of treatment, the rate of bone maturation8 x" N8 e2 D* U& {: W
decelerates and gradually returns to normal.8,9
. ~- F% n6 L# X6 r- _) H" E- f* RThere are conflicting reports and controversy
$ v9 U8 r- C2 _5 P9 x0 aover the effect of early androgen exposure on adult
" A* y9 U7 [7 X+ q4 v8 J% jpenile length.10,11 Some reports suggest subnormal9 B) x7 v! @" p% ^, Z0 h) `
adult penile length, apparently because of downreg-" w  X! T& S; }* B
ulation of androgen receptor number.10,12 However,
; y) z8 W6 Q5 W; H( tSutherland et al13 did not find a correlation between
' U# q, q. C+ Q& [' R9 D8 |childhood testosterone exposure and reduced adult) z! M$ V, f. f; Z
penile length in clinical studies.4 I& ^6 y/ J% |# M8 P
Nonetheless, we do not believe our patient is& R& r7 C# n+ v
going to experience any of the untoward effects from
1 I- B3 u6 o. u0 k2 p8 O) Btestosterone exposure as mentioned earlier because" v  `# A5 F' c+ t0 ~
the exposure was not for a prolonged period of time.  F: B% n! k. h$ U
Although the bone age was advanced at the time of
0 w# M) ~5 J1 m9 x9 w# ldiagnosis, the child had a normal growth velocity at' i# B& y' R; t
the follow-up visit. It is hoped that his final adult* D$ v+ G4 P% x; L
height will not be affected.
# g8 m) y% h  C1 Y- C& X5 ?% rAlthough rarely reported, the widespread avail-  c$ `0 e3 V1 C# e6 ?2 V
ability of androgen products in our society may, R  h, [3 v5 }2 ^0 {
indeed cause more virilization in male or female/ w0 F7 ?& }( ]1 S3 \5 L! y
children than one would realize. Exposure to andro-4 ?# I3 B8 v2 y/ c: `* L) R5 K% K
gen products must be considered and specific ques-) |  c8 [; K* s: M3 A
tioning about the use of a testosterone product or8 y. V% S) f: j1 I' g' L+ r. |4 r
gel should be asked of the family members during6 h# }2 e1 p4 Z2 m
the evaluation of any children who present with vir-
3 w5 e, K7 W1 X: |ilization or peripheral precocious puberty. The diag-
7 F: q( u3 P, }8 gnosis can be established by just a few tests and by: l- R* l( f/ I7 ?, j
appropriate history. The inability to obtain such a
& t& O  f) |1 ?, _history, or failure to ask the specific questions, may
2 f" {7 J7 v* n) H* F! Xresult in extensive, unnecessary, and expensive
* H7 c( i! V4 P0 ?5 q  r& [/ N+ yinvestigation. The primary care physician should be4 r( N3 H# Z% S6 c4 S, Z$ u" V
aware of this fact, because most of these children
( y- m* v" j3 a- Ymay initially present in their practice. The Physicians’# q) N( v; ~  P
Desk Reference and package insert should also put a
" F. ?1 J$ ^) X, I4 f& b  P* Bwarning about the virilizing effect on a male or7 Y# v' ^2 R4 X0 f$ _
female child who might come in contact with some-$ y! P" c' s  R  X- N
one using any of these products.
8 r& ]- r5 S" s2 I6 QReferences! \. B8 Z/ o/ [; ]- K. z
1. Styne DM. The testes: disorder of sexual differentiation
( w. K4 Y2 {( v6 y+ j% Aand puberty in the male. In: Sperling MA, ed. Pediatric( P# w- S1 a+ ~1 n5 T
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
3 ?4 U7 m+ e  l9 f1 u# q: @2002: 565-628.
( F' h3 _! k9 d# y5 T+ i2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious1 o9 F- ?* l5 J: F
puberty in children with tumours of the suprasellar pineal
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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
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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
' Z9 A# G5 x0 @& e* A) u
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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