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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' h4 {) L7 ?8 e( ~
Boy Induced by Indirect Topical
) S+ y- J% ?* c- c" _0 YExposure to Testosterone
, x) ~% A4 p( q% G8 V6 QSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
- H. f- N' P" P- land Kenneth R. Rettig, MD1) U- m! L1 t& m. b/ r, Q
Clinical Pediatrics; `8 x: p2 W: b$ z8 K( s
Volume 46 Number 6
$ [/ C* N# T' {July 2007 540-543
( r0 q( R2 P0 M( ]© 2007 Sage Publications6 m- {- _% [6 g; I; ~% `  {, y
10.1177/00099228062966516 q9 h# U  K# _5 c
http://clp.sagepub.com% E4 t+ |0 x7 v+ v( o, p( c7 w
hosted at5 N/ \0 b  @1 M' h3 D$ W" \
http://online.sagepub.com9 o" q; I* x( x, H/ ?
Precocious puberty in boys, central or peripheral,. D8 J/ u3 w) o' N
is a significant concern for physicians. Central7 _' M  R# v5 T, U
precocious puberty (CPP), which is mediated+ ~4 }+ m. d: g+ S% N& {3 t
through the hypothalamic pituitary gonadal axis, has2 {4 W4 v$ }) n* _1 X5 T
a higher incidence of organic central nervous system2 r0 Z; v( ?. z
lesions in boys.1,2 Virilization in boys, as manifested: \1 b- Y8 n0 d" l% p) N
by enlargement of the penis, development of pubic: t+ I, ^: j1 G  h5 T# }* N
hair, and facial acne without enlargement of testi-
$ O" n* @* u, A6 y* Y2 lcles, suggests peripheral or pseudopuberty.1-3 We
0 O1 H% {# g, S2 Z8 w: z1 Xreport a 16-month-old boy who presented with the
' T: C5 l0 O" G5 y" Q2 }0 Kenlargement of the phallus and pubic hair develop-3 p% x8 C) g; _
ment without testicular enlargement, which was due0 P3 }0 ]: ?7 Q! l% ~! j
to the unintentional exposure to androgen gel used by0 [; w6 c, B, M& s- K& B
the father. The family initially concealed this infor-
! n- L& S6 S% bmation, resulting in an extensive work-up for this7 [1 q0 P7 j! j& ]* ]" J
child. Given the widespread and easy availability of# q" W3 i! @$ m# I) u, W
testosterone gel and cream, we believe this is proba-$ k1 g8 t" M! c8 h. Y7 Z
bly more common than the rare case report in the
& n; T9 X) k( H2 [" r& D1 Mliterature.4
8 P3 i. ~' x6 }6 `Patient Report( z8 |8 }; x( N( c* O4 h
A 16-month-old white child was referred to the/ d3 S( Y5 z( h' `/ ~0 V2 G
endocrine clinic by his pediatrician with the concern
8 ^6 g6 E0 H7 H$ J/ ~of early sexual development. His mother noticed" O6 x6 a% m6 C0 o7 ]
light colored pubic hair development when he was! e+ v5 _1 W- V8 u* ~9 ^& O
From the 1Division of Pediatric Endocrinology, 2University of0 F$ |& w: C) K8 ~
South Alabama Medical Center, Mobile, Alabama.
2 W9 ^/ l# x* j8 L, a8 V- x9 dAddress correspondence to: Samar K. Bhowmick, MD, FACE,
0 i  N# D9 k9 s* J7 ]Professor of Pediatrics, University of South Alabama, College of+ S/ ?: V5 _, \1 i
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
0 w* q. Q1 w; P' k' z$ Ue-mail: [email protected].
0 E5 a3 N1 V% [* X. q# J1 [about 6 to 7 months old, which progressively became
$ u( E* Z$ p! rdarker. She was also concerned about the enlarge-
( D. B8 }- ^: E/ M- bment of his penis and frequent erections. The child
* j; \! q" \. o' g' Twas the product of a full-term normal delivery, with: ^% P8 G7 c0 r) H0 c7 Q+ P7 a
a birth weight of 7 lb 14 oz, and birth length of
: B' L2 r  [  A; z% z9 Z20 inches. He was breast-fed throughout the first year
8 y) x8 j1 p6 d7 U  ?0 }of life and was still receiving breast milk along with0 w1 g' X+ J5 q/ N3 h: y5 [
solid food. He had no hospitalizations or surgery,, Y: E# ~5 L1 U& N4 _
and his psychosocial and psychomotor development
; ?+ D% T; w0 y  u$ H% Owas age appropriate.0 _) ~+ u4 k, k3 X- r
The family history was remarkable for the father,
5 M2 N! K  x- O& L0 Vwho was diagnosed with hypothyroidism at age 16,( F0 |& K8 O0 ]
which was treated with thyroxine. The father’s% }- y# N  m7 o) g3 v
height was 6 feet, and he went through a somewhat
9 f8 B+ ^$ `5 P  Bearly puberty and had stopped growing by age 14.
+ K, I; _$ f0 P4 m5 gThe father denied taking any other medication. The
' M9 @* q) }. [! m/ ^child’s mother was in good health. Her menarche1 J4 w/ x' f- G0 @% d- Q
was at 11 years of age, and her height was at 5 feet# @7 r  m9 r  n
5 inches. There was no other family history of pre-
$ A, e: n$ b- ycocious sexual development in the first-degree rela-5 R: Z4 U7 q; m1 U
tives. There were no siblings.4 S" S; k; d6 g! w
Physical Examination
/ M1 N/ J- _- Q* w6 kThe physical examination revealed a very active,
" y2 b! p$ [1 Q! Jplayful, and healthy boy. The vital signs documented8 H. I( W, @$ N
a blood pressure of 85/50 mm Hg, his length was
" k) o( `8 r/ W, v5 \90 cm (>97th percentile), and his weight was 14.4 kg
7 d+ U( K' z% Z: b' U% I(also >97th percentile). The observed yearly growth/ Y; f; i9 G( q- n
velocity was 30 cm (12 inches). The examination of% a7 W  K' b. F9 Y$ S" F) t1 ^" A( s
the neck revealed no thyroid enlargement.( D! b6 \! j# T7 P: R7 i$ ^, q
The genitourinary examination was remarkable for
/ y9 ^8 q( ~# `  Xenlargement of the penis, with a stretched length of
" m3 l, d' [5 M  q8 cm and a width of 2 cm. The glans penis was very well8 s6 {2 B' M3 y8 h
developed. The pubic hair was Tanner II, mostly around/ e- X; u2 C: R. Z5 X; a
540$ v+ x2 V* p7 c2 A& \. q! e( L
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
2 R8 I0 @% U  s. v/ Z3 C! l& Athe base of the phallus and was dark and curled. The
6 O( a0 s" f) F: f- xtesticular volume was prepubertal at 2 mL each.3 ]% l, B6 F! g1 D# v
The skin was moist and smooth and somewhat
) `2 z% U6 }0 \5 {3 b% }oily. No axillary hair was noted. There were no
" E6 p5 L, d3 z8 n# Y1 rabnormal skin pigmentations or café-au-lait spots.( B6 n, M( o. T) ~. t$ E
Neurologic evaluation showed deep tendon reflex 2+
  I  W! I: o  @, ?bilateral and symmetrical. There was no suggestion9 R4 m1 p9 s2 ~
of papilledema.
3 i: h5 F; g# }" J- E/ n, ALaboratory Evaluation
# n; Q; T. b. h& zThe bone age was consistent with 28 months by8 R+ M2 `1 X, \- ~- ]; C/ Q
using the standard of Greulich and Pyle at a chrono-
8 ~4 d8 T* x6 _$ p( h- s. T' `% {logic age of 16 months (advanced).5 Chromosomal
& s7 ]3 F; l9 W* vkaryotype was 46XY. The thyroid function test6 n$ \, k, x' o+ T
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
( U3 L0 J. l! w' E" [2 alating hormone level was 1.3 µIU/mL (both normal).
9 X8 K% @, i+ N* l- c7 C2 qThe concentrations of serum electrolytes, blood
- j3 h9 C$ y' M5 K4 D1 _+ K3 {urea nitrogen, creatinine, and calcium all were
0 F! P2 M' X- F% b% S; hwithin normal range for his age. The concentration
- u9 }* C- V7 L7 ]8 K' oof serum 17-hydroxyprogesterone was 16 ng/dL  \( M( k$ x# A  ]6 {
(normal, 3 to 90 ng/dL), androstenedione was 20% \* E: V) _8 K& e
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-; X* R' R1 z+ y
terone was 38 ng/dL (normal, 50 to 760 ng/dL),+ T2 G; i: Z6 [$ Q/ S
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
! H- ~8 B% w" g* D4 o" v49ng/dL), 11-desoxycortisol (specific compound S)! R) y' P- ?+ D' S" r) v
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-: J. |4 |$ _' @- \0 p1 W2 `# {2 l9 c0 K
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
* X% ^; _2 f" ^# Atestosterone was 60 ng/dL (normal <3 to 10 ng/dL),) z8 T! i% O5 V, P, ~' }6 a. n2 q- u2 z
and β-human chorionic gonadotropin was less than2 q6 ~$ r  q8 x: A! ^/ ]  k) u: ~
5 mIU/mL (normal <5 mIU/mL). Serum follicular
! {; m- ~1 M6 W/ b; C" U* Fstimulating hormone and leuteinizing hormone
+ E4 q1 q6 X* R3 W# d2 q0 iconcentrations were less than 0.05 mIU/mL
  m$ b% w8 D) I% e5 E(prepubertal).
' D3 S& X3 Q: |) W. r; jThe parents were notified about the laboratory# Q4 A  U3 M- b  Y( L4 _2 K
results and were informed that all of the tests were
: p- ]7 K$ m1 ^normal except the testosterone level was high. The
5 c; U& z. z4 \1 a4 afollow-up visit was arranged within a few weeks to% H0 `9 N( s& h) i# `
obtain testicular and abdominal sonograms; how-
' H; `1 u5 Y  b' Hever, the family did not return for 4 months.( z! l( B; H  V3 {! c7 [& p/ ^+ o
Physical examination at this time revealed that the1 j1 }* T: G4 S- f( J( X- H
child had grown 2.5 cm in 4 months and had gained
5 M# ]: |, x. S- |. d2 kg of weight. Physical examination remained  I/ F2 m4 P# K7 @9 G
unchanged. Surprisingly, the pubic hair almost com-! q2 _% z+ ^# f
pletely disappeared except for a few vellous hairs at# u" [1 P4 O1 {  S) E! Q' @* n
the base of the phallus. Testicular volume was still 2$ C4 k/ r7 c' L* C
mL, and the size of the penis remained unchanged.
1 Z" c0 n/ n. i" P* dThe mother also said that the boy was no longer hav-% e* s, m8 \2 r0 w% z8 }
ing frequent erections.
# U+ u- R) |6 N7 i  @8 [Both parents were again questioned about use of
4 _# e. K! e- ^+ gany ointment/creams that they may have applied to
; v& Z% i% @- ]4 a$ J4 ?0 Xthe child’s skin. This time the father admitted the3 C+ t. H$ K3 Y- T  m" x# {
Topical Testosterone Exposure / Bhowmick et al 541( ?' m2 G: p7 [, ?* j" ]5 \8 p0 s6 _
use of testosterone gel twice daily that he was apply-
! L; r* n$ t; c  Y8 I$ king over his own shoulders, chest, and back area for
6 i: D, T4 A2 |" j: a0 ?- L4 V/ V# ia year. The father also revealed he was embarrassed7 j: R  Q3 P( z( i  _) Q
to disclose that he was using a testosterone gel pre-
$ F2 l: d: f$ v7 D: kscribed by his family physician for decreased libido
) N. }1 ^. G. _6 ^& f- T0 zsecondary to depression.; J/ `: F# Q. U6 h) m4 B
The child slept in the same bed with parents.6 `/ ^& U9 V: n8 |
The father would hug the baby and hold him on his: p5 t4 o+ B: j1 q+ a8 {/ ]" r
chest for a considerable period of time, causing sig-
& d; h" e- _  \2 a0 u, dnificant bare skin contact between baby and father.4 Q% h! U8 t" b" U% W. G
The father also admitted that after the phone call,- u  g2 R* I4 M# N0 o1 l
when he learned the testosterone level in the baby- Y; M/ x/ |# j" X
was high, he then read the product information3 N( ^) F# H* ]) C; _
packet and concluded that it was most likely the rea-$ u3 p$ w! [) e9 j  b
son for the child’s virilization. At that time, they
+ Z; Y3 b- R) d4 b/ `decided to put the baby in a separate bed, and the
- r( ~6 c; C$ z4 ]father was not hugging him with bare skin and had
0 E4 P% W+ i/ N8 Y* `. m  c3 n- R/ Xbeen using protective clothing. A repeat testosterone9 u% q. c* k- _+ G
test was ordered, but the family did not go to the0 t+ o" m$ l5 M& r. Y
laboratory to obtain the test.
* V2 u6 e  p" \4 S. v/ {Discussion
* }/ T# r- X, A7 y) Z0 X& g2 `Precocious puberty in boys is defined as secondary
1 B$ K- H. a( p; ~& ksexual development before 9 years of age.1,41 O3 d6 {& G' o( q9 {4 O; ~3 b
Precocious puberty is termed as central (true) when. C+ `5 I/ J. Z9 P/ e
it is caused by the premature activation of hypo-: }6 g4 l, i2 E$ t) _, ~
thalamic pituitary gonadal axis. CPP is more com-
/ `9 h- P( {5 umon in girls than in boys.1,3 Most boys with CPP
3 x, V1 D2 K* N4 Vmay have a central nervous system lesion that is
( Z0 \! E+ s$ y- }responsible for the early activation of the hypothal-" p8 ]: j9 {' G4 ?* w2 o* {$ k  [
amic pituitary gonadal axis.1-3 Thus, greater empha-
) |; i8 ^  L1 psis has been given to neuroradiologic imaging in6 {! R# ?1 O  v
boys with precocious puberty. In addition to viril-
2 h, g% k6 k# {) N4 [" A5 ?7 Dization, the clinical hallmark of CPP is the symmet-( [- l/ ]. k0 k1 u0 U$ W' b4 c3 v6 U
rical testicular growth secondary to stimulation by- ]; J8 J4 Z1 t% x$ M0 {8 \# u
gonadotropins.1,3) \2 o2 I7 a4 J. c% R
Gonadotropin-independent peripheral preco-! W' c; H# ]1 M7 E/ z$ e
cious puberty in boys also results from inappropriate; n+ V% N  o# H+ _9 @0 K8 ?
androgenic stimulation from either endogenous or
3 H( E* l: \; w& |exogenous sources, nonpituitary gonadotropin stim-
* }& R# z0 @( ]3 W& sulation, and rare activating mutations.3 Virilizing8 G2 Z: B  X0 c5 k
congenital adrenal hyperplasia producing excessive
3 ^3 I9 `& E1 s1 Vadrenal androgens is a common cause of precocious
, U6 T; y& B% h' T+ q, w0 `puberty in boys.3,4
& b8 K" W" R7 h; A  _  FThe most common form of congenital adrenal
+ z  u7 x6 b' p- j3 e6 B0 zhyperplasia is the 21-hydroxylase enzyme deficiency.
4 Y  b$ g3 B9 M2 J, C, HThe 11-β hydroxylase deficiency may also result in
! b% o8 R3 R. s  B& pexcessive adrenal androgen production, and rarely," m1 a! Y* t+ d7 A9 n$ c
an adrenal tumor may also cause adrenal androgen
( d1 I3 u; r* D' r3 o$ Y' g4 Cexcess.1,3
: _  `, r0 l+ E* Q! G8 r/ qat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
9 u, U- j' D9 ]6 j( C9 x542 Clinical Pediatrics / Vol. 46, No. 6, July 2007, `+ D4 n7 r' j( p) O- ]3 o
A unique entity of male-limited gonadotropin-1 e! p9 {$ J6 Y; `5 {* v6 i' [
independent precocious puberty, which is also known
" K+ L6 r+ t& B/ m5 m( aas testotoxicosis, may cause precocious puberty at a
4 O! _2 Z& u1 P/ avery young age. The physical findings in these boys3 p* E6 l' ^; b1 N* b
with this disorder are full pubertal development,# _3 i' g* n5 C8 ^. |( `
including bilateral testicular growth, similar to boys3 _, N1 z7 R. T9 r4 t4 Y. B7 {
with CPP. The gonadotropin levels in this disorder) J% j* Q! z$ S$ [- q2 y
are suppressed to prepubertal levels and do not show3 {8 b+ j  A  u" j. B
pubertal response of gonadotropin after gonadotropin-
. K" J% j  g" @- V; O6 k! g- H' \, ]' treleasing hormone stimulation. This is a sex-linked
% @; H6 g9 j8 ]" ~autosomal dominant disorder that affects only
3 G7 U, J1 H3 H! Rmales; therefore, other male members of the family0 K3 ^9 n! x* \9 @+ }
may have similar precocious puberty.3  X" s  m$ Q2 l. X$ n: x- v5 E
In our patient, physical examination was incon-/ @2 i3 R3 ?( P% X2 E) j. O
sistent with true precocious puberty since his testi-, [. Z6 W! K- T2 _% ?8 ?, {/ A  [5 V
cles were prepubertal in size. However, testotoxicosis
) N4 Q; \+ G' _; [9 kwas in the differential diagnosis because his father
) a6 t' u. r/ @/ ?5 Nstarted puberty somewhat early, and occasionally,
" b# K: [2 [! `, O% Htesticular enlargement is not that evident in the
+ w5 s' Q* Q' Q# lbeginning of this process.1 In the absence of a neg-4 b) Y! E' ?* @1 H5 |
ative initial history of androgen exposure, our
9 N% |; g- u8 Q. B8 p5 c8 nbiggest concern was virilizing adrenal hyperplasia,. g0 G$ S" I+ p
either 21-hydroxylase deficiency or 11-β hydroxylase6 c0 ~8 k2 Q# ^) u& W5 U0 `) \
deficiency. Those diagnoses were excluded by find-
$ R; P4 Y" |5 F5 `9 x# J- A2 `! E; iing the normal level of adrenal steroids.; D2 U2 T# C5 `
The diagnosis of exogenous androgens was strongly+ o5 h) B, `4 X* e; m' B' z
suspected in a follow-up visit after 4 months because
4 B# S$ n# |! ~/ U8 Nthe physical examination revealed the complete disap-
( ^8 ]' E/ h1 M- Qpearance of pubic hair, normal growth velocity, and
" j, g/ M/ B: W5 ?) ]8 ]7 Bdecreased erections. The father admitted using a testos-4 s6 o) u0 u2 b3 y
terone gel, which he concealed at first visit. He was
- L9 ?. C% r4 C* c) Wusing it rather frequently, twice a day. The Physicians’
9 n$ R: C( t4 n, n0 |/ ZDesk Reference, or package insert of this product, gel or+ Z' B0 f0 @8 V0 b1 i0 B2 D
cream, cautions about dermal testosterone transfer to9 o6 o3 W9 n, c. A& p& R$ |; N
unprotected females through direct skin exposure.
8 ~" Y# W# \4 R3 nSerum testosterone level was found to be 2 times the
5 N3 C( k* J/ T8 d, ebaseline value in those females who were exposed to
9 [; W+ a/ w9 h9 k& ^even 15 minutes of direct skin contact with their male
; }% E; n9 _4 _. Npartners.6 However, when a shirt covered the applica-
* z2 `  h& x0 a% ltion site, this testosterone transfer was prevented.1 v" ?4 X8 g4 U
Our patient’s testosterone level was 60 ng/mL," g8 x. C4 E) |9 S( w
which was clearly high. Some studies suggest that7 t5 W9 g4 n2 {1 D, F0 ]
dermal conversion of testosterone to dihydrotestos-% y! y7 s; F( V3 X; H: F1 A2 p
terone, which is a more potent metabolite, is more; U9 I# G) M0 D0 R
active in young children exposed to testosterone
5 N/ Y. k6 y0 w3 k. E, |exogenously7; however, we did not measure a dihy-0 e0 ^+ }4 r1 h9 ~' w7 T
drotestosterone level in our patient. In addition to
! x1 E$ S5 O& B9 R! W: Tvirilization, exposure to exogenous testosterone in: N8 f; ]. Y- [! m. V( l+ Y
children results in an increase in growth velocity and
, |. ]% T" n/ Y1 gadvanced bone age, as seen in our patient.% ?, `6 B( ]! r  o6 n3 D% w, f5 {
The long-term effect of androgen exposure during
) a; x' Y" F; @' u+ u8 ]( d4 kearly childhood on pubertal development and final) g2 f% U5 y% P0 l$ Y
adult height are not fully known and always remain
( x. P# a& g; [% {7 I/ la concern. Children treated with short-term testos-4 M7 j2 ]; U% I- G" }: v
terone injection or topical androgen may exhibit some
. i8 t) `. {7 W, [' jacceleration of the skeletal maturation; however, after
9 J- `2 B8 r4 }8 g3 v6 Ecessation of treatment, the rate of bone maturation
/ n. M- K5 I! }1 {2 y) hdecelerates and gradually returns to normal.8,9# m1 p. s" w* Z
There are conflicting reports and controversy0 b' p; L7 k2 K% C. ~0 b% {3 D) W5 c
over the effect of early androgen exposure on adult6 E* j7 E" l  U% g
penile length.10,11 Some reports suggest subnormal
+ i3 s( q! G5 J; U8 v/ Uadult penile length, apparently because of downreg-
$ j( H- n! k0 t3 u6 J$ h# {7 i9 vulation of androgen receptor number.10,12 However,
4 F9 Q' P) S* t$ x* R" GSutherland et al13 did not find a correlation between# {( R0 l& P- L" {3 p6 o. ?3 P
childhood testosterone exposure and reduced adult4 H: q7 U% u7 w8 j
penile length in clinical studies.0 G* {/ S* Z  F& j( V8 Z
Nonetheless, we do not believe our patient is% r+ n; i' K( a4 G
going to experience any of the untoward effects from6 C. Q" K8 K8 F2 D: f* |
testosterone exposure as mentioned earlier because
: @; @" E6 `$ u# uthe exposure was not for a prolonged period of time.
( `) d" i8 w3 i. J3 Z' TAlthough the bone age was advanced at the time of
& d1 k. w6 d' o2 y* qdiagnosis, the child had a normal growth velocity at
, p: Q4 t# d- R( z$ N1 {the follow-up visit. It is hoped that his final adult
! z2 ]. q7 W: N) H& Q, wheight will not be affected.
4 J* t% x+ ^3 ?5 EAlthough rarely reported, the widespread avail-
6 e0 B0 m% v  G- w5 q/ aability of androgen products in our society may
* @1 u+ L  i" a9 F; g7 n& E- Cindeed cause more virilization in male or female
( a0 H( {' [) b: T2 ^8 Y$ `children than one would realize. Exposure to andro-
% O7 @- j3 z0 u; X( w3 kgen products must be considered and specific ques-
+ q) K! W2 L, k2 g* Q5 j% }tioning about the use of a testosterone product or9 o5 d- X, _5 [6 ]2 N
gel should be asked of the family members during; ^' G' t0 T  Q; N% ^" z
the evaluation of any children who present with vir-/ I( Z& [7 Y' v6 h2 \; a
ilization or peripheral precocious puberty. The diag-
6 T$ z3 ^1 C3 ^; knosis can be established by just a few tests and by" a, }# B/ G; c; I. P0 |6 q
appropriate history. The inability to obtain such a, Z. m* r! m& I8 G1 @, A
history, or failure to ask the specific questions, may7 s  K& q' h& ?, b+ d* D
result in extensive, unnecessary, and expensive
; F3 l7 c$ N( p4 Z( a2 ^investigation. The primary care physician should be4 l+ a$ P7 f8 D3 T4 P
aware of this fact, because most of these children
1 p7 \% l8 e3 b% r/ F, K# Fmay initially present in their practice. The Physicians’% z% g3 R- a2 w3 f% w( }  k0 Y
Desk Reference and package insert should also put a& A9 E/ A( B0 V1 J6 A% r
warning about the virilizing effect on a male or$ I" z2 o1 m) y( `
female child who might come in contact with some-
( a* M* _% U" L6 g2 @- G" G+ Gone using any of these products.8 p5 O$ [9 v" d0 D4 I: ^
References
; D& L+ W& i; ]1. Styne DM. The testes: disorder of sexual differentiation# h0 C: e0 y) q+ c- A" f' T
and puberty in the male. In: Sperling MA, ed. Pediatric; W+ @$ E7 H! r! B" Y
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
, `& J# \2 W" i2002: 565-628.
' i! e6 s8 u3 a3 _) s3 [2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
' Z  Y/ T" m: ^6 }puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
: _! @% h! G4 t5 {9 eBoy Induced by Indirect Topical6 P3 q$ J, c3 i5 U& S+ K" B
Exposure to Testosterone
) [: c# k9 r! Z7 y5 S9 H& Q+ ~7 PSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,23 \  s1 o5 L& i0 y
and Kenneth R. Rettig, MD10 }- R- D! I9 E9 M, c8 T- ~( N
Clinical Pediatrics2 Y" g7 P; _. N( E: c$ ]' U
Volume 46 Number 6/ v. u5 r5 g/ \* A* w- H
July 2007 540-543
% Q* P5 @3 {* U2 E; K- N© 2007 Sage Publications( B; h# Z3 d2 [9 D3 ^
10.1177/0009922806296651& |# @. t% o$ [) I3 }$ t
http://clp.sagepub.com0 m/ j& Q8 J. F! u/ @& k: k5 F
hosted at" B4 E8 F! }. O# S7 F* q
http://online.sagepub.com# |. d3 l' M4 R% M
Precocious puberty in boys, central or peripheral,
2 }1 F* L/ f* r' a' w5 }) R' Iis a significant concern for physicians. Central3 D% j- L0 O+ ~9 R9 F
precocious puberty (CPP), which is mediated5 ~& d, K3 d: K3 r, `) V7 J* I
through the hypothalamic pituitary gonadal axis, has9 L) w. p4 d- }0 S$ f6 h% l
a higher incidence of organic central nervous system
/ U5 x+ G& n/ Q4 U: X! Plesions in boys.1,2 Virilization in boys, as manifested
" R8 u+ z) X( }1 u9 R" Pby enlargement of the penis, development of pubic# ]' s& y- S" t! P, Q. M/ \: h8 C9 Q% V
hair, and facial acne without enlargement of testi-
) ~1 c7 m( Z' n2 G+ k' M! v$ s  ncles, suggests peripheral or pseudopuberty.1-3 We
( ]  f. x. S8 c7 z* E9 w! X7 ireport a 16-month-old boy who presented with the3 J9 m) z' F  ~5 W: M
enlargement of the phallus and pubic hair develop-
0 m* q( s5 K/ Sment without testicular enlargement, which was due' o& ^1 d% w( s* \. K. |! H" b
to the unintentional exposure to androgen gel used by( a' L% l5 }. X0 }$ U5 `! ]: b, @+ {
the father. The family initially concealed this infor-
" S( C# P- I$ N2 Y+ E0 M0 I$ @mation, resulting in an extensive work-up for this
" L/ o: b, r1 X& x6 x5 t+ cchild. Given the widespread and easy availability of
5 ^4 c- ~, `2 B" I. A  \0 Ktestosterone gel and cream, we believe this is proba-4 c2 c/ b/ G+ B) ^* f- Y, C
bly more common than the rare case report in the
# [+ W) J* x: L% D# m& I8 mliterature.45 x, H  p2 x4 t2 _5 O5 J
Patient Report& `' J1 j+ ]4 _3 V  ~# J
A 16-month-old white child was referred to the  K$ J6 b$ o% E
endocrine clinic by his pediatrician with the concern
0 U/ y4 @+ b1 Lof early sexual development. His mother noticed
0 L9 F, w+ n. t: q8 K0 D3 ~light colored pubic hair development when he was
9 c6 k9 V/ P  o8 Z4 w* xFrom the 1Division of Pediatric Endocrinology, 2University of
: s) K0 g. \# N6 BSouth Alabama Medical Center, Mobile, Alabama.
( t7 e1 T2 X. H$ Q- |Address correspondence to: Samar K. Bhowmick, MD, FACE,
( i- J8 b3 v+ e' `) a/ O9 U6 iProfessor of Pediatrics, University of South Alabama, College of) B, x$ R5 B' [5 R
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
- U& W" G& q1 D8 j1 W7 \e-mail: [email protected].
4 V/ S4 F* m& R/ cabout 6 to 7 months old, which progressively became
8 [. D% r% I- {/ @& u" e0 ]" cdarker. She was also concerned about the enlarge-+ e, x. r8 F9 s) }1 T0 Y1 m
ment of his penis and frequent erections. The child6 s. R& _- \: @. w9 A+ m
was the product of a full-term normal delivery, with
  ]) ?$ Y: e+ Wa birth weight of 7 lb 14 oz, and birth length of
6 ~! }/ U6 y; A) T# M/ a; g  q20 inches. He was breast-fed throughout the first year: Y6 U# D, u+ M3 ]& ^' K
of life and was still receiving breast milk along with
0 M3 V: w1 D9 d! gsolid food. He had no hospitalizations or surgery,6 @# Y1 d9 y9 ~& `7 Q
and his psychosocial and psychomotor development
, v& i; e+ M8 E+ N% Jwas age appropriate.( O3 Y# z: {/ p! t! ~8 Q
The family history was remarkable for the father,
) i0 \2 q5 l; ~who was diagnosed with hypothyroidism at age 16,
# n  ~9 y8 {* g4 cwhich was treated with thyroxine. The father’s( Q( v) j& ~, ?: m# i$ [5 Y1 w
height was 6 feet, and he went through a somewhat
3 g5 O$ }" N- \0 K* Y. v) K$ tearly puberty and had stopped growing by age 14.' p- s5 ~4 [/ ^* X0 R4 }; B* E3 I0 n7 q
The father denied taking any other medication. The
: L9 w& a) q: k' w1 r0 A" gchild’s mother was in good health. Her menarche
2 _  [& P$ {1 R3 bwas at 11 years of age, and her height was at 5 feet; y6 L$ N6 x" |% t) w
5 inches. There was no other family history of pre-8 n9 V7 ^" _4 w# e: R
cocious sexual development in the first-degree rela-! r' m" {: j) ?, _- u: ^9 X1 l/ }
tives. There were no siblings.
* m; p8 u" s- L1 J8 c+ `2 ~$ j* FPhysical Examination0 z9 S5 |1 u: O' t
The physical examination revealed a very active,
1 d7 `  a' z6 M$ j0 x4 Oplayful, and healthy boy. The vital signs documented
+ K+ H5 G  L0 w. K+ Na blood pressure of 85/50 mm Hg, his length was2 ~3 i& D5 {- T. l
90 cm (>97th percentile), and his weight was 14.4 kg3 t8 G# l4 b7 X) |8 I+ |5 k/ ]
(also >97th percentile). The observed yearly growth/ b! m7 c0 n$ i2 v+ p
velocity was 30 cm (12 inches). The examination of
, ^/ O& G2 E6 w& k6 x; L! Sthe neck revealed no thyroid enlargement.7 H4 ^5 V+ l) O" S, a$ u
The genitourinary examination was remarkable for
; e+ s: Q$ Y. @5 N7 ]enlargement of the penis, with a stretched length of
: ^; P2 {- R# \/ f8 cm and a width of 2 cm. The glans penis was very well4 N1 [7 X2 p( W' h
developed. The pubic hair was Tanner II, mostly around% f& t8 U" d, S6 A& N" B
540
7 `% L4 C# e0 w, J4 w  zat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from9 O& k' j' Y$ q
the base of the phallus and was dark and curled. The
/ a3 ~$ r/ T% L( K7 xtesticular volume was prepubertal at 2 mL each.- y) {1 R, Y3 A4 G2 \6 K4 M3 |9 {% ]
The skin was moist and smooth and somewhat8 g: T" p9 j2 v
oily. No axillary hair was noted. There were no
" C( w& N4 t8 ]6 uabnormal skin pigmentations or café-au-lait spots.$ a2 }! y/ f* H+ w& q
Neurologic evaluation showed deep tendon reflex 2+/ L1 S* x1 |% L' a- _9 I' R* P5 l: v
bilateral and symmetrical. There was no suggestion8 L5 g& V" r, d, B
of papilledema./ E( ]" c$ A8 c, `; l2 |
Laboratory Evaluation
: R; g. n+ Y) P( C" w* s, i, BThe bone age was consistent with 28 months by- ?" I; X1 A& R- `* c# D
using the standard of Greulich and Pyle at a chrono-3 w% M# R; s4 Z! z- F6 ^' c% p
logic age of 16 months (advanced).5 Chromosomal
" V9 W+ ~: }9 q9 J, |0 }karyotype was 46XY. The thyroid function test( s$ z0 W$ u3 r! A
showed a free T4 of 1.69 ng/dL, and thyroid stimu-, m" ?7 l$ c, K0 }1 ?) @
lating hormone level was 1.3 µIU/mL (both normal).; s2 W' n- h/ E( D" ^) r
The concentrations of serum electrolytes, blood
; h  p( G; S3 Y. o6 J( Rurea nitrogen, creatinine, and calcium all were
8 f( T" m" V" Iwithin normal range for his age. The concentration$ T1 ]/ ]0 q0 J# F5 E5 X* [
of serum 17-hydroxyprogesterone was 16 ng/dL$ v% N/ s1 O4 k
(normal, 3 to 90 ng/dL), androstenedione was 20! P' p6 A" g2 b2 g
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-5 ?. z* [1 W+ J' v
terone was 38 ng/dL (normal, 50 to 760 ng/dL),4 h. m6 U: W* E, h2 r
desoxycorticosterone was 4.3 ng/dL (normal, 7 to- ]8 D  w4 D2 q& [* w; }
49ng/dL), 11-desoxycortisol (specific compound S)4 }" T; X, W6 Q4 d5 [/ E9 v+ p' X' L
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-0 [% e) n' v' W# g1 ]: l
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total1 o! R/ Z5 H3 R# n. j& q6 i$ _- S" W
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),  S% \( U4 _6 W% p8 h  o
and β-human chorionic gonadotropin was less than
  ^8 p# k( v$ s% K5 mIU/mL (normal <5 mIU/mL). Serum follicular
$ t8 ~) a/ J- istimulating hormone and leuteinizing hormone
6 K2 W5 n$ g& tconcentrations were less than 0.05 mIU/mL+ e6 v$ a* X1 P2 w4 I
(prepubertal).
0 u- S# I8 p- S* K- j7 G  P% SThe parents were notified about the laboratory" G6 ]' _3 q2 ]  [2 I5 ~. D
results and were informed that all of the tests were
9 N- q# W; R: l2 T" A. anormal except the testosterone level was high. The
2 X' |9 S/ @9 G2 r( T8 j3 y$ {5 \follow-up visit was arranged within a few weeks to8 s3 i; [! a) @$ e& T
obtain testicular and abdominal sonograms; how-3 E! h, R0 D. s+ J4 q
ever, the family did not return for 4 months.
/ [* k0 C6 {8 T/ J3 q! vPhysical examination at this time revealed that the
$ _3 V' n/ v! G+ w' _' @# Lchild had grown 2.5 cm in 4 months and had gained
( @0 @: H" j( ]# u2 kg of weight. Physical examination remained
4 z$ g  C: c3 g8 n# b; Lunchanged. Surprisingly, the pubic hair almost com-
8 i- |) z8 @0 j( B: ipletely disappeared except for a few vellous hairs at
6 ?) T- n+ L* B9 F( u0 ithe base of the phallus. Testicular volume was still 2
9 Q8 x5 v& t& u& v: @, G  emL, and the size of the penis remained unchanged.) t, w  b. h8 Z) l
The mother also said that the boy was no longer hav-
& ]: W8 O1 G3 O( K$ ^8 X& i: Ring frequent erections.( x8 n: U6 v/ C5 Y- U' l/ i
Both parents were again questioned about use of
* v) C; {4 W( q; }9 N5 Uany ointment/creams that they may have applied to7 u0 m  T- s0 p( b4 Q( k
the child’s skin. This time the father admitted the1 u. n8 h2 A5 U) r) z. E: B
Topical Testosterone Exposure / Bhowmick et al 5411 }+ E) ?( F* F# S' o
use of testosterone gel twice daily that he was apply-
9 L0 Y6 b  P6 {6 P7 g" c# \7 King over his own shoulders, chest, and back area for
: g( ]4 D. r2 @& `* J& V- t( ]% a/ ra year. The father also revealed he was embarrassed
0 `' c# b- C: r0 x1 A* mto disclose that he was using a testosterone gel pre-  B5 R, d! U2 ~! d0 E' C
scribed by his family physician for decreased libido' [& @4 |, a9 a0 d
secondary to depression.4 V! e" a7 ?8 w* q
The child slept in the same bed with parents.. b8 K6 T  }' v# E8 b  s& c
The father would hug the baby and hold him on his
6 e# r' w! c5 ?; X1 D3 e3 T/ Cchest for a considerable period of time, causing sig-- `7 r7 Y# e/ ^4 Z. r4 L- S0 P
nificant bare skin contact between baby and father.
# [" T- o" e  n) W" wThe father also admitted that after the phone call,- l% e" h" _" {5 Y2 q& U1 I
when he learned the testosterone level in the baby% H) Q5 S1 z- \( D
was high, he then read the product information/ ~' F& }8 l$ J" M/ O
packet and concluded that it was most likely the rea-
- ^9 r7 n; n* D# _4 m7 n! S; M8 Json for the child’s virilization. At that time, they8 q" B$ L2 {9 V( z3 Y5 Y
decided to put the baby in a separate bed, and the
) m0 s; c6 U% s0 ^5 m5 z! O8 ~father was not hugging him with bare skin and had
5 Q  |8 O' y. A' |4 Pbeen using protective clothing. A repeat testosterone
8 y1 h7 o# @$ {  }/ ^8 ^9 Vtest was ordered, but the family did not go to the" g5 z9 O' w/ \
laboratory to obtain the test.% I( g; Q* w& Z/ V% O
Discussion
, m1 e6 b1 s8 [4 oPrecocious puberty in boys is defined as secondary* o2 j( G' \, p" t8 R( I: m- E
sexual development before 9 years of age.1,4" o. ?# }& [5 `8 u5 w+ }
Precocious puberty is termed as central (true) when5 v# Y# V, \8 a' V# @7 Y3 I: a
it is caused by the premature activation of hypo-
* J! _  i+ P5 m% v& A/ m! f& sthalamic pituitary gonadal axis. CPP is more com-- C! ?' R! g% o- j; B' N
mon in girls than in boys.1,3 Most boys with CPP
! a2 J5 G* C! s( o. i% Q& Amay have a central nervous system lesion that is4 v  x: }+ v5 Y( P9 o) P
responsible for the early activation of the hypothal-& r1 ]2 t5 T7 g
amic pituitary gonadal axis.1-3 Thus, greater empha-% n) M0 v8 m5 ?( N
sis has been given to neuroradiologic imaging in
' I! h' O0 `) {boys with precocious puberty. In addition to viril-
7 ~- \( u& Z- g, P' Gization, the clinical hallmark of CPP is the symmet-( G9 [6 V6 \+ u  ?& c5 \
rical testicular growth secondary to stimulation by. \3 \# g3 n- V6 N2 e7 |7 Q* w
gonadotropins.1,35 d5 L  \( D6 U% c  i$ r8 H/ u3 I/ F: R
Gonadotropin-independent peripheral preco-" K5 N  b2 b' b8 T
cious puberty in boys also results from inappropriate
- R# j4 |+ p8 O% V% xandrogenic stimulation from either endogenous or
6 H: w9 m2 c0 mexogenous sources, nonpituitary gonadotropin stim-
; Y- ~" Z) X3 p7 ]8 m$ gulation, and rare activating mutations.3 Virilizing- ~& U6 _5 Q$ x6 n0 p! l
congenital adrenal hyperplasia producing excessive
4 ^) y- Z7 R  Q1 t+ U- Badrenal androgens is a common cause of precocious8 `) S7 s( R; y7 e! x4 [
puberty in boys.3,4; \) s* D# z# [
The most common form of congenital adrenal- m8 B4 L' F* m: R( h- _2 o
hyperplasia is the 21-hydroxylase enzyme deficiency.
. \) o) M' ]! YThe 11-β hydroxylase deficiency may also result in& ?* v6 t8 ]1 F, {, n: M+ ]( C& C7 l
excessive adrenal androgen production, and rarely,! i) Q* t+ c9 j& Q8 g1 Z
an adrenal tumor may also cause adrenal androgen
7 A) {, H* s4 \. U7 t8 n# Bexcess.1,3; ^6 ~( i( r0 Z7 P  U& @
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
- h% Z3 P5 W7 X3 B* X# H2 B542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
1 }+ K5 f( a; P( w' [. lA unique entity of male-limited gonadotropin-  F/ X' H$ k$ }" V( B
independent precocious puberty, which is also known6 b6 \1 G/ e: j* w
as testotoxicosis, may cause precocious puberty at a- ]; j) G; ]& s
very young age. The physical findings in these boys9 y0 i* l: ^. e, T: r4 E
with this disorder are full pubertal development,
  v: ?3 P0 [7 c0 Vincluding bilateral testicular growth, similar to boys
: A* g7 f6 V. b# Lwith CPP. The gonadotropin levels in this disorder" m" _0 z6 H7 F$ ^
are suppressed to prepubertal levels and do not show
0 C' {/ l; c' Q/ W" y2 g0 r3 S  R; a3 bpubertal response of gonadotropin after gonadotropin-
2 a+ I7 w  O! vreleasing hormone stimulation. This is a sex-linked
1 V- Z4 {0 }) @# S, ?$ Z9 Sautosomal dominant disorder that affects only# n# ~' x# }( d- c2 t0 U: M. S4 ]
males; therefore, other male members of the family
0 q1 \9 b% w! emay have similar precocious puberty.3) x. B. v; K0 E
In our patient, physical examination was incon-
" ^6 o5 x4 F- }# S% M+ h) ]sistent with true precocious puberty since his testi-
5 W1 P1 C2 m' h$ z; r4 b  E$ G  Zcles were prepubertal in size. However, testotoxicosis  `  f3 M* P8 h4 ^% z" n+ p, g
was in the differential diagnosis because his father( _4 W6 C" V% `
started puberty somewhat early, and occasionally,
) ~% P4 ^. I: {# J. a: z5 V# Xtesticular enlargement is not that evident in the" d# y3 `0 d. \5 c* R" \
beginning of this process.1 In the absence of a neg-
# D) R+ ?, _' U5 u9 C- A- Tative initial history of androgen exposure, our9 X% t7 c5 P. g  n# T
biggest concern was virilizing adrenal hyperplasia,
- f6 U9 J4 N0 f- ^2 |+ m: q+ Oeither 21-hydroxylase deficiency or 11-β hydroxylase
0 |; _9 E) J( U" |deficiency. Those diagnoses were excluded by find-
  r7 d% M( x" B: Z) Wing the normal level of adrenal steroids.
. S# q( S! j% mThe diagnosis of exogenous androgens was strongly
0 q& t2 F/ ?5 J/ r& s4 T  Dsuspected in a follow-up visit after 4 months because
9 n5 ^; \: y( O  d* K0 Hthe physical examination revealed the complete disap-
1 H/ z5 Y4 O/ N0 S, V3 s0 }5 epearance of pubic hair, normal growth velocity, and
2 j5 t8 Y" ?& f# @3 p+ Z/ ddecreased erections. The father admitted using a testos-, B  }- I( f4 _) j; C
terone gel, which he concealed at first visit. He was5 P3 d5 _( R. k7 q# f% M6 P9 T
using it rather frequently, twice a day. The Physicians’
  l2 G2 h+ i, qDesk Reference, or package insert of this product, gel or# ]5 x% e# H5 r# W0 _) y
cream, cautions about dermal testosterone transfer to8 h8 t! c& {4 R9 c9 X3 D3 A4 Y
unprotected females through direct skin exposure.
; @. W; J3 Z* @* f  w& \Serum testosterone level was found to be 2 times the
7 O7 Z. l) v0 }2 v$ T7 D4 i/ |4 G  t. ?baseline value in those females who were exposed to; T7 M- Q7 W7 w
even 15 minutes of direct skin contact with their male6 C- w2 z. B$ b& f
partners.6 However, when a shirt covered the applica-( W) ^& g+ u& g+ a
tion site, this testosterone transfer was prevented.% S# o5 C% q( `
Our patient’s testosterone level was 60 ng/mL,
* r7 o+ P4 k2 a* [3 w- L- Qwhich was clearly high. Some studies suggest that
- A7 L, U& A3 E: D8 x7 d! mdermal conversion of testosterone to dihydrotestos-: P6 u8 Z' g2 r: u9 W0 O) w3 A
terone, which is a more potent metabolite, is more" M) M/ u9 M2 X# F; h
active in young children exposed to testosterone
8 s8 Z: ~, Q  c# c! O5 j. dexogenously7; however, we did not measure a dihy-- k+ z) a, M" n
drotestosterone level in our patient. In addition to! v$ e6 ~( U, A# Q- F9 Y8 C
virilization, exposure to exogenous testosterone in! A5 h- c. z# u& M4 j
children results in an increase in growth velocity and  R1 R1 W! Y" E  n& s7 l: L/ m
advanced bone age, as seen in our patient.
5 T! H7 G4 X3 `: Y$ tThe long-term effect of androgen exposure during
1 a1 l" }& e' P+ }8 z, `8 A7 x7 t& n  gearly childhood on pubertal development and final
; j3 H! ~3 r3 V8 ]adult height are not fully known and always remain; t9 a& c& }4 m1 f% Z
a concern. Children treated with short-term testos-* W: ]3 n/ l1 m7 {. R. J
terone injection or topical androgen may exhibit some) E- m% X: y0 u
acceleration of the skeletal maturation; however, after5 ]; u1 d+ f, N3 l, S- g
cessation of treatment, the rate of bone maturation
) _- s/ f# p- T8 O, r+ {decelerates and gradually returns to normal.8,9
6 V4 U. ?6 i2 t% h, i, w! GThere are conflicting reports and controversy
& F, k0 o3 k% X: Y, o$ oover the effect of early androgen exposure on adult
& k% J4 t* d7 y$ R0 Mpenile length.10,11 Some reports suggest subnormal
8 }, ]7 f# ^6 G7 Yadult penile length, apparently because of downreg-
$ c# A- J) X% R! b' @ulation of androgen receptor number.10,12 However,
' O( q6 {* o; M. CSutherland et al13 did not find a correlation between. K( d' A3 n% R- G3 k3 U3 L
childhood testosterone exposure and reduced adult; Q, Q# Y4 ?# d: z% [, [7 a
penile length in clinical studies.
6 S: i; m' y6 v$ `' DNonetheless, we do not believe our patient is
6 K2 Y' D. Q) kgoing to experience any of the untoward effects from, Y" @, Z- L& W$ b
testosterone exposure as mentioned earlier because
/ v, x  l1 T4 t% kthe exposure was not for a prolonged period of time.6 Z7 M2 }7 Z+ H  t8 U3 J  ]# _
Although the bone age was advanced at the time of% g1 V& h6 T- Z5 o8 c
diagnosis, the child had a normal growth velocity at. G& R: m7 H- K0 d+ x, s: x
the follow-up visit. It is hoped that his final adult
( Y" w* g% P4 ?7 i+ D+ Pheight will not be affected.' p1 Z, X5 [( ?* [  @. _
Although rarely reported, the widespread avail-
) m4 Z( V& L/ ]. S; o" D! \$ sability of androgen products in our society may
9 Z2 n2 [5 k# C5 a) g# V/ W2 Oindeed cause more virilization in male or female/ Z+ N  B4 m9 s! }+ k) s
children than one would realize. Exposure to andro-
, P; d! ^- v  h, o. W; g9 p! n% Jgen products must be considered and specific ques-
' O% \. o6 ?# u5 a3 r9 Utioning about the use of a testosterone product or2 z, ]6 }1 D9 P# v9 q4 T
gel should be asked of the family members during
4 |6 Z+ w  i0 w5 V1 [) mthe evaluation of any children who present with vir-, M0 G0 w9 ^' K' V, r
ilization or peripheral precocious puberty. The diag-
4 {! F/ R9 w, A% s4 A$ `0 ?& ?5 Fnosis can be established by just a few tests and by
, k9 L, I+ X2 h" M: x9 G( dappropriate history. The inability to obtain such a
# }5 P& q) O4 [history, or failure to ask the specific questions, may2 E( O+ _( ], W0 g6 y$ A6 k; a
result in extensive, unnecessary, and expensive
6 Z8 a8 \% R; ]7 @* o( }% Tinvestigation. The primary care physician should be  p# Q' c  U2 v4 X! h
aware of this fact, because most of these children9 v: @: P' E/ T$ X$ S" M) f  K
may initially present in their practice. The Physicians’
/ W, `+ r/ O$ r5 }( M5 e( RDesk Reference and package insert should also put a
# F: U$ z& A7 G5 \' T6 R/ U4 rwarning about the virilizing effect on a male or
0 g: B1 b: I: _5 r' T; ~! ^: afemale child who might come in contact with some-' A2 t: f" N$ i5 @5 {2 l+ F3 v
one using any of these products.
! U; v# m+ h( m( |; [References
. m, f3 d6 I9 ]( E% C" h& ]( y1. Styne DM. The testes: disorder of sexual differentiation
$ [6 v: P: ]8 h- ]and puberty in the male. In: Sperling MA, ed. Pediatric
9 M7 p9 B9 Q; LEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
# X! Q& T  ]3 A; M5 z& ]) A1 B6 W% F2002: 565-628.
& `, @2 _8 T, g. U2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
1 K" v# _. G2 }6 L6 q" Q0 y. apuberty 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
: b( k0 `5 w6 g$ Z6 P: }
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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