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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
6 L/ \: F' _. h% E3 x6 [Boy Induced by Indirect Topical3 y( r7 }# w$ O, g* ?$ {
Exposure to Testosterone' s2 T- B2 J& [. g, n- z6 S
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
' m7 j1 H) Y  I+ Q& m, t) jand Kenneth R. Rettig, MD1
4 B$ a3 V5 f# q; X* oClinical Pediatrics
! F# K1 D9 R; k5 I1 C0 oVolume 46 Number 63 v  N* y: B5 D* q& u$ m
July 2007 540-543
& c1 h0 D! x+ t9 x4 F( w8 E© 2007 Sage Publications
* M  ^' G* c! p2 u% S' g% @2 k10.1177/0009922806296651
% z* w7 t. r" ?3 {http://clp.sagepub.com4 \/ I, q1 F) l' t6 `2 L. r
hosted at) x3 l3 S; O7 w! R* i" L5 n2 D
http://online.sagepub.com
! a9 W# ~8 S! f  ^# D, }. cPrecocious puberty in boys, central or peripheral,
" D1 b" [% B  @* B, _: Wis a significant concern for physicians. Central
1 T# M3 I+ E- X+ b8 v# e$ aprecocious puberty (CPP), which is mediated) S" G2 n9 O! |; P3 `/ }
through the hypothalamic pituitary gonadal axis, has
* q* a0 D) D+ Sa higher incidence of organic central nervous system2 y0 p. Y: i. a, a
lesions in boys.1,2 Virilization in boys, as manifested
  F# A; x3 Z: O6 t  }  k; Xby enlargement of the penis, development of pubic* y% h0 a+ }8 [! U; t! P% ~1 g
hair, and facial acne without enlargement of testi-7 H: N$ L3 ?+ h& u
cles, suggests peripheral or pseudopuberty.1-3 We
0 v& x+ g' U. Z% |+ j6 @report a 16-month-old boy who presented with the- N# q) a6 x7 e! H  k9 w( D
enlargement of the phallus and pubic hair develop-
0 L/ S/ G  {. Y( @6 }ment without testicular enlargement, which was due' [# W2 |+ ?0 R( T! L
to the unintentional exposure to androgen gel used by* q+ B. r; F1 ~! O9 `3 ]
the father. The family initially concealed this infor-
8 B6 B0 c- r4 c5 E# A# {mation, resulting in an extensive work-up for this
: R$ I# f& n% i2 b1 {child. Given the widespread and easy availability of
- R2 n2 |; c, c8 \/ Jtestosterone gel and cream, we believe this is proba-* h% e# l" _  }5 ?! v: K
bly more common than the rare case report in the* B7 r) r1 C" u6 I9 Y5 t; M
literature.4
; E5 C6 F3 F' m8 }  CPatient Report- m# y& |) g0 Q5 Q
A 16-month-old white child was referred to the
0 V! P8 H  g# ~  P2 P/ Vendocrine clinic by his pediatrician with the concern
$ e/ n, g9 S8 i! w# i: P8 yof early sexual development. His mother noticed8 E0 l  w( p! F3 y+ q5 @  e/ q
light colored pubic hair development when he was
" {0 G9 ]8 k1 ?) ~3 Y+ E- T. lFrom the 1Division of Pediatric Endocrinology, 2University of
. S9 P) w/ |1 t+ FSouth Alabama Medical Center, Mobile, Alabama.
3 d3 T  g- Y: LAddress correspondence to: Samar K. Bhowmick, MD, FACE,; ^1 C0 X, [6 k7 ^% ]6 V$ R
Professor of Pediatrics, University of South Alabama, College of- H; T- B" k0 C, {5 f' {
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;( T/ G6 E( P8 l4 ?, b/ @9 M
e-mail: [email protected].
! v  Q4 c( A3 [( l. T3 y, R/ rabout 6 to 7 months old, which progressively became1 M1 B3 O9 T* o- t
darker. She was also concerned about the enlarge-: f" L5 X+ j) _, X  y5 S
ment of his penis and frequent erections. The child
% v# m4 Z* U  C- ^" \( `was the product of a full-term normal delivery, with- e" r; }* o: |" Q
a birth weight of 7 lb 14 oz, and birth length of/ G, G, }" v/ K2 z& G
20 inches. He was breast-fed throughout the first year0 |- p7 }# ~3 V1 ^! g- p
of life and was still receiving breast milk along with
7 D% R% B( h& p2 N  ksolid food. He had no hospitalizations or surgery,( U- ^7 [% e' M2 o' B3 T: v
and his psychosocial and psychomotor development$ F/ q# s% ]$ P& A2 \6 |+ t3 {
was age appropriate.
# b& C+ C  v# f) i- H& QThe family history was remarkable for the father,
) _# u4 f3 I* K! `) a; G9 @3 b$ {who was diagnosed with hypothyroidism at age 16,
6 ~7 U* S8 {$ s3 o6 Qwhich was treated with thyroxine. The father’s
8 r; X  _, l5 }, z  Z; ~height was 6 feet, and he went through a somewhat6 Q" i1 ?6 m' j$ [, b" S
early puberty and had stopped growing by age 14.
/ c7 [1 M- J- h* p  b3 w" NThe father denied taking any other medication. The; q+ d- P, v6 E/ I  |
child’s mother was in good health. Her menarche- ]; m( D) n1 D' o: o
was at 11 years of age, and her height was at 5 feet4 ^6 {' L8 e' \' h1 v* {) X" W
5 inches. There was no other family history of pre-6 F3 J7 C- h$ ]7 f4 X& [" z- m
cocious sexual development in the first-degree rela-8 k: K0 n7 o' z' n
tives. There were no siblings.
" j- j8 E& i4 KPhysical Examination
3 X# X6 b# D1 k' a+ EThe physical examination revealed a very active,. b/ E! ^* {% D2 z7 F
playful, and healthy boy. The vital signs documented
$ |) b3 m- P4 ua blood pressure of 85/50 mm Hg, his length was4 f7 c6 z( x( w9 z% z' W' ^
90 cm (>97th percentile), and his weight was 14.4 kg
, t6 m, H5 H9 S(also >97th percentile). The observed yearly growth. W8 a+ s  }* ^$ P- i) P1 q- T
velocity was 30 cm (12 inches). The examination of
% ]' P' g  r- Ithe neck revealed no thyroid enlargement.
( x2 P6 K, i  x/ S9 |The genitourinary examination was remarkable for
3 u9 l; V8 B6 v( menlargement of the penis, with a stretched length of+ {0 L; d' P  M  u% Z" r
8 cm and a width of 2 cm. The glans penis was very well1 k9 y7 j! a; a4 c6 B9 D
developed. The pubic hair was Tanner II, mostly around& c3 ^$ Z+ i5 H, x1 N2 h% P3 G
5405 M% F* e* j' n# S0 E& C
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from& L1 d7 \7 h) L7 m
the base of the phallus and was dark and curled. The
1 f" R& C" }; f3 F6 ?testicular volume was prepubertal at 2 mL each.  B# R; B) N; @# A- k/ X
The skin was moist and smooth and somewhat
& o6 d$ i. j4 Y! R4 D; x  p6 \6 Coily. No axillary hair was noted. There were no
9 [! b2 `( z0 Q. @0 d, L- dabnormal skin pigmentations or café-au-lait spots.0 _* }& P2 S/ D' f# H8 o# n' ^  U
Neurologic evaluation showed deep tendon reflex 2+, t% z3 d$ h6 v) k' y6 |
bilateral and symmetrical. There was no suggestion/ i. u/ ?% r/ `) A: x5 }
of papilledema.
7 V( v; l+ v5 s* I% x3 ?Laboratory Evaluation7 E/ T' Z  w) i( W3 j6 L  H+ ]- O
The bone age was consistent with 28 months by+ I9 h  g: e2 l  t' d
using the standard of Greulich and Pyle at a chrono-7 N+ {6 `9 R7 C% @  d  u
logic age of 16 months (advanced).5 Chromosomal: Q0 q+ x- ?: p0 D; v/ d
karyotype was 46XY. The thyroid function test5 v% U- ^1 }; S# ^
showed a free T4 of 1.69 ng/dL, and thyroid stimu-, C$ _: S% k- ^
lating hormone level was 1.3 µIU/mL (both normal).
  Q2 @$ r6 g) d6 sThe concentrations of serum electrolytes, blood" R5 n& \; o( X$ W5 U
urea nitrogen, creatinine, and calcium all were- Z' {1 \; M5 e! c" E, w! e
within normal range for his age. The concentration
  g. @4 t- ~' m0 W) ?7 ]; L! t% zof serum 17-hydroxyprogesterone was 16 ng/dL# }7 X9 P, ^- u6 d0 y
(normal, 3 to 90 ng/dL), androstenedione was 20& m0 n* B2 r+ C( C6 {' a- \( s. B
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
* @$ M, x; ^  Rterone was 38 ng/dL (normal, 50 to 760 ng/dL),
9 _4 L1 B' w7 E# ^desoxycorticosterone was 4.3 ng/dL (normal, 7 to7 \& ?4 W' o6 P
49ng/dL), 11-desoxycortisol (specific compound S)0 ~  c) r% y2 J5 l2 y3 p2 ~1 ]
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-. \* f3 ^" j6 Q
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total- O, m, x; o% E5 h( j
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
6 c0 Q# ]+ j& H4 X# @& Land β-human chorionic gonadotropin was less than1 n: Q: h: ^. J3 e5 N
5 mIU/mL (normal <5 mIU/mL). Serum follicular' X* @8 z  p6 Q! r& w/ o- x$ ~
stimulating hormone and leuteinizing hormone
; y1 d7 ?4 {* N7 R  h) ]* w+ j& econcentrations were less than 0.05 mIU/mL- @" e9 @. Z: k& C
(prepubertal)." b6 f; a( B" j1 C* D- S5 y. N
The parents were notified about the laboratory
. H( W0 }0 R! \. J/ [1 Q2 x+ xresults and were informed that all of the tests were
$ y8 Q. b* o& V  Z  ~normal except the testosterone level was high. The
" f1 `8 ^4 t1 }$ A+ L+ U& mfollow-up visit was arranged within a few weeks to" Y$ H0 A8 `4 f: m4 }0 P: l7 {2 H$ m# x
obtain testicular and abdominal sonograms; how-7 i5 `$ P7 x1 [$ h
ever, the family did not return for 4 months.; x# n  l7 Y* O/ I
Physical examination at this time revealed that the
, ~' n" }" \/ _child had grown 2.5 cm in 4 months and had gained
$ Z5 g4 t* w1 X+ a& q% [2 kg of weight. Physical examination remained
7 p- x8 \3 l5 ?& ounchanged. Surprisingly, the pubic hair almost com-
+ o1 O8 a3 e. g" a* {. q2 xpletely disappeared except for a few vellous hairs at
# j& i  w. q& Q. Z% d. Hthe base of the phallus. Testicular volume was still 2
5 @% i) ?0 W0 y* i8 DmL, and the size of the penis remained unchanged.
+ M* P+ u. ~  _" B% UThe mother also said that the boy was no longer hav-
( L7 n* C" d# s! A+ Eing frequent erections.
. l& f3 ]# K+ t) b; |Both parents were again questioned about use of7 Z$ Z+ r4 n1 W* y  p& v6 ~$ A
any ointment/creams that they may have applied to" R2 k- ]1 Z, b+ O8 I7 ?
the child’s skin. This time the father admitted the
3 S, o( J4 |2 g! YTopical Testosterone Exposure / Bhowmick et al 541
7 y5 N! S7 ~" |% ^! ruse of testosterone gel twice daily that he was apply-( }) G( m" I. u* A' H
ing over his own shoulders, chest, and back area for
: j- E/ [4 F9 D* }3 m- ?" xa year. The father also revealed he was embarrassed" i0 a+ r# r/ I, v# v% Z% A
to disclose that he was using a testosterone gel pre-# w- ?! W$ @2 T" w& J) o) g
scribed by his family physician for decreased libido$ g( n9 w) ?3 r) t1 A  J
secondary to depression.+ q% l! w- X/ B4 H# x# w+ n
The child slept in the same bed with parents.
: L. H7 {0 v  l5 U- \The father would hug the baby and hold him on his/ U4 b7 V" ~7 H* Z  m- _
chest for a considerable period of time, causing sig-' u! L3 ^- [" F% [" O
nificant bare skin contact between baby and father." A' x% I6 C7 j* v3 h
The father also admitted that after the phone call,$ _% V) J+ X' z- t
when he learned the testosterone level in the baby
  {+ w' ~- [! }  Ewas high, he then read the product information# A  l. a) E+ E; |- j
packet and concluded that it was most likely the rea-  m' H+ c1 G, s8 o
son for the child’s virilization. At that time, they
# b; J# e8 d' `' Wdecided to put the baby in a separate bed, and the
& n8 S/ Z0 \! W8 efather was not hugging him with bare skin and had; E) ?" w. j  }, W+ H
been using protective clothing. A repeat testosterone
+ D5 _: }! O9 T! K+ Z' k+ m- S3 utest was ordered, but the family did not go to the
2 h+ a& m  S% t1 a6 Xlaboratory to obtain the test.
' ?9 o9 T0 ?! p$ O5 zDiscussion
7 \1 _' W) F- U: ?3 H- _0 uPrecocious puberty in boys is defined as secondary. {% I+ W  O, c7 d1 g8 d
sexual development before 9 years of age.1,4
  F/ _' ^6 n0 S% J& YPrecocious puberty is termed as central (true) when9 T. I% x" }* @  W, K( @+ Q  H
it is caused by the premature activation of hypo-5 x8 v0 p  a) V! \% M; ^( ], B; C7 k
thalamic pituitary gonadal axis. CPP is more com-& y& w* j8 j* |" T1 [! f7 L& }) f
mon in girls than in boys.1,3 Most boys with CPP
1 `9 _! O! X+ rmay have a central nervous system lesion that is
$ l' I, T: m6 E9 V8 a2 K: t! }$ y% t# |responsible for the early activation of the hypothal-
/ M$ n, G* m/ p0 Vamic pituitary gonadal axis.1-3 Thus, greater empha-
6 Y( s$ t* m. w7 o  v+ F4 X) osis has been given to neuroradiologic imaging in1 ?% C0 x9 N7 e( e9 {3 p+ r
boys with precocious puberty. In addition to viril-- M# Y) S+ N' l6 a! {6 W
ization, the clinical hallmark of CPP is the symmet-
7 f# r, ~  |# Brical testicular growth secondary to stimulation by
: O2 K3 v4 Q/ h" X6 E; l( U' U& E8 s9 \# _8 Xgonadotropins.1,37 ~% V' H$ H, \$ G4 x& p
Gonadotropin-independent peripheral preco-; `1 {* }8 A  X1 h& R5 p5 P
cious puberty in boys also results from inappropriate7 k) ~$ R* ~. o. S  I
androgenic stimulation from either endogenous or# o- @3 l$ O4 H4 b- O; v
exogenous sources, nonpituitary gonadotropin stim-
. f# ]& X! ~6 H& Julation, and rare activating mutations.3 Virilizing" j. N" s5 D' g. g$ @
congenital adrenal hyperplasia producing excessive9 U; {% a. L+ ^5 f
adrenal androgens is a common cause of precocious
+ e% s/ r( N. Zpuberty in boys.3,4
1 q, q! |; H% p& RThe most common form of congenital adrenal
# m" E  j: Z! @5 Whyperplasia is the 21-hydroxylase enzyme deficiency.0 d$ Q6 V1 r6 w+ H) H" l' K7 @
The 11-β hydroxylase deficiency may also result in
: \( |: g( {+ ~* Lexcessive adrenal androgen production, and rarely,
- P  V- i# b; ]( U0 B+ r& aan adrenal tumor may also cause adrenal androgen
9 w$ ~- I3 D! s/ i+ bexcess.1,3
8 m0 O: R7 R) xat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
  e; {& d- @% ?$ A! z542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
5 B: I6 }6 x: `$ w* q4 D( oA unique entity of male-limited gonadotropin-+ _* I! e! Y) a0 C1 Z: T0 a
independent precocious puberty, which is also known9 M( Q1 O) M! K& I
as testotoxicosis, may cause precocious puberty at a+ Y/ d1 ?& }0 R5 O0 Z4 ^
very young age. The physical findings in these boys$ `* H" O* Z' b5 b$ L
with this disorder are full pubertal development,
0 v5 c( P* {* o2 \  _; nincluding bilateral testicular growth, similar to boys
  C. S' F" \( ~with CPP. The gonadotropin levels in this disorder- r( U3 A: a" I4 I
are suppressed to prepubertal levels and do not show) j2 U: \' Y% n( z6 X3 o
pubertal response of gonadotropin after gonadotropin-
; f# B3 a2 B1 S3 ]& Oreleasing hormone stimulation. This is a sex-linked9 g7 l4 G5 L" ^2 Z7 \
autosomal dominant disorder that affects only
. A* B4 u6 G% c; `) d* M4 emales; therefore, other male members of the family$ n! _- Z9 t% |9 x8 V7 b
may have similar precocious puberty.3
5 a- y8 ]6 E1 ~* _8 I; xIn our patient, physical examination was incon-% V/ e7 @5 E1 M0 q
sistent with true precocious puberty since his testi-: [1 w2 B9 h; P" m
cles were prepubertal in size. However, testotoxicosis) V4 r+ d) l0 U; v8 y
was in the differential diagnosis because his father
) P6 }1 j3 \! nstarted puberty somewhat early, and occasionally,
% J6 i; x% f  \testicular enlargement is not that evident in the8 Z9 y8 Z& G% c. @0 P  G5 e, I' Y( J
beginning of this process.1 In the absence of a neg-6 D" W* a5 i" a* ]3 j
ative initial history of androgen exposure, our
+ B9 X/ v0 P9 t$ f1 N8 X5 ~! ebiggest concern was virilizing adrenal hyperplasia,
/ Y6 _# p0 {- V' Ceither 21-hydroxylase deficiency or 11-β hydroxylase9 r" E8 P$ q$ Q; Y# u. ^
deficiency. Those diagnoses were excluded by find-! N' q" ^! D! I/ _0 W+ _
ing the normal level of adrenal steroids.
) ~* |0 Z1 V+ z% w, ]8 q$ FThe diagnosis of exogenous androgens was strongly% `" t4 h9 C. t2 x1 A' G1 W; Y
suspected in a follow-up visit after 4 months because
- p5 h4 W5 F1 @, {. vthe physical examination revealed the complete disap-- A* U+ a0 \9 ]& U* J
pearance of pubic hair, normal growth velocity, and
- w6 h. H3 x$ Ydecreased erections. The father admitted using a testos-  d5 O& F% Q  m  P) b2 z
terone gel, which he concealed at first visit. He was
4 H$ E/ |0 S5 ]* h2 Fusing it rather frequently, twice a day. The Physicians’
5 T( Z7 H2 B6 B6 w# Q0 T4 o4 gDesk Reference, or package insert of this product, gel or8 s* ]+ \& m7 [3 n, A* K4 o
cream, cautions about dermal testosterone transfer to& t5 X: `1 E4 f
unprotected females through direct skin exposure.
6 q9 l: [0 u* l2 DSerum testosterone level was found to be 2 times the
7 k3 V/ I8 b4 h! f1 A. _baseline value in those females who were exposed to4 P- U) @& N0 O) |+ r: ?
even 15 minutes of direct skin contact with their male, W; o" ]9 x6 l: ~
partners.6 However, when a shirt covered the applica-
8 b( t6 m8 S  Etion site, this testosterone transfer was prevented.& |6 r. {+ G! K3 B0 ~
Our patient’s testosterone level was 60 ng/mL,
% |( V2 h5 ?  S2 \9 @& |7 H4 Jwhich was clearly high. Some studies suggest that; X" `3 |. x6 W- W
dermal conversion of testosterone to dihydrotestos-
: m8 C, B& v; V, ^terone, which is a more potent metabolite, is more
3 x% P. H, R7 N8 ?active in young children exposed to testosterone# A" [  A- \  ^0 w
exogenously7; however, we did not measure a dihy-) Y9 H! H, X) m* F+ }
drotestosterone level in our patient. In addition to+ G+ Z% r$ ]& s9 A
virilization, exposure to exogenous testosterone in
6 [' Y" F- r3 t' m0 R: B" o; schildren results in an increase in growth velocity and
  }/ t5 m5 I! G0 U+ y6 Madvanced bone age, as seen in our patient.
! z8 p+ `2 L/ B4 G! V" K9 v$ ~$ AThe long-term effect of androgen exposure during: @/ p  E6 j3 i
early childhood on pubertal development and final
2 p2 m0 ?* D9 A( p0 [adult height are not fully known and always remain7 ^/ W  F. u8 g- {  e! H( V
a concern. Children treated with short-term testos-# {: Y  l# D8 E+ k
terone injection or topical androgen may exhibit some
. \) V. p# F& _& U2 I  Z8 Z5 Uacceleration of the skeletal maturation; however, after
; n2 h0 c. }1 W- u1 _2 }  b0 Vcessation of treatment, the rate of bone maturation
( P3 }, Q) K4 B6 l# C* r( Q+ H% }1 pdecelerates and gradually returns to normal.8,91 I! D- ~% t- a+ A$ l
There are conflicting reports and controversy. j0 f6 \( Y  i2 z$ {5 I' t" k
over the effect of early androgen exposure on adult: p" D1 @) S* _6 S9 m- \) h
penile length.10,11 Some reports suggest subnormal* o1 f3 D  R9 W4 i. g4 i
adult penile length, apparently because of downreg-$ k# I" {8 I1 n7 K; Q% {! G3 u; [
ulation of androgen receptor number.10,12 However,& X& |7 I& k1 q0 e
Sutherland et al13 did not find a correlation between4 e) L, n9 e  n/ @6 p( g2 i5 L
childhood testosterone exposure and reduced adult
# s& t4 q, B9 Ipenile length in clinical studies.
8 S3 _# B8 _$ H8 W  d; ENonetheless, we do not believe our patient is/ }& N" t2 X' x$ J- S4 R9 l
going to experience any of the untoward effects from( m% H: i( [& i/ T; M. F; ^
testosterone exposure as mentioned earlier because
0 I4 `$ ]5 b) z+ y/ b" Athe exposure was not for a prolonged period of time.
6 ~- O2 h) ]& S$ PAlthough the bone age was advanced at the time of$ L( F* T* k$ o9 J- Q
diagnosis, the child had a normal growth velocity at/ P) |2 Q9 V: O$ v9 w
the follow-up visit. It is hoped that his final adult
" o$ C9 t1 ]( F+ l, sheight will not be affected.
# V6 Z$ `4 E2 Q9 X9 m+ Y$ UAlthough rarely reported, the widespread avail-4 I3 R1 G  X8 ]# ~
ability of androgen products in our society may
8 D% U/ L- v" H" Z1 ~; a2 uindeed cause more virilization in male or female
2 e" L2 ^, ~* p$ J  Xchildren than one would realize. Exposure to andro-
% e8 F% T' W; Q/ y$ Hgen products must be considered and specific ques-
/ q$ n# E9 A, `: P$ ?7 Ztioning about the use of a testosterone product or# Z8 d# s; Y8 u9 Q! H: U8 ?% X- m( G" y
gel should be asked of the family members during) |3 D# d5 g+ m3 c% e0 Q
the evaluation of any children who present with vir-
2 t7 b2 H% R1 i0 o: r" |/ x5 [ilization or peripheral precocious puberty. The diag-
( L1 ^# Q$ p# _6 c+ a7 ?/ Vnosis can be established by just a few tests and by0 `* ]) u7 F0 s! R* f1 Z
appropriate history. The inability to obtain such a
8 `% ^$ L% d$ z) W' Nhistory, or failure to ask the specific questions, may
2 r) U6 R7 d+ C& X& u3 x# n. @& jresult in extensive, unnecessary, and expensive
4 |: H" N8 O, q; x  x- ]investigation. The primary care physician should be
6 ~# {* N& g  V8 C! u/ faware of this fact, because most of these children
1 n3 v" L$ F# Q4 Zmay initially present in their practice. The Physicians’
2 z! N  O$ n7 oDesk Reference and package insert should also put a7 P8 k2 t( `9 C6 v6 |5 [7 c6 m
warning about the virilizing effect on a male or; h# [5 m' @& x0 u" O& t
female child who might come in contact with some-' m4 c3 q( h& p5 i; }! L& {) l
one using any of these products.' l/ E, z" N- Q2 c& _0 n
References
! r( l1 V& G, z1. Styne DM. The testes: disorder of sexual differentiation7 z! k. X( k  L( S
and puberty in the male. In: Sperling MA, ed. Pediatric
# D3 u' D. I( T/ R' D% x7 J' wEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;5 `) W; W9 q% K# d7 n& @
2002: 565-628.- u6 G# \) E3 ]. ]. z
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
; v+ M9 n& i* ^puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old8 M8 I+ I2 e8 \# w, u
Boy Induced by Indirect Topical
2 I4 Y" y/ ^  M/ M, a5 gExposure to Testosterone
. A. w$ s+ U# y: U: GSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
9 P) k2 Y; A1 a8 d9 t' Mand Kenneth R. Rettig, MD1
% z8 C" K. Q4 kClinical Pediatrics
7 P9 E7 V; Y% V; M* @1 K' ?Volume 46 Number 67 z8 J, [! ^3 V( n8 d8 i: B+ l  O
July 2007 540-543) t# T  j. ^8 o- f  x
© 2007 Sage Publications! y! k* ~8 V0 b, S$ t4 q! C/ e
10.1177/0009922806296651" M" j: G' j3 S2 j
http://clp.sagepub.com9 G/ }! k1 N! I% F! k' o
hosted at
. @7 z7 D6 o% U% l. x! N- h) Qhttp://online.sagepub.com4 s+ b& V6 w+ ]3 u; J
Precocious puberty in boys, central or peripheral,1 {* \$ q4 w9 ?8 N+ d0 P' k
is a significant concern for physicians. Central5 F# M" u  R- T3 y# T; _4 I
precocious puberty (CPP), which is mediated
; z/ r/ t8 R& c! I1 b5 x: e3 Hthrough the hypothalamic pituitary gonadal axis, has( S+ T0 `2 z' x: ?3 r2 C% b
a higher incidence of organic central nervous system
. Q  _7 o6 L3 q8 y/ [lesions in boys.1,2 Virilization in boys, as manifested
. \, n4 y9 l# |7 mby enlargement of the penis, development of pubic6 ~9 H5 C: o/ ]; d  _% [5 W
hair, and facial acne without enlargement of testi-# _& q+ @6 H, o* C+ w
cles, suggests peripheral or pseudopuberty.1-3 We8 Q; J( B: b5 K3 e: _, w$ V
report a 16-month-old boy who presented with the. E3 Z& \( j8 r% }" ~
enlargement of the phallus and pubic hair develop-) o* y8 Y5 C( t' A) P) G1 c
ment without testicular enlargement, which was due5 R: W9 V9 v. ]/ G! G3 }) w
to the unintentional exposure to androgen gel used by, V% r+ P# ~! T+ g! ~
the father. The family initially concealed this infor-& r8 \0 z# |6 U: }' `
mation, resulting in an extensive work-up for this
8 V! ?( l/ ]3 Kchild. Given the widespread and easy availability of
3 B4 A' ?* |# a' @: Z# Q; jtestosterone gel and cream, we believe this is proba-
8 V$ h0 l; }) q3 E$ cbly more common than the rare case report in the) k4 m8 U! _# v. d1 x
literature.4
' X, q5 {& M: `# e" K, FPatient Report
# G5 Z8 z" V2 d5 rA 16-month-old white child was referred to the6 n# t/ Y6 g) k! a8 c
endocrine clinic by his pediatrician with the concern3 v9 E; A0 ?3 O: m
of early sexual development. His mother noticed" ]- y( b1 r9 a  \% `
light colored pubic hair development when he was
, O, W/ X$ O! ?; p  T; l% ~7 C" KFrom the 1Division of Pediatric Endocrinology, 2University of
& i  ]. E) p5 t' \; w% dSouth Alabama Medical Center, Mobile, Alabama.9 {! g+ S4 y& Q+ J$ K0 m6 x6 t
Address correspondence to: Samar K. Bhowmick, MD, FACE,1 B0 }8 ]' K# u( a, Z' t: ?
Professor of Pediatrics, University of South Alabama, College of
( P9 y; ?4 A" ~Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;4 i9 A3 Z! R1 c  f% f
e-mail: [email protected].
" |$ I; A; K4 H" W& z  Kabout 6 to 7 months old, which progressively became" s' ^0 ^" Y+ o: g& }' j' q
darker. She was also concerned about the enlarge-: q/ W: i/ f2 `' v& _: U
ment of his penis and frequent erections. The child
9 n1 D8 `( {, H/ T9 G+ \was the product of a full-term normal delivery, with
! V, M5 H8 G! c0 e$ T- ba birth weight of 7 lb 14 oz, and birth length of9 K5 `( ^* a4 t) ]' G
20 inches. He was breast-fed throughout the first year( w0 H; L2 v+ f: h) G
of life and was still receiving breast milk along with
3 r# |: l3 `2 \0 {0 G; Esolid food. He had no hospitalizations or surgery,' r: m$ t9 R1 A9 p) b5 `# L1 s% H
and his psychosocial and psychomotor development5 ?0 m& d; o+ u) t
was age appropriate.
) _7 i5 U6 S$ g) P) Y0 p3 NThe family history was remarkable for the father,  M7 z7 P4 q8 g$ w
who was diagnosed with hypothyroidism at age 16,
) f0 m5 J- U  e3 l0 [( X% Iwhich was treated with thyroxine. The father’s
. @9 Z7 ~$ E# B5 v! H1 zheight was 6 feet, and he went through a somewhat
# s" g3 m. f2 I7 E$ L8 qearly puberty and had stopped growing by age 14.
2 a& Q3 ~) m5 a4 v, t: y- ZThe father denied taking any other medication. The+ L9 L7 w8 c* F! ]( M0 [4 E
child’s mother was in good health. Her menarche# P9 c0 `9 a4 o! m: O
was at 11 years of age, and her height was at 5 feet, c2 y: Q4 u" F
5 inches. There was no other family history of pre-  y' o; S" C8 j; {0 {
cocious sexual development in the first-degree rela-
% R& M5 X. R+ ]8 p0 ?* A2 ^tives. There were no siblings.3 p4 B  m& ^( j
Physical Examination0 L# t3 l1 j) y1 f
The physical examination revealed a very active,. ~3 ], l: A1 Z& p
playful, and healthy boy. The vital signs documented/ e: r. R) `: E0 {: K+ m
a blood pressure of 85/50 mm Hg, his length was
: p6 B5 U# ~7 y6 }90 cm (>97th percentile), and his weight was 14.4 kg5 L$ x  [9 S% M/ ~1 N( I
(also >97th percentile). The observed yearly growth3 Q& _& B, e' S6 x' ^% x
velocity was 30 cm (12 inches). The examination of
9 z3 p4 N( Y5 o# r* B) ~; Hthe neck revealed no thyroid enlargement.' b0 Z& E, d: f- |1 Q, \
The genitourinary examination was remarkable for  G% _# k7 k/ m+ l) ], J
enlargement of the penis, with a stretched length of
- O  v6 Q- p. K, e9 x! G8 cm and a width of 2 cm. The glans penis was very well
$ T) V; P& n# V/ J6 M+ Pdeveloped. The pubic hair was Tanner II, mostly around0 b5 O3 J& |9 c/ V: F7 f$ P( \" Z
540
# P9 Z) r3 N7 q* u+ d9 Oat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from2 m* g$ ^2 g# C, _
the base of the phallus and was dark and curled. The
' o$ N) V2 m3 I: s/ gtesticular volume was prepubertal at 2 mL each.
: l& h/ w* c8 T& i- uThe skin was moist and smooth and somewhat' w/ X) @& ^# m5 k, Y- |) E) b
oily. No axillary hair was noted. There were no
( Y0 d, {+ _6 l! |3 Mabnormal skin pigmentations or café-au-lait spots.1 n" u( y1 L& ]7 z1 j& p
Neurologic evaluation showed deep tendon reflex 2+
: O/ |0 ~4 u$ u- Dbilateral and symmetrical. There was no suggestion- k1 |- F* j% q' d/ f, N9 P2 [% k
of papilledema.
! E3 V0 V* O3 E. G+ PLaboratory Evaluation
- v/ g3 l; F3 N4 A: U' b" EThe bone age was consistent with 28 months by
" L# d) O, _# W- T; Z) t! Husing the standard of Greulich and Pyle at a chrono-
: }; \# |% f4 m9 e( P5 |logic age of 16 months (advanced).5 Chromosomal
- }: m2 t( d$ }* h& ]karyotype was 46XY. The thyroid function test. Z1 C+ e/ O1 \" m& U: {
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
, ?' f3 S0 v) Blating hormone level was 1.3 µIU/mL (both normal).1 Y1 x& i  [1 d+ u, @7 A  p! k
The concentrations of serum electrolytes, blood' V5 C9 g* Q% R  y2 h0 s
urea nitrogen, creatinine, and calcium all were
! l6 O$ \1 P' }4 Vwithin normal range for his age. The concentration
4 [' z9 d  q# W5 K# d/ Hof serum 17-hydroxyprogesterone was 16 ng/dL
7 Y+ X# N# w" d/ {2 w, ^* \(normal, 3 to 90 ng/dL), androstenedione was 20
+ n7 f9 Q' `8 w, i9 w; z- {$ Png/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
" k0 O. ^0 Q* h! {% hterone was 38 ng/dL (normal, 50 to 760 ng/dL),9 g7 R6 p" O9 F$ I3 K4 W. f
desoxycorticosterone was 4.3 ng/dL (normal, 7 to+ ~$ V& W5 J4 D: v
49ng/dL), 11-desoxycortisol (specific compound S)6 X& l7 ?) B- N/ U0 g5 a5 `
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-/ `6 i; w0 P+ s8 w. |) O9 ^! e
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
$ G& C( C# n' ?8 U$ j- ytestosterone was 60 ng/dL (normal <3 to 10 ng/dL)," W  d; r# W: z, d  R. D0 }
and β-human chorionic gonadotropin was less than
+ L: I. u' @/ H5 mIU/mL (normal <5 mIU/mL). Serum follicular
$ `& i* v6 N7 I- v  I9 pstimulating hormone and leuteinizing hormone
. U8 C. B% \6 @4 V+ c- [: g3 S# {concentrations were less than 0.05 mIU/mL' \" ^- Y1 ]5 H& Q
(prepubertal).
3 D' M: [% C1 O: q, q( y& yThe parents were notified about the laboratory$ f# A1 E2 C2 ^- z
results and were informed that all of the tests were# z7 _1 O& Y3 L% ?2 s1 D$ k
normal except the testosterone level was high. The& i+ ~' s  l( R1 x) I/ Q' ?
follow-up visit was arranged within a few weeks to! m. _$ ]- n- H5 @  ]8 _
obtain testicular and abdominal sonograms; how-
6 r% ?" C- a. v  N5 [+ p! {: Fever, the family did not return for 4 months.7 b2 y4 p0 G# \5 q' s, f9 r: L
Physical examination at this time revealed that the
% y+ j& D2 }8 T* f" d6 X( ~child had grown 2.5 cm in 4 months and had gained
- P4 l: d) ~9 R, [2 kg of weight. Physical examination remained" R8 l" u0 N9 E6 ]
unchanged. Surprisingly, the pubic hair almost com-
* C" J# L. L8 C. H! p" Gpletely disappeared except for a few vellous hairs at$ Z' I; B- J. \( p2 d: \
the base of the phallus. Testicular volume was still 2( C$ n9 Q! Q2 k* y# E# {( b
mL, and the size of the penis remained unchanged.
3 ?7 \$ J) j5 v9 GThe mother also said that the boy was no longer hav-/ p. N' s/ V- \0 @4 ^+ z
ing frequent erections.
! L& ?, B0 ~- e3 P0 c0 q) Z* _, [Both parents were again questioned about use of& c  N' E, \; ^9 [; z# K
any ointment/creams that they may have applied to* h$ y- T) D6 b3 ?& f
the child’s skin. This time the father admitted the
9 A: N8 w1 D. Q, y8 E4 o" }Topical Testosterone Exposure / Bhowmick et al 541
6 o/ m% f" R% wuse of testosterone gel twice daily that he was apply-
0 v3 Z/ _9 v* k' Z4 y1 Sing over his own shoulders, chest, and back area for
4 s3 \) s! n  e" ^& S& _a year. The father also revealed he was embarrassed% J# m# L0 _" H( C3 y0 ~& t
to disclose that he was using a testosterone gel pre-) H# }3 w: k3 p
scribed by his family physician for decreased libido
* R0 o- x/ \9 b" F  Wsecondary to depression.
' V: Y$ V3 G* h# vThe child slept in the same bed with parents." E1 e6 q- \# z+ k
The father would hug the baby and hold him on his
! v4 r) \  s0 P5 v# C* ~chest for a considerable period of time, causing sig-) W8 z, C! m# g- R1 c
nificant bare skin contact between baby and father.
; Q9 A/ B5 e7 t( PThe father also admitted that after the phone call,
1 B( X5 _* p1 C1 t! V1 w! S  hwhen he learned the testosterone level in the baby7 W2 K0 g5 ^: E, f' y  [$ o
was high, he then read the product information2 M) n6 x( E7 }
packet and concluded that it was most likely the rea-6 R- Y. e" D5 Y- l
son for the child’s virilization. At that time, they
% S: @  P2 W5 Q  W" wdecided to put the baby in a separate bed, and the
9 u; r" n2 i- N2 H& Y* wfather was not hugging him with bare skin and had
3 y) ^# A" s; R6 Cbeen using protective clothing. A repeat testosterone& ?  ~# ?3 i1 H+ b% n. }  r
test was ordered, but the family did not go to the& m0 B1 G% e+ y# c
laboratory to obtain the test.
/ p( N: V1 j6 }9 YDiscussion2 C6 c! {0 {, W. Z' r( {# @4 ?' _# L
Precocious puberty in boys is defined as secondary
  J2 [, K, m. Fsexual development before 9 years of age.1,46 g4 L3 F) l% K) u" \
Precocious puberty is termed as central (true) when% n7 d1 Y' X8 P$ h
it is caused by the premature activation of hypo-
) n9 r5 ?0 C( S5 o- _6 xthalamic pituitary gonadal axis. CPP is more com-' l, L, ?: u- E
mon in girls than in boys.1,3 Most boys with CPP9 F- A  L; o7 X4 H
may have a central nervous system lesion that is5 T$ A' ?$ M! B
responsible for the early activation of the hypothal-
$ E* E  M, M; jamic pituitary gonadal axis.1-3 Thus, greater empha-3 j9 o  H8 \- U9 {$ U5 c6 o
sis has been given to neuroradiologic imaging in: G. n2 ?2 |, e3 C- H
boys with precocious puberty. In addition to viril-$ h& `  L% l) l* ~  O8 y  o
ization, the clinical hallmark of CPP is the symmet-
0 L# f' x/ L7 C9 n/ L  a9 drical testicular growth secondary to stimulation by
1 N5 Z) c+ p; w9 @) B. v" @7 pgonadotropins.1,37 d6 E9 P  h/ W/ ]( ~
Gonadotropin-independent peripheral preco-2 F% g6 X4 M4 K. a
cious puberty in boys also results from inappropriate
$ L$ X" @  H  y" ?0 q+ {* Fandrogenic stimulation from either endogenous or3 S1 n% s& o3 k8 S
exogenous sources, nonpituitary gonadotropin stim-
& p; H, P/ Z1 W+ X$ `6 |; tulation, and rare activating mutations.3 Virilizing
8 L' M( S6 V0 G6 t3 b" J  Scongenital adrenal hyperplasia producing excessive" X% D- m* r5 ?% _. F9 q5 a
adrenal androgens is a common cause of precocious; x/ i+ \% v- ~/ e1 ]+ J% x
puberty in boys.3,4$ h( J) x0 U: x  A( j
The most common form of congenital adrenal! A9 Y3 K1 U; g5 a
hyperplasia is the 21-hydroxylase enzyme deficiency.: l, j) u+ t5 f# C1 `4 p: S+ m
The 11-β hydroxylase deficiency may also result in
, U6 x' L. a* B! b2 u# [excessive adrenal androgen production, and rarely,$ X3 O. M" |/ h" M- \/ I9 Q/ D
an adrenal tumor may also cause adrenal androgen9 D3 E3 R3 K9 M
excess.1,3
0 r+ i4 e; ~& V6 ^  P9 m2 iat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
8 c, F3 D, _0 Q' E542 Clinical Pediatrics / Vol. 46, No. 6, July 20073 w7 Q- P) j4 s: h8 i
A unique entity of male-limited gonadotropin-6 X" X7 W  S- o: H7 ^, J: O0 L# m
independent precocious puberty, which is also known. @: j0 I* I3 p+ J- d0 N
as testotoxicosis, may cause precocious puberty at a* ~% D5 }$ M5 [6 [9 N# U+ G
very young age. The physical findings in these boys6 |, Y. n, b7 x7 D
with this disorder are full pubertal development,
3 V  t0 V& Q* M! g% v; q) |1 jincluding bilateral testicular growth, similar to boys( ~0 e8 h% O5 e" P
with CPP. The gonadotropin levels in this disorder
8 a- D: O+ G* h1 [/ W0 w4 e% Zare suppressed to prepubertal levels and do not show8 P6 A; L5 j3 ^  N, {. k: Q
pubertal response of gonadotropin after gonadotropin-
+ u- e* j9 \5 {* S4 i1 rreleasing hormone stimulation. This is a sex-linked
+ G! D% J) e: j' z: C& f$ p4 aautosomal dominant disorder that affects only
7 g1 ^  c: w0 o) M; F# N" Mmales; therefore, other male members of the family
+ _7 u- V) e/ E/ [* i) ?9 Y" {may have similar precocious puberty.30 n8 Q* p1 a9 N6 B" T8 {: e; i
In our patient, physical examination was incon-7 e$ D: X  E, w) ^4 u4 P9 e
sistent with true precocious puberty since his testi-; u* F1 a0 K4 n# N4 T* e
cles were prepubertal in size. However, testotoxicosis7 M0 L' J$ O% Y; H
was in the differential diagnosis because his father& Y( ]7 f( @, c
started puberty somewhat early, and occasionally,- ^4 L& i7 _- P2 C" N: b
testicular enlargement is not that evident in the
* P  {& R4 n" ]  G" v! Pbeginning of this process.1 In the absence of a neg-7 O' |  h* z- D! O: w
ative initial history of androgen exposure, our4 g+ ?4 n+ X, W% a
biggest concern was virilizing adrenal hyperplasia,
$ m4 l- B5 E5 ^) Jeither 21-hydroxylase deficiency or 11-β hydroxylase
6 N. h! Z2 }8 K+ U1 A# Sdeficiency. Those diagnoses were excluded by find-
" o; M; b8 ^. \3 bing the normal level of adrenal steroids.
; {2 L$ {" i5 i; aThe diagnosis of exogenous androgens was strongly
) Q( T' L! j. W$ Bsuspected in a follow-up visit after 4 months because* f6 v: E# X1 g+ @& @
the physical examination revealed the complete disap-
3 a1 U8 ?  M/ ]$ i. e7 Zpearance of pubic hair, normal growth velocity, and& r: w8 U+ R- I/ j+ ^: h7 M
decreased erections. The father admitted using a testos-' f& o! _2 a& X" N9 M+ K' f* Z
terone gel, which he concealed at first visit. He was
. w' }+ ~7 _! g. E: Ausing it rather frequently, twice a day. The Physicians’
" h1 g5 W; W" k8 T" R$ M8 tDesk Reference, or package insert of this product, gel or! @, H5 G+ r4 L
cream, cautions about dermal testosterone transfer to; r  c! M4 w$ b
unprotected females through direct skin exposure.7 d$ i! r4 Q9 Q" e5 w7 b2 S0 U" w8 {6 g4 L
Serum testosterone level was found to be 2 times the
9 U  k" x3 n( ~% b+ a$ c7 l  hbaseline value in those females who were exposed to
4 i+ z6 S" f* |even 15 minutes of direct skin contact with their male
' Q0 \+ ~, _) gpartners.6 However, when a shirt covered the applica-
9 v1 \# o) [: b+ `& e2 N! o9 H/ Mtion site, this testosterone transfer was prevented.
9 P8 r5 A) Q, D2 V3 z* T. ^Our patient’s testosterone level was 60 ng/mL,9 K7 f6 w6 x8 i/ m. y
which was clearly high. Some studies suggest that
) n% @0 |+ M9 u( }( \8 ?8 J/ Edermal conversion of testosterone to dihydrotestos-$ O, `4 ?9 t3 T6 E- s( d
terone, which is a more potent metabolite, is more0 H1 J# r" I/ [8 ~
active in young children exposed to testosterone& ^. m0 m) \2 d# @/ r' @0 j" x
exogenously7; however, we did not measure a dihy-! E& L' v% S/ E/ O2 v4 G5 q' p
drotestosterone level in our patient. In addition to
, c4 u( P7 k1 O" D- D' [virilization, exposure to exogenous testosterone in; k: k6 n- {) j
children results in an increase in growth velocity and
  v( N+ H# M& C. ?- l. q! \advanced bone age, as seen in our patient.
* M2 y) l6 d3 ?The long-term effect of androgen exposure during
0 z3 N8 s2 f* Z9 i: hearly childhood on pubertal development and final
% y# d, n! c3 f0 w: hadult height are not fully known and always remain
- |# B, L2 A9 D/ N3 ~7 Na concern. Children treated with short-term testos-
6 ]; |" y' ]  q. wterone injection or topical androgen may exhibit some
& G) A# w5 F1 |0 V' U. |acceleration of the skeletal maturation; however, after) V6 u3 Q( r: v
cessation of treatment, the rate of bone maturation
" e6 F: \/ F$ \% z9 t9 jdecelerates and gradually returns to normal.8,9
* R5 t" G- j' }) bThere are conflicting reports and controversy
1 }# k& T2 n* {- [# v  Eover the effect of early androgen exposure on adult
- ?: M6 o: S) m/ Y( _penile length.10,11 Some reports suggest subnormal3 d; k3 s& |' u7 `
adult penile length, apparently because of downreg-$ C6 W% e" P, S  e1 w* }, ]' N
ulation of androgen receptor number.10,12 However,6 R' p$ r$ [0 N# O' }, C
Sutherland et al13 did not find a correlation between" V5 P) K3 z% i; V9 c- ]) \
childhood testosterone exposure and reduced adult
7 c/ ^  D$ ^. A6 E7 Dpenile length in clinical studies.
3 A4 a5 Y/ E# Y8 B7 N; oNonetheless, we do not believe our patient is3 R9 p6 I3 ^( J8 |
going to experience any of the untoward effects from
+ B) U0 r: \& F! f( F  R: Ctestosterone exposure as mentioned earlier because
" A- F3 `' l3 Xthe exposure was not for a prolonged period of time.
% b; d# Z# Z6 e: ~5 p# i9 RAlthough the bone age was advanced at the time of
& ]  i+ d7 x  o: T/ B$ _6 gdiagnosis, the child had a normal growth velocity at
! E" D  {' K+ f; m1 G8 |4 kthe follow-up visit. It is hoped that his final adult4 c: B  P- _: q' e
height will not be affected.
1 e, Z3 b( N& P5 D) jAlthough rarely reported, the widespread avail-
+ T( ^: f9 W; }) u; Lability of androgen products in our society may; X/ V2 I% Q: k* L
indeed cause more virilization in male or female' C# I: y' p/ z7 a) |
children than one would realize. Exposure to andro-" q5 k* h- b% ]6 v, _6 o' W5 U
gen products must be considered and specific ques-
% }0 c( w0 _, ntioning about the use of a testosterone product or
, w& G5 W8 Q: L- \  S) v' [gel should be asked of the family members during* q/ c1 u7 W  D
the evaluation of any children who present with vir-
6 [6 B, U* s' R( @ilization or peripheral precocious puberty. The diag-/ |6 d7 \( F" Q) d1 U
nosis can be established by just a few tests and by
  I& {6 ~, ]% p. jappropriate history. The inability to obtain such a/ W  {7 r3 c9 x4 Q5 z; @" \
history, or failure to ask the specific questions, may
$ z# J2 y: i( I; _" H% b2 p- Lresult in extensive, unnecessary, and expensive& |7 L- T& B! }3 n# ~5 K! n
investigation. The primary care physician should be+ ?0 W/ T1 n9 ]) ]7 {* ?
aware of this fact, because most of these children0 H9 z  U2 s+ b0 o+ F& T
may initially present in their practice. The Physicians’
' o4 f/ l$ |9 M7 E- U  }Desk Reference and package insert should also put a) |0 W4 s  \9 R) x
warning about the virilizing effect on a male or! n' c/ V% u4 u* v4 Z
female child who might come in contact with some-1 z1 x0 w. e0 P' i! T6 J4 w
one using any of these products.
5 V$ f( a" k. p" K4 B6 @& w  U; fReferences; d. `( h7 A0 |0 X; t8 L+ y5 [( g5 d
1. Styne DM. The testes: disorder of sexual differentiation
* z4 F1 z6 o1 r6 e  ~/ L% Gand puberty in the male. In: Sperling MA, ed. Pediatric3 p& ]% K+ L6 w- y+ n" B; V  V5 s
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;) r, {7 t# f0 z& h& E, C
2002: 565-628.
0 E# h+ ^# H* f2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious6 ]2 U/ E  ?7 b/ i7 b
puberty in children with tumours of the suprasellar pineal
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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
- X6 g2 D! p' X: u6 Z
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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