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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
4 ?. L# W' B+ C/ w1 g3 n! [9 QBoy Induced by Indirect Topical( O7 q& h% y! _' g
Exposure to Testosterone9 m' |; j1 o, D
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
9 \6 E: B9 U* E6 e% U( [6 P; Xand Kenneth R. Rettig, MD1' `) T6 r' o  G7 y& S# T- C% ~- v
Clinical Pediatrics7 `0 u) W$ J- s1 }" j$ w1 R8 l$ }
Volume 46 Number 6! Z6 L) E% c4 i- ?' q
July 2007 540-543
! k& u( P4 F( k2 q! Z3 l" K/ u) C© 2007 Sage Publications
; O" U! @/ d3 w+ N10.1177/0009922806296651
. O9 [* `+ g' ~  s7 ?9 v: khttp://clp.sagepub.com
+ E0 s: |3 ^& U  @' |2 ahosted at' D# Z0 p# I  z5 S' ^
http://online.sagepub.com! K" S2 |- E" Y
Precocious puberty in boys, central or peripheral,! q! W; X. ~: m1 J
is a significant concern for physicians. Central
, R! k/ {0 T, g% [! F0 Pprecocious puberty (CPP), which is mediated2 x6 Q. R# w" i
through the hypothalamic pituitary gonadal axis, has
! u) Z; o7 E# e5 x; f, U& O/ Fa higher incidence of organic central nervous system
" Z! V8 t3 s) m9 Mlesions in boys.1,2 Virilization in boys, as manifested
: i; [" |: E4 _* O$ n% ]6 Iby enlargement of the penis, development of pubic
! \+ ^9 t+ _/ ^5 T0 R: phair, and facial acne without enlargement of testi-
% n. p" D' z! n! B. e$ h7 h' ?cles, suggests peripheral or pseudopuberty.1-3 We
8 ~9 J2 Y4 Y* B: E' m  \  u- r8 preport a 16-month-old boy who presented with the
4 [6 V! u2 F2 Kenlargement of the phallus and pubic hair develop-, z, c+ z- f% H6 f& W: C' C0 k6 S
ment without testicular enlargement, which was due
+ i8 Z2 G. q) m+ K9 {2 wto the unintentional exposure to androgen gel used by
8 ]7 b* U% w# b. U3 B8 Y5 nthe father. The family initially concealed this infor-! w) l( M, j$ I8 H8 R: t
mation, resulting in an extensive work-up for this
6 u- M% K' p& v( c7 nchild. Given the widespread and easy availability of
- ~; @  V! S9 M; T9 g4 x1 H% atestosterone gel and cream, we believe this is proba-
  }  t4 [- N" E3 N2 Xbly more common than the rare case report in the
8 B! U/ X  C. X. Q) Hliterature.4
3 r% \! s. T+ m9 i$ E. @  l8 IPatient Report9 e& y- O0 i; g3 R6 `" V% X
A 16-month-old white child was referred to the% E: r& |: A- `. F3 n6 p1 x1 j5 r
endocrine clinic by his pediatrician with the concern
1 ^' @2 L0 V, |+ ]of early sexual development. His mother noticed
/ i9 p% P8 i9 o( v+ z( n. u! dlight colored pubic hair development when he was# \  a+ }5 P  q
From the 1Division of Pediatric Endocrinology, 2University of- I, a3 N9 L$ r7 R: _% g
South Alabama Medical Center, Mobile, Alabama.' i: m# k! B2 u0 A5 r
Address correspondence to: Samar K. Bhowmick, MD, FACE,
6 N: F- I# _: B8 X( M  O) ]Professor of Pediatrics, University of South Alabama, College of; {; J9 E% b/ }( B
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;# A" k, P2 M+ W5 ]- [* I
e-mail: [email protected].
+ R5 V  O2 e' Xabout 6 to 7 months old, which progressively became
4 G' V- P; r- p( _, N, adarker. She was also concerned about the enlarge-6 m, B$ Z, V& o9 W! ^  {! J
ment of his penis and frequent erections. The child: V! a* a$ p$ R% r! W3 ~
was the product of a full-term normal delivery, with
4 D3 z+ G- p5 s/ y7 V8 |3 V5 {a birth weight of 7 lb 14 oz, and birth length of
0 W6 {9 ?  U. ]- N20 inches. He was breast-fed throughout the first year; ~( J6 {7 _/ Q/ Y0 h* N
of life and was still receiving breast milk along with- O+ }- J+ R- L; x! K
solid food. He had no hospitalizations or surgery,
+ v# D" z2 x) ~and his psychosocial and psychomotor development" W7 r, J; D- P( Q" S8 V0 Q0 l
was age appropriate.
9 {2 b/ m, j0 v# ^- @The family history was remarkable for the father,& C( Y$ |- S" \6 P4 F/ |- I; Z
who was diagnosed with hypothyroidism at age 16,  a# O3 }& J; R( w: E
which was treated with thyroxine. The father’s
$ s% d/ V6 a3 g" F0 Oheight was 6 feet, and he went through a somewhat! y/ \* ^- V9 X7 p9 z5 x
early puberty and had stopped growing by age 14.
6 ~$ M4 R/ A" P. TThe father denied taking any other medication. The" \8 e5 M/ K; w+ z: E
child’s mother was in good health. Her menarche  p7 F6 c4 L( M7 n- a" n: M) W) ]
was at 11 years of age, and her height was at 5 feet5 U1 A% J5 u- [, y" O
5 inches. There was no other family history of pre-1 k# X. R$ o6 l* s* b
cocious sexual development in the first-degree rela-- p8 b+ F9 R; [( z3 N) a. u9 G6 X
tives. There were no siblings.
+ M; ]) {' S; f" ePhysical Examination( X% s6 Y' K& Y( V
The physical examination revealed a very active,  ?0 x2 y# w2 w, n0 h% Z; a
playful, and healthy boy. The vital signs documented
# p/ m! L3 M, Sa blood pressure of 85/50 mm Hg, his length was3 `, S( s1 u0 M
90 cm (>97th percentile), and his weight was 14.4 kg. Q1 t& b( \/ `
(also >97th percentile). The observed yearly growth
, P& s9 |( B& Z5 E* C9 Gvelocity was 30 cm (12 inches). The examination of( q1 r$ J0 {/ w2 e: I/ i
the neck revealed no thyroid enlargement.' {3 v4 c! W5 p( W+ |
The genitourinary examination was remarkable for
) W* m9 ]% \; g4 X, E) Senlargement of the penis, with a stretched length of
+ T2 V4 j5 |3 s! D8 cm and a width of 2 cm. The glans penis was very well
, v* p4 b; u; P: rdeveloped. The pubic hair was Tanner II, mostly around$ ^, b, U/ k. l8 s" f
540  g+ `# ?: i4 f! E, P  L/ Y! m+ A
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from% f1 X& w! B  W, a
the base of the phallus and was dark and curled. The- Z" h' U) T8 \$ P/ ~
testicular volume was prepubertal at 2 mL each.
' B$ N& P- e+ E/ \  kThe skin was moist and smooth and somewhat, C" w0 o$ U4 @) C" s" C
oily. No axillary hair was noted. There were no  A' M% b4 B  g/ l0 i+ ^
abnormal skin pigmentations or café-au-lait spots.' V( v+ v) X& S1 o; F# Q
Neurologic evaluation showed deep tendon reflex 2+( W7 i. i5 A& h+ T
bilateral and symmetrical. There was no suggestion" Y4 r3 \; M7 I  f0 e5 _: A# J- H
of papilledema.
$ X, ?2 D1 r1 X: z1 C" c7 w! ^Laboratory Evaluation
) O7 j" x" K# Y2 I0 a: v( S. RThe bone age was consistent with 28 months by
) j7 o4 x! |2 L6 Nusing the standard of Greulich and Pyle at a chrono-
3 U( j+ f( @: U. |logic age of 16 months (advanced).5 Chromosomal
1 l! x9 S% z' R5 akaryotype was 46XY. The thyroid function test' w. q& V, Z2 N! K
showed a free T4 of 1.69 ng/dL, and thyroid stimu-+ M" ?7 J. z9 b
lating hormone level was 1.3 µIU/mL (both normal).) F& r+ c4 I- e' B/ }) w
The concentrations of serum electrolytes, blood
; W; s: O2 x0 [" U3 \, D9 D# T$ uurea nitrogen, creatinine, and calcium all were* {: T2 O1 R( c8 _# C9 ^1 q
within normal range for his age. The concentration
( k3 Z: Z; M+ p# w: a6 _of serum 17-hydroxyprogesterone was 16 ng/dL
& b4 g0 F" d: j/ O* I' V(normal, 3 to 90 ng/dL), androstenedione was 20* S( n9 |# v$ q1 c6 ?! S( J: s4 r
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-8 `7 c  `! \* Y4 D; _; x
terone was 38 ng/dL (normal, 50 to 760 ng/dL),. p, }2 {! I5 P; B. z. V, t
desoxycorticosterone was 4.3 ng/dL (normal, 7 to! \1 b4 g# T( U1 D
49ng/dL), 11-desoxycortisol (specific compound S)% v/ f0 p# y, _* z3 z3 c/ ?' e# H4 W! N
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-# }" U0 s) v6 N
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total4 H0 k0 v/ u- n( P% f! ?
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),$ d" O% ?0 T  o
and β-human chorionic gonadotropin was less than( |7 ~5 m1 \& ?3 ~- H
5 mIU/mL (normal <5 mIU/mL). Serum follicular
7 Y* h7 J, g2 l/ K- D* W4 y+ Jstimulating hormone and leuteinizing hormone
6 @6 R8 \/ a# i8 Jconcentrations were less than 0.05 mIU/mL
8 z( t4 Q8 Z% m% ?(prepubertal).
# ^) \7 X* D( V* e! ~+ iThe parents were notified about the laboratory
/ m: d! _) ]$ J4 z: Qresults and were informed that all of the tests were
. C1 j  r' t* c% w2 Wnormal except the testosterone level was high. The2 A0 k! s( f+ ~" t9 U! w% o" t+ J
follow-up visit was arranged within a few weeks to
, Z- w/ e, }8 nobtain testicular and abdominal sonograms; how-
) L, L" i# t+ W+ o3 _ever, the family did not return for 4 months.) g/ V, H- K/ A& }& e
Physical examination at this time revealed that the. L% r# X: `& M- y
child had grown 2.5 cm in 4 months and had gained3 }6 |0 B/ f) @1 u  Q
2 kg of weight. Physical examination remained1 |: u' y0 M- a6 u7 a" H; Z% {
unchanged. Surprisingly, the pubic hair almost com-
: i1 }/ Z% s0 Q: h( n4 gpletely disappeared except for a few vellous hairs at
) d, h) W6 j4 C! @' ], O5 Z: ?the base of the phallus. Testicular volume was still 2& M1 H  Z6 V; L. w+ H
mL, and the size of the penis remained unchanged.
6 d5 _  n' W* l/ |9 V% XThe mother also said that the boy was no longer hav-
- O+ F8 d, a8 d6 W' ~* C" f7 Ring frequent erections.
- w) V7 i/ \! ~2 A: QBoth parents were again questioned about use of+ J3 n9 G) h# Q  W0 X
any ointment/creams that they may have applied to
) ?* S% h7 _) X& Q5 P/ qthe child’s skin. This time the father admitted the8 O- Y' J. Y  J) B7 Y; r
Topical Testosterone Exposure / Bhowmick et al 541* e! m9 g  p  Y# Q. l
use of testosterone gel twice daily that he was apply-
) r+ `4 _5 i  s5 ting over his own shoulders, chest, and back area for
" ~2 c9 Y+ B' ]& c9 z, g$ @( ?) Aa year. The father also revealed he was embarrassed
9 C& |8 H( D! m8 \; y6 v, _( Rto disclose that he was using a testosterone gel pre-
2 D, E5 e, A9 ~: Gscribed by his family physician for decreased libido! x# ~/ R7 [) W3 K- J* N. J; U
secondary to depression.
2 C8 O$ u! g4 v9 h% k3 T4 wThe child slept in the same bed with parents.
/ j8 _- i7 H! h) A- KThe father would hug the baby and hold him on his5 w7 x1 I9 U& U0 d  k) S8 c4 }
chest for a considerable period of time, causing sig-
* X: e7 O3 F; h3 gnificant bare skin contact between baby and father." k1 {7 `- h9 ~8 m3 T" S
The father also admitted that after the phone call,, a" P+ l: O8 t) s
when he learned the testosterone level in the baby5 G# l; Q* `! A1 J7 c4 q4 U/ s
was high, he then read the product information
& U, i/ H$ \' @  K7 J4 xpacket and concluded that it was most likely the rea-6 @2 T/ o4 E6 g
son for the child’s virilization. At that time, they+ s1 \9 q8 V1 q3 s6 \4 ~
decided to put the baby in a separate bed, and the/ H0 L' L& G  b* O
father was not hugging him with bare skin and had
  e* g) p2 F) Z3 y) Q6 F! ~been using protective clothing. A repeat testosterone
+ T" |; {: ^1 d* B# V0 Ktest was ordered, but the family did not go to the& f. x: F$ [6 X* C; E/ P
laboratory to obtain the test.
3 t% b5 W2 `  `Discussion3 }) Y$ {, k! `6 b' X8 W
Precocious puberty in boys is defined as secondary( R; `3 [5 v* U: W( |/ s, k
sexual development before 9 years of age.1,40 ~1 T6 _" R& b6 O0 [/ K- i) Z6 X+ }
Precocious puberty is termed as central (true) when
: \) u/ W' e1 {4 Tit is caused by the premature activation of hypo-
- {; I/ P# k4 K& P" a8 dthalamic pituitary gonadal axis. CPP is more com-, N1 q% U# Z' r) _1 t
mon in girls than in boys.1,3 Most boys with CPP# ~5 y  s8 s( w: `" f
may have a central nervous system lesion that is
0 N8 h' d# I- [. P2 aresponsible for the early activation of the hypothal-
, @5 x' W+ M- g2 G! Z0 Hamic pituitary gonadal axis.1-3 Thus, greater empha-9 @: G& ~  }' j7 Y$ D' l3 n
sis has been given to neuroradiologic imaging in
6 l, [5 r. z; |1 @" C% Gboys with precocious puberty. In addition to viril-
! [) l) C: W) P# A% R6 @ization, the clinical hallmark of CPP is the symmet-
$ |/ }2 h5 E, l8 lrical testicular growth secondary to stimulation by, d+ o' @2 i; Q# F+ M9 u8 |, G4 W
gonadotropins.1,3
* M$ Z6 T8 r; |' K  {4 TGonadotropin-independent peripheral preco-9 Q5 N2 C: b9 f. Z
cious puberty in boys also results from inappropriate, l) {0 x1 f$ X7 F. j6 y
androgenic stimulation from either endogenous or
" f8 Q3 O) G' `* ]4 ?+ texogenous sources, nonpituitary gonadotropin stim-
2 I' S! e$ K0 k" V( e! C, Oulation, and rare activating mutations.3 Virilizing
) T( b" e# o4 S  {4 Lcongenital adrenal hyperplasia producing excessive) j' }# U, F. J- v0 j8 y9 r
adrenal androgens is a common cause of precocious
7 e8 }9 \$ C: W. F8 w5 ]5 P/ y- Fpuberty in boys.3,4- \8 O& P6 o# y( F5 R- f2 g
The most common form of congenital adrenal" B. i$ r6 @1 E7 j" X* `$ Y6 m% I, C
hyperplasia is the 21-hydroxylase enzyme deficiency.4 F4 K" ~$ [4 r
The 11-β hydroxylase deficiency may also result in: |5 f. W: ^+ K; O  U
excessive adrenal androgen production, and rarely,
  J( C8 U4 v+ M# xan adrenal tumor may also cause adrenal androgen. E9 z$ l8 ^! J; L
excess.1,3( @- S4 g$ e' x% P3 }
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from- L) j: A  A0 N- }; Q; H
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
0 c( P  h4 E4 @  O/ rA unique entity of male-limited gonadotropin-: E, o. f8 y: R& @* P( j3 R( F
independent precocious puberty, which is also known
$ u5 H/ H6 \$ }as testotoxicosis, may cause precocious puberty at a* ?+ U& B+ m* c9 b5 g
very young age. The physical findings in these boys
# D6 r7 S8 M7 r& I$ v( T( D5 V6 Cwith this disorder are full pubertal development,5 d; G0 O" c4 o# P( I
including bilateral testicular growth, similar to boys
7 K4 Y% ^1 \8 W! K, _; b7 j& M  Owith CPP. The gonadotropin levels in this disorder
1 b2 l$ `+ C1 ]! ]* ~/ o/ Yare suppressed to prepubertal levels and do not show
0 X0 G: g4 T( A7 R! ]: _1 O! ipubertal response of gonadotropin after gonadotropin-
: H% m. w  L& {7 [releasing hormone stimulation. This is a sex-linked
  H- Y( A- E$ p# G0 r4 d& j( pautosomal dominant disorder that affects only
; d2 v9 ?1 s  _& P. k+ k8 Q2 k/ Umales; therefore, other male members of the family; ^6 k+ l" y: w5 h. j! E2 O5 q5 C
may have similar precocious puberty.3
0 O( i1 {0 X- \, r$ T: i7 kIn our patient, physical examination was incon-
* n3 ^% y8 l/ G5 h# p$ ]sistent with true precocious puberty since his testi-7 J3 h. m0 F" l1 s  Y7 q
cles were prepubertal in size. However, testotoxicosis7 W) T+ G% k- K5 v6 t. k  r3 M
was in the differential diagnosis because his father
% H$ v* @8 B7 R1 Ustarted puberty somewhat early, and occasionally,7 A! |! y& q  I# s+ z& p& o6 W4 {
testicular enlargement is not that evident in the! d1 T; Q/ R$ ^; }% l
beginning of this process.1 In the absence of a neg-& o2 Z& [. e; c9 S4 U$ ^/ R
ative initial history of androgen exposure, our2 w. f( n4 o6 M+ ~
biggest concern was virilizing adrenal hyperplasia,
$ f: q8 a+ b4 N! b) \either 21-hydroxylase deficiency or 11-β hydroxylase
7 Q9 @  s( g) Wdeficiency. Those diagnoses were excluded by find-  l8 s1 M; m* [1 i" E' V# b) [
ing the normal level of adrenal steroids.
8 U2 I' {0 H. A; g. H+ u7 x5 F( @The diagnosis of exogenous androgens was strongly' y" o# e- ?2 E. E
suspected in a follow-up visit after 4 months because* Y/ o( Y2 l, q# f, w
the physical examination revealed the complete disap-
% s: m) B8 @7 @pearance of pubic hair, normal growth velocity, and
8 W3 t  ]8 e  m* j% pdecreased erections. The father admitted using a testos-
  f$ G/ Y! J+ D) {5 @; d# _/ ^terone gel, which he concealed at first visit. He was
4 E( A( A" W/ [! m: f3 x. J% Z$ Zusing it rather frequently, twice a day. The Physicians’4 D; R  [" e* @
Desk Reference, or package insert of this product, gel or# a7 R; o3 g- L2 Y/ ]
cream, cautions about dermal testosterone transfer to1 S0 z8 Q, O# q
unprotected females through direct skin exposure.
* ]$ d! {$ n% [$ g. Q& _+ QSerum testosterone level was found to be 2 times the# q, G- P0 x: v! E& y; y/ g6 q
baseline value in those females who were exposed to. X* F+ V! X0 e- C- E9 w
even 15 minutes of direct skin contact with their male8 w$ s  h) m6 }' k
partners.6 However, when a shirt covered the applica-
6 |. B" k5 O( ]& K3 Rtion site, this testosterone transfer was prevented.; P0 u0 a4 f$ y! m- Z+ t
Our patient’s testosterone level was 60 ng/mL,% p, l) M* d( G! g" R9 r* Z5 Z
which was clearly high. Some studies suggest that
( `# D# ^4 Q6 [dermal conversion of testosterone to dihydrotestos-8 y6 C* ~1 g9 j& K. w
terone, which is a more potent metabolite, is more: c* e- [7 C. Q+ F; H
active in young children exposed to testosterone  F4 g2 o& B& a# |* ?5 j
exogenously7; however, we did not measure a dihy-" z% T7 f5 T/ S0 |6 K. _( W
drotestosterone level in our patient. In addition to/ l  n% \8 K' a/ z
virilization, exposure to exogenous testosterone in0 z5 E& e( L+ L/ G! m; u, f0 G/ _
children results in an increase in growth velocity and
0 m$ w8 F# E% m' @advanced bone age, as seen in our patient.8 |' X+ L8 R& o; r4 H$ u
The long-term effect of androgen exposure during
( G9 ]0 d4 o" t( t- N3 xearly childhood on pubertal development and final
! R8 y% F) i+ a2 t+ M" W( Oadult height are not fully known and always remain' r+ |/ Y# e9 F* b' O
a concern. Children treated with short-term testos-
3 _4 Y: I6 `) S* z4 q1 Lterone injection or topical androgen may exhibit some1 X! T! M7 o; u  W. s
acceleration of the skeletal maturation; however, after
* Z3 g/ J% a  vcessation of treatment, the rate of bone maturation+ r2 J) K) w7 t$ }5 c7 ^
decelerates and gradually returns to normal.8,9
/ P, r& C  L8 ]There are conflicting reports and controversy
9 `# d/ }# g# z# E  U9 y0 ?7 }, Gover the effect of early androgen exposure on adult! |6 |9 E' P; \* A! e# ^% z/ A
penile length.10,11 Some reports suggest subnormal
/ m& }5 f. T. r. m% Sadult penile length, apparently because of downreg-
4 r* Z4 D6 P7 z, r; U( p. lulation of androgen receptor number.10,12 However,; K) V# R7 b/ h% a
Sutherland et al13 did not find a correlation between
  i8 I& ^( y4 M7 ]; U3 [7 U2 M# Jchildhood testosterone exposure and reduced adult
4 ^+ W5 `; }4 h; S) o! Ypenile length in clinical studies.
+ v2 i& B8 |4 x0 rNonetheless, we do not believe our patient is7 x0 H* x* F5 j+ P0 o
going to experience any of the untoward effects from
; q% y. w4 G3 I% N/ h2 dtestosterone exposure as mentioned earlier because
  U/ O* c- q0 k7 E4 qthe exposure was not for a prolonged period of time.
% p: f5 O+ z7 {* M/ b* dAlthough the bone age was advanced at the time of1 O# L! z- }+ P3 S
diagnosis, the child had a normal growth velocity at
; Z2 Z6 V- i/ L. {the follow-up visit. It is hoped that his final adult
5 _4 f  n( ~7 ?$ L6 V* R  {height will not be affected.- c) ~5 y  J! q
Although rarely reported, the widespread avail-
! ^  C5 S3 g4 G) t1 }  Z% R0 S3 G2 Wability of androgen products in our society may, n" n1 n# j" V) I) P
indeed cause more virilization in male or female, @& b4 P" a  Y9 c
children than one would realize. Exposure to andro-
/ h3 i* p0 }: p" dgen products must be considered and specific ques-
  \8 U- d/ H: H/ f  Stioning about the use of a testosterone product or/ Q. g( I; m& I2 Z, m. e# f; ?& Y
gel should be asked of the family members during. B+ V) G- a, l" c
the evaluation of any children who present with vir-
, B1 v, \! Z+ P* @" a0 Yilization or peripheral precocious puberty. The diag-
7 v* Q* B5 @0 J3 C$ xnosis can be established by just a few tests and by
6 _& l% N( ~4 g) C- c* aappropriate history. The inability to obtain such a
" ]# n9 F7 }# U- v$ i$ W; l) chistory, or failure to ask the specific questions, may+ s- k1 f  O) [
result in extensive, unnecessary, and expensive; g! ?9 k8 m' Y
investigation. The primary care physician should be' k! M9 }/ q' c3 O1 s- G) @
aware of this fact, because most of these children
! Q& U. d% b$ ~& i  u1 U0 ?% ^may initially present in their practice. The Physicians’
( p0 T  t# y6 N8 c# nDesk Reference and package insert should also put a
( Y. R# k: C  v# Lwarning about the virilizing effect on a male or0 i6 h: C* g( c% ^
female child who might come in contact with some-
: n! v$ T; r8 Q" _one using any of these products.8 l$ i  }8 K( \+ s
References+ J2 {( e& U! l- ]8 I9 C
1. Styne DM. The testes: disorder of sexual differentiation; N7 c6 S. @" R5 d+ m" R7 [
and puberty in the male. In: Sperling MA, ed. Pediatric( z9 X) z6 u! Q4 D  b6 f
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;: L& s7 P1 b$ U/ {' a
2002: 565-628.
2 f3 ?: p& }; W* [' ~2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious, m& @0 x& P; G) W& }
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old' E- i4 G- ^" G9 Y2 ]
Boy Induced by Indirect Topical
3 C3 f3 \2 i  V; IExposure to Testosterone0 X' c, D/ {! ~5 `
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,25 T% ~3 }% _7 Y: y0 B2 V
and Kenneth R. Rettig, MD1
' z  X! ^% B. L6 ?8 \2 _' F( cClinical Pediatrics
! U5 L* P# G5 r1 q6 v3 kVolume 46 Number 6
6 }5 ]- X7 W0 w. {) t1 l% C1 Y% u8 BJuly 2007 540-543
0 H9 }# D& C" H© 2007 Sage Publications' _; k( n8 O/ I8 a) I$ Y
10.1177/00099228062966510 I0 O' @6 l9 o  b, Z0 w  `
http://clp.sagepub.com" T3 Z; z5 v% f# W8 j, |
hosted at
1 y$ @; g- P0 t9 H& Q. k( V7 Dhttp://online.sagepub.com
3 l5 V' h; ~6 X, S  e: NPrecocious puberty in boys, central or peripheral,
1 X/ a  ^2 b5 e9 r1 gis a significant concern for physicians. Central
: {1 V- p8 G$ u1 R  ]0 e( m# ?2 ?4 aprecocious puberty (CPP), which is mediated6 m4 t/ Z' r9 P% s1 J
through the hypothalamic pituitary gonadal axis, has
! }, J' m4 a& ~$ W6 U9 q9 la higher incidence of organic central nervous system; F8 K, E+ l. g+ V) T# _
lesions in boys.1,2 Virilization in boys, as manifested' d+ M9 r: T7 Y
by enlargement of the penis, development of pubic2 K! r- t* P* q* l* n: W. L
hair, and facial acne without enlargement of testi-
, A" W* t6 b0 U, ycles, suggests peripheral or pseudopuberty.1-3 We% l; i& l( F9 o' K
report a 16-month-old boy who presented with the
# @, p4 Y. z. H+ ]enlargement of the phallus and pubic hair develop-
  B3 ?; Z- ?! fment without testicular enlargement, which was due
  b" l4 ]& o+ K% Q4 g( U' Ito the unintentional exposure to androgen gel used by! j: L8 y* S! v' b4 i
the father. The family initially concealed this infor-
. ^/ F) X: u1 \mation, resulting in an extensive work-up for this
% {+ v# C' A6 A2 ?3 }1 _& Q. Echild. Given the widespread and easy availability of
% |& J1 C( H( C6 Atestosterone gel and cream, we believe this is proba-
- z8 ]: H+ S! V8 obly more common than the rare case report in the! l) @$ f. z, U/ w( }2 L
literature.41 B" l# z+ d1 d3 L3 Y) D& K
Patient Report4 Z9 H7 c2 ~6 F$ c, V
A 16-month-old white child was referred to the4 n' y, M: D" N* Y0 @% j
endocrine clinic by his pediatrician with the concern
/ _/ U8 r$ G+ u/ y% _  ^1 v3 ^of early sexual development. His mother noticed
; g* f5 w, p0 b( @light colored pubic hair development when he was% Y: L9 u; V+ G, B8 ?3 ?
From the 1Division of Pediatric Endocrinology, 2University of
3 O% G5 |% X: _South Alabama Medical Center, Mobile, Alabama.5 B1 Y+ e. i7 _. _# q7 [. L$ |$ v
Address correspondence to: Samar K. Bhowmick, MD, FACE,. N( E' Q0 Z# J/ @: [$ b# ?
Professor of Pediatrics, University of South Alabama, College of
( R" D3 W6 ]/ c% n5 ]Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
! f9 D/ g# ~3 h9 D: P0 Y4 @- f, U& re-mail: [email protected].# Q& e! F4 e5 G" o; g  c
about 6 to 7 months old, which progressively became) }- n3 n1 B3 \' a0 o& f& h
darker. She was also concerned about the enlarge-
* A- N- b5 _0 X. v, `4 Hment of his penis and frequent erections. The child; E3 O: O7 d  O' L: m3 M
was the product of a full-term normal delivery, with
* ]3 K, `- \: D6 Z- J/ s- ^, Za birth weight of 7 lb 14 oz, and birth length of
$ q" R) }. {. _. w20 inches. He was breast-fed throughout the first year
: J- L4 U3 S; X. ~of life and was still receiving breast milk along with% n/ C8 S& L$ @6 O5 @0 Y6 @5 {
solid food. He had no hospitalizations or surgery,
0 W5 |0 K' ]* E6 x: O0 @3 Jand his psychosocial and psychomotor development) `" t& b$ n9 }1 m" H1 P, P
was age appropriate., |$ w* f, }* ]) B
The family history was remarkable for the father," C# Y  O; x: x4 s% R( Q7 J' W
who was diagnosed with hypothyroidism at age 16,
+ H6 d, J' ]. l, O2 twhich was treated with thyroxine. The father’s
2 u, S/ \" b0 x# F" o% wheight was 6 feet, and he went through a somewhat
% j( y: z8 V' i# {2 b% ?early puberty and had stopped growing by age 14.
# G. ]1 \& B# h; vThe father denied taking any other medication. The
' Q, ]$ J3 |6 v, K* Lchild’s mother was in good health. Her menarche+ u  y: @$ M3 w$ ^  Q/ j. p
was at 11 years of age, and her height was at 5 feet
- l- \- i$ `# H* Y; v$ X  F8 w5 inches. There was no other family history of pre-0 i( `3 v- |/ l) C% u. H
cocious sexual development in the first-degree rela-
' i( d$ G- B. X7 L# L# O% X9 n$ Ltives. There were no siblings.2 s! @% Y8 [- a# D# ^9 p% ?" ?9 d/ b
Physical Examination: l# W/ t9 u/ }3 y
The physical examination revealed a very active,
' R& @* e+ B: Z+ C' {2 X. F/ Oplayful, and healthy boy. The vital signs documented
  {6 m. P7 |8 g5 Q! Z) ha blood pressure of 85/50 mm Hg, his length was: s; q- P% A# o, Q
90 cm (>97th percentile), and his weight was 14.4 kg
* i* ^9 x# X, r) ~8 G& a5 S(also >97th percentile). The observed yearly growth1 c5 f, f. ^$ E5 b9 g; b( x/ y6 G
velocity was 30 cm (12 inches). The examination of8 _7 Y0 x% ]5 j0 _' k
the neck revealed no thyroid enlargement.
% ?) S7 e8 {$ X5 HThe genitourinary examination was remarkable for
% t3 M3 U; j$ R* |% O& renlargement of the penis, with a stretched length of
4 k( A0 r3 Y8 U. R# {& V* P8 cm and a width of 2 cm. The glans penis was very well: \& p! w1 n- J1 t, L1 n
developed. The pubic hair was Tanner II, mostly around" s  z/ \) y# C9 q: K* C8 o
540
. g; T' |' K$ N9 h' u' `1 \1 Cat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from9 |: O* |5 Z" E3 m7 P" x
the base of the phallus and was dark and curled. The5 x9 U8 N6 T( e+ h5 |+ X
testicular volume was prepubertal at 2 mL each.- I1 t9 m& V, ]( }, y" [
The skin was moist and smooth and somewhat+ r& b7 v0 f/ @4 g
oily. No axillary hair was noted. There were no7 D& r- m( m1 y+ z+ z# q
abnormal skin pigmentations or café-au-lait spots.. m/ i" e7 Z" h4 L/ R% ^
Neurologic evaluation showed deep tendon reflex 2+; N. R- e3 B& I8 k) n9 V
bilateral and symmetrical. There was no suggestion2 A7 L7 R  B- G* `
of papilledema.2 |. H( H, R* s! D' a2 P
Laboratory Evaluation
9 C. _# r" t# a# v+ ZThe bone age was consistent with 28 months by; X4 J% ^6 g: U
using the standard of Greulich and Pyle at a chrono-
4 d2 z- D7 |+ A; z6 ~3 H% Y1 C/ Llogic age of 16 months (advanced).5 Chromosomal7 O! B7 S, ?, }4 @! P
karyotype was 46XY. The thyroid function test; f; U( q" s! X3 N, i- d
showed a free T4 of 1.69 ng/dL, and thyroid stimu-# P6 p8 U0 l0 c) Z  i
lating hormone level was 1.3 µIU/mL (both normal)." h$ _/ g, X; N3 J( V; e
The concentrations of serum electrolytes, blood
2 x+ l- b$ F$ Z; c$ jurea nitrogen, creatinine, and calcium all were
+ c9 b1 n: [+ Wwithin normal range for his age. The concentration
" X3 i& X5 \# b' sof serum 17-hydroxyprogesterone was 16 ng/dL
( a7 v( j1 X5 J# H/ m(normal, 3 to 90 ng/dL), androstenedione was 206 r+ ^( g" z' `9 E
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
& j" G, n- K$ U" p! Q+ S6 kterone was 38 ng/dL (normal, 50 to 760 ng/dL),& ]0 ?! e: C! H8 W& o
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
8 ^6 e2 `* C3 i$ n: |49ng/dL), 11-desoxycortisol (specific compound S)
4 [0 s4 n) G2 k6 q. v- Ywas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-) m( _3 A4 d& A+ p6 z9 o2 X* h
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
- ]- r$ i* A% @* wtestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
3 e0 d! |1 C" D: ^and β-human chorionic gonadotropin was less than
$ ?  a  F* W& ?5 mIU/mL (normal <5 mIU/mL). Serum follicular, Q# i, A' b$ `+ u) _0 [+ n' ^
stimulating hormone and leuteinizing hormone! }. J0 i% c! d% c
concentrations were less than 0.05 mIU/mL% j2 q# b. e4 f1 U
(prepubertal).
0 n& s" X: A9 ~1 @8 QThe parents were notified about the laboratory5 |- E- q  _  D9 o& |5 o- c8 j
results and were informed that all of the tests were
8 K. F; }/ f3 i2 gnormal except the testosterone level was high. The: p* ?; ~9 c" |* c/ v7 k( v
follow-up visit was arranged within a few weeks to$ x" z2 C5 ~/ v( s+ e5 X
obtain testicular and abdominal sonograms; how-
  X7 J' N1 A+ \: P4 }8 o; o; _. l. V% Rever, the family did not return for 4 months.
& G9 _4 W1 ^/ z$ `- o( U: aPhysical examination at this time revealed that the
; V' H# E1 q# o0 s) L. _% D- s7 |child had grown 2.5 cm in 4 months and had gained3 \, W. ]8 X0 ~
2 kg of weight. Physical examination remained  H9 ^. V' I" b- N; C' `7 C
unchanged. Surprisingly, the pubic hair almost com-" n" k2 K1 l0 i0 r2 v
pletely disappeared except for a few vellous hairs at% m% h8 S6 P: ^4 T* R9 v9 n8 D8 G6 J
the base of the phallus. Testicular volume was still 2, X' n, l  R- H, I7 _: |
mL, and the size of the penis remained unchanged.' j) I. l! O4 O5 [
The mother also said that the boy was no longer hav-
! \4 }  v) M& L- j! oing frequent erections.
/ j+ W/ i* m# s9 r6 X5 r* yBoth parents were again questioned about use of
1 D( Z9 H8 [: m2 i) ^any ointment/creams that they may have applied to
4 d( j0 S' w/ v2 ~- ?4 }( Rthe child’s skin. This time the father admitted the; E- o$ ^) ^6 j4 u0 L% X
Topical Testosterone Exposure / Bhowmick et al 541
5 m6 W9 J7 Y4 o  Y% q/ |) quse of testosterone gel twice daily that he was apply-
% F( _% h' p8 p# h7 l5 c; sing over his own shoulders, chest, and back area for7 W; u6 ]3 _) U; D0 S6 D
a year. The father also revealed he was embarrassed
8 _/ k) f/ Y4 F" Gto disclose that he was using a testosterone gel pre-/ Z! v. i/ g) ]5 g$ s
scribed by his family physician for decreased libido0 q+ w+ y/ b/ ?; |6 l7 f
secondary to depression.
- }: [' s4 y' D" RThe child slept in the same bed with parents.  z/ Q; s( t, E. `
The father would hug the baby and hold him on his) v, _9 d/ `6 d  {5 p
chest for a considerable period of time, causing sig-- T. M4 v* w' S. c: c/ j
nificant bare skin contact between baby and father.
! K  x: L5 T, C3 {" ~4 q8 A* YThe father also admitted that after the phone call,4 A4 @" {/ r& X. y3 X9 u
when he learned the testosterone level in the baby& G; a+ E# A1 q4 J0 f9 u+ e. H" d
was high, he then read the product information
  b, }: m  x4 A, C  Vpacket and concluded that it was most likely the rea-8 z* M$ P* G3 U& d! v* l9 v
son for the child’s virilization. At that time, they- ]& p# e% c, v& d, e* A
decided to put the baby in a separate bed, and the
2 W1 B+ t3 A, ?" C9 ~: k5 ~father was not hugging him with bare skin and had: I1 r5 s/ i  s5 o# r: m$ z$ M4 n
been using protective clothing. A repeat testosterone' Y  X# w5 S0 [& i
test was ordered, but the family did not go to the
: n6 P; g6 U$ A! Rlaboratory to obtain the test.
9 K: ^7 P5 i& }4 m; GDiscussion
4 U- I/ t) l* `" [. t! Z* F2 z/ e8 W2 fPrecocious puberty in boys is defined as secondary
6 R0 X- L+ h7 h' _: X3 o) e+ tsexual development before 9 years of age.1,4# |* B0 D! \9 O+ a3 C1 u
Precocious puberty is termed as central (true) when
7 F* b% @4 T1 ]( uit is caused by the premature activation of hypo-
6 h  B. {% g3 C  P5 E5 S5 v% qthalamic pituitary gonadal axis. CPP is more com-" X& U, s) |% B
mon in girls than in boys.1,3 Most boys with CPP
+ |) n* w; v2 L' y4 J; @may have a central nervous system lesion that is' p) F* I/ n: a9 M' x9 ]1 t+ k  V
responsible for the early activation of the hypothal-: o) [" P; c# U4 {. _1 y
amic pituitary gonadal axis.1-3 Thus, greater empha-
3 ]5 q/ q6 s, j$ f2 ]( w# Rsis has been given to neuroradiologic imaging in0 {/ p" m; U! {) @
boys with precocious puberty. In addition to viril-5 R' h% X6 d, h
ization, the clinical hallmark of CPP is the symmet-/ o7 m, h$ L+ i; g- z
rical testicular growth secondary to stimulation by" q1 X6 y$ W" L+ G- H6 J* U
gonadotropins.1,3; d3 r2 R9 t/ r3 x
Gonadotropin-independent peripheral preco-
# Y2 F' V2 }1 R5 @) b, }+ kcious puberty in boys also results from inappropriate5 @5 {) s" T8 ~
androgenic stimulation from either endogenous or" t  Z, y3 j% c9 Y( @' z) l1 b
exogenous sources, nonpituitary gonadotropin stim-1 ?- ?5 S6 P, T
ulation, and rare activating mutations.3 Virilizing) Q$ a8 P4 ?7 |+ I/ q* X8 J8 X
congenital adrenal hyperplasia producing excessive
( }8 o! i7 \4 j+ a6 k- dadrenal androgens is a common cause of precocious+ _7 z8 v! |$ e; m0 l( I$ x3 D
puberty in boys.3,45 H; \9 Y- ?. f9 y+ M: ]3 j
The most common form of congenital adrenal
0 z8 k9 C9 S6 l! ?, h$ Fhyperplasia is the 21-hydroxylase enzyme deficiency.' ^2 [! w( m' _, Y) A6 F
The 11-β hydroxylase deficiency may also result in
5 q" r- d; s- L, R3 u: B) Q+ k/ ~+ rexcessive adrenal androgen production, and rarely,
) }5 A) C. l) a4 V9 K, Xan adrenal tumor may also cause adrenal androgen9 M% p! v! i1 R  E5 P* e& x
excess.1,3
- Q% M5 T) |- s- p; xat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from9 i1 k) j. B2 [( ?% V- g
542 Clinical Pediatrics / Vol. 46, No. 6, July 20076 E9 e0 o# _0 l- h
A unique entity of male-limited gonadotropin-
. }0 \' |0 u/ a$ `. B2 Xindependent precocious puberty, which is also known
7 Q" y1 p& [5 Oas testotoxicosis, may cause precocious puberty at a; Q$ U) f7 d; }: U% g
very young age. The physical findings in these boys! S( ^7 y  B5 _$ ], y
with this disorder are full pubertal development,
" m- O) N7 D8 `6 t, f$ Bincluding bilateral testicular growth, similar to boys
$ o1 S; i) P' f/ i* Owith CPP. The gonadotropin levels in this disorder0 A$ t1 i( ?/ l& p
are suppressed to prepubertal levels and do not show8 i6 y0 L( d7 P: E
pubertal response of gonadotropin after gonadotropin-* \8 E" k4 Y3 P; A7 a
releasing hormone stimulation. This is a sex-linked# w1 B+ X/ \8 `& |
autosomal dominant disorder that affects only
4 \* C9 m  D* [' q# Gmales; therefore, other male members of the family
9 j: e9 _" y2 `* \: L. Fmay have similar precocious puberty.3; v& e$ }! c9 a6 ?/ }
In our patient, physical examination was incon-* Q4 w- v3 z, j
sistent with true precocious puberty since his testi-
# _, d6 V7 g: X. K2 e8 xcles were prepubertal in size. However, testotoxicosis4 q& K7 m7 C' E+ |
was in the differential diagnosis because his father
/ [- Z% b9 `6 S* h( p, L7 Qstarted puberty somewhat early, and occasionally,0 ]+ |) d% K# H) V' i# x  f% {& p1 Z5 D
testicular enlargement is not that evident in the
0 u4 w! u% M0 r2 P' l/ lbeginning of this process.1 In the absence of a neg-  T* _# Y7 C8 O% D
ative initial history of androgen exposure, our
; h) u& c, v9 v5 i2 ebiggest concern was virilizing adrenal hyperplasia,' j& S* q. b; ^$ _) J5 N  e% _, k7 q
either 21-hydroxylase deficiency or 11-β hydroxylase# v& \; v! }" z1 [) `; \
deficiency. Those diagnoses were excluded by find-
5 }  W: Q- l( m6 A; Eing the normal level of adrenal steroids.
- S2 a$ J: b3 D/ i/ U: nThe diagnosis of exogenous androgens was strongly2 U: g- ~2 L2 ^1 t) W
suspected in a follow-up visit after 4 months because
( S4 q/ |9 T# k+ J: T3 ]the physical examination revealed the complete disap-
1 T$ \" D) Z9 \pearance of pubic hair, normal growth velocity, and
/ T6 l* a+ H% y0 u: z9 s. wdecreased erections. The father admitted using a testos-
0 _/ X- X( {/ U: c& ^' pterone gel, which he concealed at first visit. He was) y9 v" K# t& R( @3 P6 r7 C
using it rather frequently, twice a day. The Physicians’
2 W+ _* C1 F/ b( U& S5 F; g- Q5 z4 }Desk Reference, or package insert of this product, gel or
5 j* I; d2 [, o% j7 w5 dcream, cautions about dermal testosterone transfer to
- u8 o) Q  u% a* m% Punprotected females through direct skin exposure.
5 s9 C# f7 M+ Y8 |Serum testosterone level was found to be 2 times the
* ^& O, @8 s5 s! p+ W: j3 G, jbaseline value in those females who were exposed to
2 R0 ^) D2 _( H- g7 `even 15 minutes of direct skin contact with their male! X0 O  t8 `6 }3 n4 n; i
partners.6 However, when a shirt covered the applica-
. F  E/ i5 W4 J4 \tion site, this testosterone transfer was prevented.
0 L9 ?3 f2 n, u  Z8 |( J; K6 j- SOur patient’s testosterone level was 60 ng/mL,6 I- ?) t, n- y; f
which was clearly high. Some studies suggest that
& Q+ T' \- O8 Z0 H$ ydermal conversion of testosterone to dihydrotestos-
% i* m, _7 a6 f" q  xterone, which is a more potent metabolite, is more& u2 B" s, B: h  ?) }2 J% T4 T6 v8 N
active in young children exposed to testosterone
, O6 `: A! E- i; Nexogenously7; however, we did not measure a dihy-8 y  t1 X6 v9 G$ s: A+ z0 k
drotestosterone level in our patient. In addition to
, N7 n8 J) I! V8 I5 p* _# qvirilization, exposure to exogenous testosterone in8 `$ P0 i" B9 P/ d% f% ^# }+ g
children results in an increase in growth velocity and( M; {, J9 A7 K3 ]0 s. u( y" a
advanced bone age, as seen in our patient.) v" h7 A) ]4 Q9 j
The long-term effect of androgen exposure during
4 d& ~1 }5 o: j' Cearly childhood on pubertal development and final
6 X5 M& z: s8 U9 |adult height are not fully known and always remain
: C' Z. T8 C. P1 O: ~( `4 Za concern. Children treated with short-term testos-
) z, T* Z( J+ I/ N( z+ i, \terone injection or topical androgen may exhibit some6 O1 R! l  M# o
acceleration of the skeletal maturation; however, after
) A3 z, x" O# k6 L! ]% l) k  H- Hcessation of treatment, the rate of bone maturation4 ^; x" O, E" |( z! C9 B
decelerates and gradually returns to normal.8,9
. a( C, ?/ L: Y# v# YThere are conflicting reports and controversy
; R2 W  W, w6 U' o1 }1 M( m: \7 kover the effect of early androgen exposure on adult+ N8 b+ O+ T: @
penile length.10,11 Some reports suggest subnormal+ M; ]. Y$ U  z- F. k5 d# o! k
adult penile length, apparently because of downreg-
7 h0 u' K8 |! M) `ulation of androgen receptor number.10,12 However,
2 W' a& r/ v. v- j( t: M2 e; k6 I& `) QSutherland et al13 did not find a correlation between
* p% G) w; u3 F0 \childhood testosterone exposure and reduced adult
$ Z. T% n: N  H9 u5 `5 ppenile length in clinical studies." R2 \$ F; I7 T
Nonetheless, we do not believe our patient is
5 [7 a: M/ c1 P- b: N4 Igoing to experience any of the untoward effects from. \8 @: g( r& w
testosterone exposure as mentioned earlier because
3 I  Y/ N9 L$ U+ t: M2 Vthe exposure was not for a prolonged period of time.
; f* i  }+ s6 k6 ?Although the bone age was advanced at the time of
1 h+ `; d- M, m# |; N9 {! vdiagnosis, the child had a normal growth velocity at
! x+ [3 Z$ S: i3 {9 othe follow-up visit. It is hoped that his final adult9 d2 x( V& J1 a+ c3 p
height will not be affected.
6 h3 _( Y! z4 M! E; X7 M5 ^Although rarely reported, the widespread avail-% n( a" j) g7 |( n; d
ability of androgen products in our society may& u* @' ?+ L, r& |. z0 n
indeed cause more virilization in male or female# P; D( F' \  t$ g% E) Q2 V
children than one would realize. Exposure to andro-5 E, K  m7 J, t8 ?9 l# P
gen products must be considered and specific ques-
  n- v3 r% R9 L0 ytioning about the use of a testosterone product or
# N4 l8 I% h8 z, T/ M2 v, zgel should be asked of the family members during
$ s6 D+ B* ]  a& v0 Hthe evaluation of any children who present with vir-
' j6 c" _$ n: d$ i3 bilization or peripheral precocious puberty. The diag-
: p" n* v+ y0 N: J- P, h- P/ E- Vnosis can be established by just a few tests and by
7 B6 z0 |2 J# s0 U4 _+ |appropriate history. The inability to obtain such a
4 a( m- X1 F9 J8 j1 d6 i' Ehistory, or failure to ask the specific questions, may7 c* B9 e0 d) b) E
result in extensive, unnecessary, and expensive
& U) U7 S2 y. s) jinvestigation. The primary care physician should be
0 C3 e2 G" @- e. J: m0 x/ u' Gaware of this fact, because most of these children
- D. W2 |$ c- D/ V5 z0 rmay initially present in their practice. The Physicians’& ]0 W7 T% y& A2 Q5 c% h
Desk Reference and package insert should also put a7 o3 ~- ]# A- G' V& b- g
warning about the virilizing effect on a male or
# Q3 y! x: \0 wfemale child who might come in contact with some-
7 o: V8 l, n) F; k! Hone using any of these products.
8 V( Q) `2 W5 ], q/ N; y) iReferences
$ W) y. L: o* I$ |! Q6 f* F1. Styne DM. The testes: disorder of sexual differentiation
0 f. G0 b4 u  xand puberty in the male. In: Sperling MA, ed. Pediatric3 ]  S2 h, ~  q4 t
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
4 g$ q5 A2 c. _- y% \. C: X* |  d+ M! K2002: 565-628.
7 P: ]4 W' q& R2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
; ~* s& g1 Q* c, kpuberty 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

7 [, d0 j& S" j" g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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