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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
2 N7 s! z% H& ~( p( mBoy Induced by Indirect Topical) q/ l: t, @  x
Exposure to Testosterone- Z: V4 y, [7 i* V% W! ]) E7 ^
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,20 g: l5 j6 {$ S# Q' d
and Kenneth R. Rettig, MD19 W. X6 Y7 |' _* B  Z7 \
Clinical Pediatrics
6 R5 X3 u0 E# |: x7 Z* OVolume 46 Number 6* C. b: x& I9 z$ U( H
July 2007 540-543% f; C6 O/ p+ Z$ n$ E7 W5 L4 [
© 2007 Sage Publications
2 P" O' d/ G" B, [# R3 g+ y8 Q* I10.1177/0009922806296651/ @+ E2 H4 a; @+ m- p  V. I
http://clp.sagepub.com
- C9 ^+ z& ^7 nhosted at$ N- @+ W9 J2 I) `. k
http://online.sagepub.com
, O5 L3 }: f) XPrecocious puberty in boys, central or peripheral,
5 h2 [* ^6 G' z, }9 S- Iis a significant concern for physicians. Central
3 j! E) i! W5 ]( G5 {9 y: ^2 n) uprecocious puberty (CPP), which is mediated
! y* c6 m$ i) d3 `through the hypothalamic pituitary gonadal axis, has7 L  z' x2 Y/ H. {9 ~- [1 s  K0 T/ j0 N
a higher incidence of organic central nervous system
+ X% x, m5 i$ r  \8 c+ R! Olesions in boys.1,2 Virilization in boys, as manifested' b- O9 P5 Q  j% h1 `
by enlargement of the penis, development of pubic
" f$ S( \: T4 y7 ]5 Z/ Shair, and facial acne without enlargement of testi-# P# C# Y6 B+ `( M- u& {( e4 O
cles, suggests peripheral or pseudopuberty.1-3 We
9 A8 `  i2 @) @report a 16-month-old boy who presented with the
, F& ]' ], I; u, R& kenlargement of the phallus and pubic hair develop-
5 s" _; z8 l* _4 f* _ment without testicular enlargement, which was due
# h* K" @& o3 W; H; q2 Sto the unintentional exposure to androgen gel used by
+ J# G3 V/ h0 s, T; M5 Kthe father. The family initially concealed this infor-# i" U- ~" |, z* ~  Z7 r: H+ i9 h
mation, resulting in an extensive work-up for this
7 o* S% ?) l2 p& M0 ~2 A* kchild. Given the widespread and easy availability of* Q3 _3 b* z, [- o. _
testosterone gel and cream, we believe this is proba-7 y4 m/ y) U5 }
bly more common than the rare case report in the" `/ e5 u" @8 b4 P
literature.4  }* N2 w) p8 A3 t0 x& b
Patient Report
0 K: j8 T+ U8 s0 kA 16-month-old white child was referred to the
$ L! F, S, t) T9 t4 i; uendocrine clinic by his pediatrician with the concern
+ q# \/ i7 K0 y) {% Tof early sexual development. His mother noticed
% D+ ^3 ]; ^2 b6 Mlight colored pubic hair development when he was# G  C. q# H% u2 a2 z
From the 1Division of Pediatric Endocrinology, 2University of
& u, B* J$ ^, U" b! F5 D0 NSouth Alabama Medical Center, Mobile, Alabama.
2 y5 I8 {# z1 u) dAddress correspondence to: Samar K. Bhowmick, MD, FACE,. d' S: \$ j+ O2 L# ?4 f0 x
Professor of Pediatrics, University of South Alabama, College of2 l4 ^, O. Q7 ]- W
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
- M7 g  C$ V; a$ ~e-mail: [email protected].
  ?' W2 |6 d3 R2 Z/ ~5 `8 r7 Nabout 6 to 7 months old, which progressively became
+ h! ^7 O# H* \& Q0 m9 Gdarker. She was also concerned about the enlarge-; H8 Y& _. L- C6 _( O
ment of his penis and frequent erections. The child$ j7 Q& S4 N8 k/ I6 R
was the product of a full-term normal delivery, with
) @$ s" I4 X; v! Y, x" Qa birth weight of 7 lb 14 oz, and birth length of
( `+ d+ e3 D/ w1 A% k/ l2 ^1 a* K20 inches. He was breast-fed throughout the first year: h" {8 f9 I- B8 ^1 M1 n1 f4 w
of life and was still receiving breast milk along with
- P5 W' c# c8 D6 z% I) g# [solid food. He had no hospitalizations or surgery,
' _' K7 g3 b- ^& X3 Dand his psychosocial and psychomotor development" @4 s% a7 W0 k- u% w
was age appropriate.
& V! q1 d6 _; H% v2 z. Z& G5 j4 Q9 zThe family history was remarkable for the father,* u+ w, S7 R0 s/ R/ q$ u) O
who was diagnosed with hypothyroidism at age 16,. a, u/ C0 x3 O2 V; w# e
which was treated with thyroxine. The father’s
8 k1 E! T0 z1 }( [height was 6 feet, and he went through a somewhat' i7 }2 N7 M$ l  Z: z
early puberty and had stopped growing by age 14.- h" D( p2 d( e
The father denied taking any other medication. The" _" t+ t! s, _9 N* e6 F! F  i: k
child’s mother was in good health. Her menarche4 ~2 J& Y& q2 V- x
was at 11 years of age, and her height was at 5 feet* i& ]8 [6 f, |! Y3 a0 W  v
5 inches. There was no other family history of pre-) V2 U% `% U, `- V5 i9 O$ ^
cocious sexual development in the first-degree rela-3 f% `) T3 G8 l8 z7 z% ^( m
tives. There were no siblings.
& q% F- S/ ^. `. r2 V! cPhysical Examination( R! q% I' q7 n% O. g+ H$ {1 s
The physical examination revealed a very active,
- @# G4 ]( W! \& aplayful, and healthy boy. The vital signs documented1 c7 D5 \% l; h% b# e$ y4 c
a blood pressure of 85/50 mm Hg, his length was5 e& K4 D/ n- Q, y; N2 w
90 cm (>97th percentile), and his weight was 14.4 kg
. L2 J  H! m0 c4 `6 ]+ I9 L3 H(also >97th percentile). The observed yearly growth! Z1 X  ~# v- S* K% p% ?6 z
velocity was 30 cm (12 inches). The examination of  B6 t9 \) I. a7 a6 }8 @; G& c7 f
the neck revealed no thyroid enlargement.1 x: ^" W5 J1 ^" \# H
The genitourinary examination was remarkable for
- j# f& w! h1 _0 W* y  menlargement of the penis, with a stretched length of) S! z4 t( f# ]( x1 @$ C, p* Q
8 cm and a width of 2 cm. The glans penis was very well7 @: d6 [7 i7 z+ L* u
developed. The pubic hair was Tanner II, mostly around
, m! I& b0 q' k; m( J( k8 z7 j  M' @5408 Y5 d! p7 y2 z
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
' a; Z5 H3 p$ g' l+ m, mthe base of the phallus and was dark and curled. The9 e, U9 X0 o+ P8 X3 d8 g
testicular volume was prepubertal at 2 mL each.3 ]5 B7 E! F2 j$ u6 n: W8 l9 C2 a  j
The skin was moist and smooth and somewhat! H% ?+ u7 q3 |8 ]
oily. No axillary hair was noted. There were no
& A% ^5 O8 c/ L' Dabnormal skin pigmentations or café-au-lait spots.7 h' }" Q: e1 g# J- p
Neurologic evaluation showed deep tendon reflex 2+
7 G5 _; b6 q% P5 b) sbilateral and symmetrical. There was no suggestion7 ]+ h# X9 v0 A+ v, @% z8 d
of papilledema.
) \' R' {: G$ h) _" a$ ~. n* K% e1 b6 }Laboratory Evaluation- G& P' ]2 C# O$ Y6 n& d' L
The bone age was consistent with 28 months by- n  y0 M( y  ^* ^9 ~$ L* I& e4 o
using the standard of Greulich and Pyle at a chrono-" e3 W% x8 O0 p3 E9 M- e* q
logic age of 16 months (advanced).5 Chromosomal
* K# R# B! o" I3 ]0 r& G8 d6 Rkaryotype was 46XY. The thyroid function test& {6 O& E# _! [# W- o$ `4 \7 f: ~
showed a free T4 of 1.69 ng/dL, and thyroid stimu-3 Y" K7 t9 J2 O4 A% I
lating hormone level was 1.3 µIU/mL (both normal).
0 H6 U) z  X' o8 n/ Z7 HThe concentrations of serum electrolytes, blood% T) @9 |" Z( \4 c: ^6 O
urea nitrogen, creatinine, and calcium all were% Y; r9 f3 E+ u5 }8 m1 E+ H
within normal range for his age. The concentration
0 h- Q- C) {, _of serum 17-hydroxyprogesterone was 16 ng/dL
$ W; {+ \6 ^  t4 L  J* ~(normal, 3 to 90 ng/dL), androstenedione was 20
7 X2 p1 A( [9 Yng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
0 k9 }# z2 g, kterone was 38 ng/dL (normal, 50 to 760 ng/dL),. }& W) ?1 h  [* [. U
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
/ i* ^4 O3 E& P% _49ng/dL), 11-desoxycortisol (specific compound S)
4 K( r, `8 B0 X' D# @$ \. bwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
& g0 |1 z! p! T7 i2 X/ atisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
& L% H; x0 d2 s& x! j+ d- Ctestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
- |6 `3 r4 L* a. ~3 vand β-human chorionic gonadotropin was less than
7 I7 n3 V% Z" T7 |5 mIU/mL (normal <5 mIU/mL). Serum follicular) U6 ?  c9 \" g) |, Q0 @
stimulating hormone and leuteinizing hormone8 c4 l5 s3 ~4 b+ w
concentrations were less than 0.05 mIU/mL; M+ z: n# R; |* ]0 w" a; U4 m
(prepubertal).
( @4 W) k$ X4 K( {The parents were notified about the laboratory
# U; L% s9 p$ K4 a; Presults and were informed that all of the tests were
5 f% W1 H6 N6 a2 ~5 ~6 H" ynormal except the testosterone level was high. The
8 A2 n, ~( Z* s! W- x: x" I5 nfollow-up visit was arranged within a few weeks to
9 b5 ?, Z( @- Q5 L. w2 Jobtain testicular and abdominal sonograms; how-
0 G0 S: S. a7 R& S2 V7 Z* t5 Sever, the family did not return for 4 months.. K- ~+ p& ~2 x4 W2 T  T
Physical examination at this time revealed that the
' O3 Y8 r3 @2 Gchild had grown 2.5 cm in 4 months and had gained7 C2 M/ a3 J  _
2 kg of weight. Physical examination remained& l7 t; ]5 B7 \- m2 G6 I
unchanged. Surprisingly, the pubic hair almost com-
! m( G# p. b9 N; J% [3 p0 N: `pletely disappeared except for a few vellous hairs at8 y9 I# Q! R  j0 T* V0 P: @
the base of the phallus. Testicular volume was still 2
6 ~3 U" Z8 j3 l, N2 z2 t5 \( O- smL, and the size of the penis remained unchanged./ A" g- @, l8 K- `) m* o
The mother also said that the boy was no longer hav-
# ?: i: ^1 l, G' q3 S  Q# |5 ning frequent erections.4 n% ^+ {/ m$ b5 H9 P9 q$ D7 M4 a
Both parents were again questioned about use of2 x% K- n, q2 c2 s8 Y
any ointment/creams that they may have applied to/ G' S8 r8 c& U9 p( i: N
the child’s skin. This time the father admitted the
2 y) y0 e( k3 W1 S* kTopical Testosterone Exposure / Bhowmick et al 541
* ?% a" M: V" S+ A* G1 A8 Wuse of testosterone gel twice daily that he was apply-2 A- `- @  Q) S4 ~- Z; f
ing over his own shoulders, chest, and back area for
5 P8 c6 ~. t: ga year. The father also revealed he was embarrassed! ?2 p8 p1 G; o2 q0 f
to disclose that he was using a testosterone gel pre-
) W& X" L8 \$ R' W7 z! @scribed by his family physician for decreased libido# G; x/ ~& p" y* G5 q" X' n4 v
secondary to depression.
5 {  Y% p7 X. c  xThe child slept in the same bed with parents.
9 V! J$ E+ R) N5 G- nThe father would hug the baby and hold him on his9 v1 w5 f, K5 t
chest for a considerable period of time, causing sig-
( s: [5 M! p) C3 R3 [8 nnificant bare skin contact between baby and father.( \. v  M7 n" S( U
The father also admitted that after the phone call,
$ p& [( U6 r9 |4 t8 Nwhen he learned the testosterone level in the baby7 k. X# I5 t1 l
was high, he then read the product information
1 h2 M6 x! k8 E/ Hpacket and concluded that it was most likely the rea-6 v% H1 M, g0 b8 H5 z+ h  t5 ]9 B
son for the child’s virilization. At that time, they$ \6 U- H" g, |6 O* r  Z" F2 M+ I
decided to put the baby in a separate bed, and the/ X% ~/ Y/ q3 @! g' r
father was not hugging him with bare skin and had8 y- w3 x- f5 j: i7 n; A
been using protective clothing. A repeat testosterone
% B) T, m1 a* }% Qtest was ordered, but the family did not go to the' b' t) @: }4 Q; F2 U( j
laboratory to obtain the test.
5 d/ _& w; C% t+ y2 RDiscussion
2 k2 D% L5 k7 ~; p" P$ p! jPrecocious puberty in boys is defined as secondary
8 I* s( i. V0 O, ]) S0 esexual development before 9 years of age.1,41 u5 K, c- c: g' M& w# [+ X
Precocious puberty is termed as central (true) when
$ G1 Z8 p; x/ O3 P% |' rit is caused by the premature activation of hypo-; {. R9 m" U& T6 F
thalamic pituitary gonadal axis. CPP is more com-
  \% c: i4 U# N! r' S$ _3 @mon in girls than in boys.1,3 Most boys with CPP" `/ B4 o3 q5 {; {" p+ r1 _
may have a central nervous system lesion that is
% _/ E; r% c4 Mresponsible for the early activation of the hypothal-# u- f* J" l# C" ]* _% o3 }8 `
amic pituitary gonadal axis.1-3 Thus, greater empha-
* u# v: v8 |9 x) b5 rsis has been given to neuroradiologic imaging in
+ r# B4 s$ y( P7 tboys with precocious puberty. In addition to viril-
/ q" l) I9 k* O6 J3 jization, the clinical hallmark of CPP is the symmet-9 V; i" v0 Y" n* Q( t
rical testicular growth secondary to stimulation by
2 c" T% w! S% w/ ~0 a$ vgonadotropins.1,3
3 u& @* O+ O, Z& W1 z6 N: CGonadotropin-independent peripheral preco-* f" |2 f5 O0 l, a: ^# H0 p
cious puberty in boys also results from inappropriate
: f$ N! _3 J7 a2 ?9 oandrogenic stimulation from either endogenous or
: R- L. }; o" F7 [exogenous sources, nonpituitary gonadotropin stim-! z! A# ~7 J3 c0 D
ulation, and rare activating mutations.3 Virilizing+ a$ D0 k* [+ N7 R' p; b# K
congenital adrenal hyperplasia producing excessive6 `0 s7 ]/ J$ f% ^  d2 Q" ~
adrenal androgens is a common cause of precocious
: }! s; D) \4 }! j: p% P' Dpuberty in boys.3,4
' [. V( U: ^- _0 dThe most common form of congenital adrenal
0 E2 t$ q6 v5 b3 j/ m% D5 Bhyperplasia is the 21-hydroxylase enzyme deficiency.
# P3 S  m+ m0 R3 qThe 11-β hydroxylase deficiency may also result in, ?' s9 G0 Q6 u& ]% x; s! S7 Q) U) Q
excessive adrenal androgen production, and rarely,$ C2 Q# c5 E9 y3 U7 r# A
an adrenal tumor may also cause adrenal androgen
! F9 ?. d- E6 Pexcess.1,3
# B+ C% @4 n) L  Z% jat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from% c/ U: ?% k) t7 A" Q/ l% a
542 Clinical Pediatrics / Vol. 46, No. 6, July 20073 W+ _" }% `9 T1 Z* h3 B) d/ }5 G
A unique entity of male-limited gonadotropin-
; u2 R- V- _/ _1 e; x# mindependent precocious puberty, which is also known
/ |# e: m. [" ^  Vas testotoxicosis, may cause precocious puberty at a2 ?- \( q9 s# J) v8 J8 _
very young age. The physical findings in these boys
2 Y  r, G5 \* k0 F7 }with this disorder are full pubertal development,0 L: y4 ]' ?0 @  `: O* o
including bilateral testicular growth, similar to boys
) r+ E2 S7 d& ^0 Kwith CPP. The gonadotropin levels in this disorder
  ]% X% B1 J0 C& q! nare suppressed to prepubertal levels and do not show
1 O2 P2 _9 a; \- M0 @pubertal response of gonadotropin after gonadotropin-) X" [! v; s- [. a7 b6 ]
releasing hormone stimulation. This is a sex-linked
) ?( o/ G4 {+ }; y% K) [autosomal dominant disorder that affects only
" [& A6 c8 ~5 n  M( K$ u9 g* M' amales; therefore, other male members of the family$ P0 Q' t' T3 ?8 k, j" G
may have similar precocious puberty.3, V8 M! v7 u) a7 H: j6 ?+ z* @
In our patient, physical examination was incon-
" ^) C7 L( |6 I' O; L" Hsistent with true precocious puberty since his testi-
0 U7 S( v( E4 t, mcles were prepubertal in size. However, testotoxicosis1 A# ~/ K% Q4 O' z' j7 `2 ^
was in the differential diagnosis because his father; h7 [3 h  A1 c
started puberty somewhat early, and occasionally,
7 i( S, I  j  d2 Utesticular enlargement is not that evident in the3 q. r% H7 n. q2 I
beginning of this process.1 In the absence of a neg-
6 I4 v2 T1 J" D" k! tative initial history of androgen exposure, our
. L0 `6 b4 Y! C3 z# Wbiggest concern was virilizing adrenal hyperplasia,, q. A! Q3 {5 X; ]
either 21-hydroxylase deficiency or 11-β hydroxylase
, W& E7 ~1 k0 `! V7 n5 d! @deficiency. Those diagnoses were excluded by find-
2 k6 e5 v9 c6 f0 O" s) k  A9 ~ing the normal level of adrenal steroids.
7 c8 F, d/ r2 z) PThe diagnosis of exogenous androgens was strongly; ]+ q* ^/ K( b- M3 @+ F: }
suspected in a follow-up visit after 4 months because
5 ]) `6 _9 l) K" M8 bthe physical examination revealed the complete disap-
6 \, ]3 A% u, B9 P$ p+ ypearance of pubic hair, normal growth velocity, and
/ z( Z4 j' W" w" edecreased erections. The father admitted using a testos-8 K6 O2 \; y8 d& Y, {1 ~$ [
terone gel, which he concealed at first visit. He was3 A! F$ K) e" W
using it rather frequently, twice a day. The Physicians’
3 @! Y" A1 j4 C4 ~Desk Reference, or package insert of this product, gel or; N$ ?- E- Z0 H! M! O" E! j. W
cream, cautions about dermal testosterone transfer to; U. G2 F9 ]2 |$ R; h4 H" Z7 }
unprotected females through direct skin exposure.
# }* r9 j# A  ]/ A- j: ]3 X- ^Serum testosterone level was found to be 2 times the
& l; ]. G# C! w3 fbaseline value in those females who were exposed to
) O& H0 e, J! X. h! }2 ieven 15 minutes of direct skin contact with their male' ]6 J- C, K9 }: ^5 _0 g# r
partners.6 However, when a shirt covered the applica-
; l, o& [4 Z, @% t- e7 h) z8 ]tion site, this testosterone transfer was prevented.
: v! L/ h( n) fOur patient’s testosterone level was 60 ng/mL,
; z' c5 r8 g) Iwhich was clearly high. Some studies suggest that
9 A' v  N; z/ t" odermal conversion of testosterone to dihydrotestos-
! a$ x% d& {) y3 C% Oterone, which is a more potent metabolite, is more, z) w5 g) B  T5 n( H: d
active in young children exposed to testosterone1 p: ], y  f8 L' {8 u# v. {% L( S
exogenously7; however, we did not measure a dihy-* c. v4 Y9 c+ @# p
drotestosterone level in our patient. In addition to
$ Q: z9 I- |3 D( Uvirilization, exposure to exogenous testosterone in
- D9 p- A: g; W* @children results in an increase in growth velocity and
2 C6 v' b+ I; x. m% M0 x- D7 Uadvanced bone age, as seen in our patient.
+ A  G0 H0 r9 B; ]The long-term effect of androgen exposure during/ I0 D* G) f8 i; h- W/ @
early childhood on pubertal development and final
4 j2 Z, r8 M/ H# Q' W* V" Aadult height are not fully known and always remain
. L9 }6 t+ O( x' L1 ^; ]a concern. Children treated with short-term testos-
3 k/ x. C! B$ iterone injection or topical androgen may exhibit some
) K( e/ D: N- j+ i# K) O# Sacceleration of the skeletal maturation; however, after
: m3 L9 H" y+ W6 L8 s  H" Qcessation of treatment, the rate of bone maturation
' ~; ]/ ]6 ?1 S$ idecelerates and gradually returns to normal.8,9
! p3 x! z! Y* u: z% hThere are conflicting reports and controversy$ y1 {0 N2 Z# L/ A' Z5 I' j4 w$ g
over the effect of early androgen exposure on adult
/ u) U7 ~1 W; }penile length.10,11 Some reports suggest subnormal
1 S3 }0 a# a" ~! |% i; d8 d% T0 cadult penile length, apparently because of downreg-
" K9 C( B+ F2 ?7 W7 v  [- Vulation of androgen receptor number.10,12 However,$ [# q4 ~9 H/ r
Sutherland et al13 did not find a correlation between- F& V4 J9 V- o4 p  @
childhood testosterone exposure and reduced adult% H/ Z+ Z* ^" Q: `5 s/ R4 M
penile length in clinical studies.6 A% V( n6 K. Q( R
Nonetheless, we do not believe our patient is9 n, A, K5 h8 B/ |! c  o: ]# ^
going to experience any of the untoward effects from
" q' o- i9 W  t: X# o; K! N/ ftestosterone exposure as mentioned earlier because0 K% M) O  n5 Z5 e$ ?0 l/ C$ D% Q! z
the exposure was not for a prolonged period of time.
3 m; e0 l# K) ?Although the bone age was advanced at the time of
* v$ g+ m% J$ @) q% [2 R$ Ydiagnosis, the child had a normal growth velocity at
! q/ I4 Z; z9 l3 hthe follow-up visit. It is hoped that his final adult" f( I1 l8 _6 N
height will not be affected." U# X" K, g' T( w% L1 t
Although rarely reported, the widespread avail-& s  }) m+ O9 n( z& d: J2 P
ability of androgen products in our society may
" Q. P. w* s3 X8 o0 t2 Z/ o: eindeed cause more virilization in male or female) M$ o( N# i. ^; }/ e3 y
children than one would realize. Exposure to andro-' I5 H" d- a) N
gen products must be considered and specific ques-
, h" K& t0 [* I1 G1 b5 Ationing about the use of a testosterone product or
) q( [8 C8 a! g0 U& g' I: _gel should be asked of the family members during
6 _. G( a/ L" H# A4 F" d3 jthe evaluation of any children who present with vir-  R) c* N3 C% Q8 d* Y8 a9 A$ _
ilization or peripheral precocious puberty. The diag-) c5 `6 `1 g6 e/ Y$ |8 n
nosis can be established by just a few tests and by  m4 p  u; o4 B
appropriate history. The inability to obtain such a: J1 ~" j1 R! R$ ~  a
history, or failure to ask the specific questions, may& D! x- D  ]7 v' x3 {) s
result in extensive, unnecessary, and expensive
2 C' T' w1 C: y$ r0 a( ]investigation. The primary care physician should be
9 K. p" N3 C: W" l( kaware of this fact, because most of these children
& u0 U* k1 |! r8 P+ Z- fmay initially present in their practice. The Physicians’
: z' w" C0 q9 v/ h/ R3 NDesk Reference and package insert should also put a2 Z! t" W  ~% a" ^% e
warning about the virilizing effect on a male or
* {* u, X+ T* S3 D7 j9 tfemale child who might come in contact with some-/ X8 F! e2 r, N) u. R% W9 n
one using any of these products.
" o; ]# b+ H# H/ mReferences; K+ p" m) S' F' v
1. Styne DM. The testes: disorder of sexual differentiation+ j2 \5 I& f6 D* }* Z1 `. M
and puberty in the male. In: Sperling MA, ed. Pediatric
+ M  r- u( Z: U& |Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;, M2 W% _$ _& o0 |! n: k$ M" v
2002: 565-628.
9 [$ T* p. o2 }2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
1 K  P1 A3 g1 h: p3 K, Ppuberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
7 }# e, D& b4 h+ v9 b7 j4 y# g/ P) ~Boy Induced by Indirect Topical, `) a( Y: ?/ ~- x0 W" `9 O$ J
Exposure to Testosterone7 P3 }, n0 q' t1 ^
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
% X  C% G. j; U- {& Kand Kenneth R. Rettig, MD1
$ M- d7 P, @& M0 d5 N& L8 QClinical Pediatrics0 w" M0 T; V1 ~% O9 j% R$ f. B
Volume 46 Number 6
( P) e# A* Z7 A- tJuly 2007 540-5434 x: k( Z4 O, G5 b$ e
© 2007 Sage Publications6 }* @% j# u7 P8 g  D& J# M
10.1177/00099228062966510 }/ h/ a& ^- {
http://clp.sagepub.com+ ~: s, M& J0 S) n! `" s4 T
hosted at
& X; R6 L0 T, Ehttp://online.sagepub.com
+ `  W% j0 ]% F; }, v9 b' s6 R& A0 YPrecocious puberty in boys, central or peripheral,
) d3 E* ?& `9 B% f* x7 ]is a significant concern for physicians. Central
  Q! x" T. a# _- w0 ]precocious puberty (CPP), which is mediated
- Y: f8 r1 S% e- wthrough the hypothalamic pituitary gonadal axis, has
& K5 X8 N: V5 J0 B' B  [  J+ ~a higher incidence of organic central nervous system/ z: F, e. ?) D; k; w. J, d# N
lesions in boys.1,2 Virilization in boys, as manifested8 r9 J" Q. F+ l+ X( y# T6 P
by enlargement of the penis, development of pubic
8 i  _9 }: L3 ^( r' n. b; Khair, and facial acne without enlargement of testi-
/ \! |; ]# Q3 G8 Mcles, suggests peripheral or pseudopuberty.1-3 We
/ _9 w4 @( ^; x' b& Z% sreport a 16-month-old boy who presented with the
+ a6 A1 M% F+ oenlargement of the phallus and pubic hair develop-
: T, ~2 d$ L/ p. N; @: ~% x0 vment without testicular enlargement, which was due% m% B+ w9 R4 A
to the unintentional exposure to androgen gel used by
0 k% N1 M6 \5 L8 othe father. The family initially concealed this infor-
9 k' Q# M4 t6 |" F6 x  ]! _3 s. mmation, resulting in an extensive work-up for this
5 e( h# W. E- Pchild. Given the widespread and easy availability of
% i6 Q" s" L& M: ]; Ytestosterone gel and cream, we believe this is proba-
9 {, t0 ^; K$ F$ L2 B, tbly more common than the rare case report in the2 t" i( P5 p' V6 o
literature.46 i4 r* S, M9 k
Patient Report
9 r0 b4 F: ~% m$ g( \+ O4 pA 16-month-old white child was referred to the  B9 h. m' f: y
endocrine clinic by his pediatrician with the concern7 ~1 F. ?9 _- x/ |; H' H
of early sexual development. His mother noticed
4 E4 z/ C/ ~9 `4 S! Zlight colored pubic hair development when he was. q1 [0 D8 o' i4 J8 u9 o7 ]
From the 1Division of Pediatric Endocrinology, 2University of
6 [5 ^8 \2 K. o$ S+ C- d6 FSouth Alabama Medical Center, Mobile, Alabama.. u# M8 |# P. P( d9 p  G# s
Address correspondence to: Samar K. Bhowmick, MD, FACE,
9 K0 o! s6 h: ]8 b# XProfessor of Pediatrics, University of South Alabama, College of
4 D8 ?, |3 s6 M- [5 ^Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
# r: _: C1 ]( C9 o; }5 Ke-mail: [email protected].
3 s& a8 H3 O$ mabout 6 to 7 months old, which progressively became
0 l# |# C% O+ k2 Ydarker. She was also concerned about the enlarge-- e, F: o  |- N) |' W' P
ment of his penis and frequent erections. The child: u( m, ?8 p6 f5 _' T8 K" H
was the product of a full-term normal delivery, with
( P" ~6 X9 m. U. ha birth weight of 7 lb 14 oz, and birth length of
( Z4 m6 S, J% \1 y20 inches. He was breast-fed throughout the first year9 S& ?5 |$ K0 b! K* j7 a
of life and was still receiving breast milk along with
4 G0 v0 _. U, Nsolid food. He had no hospitalizations or surgery,( g& J; A1 e6 p: v" |
and his psychosocial and psychomotor development
. x+ `4 `5 F. B* U5 L) [was age appropriate.
$ B) H6 @- p2 x1 {7 FThe family history was remarkable for the father,
- }6 W9 U0 P% c8 H( M: R, {who was diagnosed with hypothyroidism at age 16,
4 [0 w+ G, h( iwhich was treated with thyroxine. The father’s
5 U2 V/ i, [1 D' V  w* xheight was 6 feet, and he went through a somewhat" |9 j' W) M, h* u. e5 g$ J5 }
early puberty and had stopped growing by age 14.. j2 C/ `) L" T3 N8 P( i/ q; `) Z
The father denied taking any other medication. The
6 d. [% q! V; T8 E% S+ k; Zchild’s mother was in good health. Her menarche6 ?% M' x% u& T) j/ S# O
was at 11 years of age, and her height was at 5 feet
' b, E; ^2 S0 k9 g7 v  X- B5 inches. There was no other family history of pre-
0 b2 b9 y: a# z+ L, o1 y4 Z) ~cocious sexual development in the first-degree rela-" j+ _! F6 w4 z( w
tives. There were no siblings.
+ p! W9 @: D) h8 iPhysical Examination
1 f; d  h: ~9 oThe physical examination revealed a very active,
' F2 b$ q) v9 d1 }( g) g2 B, [playful, and healthy boy. The vital signs documented
0 j; D6 ?6 N7 L- H: \a blood pressure of 85/50 mm Hg, his length was
& P; l$ s1 p1 ~6 }9 D90 cm (>97th percentile), and his weight was 14.4 kg
* p4 W, c1 e, Q/ J& t: o. w(also >97th percentile). The observed yearly growth
. S7 S' f. E! R! j" v8 b( yvelocity was 30 cm (12 inches). The examination of" w' N9 h" W& Z! ?
the neck revealed no thyroid enlargement.3 a3 R: v$ m7 r0 u/ U- E& }. l, A
The genitourinary examination was remarkable for
3 a( W4 {. X' @6 s. q0 u! g9 Ienlargement of the penis, with a stretched length of
) w7 F6 w0 v; b+ ?: U8 cm and a width of 2 cm. The glans penis was very well
0 J3 J) F1 K; [3 |2 ~developed. The pubic hair was Tanner II, mostly around
. L3 |% P- u: Z2 V5406 f4 Q0 p$ i4 V7 X+ Q' }
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
4 w8 {' E9 F! m, A' q( Rthe base of the phallus and was dark and curled. The
; h2 u3 o! H7 Z! q) v0 ~- H& atesticular volume was prepubertal at 2 mL each.
$ G* N  ~  S% F% FThe skin was moist and smooth and somewhat
- r1 j" x& k) X1 b- W: [oily. No axillary hair was noted. There were no
& V9 l' V+ e- Q  {  g) O5 E8 H/ @abnormal skin pigmentations or café-au-lait spots.  V* Z1 F  U7 G9 |8 y% I$ L2 }: S/ Q
Neurologic evaluation showed deep tendon reflex 2+- ]" A2 v2 ~. M
bilateral and symmetrical. There was no suggestion# x0 p: {8 D$ H
of papilledema.
1 N# v9 Q5 \4 rLaboratory Evaluation8 z' g( D1 B1 e$ G4 Y. i
The bone age was consistent with 28 months by' b  e& H9 a' i' Z$ ~6 `
using the standard of Greulich and Pyle at a chrono-  \7 v; e/ b2 Q2 b, d
logic age of 16 months (advanced).5 Chromosomal
- s, P9 J8 N9 s; t  Ukaryotype was 46XY. The thyroid function test
2 b4 a( o+ H4 [* D0 V! e; Rshowed a free T4 of 1.69 ng/dL, and thyroid stimu-5 s  K/ u& r% C, b. H
lating hormone level was 1.3 µIU/mL (both normal).
; P+ L) R8 J8 X9 O0 yThe concentrations of serum electrolytes, blood
0 J+ a) O  |: v* U+ Yurea nitrogen, creatinine, and calcium all were7 ?5 |" X3 d* |, v& k
within normal range for his age. The concentration
' T/ D+ Z, p- q: jof serum 17-hydroxyprogesterone was 16 ng/dL
2 Q8 y* H7 V; M(normal, 3 to 90 ng/dL), androstenedione was 20
# _- `8 R) A5 P2 ]. Sng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
" q! ]6 P. _$ c- gterone was 38 ng/dL (normal, 50 to 760 ng/dL),
; Q7 l* E4 _  Z  Q0 u, l0 v  y7 idesoxycorticosterone was 4.3 ng/dL (normal, 7 to$ m2 C/ R: u2 K, _2 ^
49ng/dL), 11-desoxycortisol (specific compound S)
$ ~9 K4 q+ ^5 R( Vwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-: N. n; v, h* E/ u9 \# u9 W
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total% Y( v9 f7 T) A5 W, w; [7 ^: J
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),8 f  N% K- @% s- @9 M
and β-human chorionic gonadotropin was less than
/ g! e; a+ D: ~9 I4 x5 mIU/mL (normal <5 mIU/mL). Serum follicular
$ E+ F" I  U0 M; \0 t7 n* e; vstimulating hormone and leuteinizing hormone! q  m1 c$ V$ z* I0 B5 L
concentrations were less than 0.05 mIU/mL' ~6 O( h) N& c( m& a; j# o  f
(prepubertal).! {5 i9 [) d6 l: n" x0 _; [3 f
The parents were notified about the laboratory% }* b! Z" Z* Q, @2 v# c7 k
results and were informed that all of the tests were7 Q7 c- y8 i7 o& X0 S5 s
normal except the testosterone level was high. The
6 G. B8 c4 m! B) h1 M( {follow-up visit was arranged within a few weeks to
+ N  A8 Q# v2 o) M7 m- ]! ]obtain testicular and abdominal sonograms; how-
9 S8 J, b+ Z& g: U" L* w; a) Wever, the family did not return for 4 months.0 N6 b0 q$ B9 |3 F9 n7 E
Physical examination at this time revealed that the
; \9 e. W# P$ g/ o; }$ qchild had grown 2.5 cm in 4 months and had gained
( g- r( H4 ]  S5 l5 D$ e2 kg of weight. Physical examination remained$ \  V* @0 v, e" ~- _
unchanged. Surprisingly, the pubic hair almost com-. {' Y4 G8 L) e
pletely disappeared except for a few vellous hairs at) r$ H0 G6 }0 d/ [& c0 J1 W' R
the base of the phallus. Testicular volume was still 2
  _! w4 I$ l4 A% ~9 g* PmL, and the size of the penis remained unchanged.) F$ \* Q. {: f3 o
The mother also said that the boy was no longer hav-
9 n1 s  N$ j0 uing frequent erections.9 H4 ~0 @/ D- i( S. x  o0 V2 N
Both parents were again questioned about use of. v( g0 }* r# U( o& t
any ointment/creams that they may have applied to2 t" E1 s* s$ W
the child’s skin. This time the father admitted the. y# R: d  g) T
Topical Testosterone Exposure / Bhowmick et al 541
" P5 }  b; _* F* ~0 x4 F' Xuse of testosterone gel twice daily that he was apply-1 ^7 d# W' j/ t) [
ing over his own shoulders, chest, and back area for* T8 {7 y/ A1 t8 X0 ]
a year. The father also revealed he was embarrassed
! j- S; V0 Z, j: _to disclose that he was using a testosterone gel pre-
+ j1 n2 c* x6 p: F! P" j1 Fscribed by his family physician for decreased libido
5 @1 i. E$ D! _* K( {, \) p- @secondary to depression./ s3 Z, ]( K9 p
The child slept in the same bed with parents.
( L8 a, ]$ r" q8 d, {( YThe father would hug the baby and hold him on his
; h/ \/ ~) j7 I, mchest for a considerable period of time, causing sig-& {. r7 D! G+ g
nificant bare skin contact between baby and father.' m: }7 a7 @7 T( J% \9 P
The father also admitted that after the phone call,2 T7 J4 G- X6 z( w. N- a* O5 g
when he learned the testosterone level in the baby" w' m2 A5 x% Z/ F- n% Z
was high, he then read the product information% P' x! I5 s+ a# ~/ |2 ]
packet and concluded that it was most likely the rea-
+ o4 a7 S5 |$ V0 @; uson for the child’s virilization. At that time, they' D" E4 v7 o8 R# L% t7 D, y
decided to put the baby in a separate bed, and the, z7 x: u; j  V/ X; f
father was not hugging him with bare skin and had+ A" P# j( `: [; w
been using protective clothing. A repeat testosterone: F" p9 M) B1 t
test was ordered, but the family did not go to the
' n# e* A/ H$ @laboratory to obtain the test.
0 `; X  L; c4 XDiscussion
  K& V& h$ r2 c6 d/ Y* R. lPrecocious puberty in boys is defined as secondary
5 k3 U* b; v# p/ csexual development before 9 years of age.1,4
: q9 {( d$ E. w$ o, ^Precocious puberty is termed as central (true) when2 C; ^0 s9 t; \2 l! e7 C( n
it is caused by the premature activation of hypo-
9 _1 s, @+ y' Z: B; ]thalamic pituitary gonadal axis. CPP is more com-) a& n  U; K9 j* W  Y. o
mon in girls than in boys.1,3 Most boys with CPP
8 W0 G, p  W+ ?9 d( z" a2 hmay have a central nervous system lesion that is4 }: q  |6 Z* l, j% g
responsible for the early activation of the hypothal-) o- e( m# x4 [2 g/ U* a. R
amic pituitary gonadal axis.1-3 Thus, greater empha-/ a1 @1 u0 V9 Q" w1 H
sis has been given to neuroradiologic imaging in; i9 F- Q2 C8 q3 a5 e7 M# ?7 k
boys with precocious puberty. In addition to viril-
# J# R! o, N% `: }( yization, the clinical hallmark of CPP is the symmet-5 |! K$ P1 c! c* `
rical testicular growth secondary to stimulation by* ]2 z3 ?4 \3 w, ^/ n* B
gonadotropins.1,34 W+ E2 p# G( _0 N
Gonadotropin-independent peripheral preco-7 s  _8 @8 b, i
cious puberty in boys also results from inappropriate1 h2 b0 i; I4 ~4 v! e
androgenic stimulation from either endogenous or
+ F* @$ [# N0 U) }) E3 F" ]$ i# z: yexogenous sources, nonpituitary gonadotropin stim-6 a4 f+ h0 m# g; o1 X3 z; ?
ulation, and rare activating mutations.3 Virilizing4 l9 Q# k7 Y3 Y& L9 v6 m( v
congenital adrenal hyperplasia producing excessive
7 [" s! R! I( }  T# L1 I1 a+ qadrenal androgens is a common cause of precocious& ?0 ]4 M, _& x% L( H. H
puberty in boys.3,4; b* T( E7 ?2 t1 O; s# f2 [
The most common form of congenital adrenal! I' i) x2 P5 S. s3 M! Z* s" E
hyperplasia is the 21-hydroxylase enzyme deficiency., Z! c, Z- a* u' w2 I$ j$ ]
The 11-β hydroxylase deficiency may also result in
( P0 H4 R; C- g. ~5 t. Y: S+ kexcessive adrenal androgen production, and rarely,
* U2 F  j! ]4 o4 @9 I' B$ L' Lan adrenal tumor may also cause adrenal androgen0 O5 [# a$ y5 L& q
excess.1,31 ^5 w6 Z% a- m4 _- c  f( J
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from. O- r' _) C# @; K) S/ u' i6 c
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
1 ^3 m; I8 n& {" l( v9 BA unique entity of male-limited gonadotropin-% k% ~7 a) E: E# V$ ]7 p
independent precocious puberty, which is also known
* G+ p2 t- ^$ S) Z# c5 f* B4 Mas testotoxicosis, may cause precocious puberty at a, N$ N* R5 q& u- |' f
very young age. The physical findings in these boys
2 a) E+ P& A1 t! p! K" Fwith this disorder are full pubertal development,7 U" C" N+ f+ E; U/ {& x6 J
including bilateral testicular growth, similar to boys( z4 j. f+ _& P6 V
with CPP. The gonadotropin levels in this disorder2 B- q- j$ _+ U  R+ [
are suppressed to prepubertal levels and do not show% Z3 n' R1 _/ N0 k# J/ R
pubertal response of gonadotropin after gonadotropin-
; G& j( I* y1 c0 Jreleasing hormone stimulation. This is a sex-linked4 I2 a$ c+ o. n
autosomal dominant disorder that affects only
" S+ `" k6 S& i2 Qmales; therefore, other male members of the family
5 G/ W/ r& z, a- m1 dmay have similar precocious puberty.30 u8 c/ x% r1 u
In our patient, physical examination was incon-
) x' ]3 n5 _& a5 zsistent with true precocious puberty since his testi-
1 d/ |6 |  n5 D' z/ R* a( F3 x, Mcles were prepubertal in size. However, testotoxicosis+ a3 L" b5 W9 K, k$ H2 W% Z# L
was in the differential diagnosis because his father9 p# j# G& t# n4 ?9 y; H
started puberty somewhat early, and occasionally,6 ?1 u- n6 z7 p  E" L
testicular enlargement is not that evident in the
8 Q! m) ]$ j9 h3 w5 ~  ybeginning of this process.1 In the absence of a neg-6 B5 p, j( y* Y6 D, B0 M
ative initial history of androgen exposure, our* o; S: ]4 ?9 e# c* a, P$ ?( g9 x, Y
biggest concern was virilizing adrenal hyperplasia,
. c4 V2 E9 x& j. Deither 21-hydroxylase deficiency or 11-β hydroxylase
7 m! ~. }$ l) B  Q8 c& Mdeficiency. Those diagnoses were excluded by find-7 Y3 {9 S. S6 Z
ing the normal level of adrenal steroids.
% M4 O) E7 r/ `; F. QThe diagnosis of exogenous androgens was strongly2 C( C- _' r' v' L
suspected in a follow-up visit after 4 months because
7 D! O' j1 q# Q, Ethe physical examination revealed the complete disap-1 c& r9 G) p# I* s- m! B; ], p
pearance of pubic hair, normal growth velocity, and+ A7 X% h9 p$ S: F
decreased erections. The father admitted using a testos-! h# Z2 [. m6 ]; U( \1 s
terone gel, which he concealed at first visit. He was4 v9 L* a) F+ v8 j  h4 c
using it rather frequently, twice a day. The Physicians’. @* T* Q+ y# m
Desk Reference, or package insert of this product, gel or( x; X3 F) d9 K# J
cream, cautions about dermal testosterone transfer to
% j( J: Y) ^. H* O8 ~2 \/ _unprotected females through direct skin exposure.
5 x3 R- N( ]+ VSerum testosterone level was found to be 2 times the" [% q/ E6 B. P* m
baseline value in those females who were exposed to3 h7 z1 r; }& t- w' }' B
even 15 minutes of direct skin contact with their male/ w) ^( \( I5 n- u* o
partners.6 However, when a shirt covered the applica-
* _: q, h/ ?) E% ^$ J- U$ otion site, this testosterone transfer was prevented.# N9 ]- u6 W- [2 Z
Our patient’s testosterone level was 60 ng/mL,4 y/ {  x: l* L8 ?. y, n) H
which was clearly high. Some studies suggest that* K6 t9 }! t% h
dermal conversion of testosterone to dihydrotestos-
- c. o( c+ p' B7 ?+ pterone, which is a more potent metabolite, is more# e4 j4 c( j& g# K
active in young children exposed to testosterone
* D8 I  ]* m2 a' v7 Rexogenously7; however, we did not measure a dihy-, x. a/ d& w; J& g5 J
drotestosterone level in our patient. In addition to
! `3 d+ j0 \/ @  z- wvirilization, exposure to exogenous testosterone in
3 ]! O2 U4 M$ nchildren results in an increase in growth velocity and
/ {9 e, }: k- q$ q9 M- Q# J" W& Gadvanced bone age, as seen in our patient.3 N( R1 w: i' L  e& a# Y
The long-term effect of androgen exposure during
' V& s* l- d) c: Oearly childhood on pubertal development and final. s9 @6 V; s5 {8 D8 q; ?
adult height are not fully known and always remain
1 h& U% A( B7 `( L: ^5 a5 S! o8 wa concern. Children treated with short-term testos-
' E! n8 ?8 t. J; Xterone injection or topical androgen may exhibit some) U5 w: J! H, x+ `: N
acceleration of the skeletal maturation; however, after
. {2 T6 @5 Q: L: k* P- }cessation of treatment, the rate of bone maturation3 K+ ~  i5 B: X! S. ~3 V3 a: k
decelerates and gradually returns to normal.8,9+ g+ _3 A& e% p; J; z6 ^
There are conflicting reports and controversy* {+ ^1 C9 H* U5 k3 z
over the effect of early androgen exposure on adult
$ S3 z, X* S5 N: N! R; Lpenile length.10,11 Some reports suggest subnormal
7 ]* m5 ?/ i, wadult penile length, apparently because of downreg-
8 x. X) |3 E0 \  E9 S: [4 M$ ?ulation of androgen receptor number.10,12 However,
4 ~9 |4 Y* f# B- N/ e1 j6 K6 nSutherland et al13 did not find a correlation between
# O# F" }  J! l% schildhood testosterone exposure and reduced adult0 G5 x) Z! _7 P
penile length in clinical studies.
( u  X* B$ z8 `; `# n6 }! t% m8 {Nonetheless, we do not believe our patient is- u! \  K$ _: ]9 B. c4 \. u
going to experience any of the untoward effects from
& y9 \$ w7 q6 z) Itestosterone exposure as mentioned earlier because
) j. C3 N8 O8 W* G: J+ U% o  zthe exposure was not for a prolonged period of time.* q) J6 `4 r1 \/ F6 o: H  n
Although the bone age was advanced at the time of
% k) n6 Y+ Q  q$ |2 }& R* Ndiagnosis, the child had a normal growth velocity at* H7 ~' d9 b$ G( Q# i) o
the follow-up visit. It is hoped that his final adult
. F" G9 ^1 g2 P: C# \- z/ H/ Fheight will not be affected.8 I. N; I$ q% H) h' @) Q
Although rarely reported, the widespread avail-5 n' }1 i; p) f' D# ~5 o
ability of androgen products in our society may5 d5 ~$ {  h$ y0 A( g
indeed cause more virilization in male or female
3 Q% L2 l: @* Ychildren than one would realize. Exposure to andro-! r7 X, S$ I& H9 Y# Q6 ]* e. n
gen products must be considered and specific ques-+ B6 Z/ m( S1 `  D( d0 x" Z
tioning about the use of a testosterone product or
$ d' d+ K: p' }gel should be asked of the family members during0 T. [# c2 g6 i. s6 I
the evaluation of any children who present with vir-
7 g* k: m4 _! K6 n+ y: wilization or peripheral precocious puberty. The diag-( T1 K0 u. R! R7 m% T$ x: c
nosis can be established by just a few tests and by; n# g. h" Q' N3 U6 X
appropriate history. The inability to obtain such a9 C5 N$ L; ?8 {7 _
history, or failure to ask the specific questions, may
8 Y. `( J1 ~, T7 Q4 m6 O) tresult in extensive, unnecessary, and expensive
  P" t+ c& H! y, N% P3 p6 [+ X. k! A7 _9 |investigation. The primary care physician should be
5 K. h% ~+ a6 r  g( f0 v# W* `( _aware of this fact, because most of these children
1 g. l( T+ x; w0 _4 pmay initially present in their practice. The Physicians’
* R' i  e" l4 h7 [Desk Reference and package insert should also put a
( U1 W: {( {' _6 xwarning about the virilizing effect on a male or; g% q7 A, r) Y  a2 U. f
female child who might come in contact with some-, ^2 \* F! M4 }3 u
one using any of these products.
1 F4 r/ S3 {0 j- b$ O2 [2 eReferences
  Z4 u, Y! B' t, H: ]1. Styne DM. The testes: disorder of sexual differentiation
: A/ _% S; R; E0 p: q8 F0 dand puberty in the male. In: Sperling MA, ed. Pediatric* |4 a. R% y, r
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
& \( Y; m* t0 R0 ^8 u/ G2002: 565-628.
6 N# G' N' E8 s8 \7 Q4 D2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
, [7 r8 |9 O* ipuberty 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
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4个什么样的?
發表於 2025-1-19 02:41:05 | 顯示全部樓層

4 p8 v0 s) B8 D- T) ?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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