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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& W" w& f$ P% J
Boy Induced by Indirect Topical
, q7 o2 R5 z. m$ SExposure to Testosterone
8 D3 X2 X- C4 m0 S4 ySamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
2 q0 S- O. T' N9 Jand Kenneth R. Rettig, MD1
( L! p7 S' u( r3 E) R3 d* i1 `, [% EClinical Pediatrics2 Y: k8 B! E7 B: n5 C7 u2 x
Volume 46 Number 6. y2 u: ^" P3 G% x6 }2 O8 ~
July 2007 540-5436 C" N, [$ @) A( g
© 2007 Sage Publications6 Z9 F& q: q2 S
10.1177/0009922806296651' e+ B' B) {( E7 g5 O3 P
http://clp.sagepub.com
" i- z* A: j' Ehosted at7 K4 c" x3 t; v$ [  z9 |
http://online.sagepub.com: a5 k- n  B& c$ i  ~9 S
Precocious puberty in boys, central or peripheral,( O% y$ K4 v  J" V% J! D
is a significant concern for physicians. Central
+ Y3 v! R  a. v4 @precocious puberty (CPP), which is mediated
( m6 g$ l8 k; B5 R8 i+ E$ C. S! k+ Wthrough the hypothalamic pituitary gonadal axis, has
. Y$ B; u+ i8 Ya higher incidence of organic central nervous system, g4 h2 L( F2 F% L; L0 l& U( d
lesions in boys.1,2 Virilization in boys, as manifested
% l1 `2 W& G( I3 p+ eby enlargement of the penis, development of pubic
' p" V/ L, b# F' C' qhair, and facial acne without enlargement of testi-1 r: s- e# Q* d; l0 M7 f
cles, suggests peripheral or pseudopuberty.1-3 We
" F! n( o: x8 M, L8 Y2 {report a 16-month-old boy who presented with the1 |6 Y7 ~6 Y9 V1 \. K
enlargement of the phallus and pubic hair develop-
7 h; N) ^8 ^& i" Zment without testicular enlargement, which was due
0 N& @6 `+ L# y8 r* L( P3 x' |to the unintentional exposure to androgen gel used by* _# j: R# k1 k/ s0 k
the father. The family initially concealed this infor-6 ^' j' L- j/ h6 N8 x
mation, resulting in an extensive work-up for this: A0 o/ d! B$ n) d, E" q9 I& f
child. Given the widespread and easy availability of% n8 _" Q/ f6 t$ p4 G1 X- w- w
testosterone gel and cream, we believe this is proba-+ P! [# \6 i8 m7 }4 u
bly more common than the rare case report in the' d3 ~. t  |! ]- w: V- a
literature.4  X% t' x% _+ e4 b+ @4 t
Patient Report% f* ^0 A+ P/ I$ t, `
A 16-month-old white child was referred to the) A+ E' |: T% b0 V$ X8 M& H
endocrine clinic by his pediatrician with the concern) w5 J3 [. L, ^9 G# e9 ^) w* q
of early sexual development. His mother noticed
5 v+ F: s* E, e% i, X; h+ I6 Rlight colored pubic hair development when he was
2 n2 U. i: T: n5 V* a+ e% W; jFrom the 1Division of Pediatric Endocrinology, 2University of
# e0 {" U& O- n- Q" Y8 KSouth Alabama Medical Center, Mobile, Alabama.
& s8 a/ I. h$ o- eAddress correspondence to: Samar K. Bhowmick, MD, FACE,
  n% r1 d; }0 D& {5 UProfessor of Pediatrics, University of South Alabama, College of
6 M8 v4 F. p  k5 mMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;' [8 o. ?3 o! e6 n% q: L1 N  K
e-mail: [email protected]./ L  N- b+ t* n* K. J" s9 {
about 6 to 7 months old, which progressively became
# S! M+ l2 A6 R) s2 bdarker. She was also concerned about the enlarge-
3 ^0 o, t& {! Vment of his penis and frequent erections. The child3 X3 U: d( R; r. d, W/ M5 u
was the product of a full-term normal delivery, with5 o" v: t# b1 S/ ?
a birth weight of 7 lb 14 oz, and birth length of
% p5 A' X! ~& o: A3 E+ b20 inches. He was breast-fed throughout the first year
% u  `9 s- M& c& f' m% c4 [/ g) K# tof life and was still receiving breast milk along with
# w6 A$ v% ^9 p: X9 ~* [solid food. He had no hospitalizations or surgery,7 X$ m- Q) C: ]4 b
and his psychosocial and psychomotor development, H: h* P# ]3 R: q% m
was age appropriate.
% _( a* M9 p! W8 c7 YThe family history was remarkable for the father,7 f# D3 ?' L- H4 ?* P( u8 p
who was diagnosed with hypothyroidism at age 16,  h3 j2 S/ Z5 `
which was treated with thyroxine. The father’s& s; O9 @6 n7 `/ h% u
height was 6 feet, and he went through a somewhat
7 B, ^# k9 F: K7 learly puberty and had stopped growing by age 14.
' y( q9 I' ?$ w) Q9 }The father denied taking any other medication. The
. i( F& B+ d$ E0 o. F/ H% jchild’s mother was in good health. Her menarche
+ P5 q! y; c& a; M) swas at 11 years of age, and her height was at 5 feet7 B" b7 Z0 y! l6 ?2 y
5 inches. There was no other family history of pre-
3 X: K' S7 }. t' F4 b2 kcocious sexual development in the first-degree rela-
$ `& Z& n/ A  m6 Jtives. There were no siblings.1 P3 }9 z  f, w( S
Physical Examination
" {' e8 p0 y- q% k9 @The physical examination revealed a very active,5 A3 ^% z6 N& z, j
playful, and healthy boy. The vital signs documented
0 E* Y1 B4 S6 H% Y: c& z' x/ [: Ra blood pressure of 85/50 mm Hg, his length was8 u4 L' h9 i7 V! ~
90 cm (>97th percentile), and his weight was 14.4 kg
  o. V  P% ~% r- U% B% R(also >97th percentile). The observed yearly growth: f( N0 \) ^) ]8 V3 ^2 `+ U
velocity was 30 cm (12 inches). The examination of7 ^# Y- D' v. H9 r4 W- \+ z4 a
the neck revealed no thyroid enlargement.+ m' B0 {0 z' V, l% M/ i- W
The genitourinary examination was remarkable for
! d8 R. v) e4 u% ?enlargement of the penis, with a stretched length of
4 o0 b; {: B4 x0 a8 cm and a width of 2 cm. The glans penis was very well
9 u4 ~( E2 _  Jdeveloped. The pubic hair was Tanner II, mostly around! y; I1 A- C' C( h3 z+ `
540- q4 M. F' y# Q9 I1 Q" r! V
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
1 Q* [5 m$ u; v% m5 [the base of the phallus and was dark and curled. The
! `# w* h6 {3 a, Y( Ttesticular volume was prepubertal at 2 mL each.: H2 K. _; X' j' v+ j4 S
The skin was moist and smooth and somewhat2 _3 t8 w- d: c  @. t
oily. No axillary hair was noted. There were no
6 I. G5 V" J/ }" p- i: jabnormal skin pigmentations or café-au-lait spots.8 r2 C: \& S: k) l3 w; t9 |- H
Neurologic evaluation showed deep tendon reflex 2+
8 \! g( v$ G2 g2 z3 M* h4 M" Z4 `bilateral and symmetrical. There was no suggestion
2 s1 p9 X0 w" P" C# `of papilledema.; |8 Q' Y! _$ z! j/ t+ I# K+ v
Laboratory Evaluation
  n+ ~8 W. [9 e* H( s4 b/ HThe bone age was consistent with 28 months by
$ s9 P# V, |/ [! i+ g  husing the standard of Greulich and Pyle at a chrono-
3 H& F/ v6 V/ x$ [* Slogic age of 16 months (advanced).5 Chromosomal# i+ h* E% k$ ^0 S' `
karyotype was 46XY. The thyroid function test, J3 N5 S. m" c# T3 q
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
% b7 S0 I  r  A" {  H, o; Alating hormone level was 1.3 µIU/mL (both normal).  ~% z% S: E/ }  F( h3 B' G/ B, g
The concentrations of serum electrolytes, blood
; n3 ?5 O; S* k+ P/ p* uurea nitrogen, creatinine, and calcium all were+ }! h- w! H( Z7 ~
within normal range for his age. The concentration, c  n9 b3 j. R8 Q* D
of serum 17-hydroxyprogesterone was 16 ng/dL
6 E& E2 P! I# D  z  |& W% Y. G(normal, 3 to 90 ng/dL), androstenedione was 20
% |1 v* \2 T8 r% H! t# [ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
) z4 ^- Y! _6 R1 iterone was 38 ng/dL (normal, 50 to 760 ng/dL),
: ?3 G6 j7 [' @, @( Vdesoxycorticosterone was 4.3 ng/dL (normal, 7 to* ]8 p  ~3 W0 M6 u' C
49ng/dL), 11-desoxycortisol (specific compound S)
6 f4 u0 W, v0 e- a& g+ X& a2 Owas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
% i$ O5 q' I, z/ k6 ]' X9 Xtisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
1 z* v3 ]- @+ O3 Xtestosterone was 60 ng/dL (normal <3 to 10 ng/dL),( s5 z: ]/ T( F( E1 a
and β-human chorionic gonadotropin was less than
9 g" F! C- c, A, W( t. `& E; O5 mIU/mL (normal <5 mIU/mL). Serum follicular8 F1 X  G0 K- d- v
stimulating hormone and leuteinizing hormone7 b7 p( i& z% x9 D8 m/ c( A
concentrations were less than 0.05 mIU/mL$ Z( @& e) H0 `' D
(prepubertal).
7 P5 a5 S' R  BThe parents were notified about the laboratory
9 L# x2 ^8 T0 A  Mresults and were informed that all of the tests were/ e; x8 G+ Q* Z8 C' ]( \
normal except the testosterone level was high. The
% \# A9 B: {) {- {# p2 bfollow-up visit was arranged within a few weeks to
1 Q" x8 ?' H. @; _  D. H1 sobtain testicular and abdominal sonograms; how-6 i9 M0 A4 y- J3 e8 w
ever, the family did not return for 4 months.6 E( A$ ]& D5 D0 [# b1 V7 s
Physical examination at this time revealed that the
3 e; ^1 E. N+ T0 m7 c5 k" y2 Lchild had grown 2.5 cm in 4 months and had gained) q& ]$ L/ s6 ^; K8 R7 C" Y# z
2 kg of weight. Physical examination remained; N! I. \! L, ~
unchanged. Surprisingly, the pubic hair almost com-
) o/ R3 z6 X. tpletely disappeared except for a few vellous hairs at: d. a: ^+ z/ T6 |
the base of the phallus. Testicular volume was still 2
0 W2 b  n6 V9 T- }mL, and the size of the penis remained unchanged.- i) }6 i) ^" ~% \8 \/ `
The mother also said that the boy was no longer hav-
7 n" d' K( ]. \0 {3 g& X" Oing frequent erections.
7 s) l$ q0 X1 m6 d4 e3 jBoth parents were again questioned about use of
. ^. w" Q. F5 l* G4 rany ointment/creams that they may have applied to" S( U" O+ {& @! L6 U5 |9 i
the child’s skin. This time the father admitted the: {6 H9 e5 p4 s" @$ X3 K# d
Topical Testosterone Exposure / Bhowmick et al 541
3 L! W' f/ ^2 n. J# ?; k! x5 c% duse of testosterone gel twice daily that he was apply-8 Q: d6 p: }- O
ing over his own shoulders, chest, and back area for
+ J; f# ~! r6 j6 D& Z1 Ka year. The father also revealed he was embarrassed
: C: U& W' n* J* K/ hto disclose that he was using a testosterone gel pre-
% U) `  V2 o  n# dscribed by his family physician for decreased libido
  t- T8 q' Z& f7 usecondary to depression.
1 X% a; b, }4 [) q$ ]" b( K8 }The child slept in the same bed with parents.8 _6 `1 K2 M5 L! P% y. X2 C6 H# g
The father would hug the baby and hold him on his
  }* D3 B0 Y$ Q, U$ v$ [; K  I  z( Ychest for a considerable period of time, causing sig-
" v/ r1 U9 T& P4 r- qnificant bare skin contact between baby and father.
9 h6 A. E# V8 l7 cThe father also admitted that after the phone call,
0 J. ?+ j3 w; K& ~0 Lwhen he learned the testosterone level in the baby
* m7 c$ P- l7 I" M4 {  \2 Jwas high, he then read the product information' X- ?1 `/ g7 I% @0 R
packet and concluded that it was most likely the rea-1 G; d. s2 |& j4 i7 `
son for the child’s virilization. At that time, they
. ^8 F9 a! H& _* f' idecided to put the baby in a separate bed, and the( G- W" P) W% [. D
father was not hugging him with bare skin and had6 w$ U4 l9 z: e! l1 |7 Z
been using protective clothing. A repeat testosterone
. ?& D" N) j$ Ptest was ordered, but the family did not go to the
& ]$ s) t1 o& ~$ T5 I* q( Glaboratory to obtain the test.
( b- D" r0 E" o4 C4 u4 y- \& @Discussion
2 P- V* S% r" R' RPrecocious puberty in boys is defined as secondary
) n, G. L# A" @; G4 asexual development before 9 years of age.1,4! L7 i3 o7 x' ?  w8 `2 d' b
Precocious puberty is termed as central (true) when
5 [" Q7 f$ H2 O& J( z3 L" d* |2 Mit is caused by the premature activation of hypo-
# m, V1 G" M" Y0 V- vthalamic pituitary gonadal axis. CPP is more com-
# r9 V* }$ ?- Z+ `" omon in girls than in boys.1,3 Most boys with CPP/ U0 W& N3 z, I, V
may have a central nervous system lesion that is; P$ |" d# S6 L1 [( ?7 {8 d  T
responsible for the early activation of the hypothal-
( \9 X% g) o; F9 namic pituitary gonadal axis.1-3 Thus, greater empha-" L5 `3 @! l+ _/ W: X+ b5 ~
sis has been given to neuroradiologic imaging in5 }2 h6 A5 P+ L4 Y9 _- Q
boys with precocious puberty. In addition to viril-8 q" l- e  g% q4 g
ization, the clinical hallmark of CPP is the symmet-
' a$ ^! x" j# h" W2 |rical testicular growth secondary to stimulation by
! `  E% A; s/ N2 j. {$ j+ Tgonadotropins.1,3$ g3 }/ G3 w: S! a! b* }8 Z
Gonadotropin-independent peripheral preco-
! ?  e. p7 e% _8 u8 bcious puberty in boys also results from inappropriate
3 G! z: R! o4 V% tandrogenic stimulation from either endogenous or
* C4 f) N6 M$ f' J- cexogenous sources, nonpituitary gonadotropin stim-
2 e+ A2 _- v$ D+ ^! m; bulation, and rare activating mutations.3 Virilizing7 ]5 j1 {7 m7 R: w$ R, j
congenital adrenal hyperplasia producing excessive
. D% Q- D: ~5 M# M" L6 h: Ladrenal androgens is a common cause of precocious% ]2 L1 I: z! }3 W- ]
puberty in boys.3,4  ~; D/ R" q& D
The most common form of congenital adrenal% B7 o) d0 o5 p  G" C9 L( J) I  v
hyperplasia is the 21-hydroxylase enzyme deficiency.
, l: \- ^$ O* q) W( q4 ]The 11-β hydroxylase deficiency may also result in
/ f9 {: \8 R& c+ v) oexcessive adrenal androgen production, and rarely,& k* k. k) ]! X
an adrenal tumor may also cause adrenal androgen# f* Z1 `" N1 Y; }- @
excess.1,32 S8 Q( P* b, ]7 d
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from- j/ [; c$ g- j9 L( p" f  ~) D% q2 }
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007- E; M5 X0 o( _4 ^
A unique entity of male-limited gonadotropin-7 h" L; K8 h9 U; u
independent precocious puberty, which is also known
' x1 o& J, }% h9 o/ p# Z* ?6 Pas testotoxicosis, may cause precocious puberty at a3 h1 P! N* U8 {; a$ t/ F
very young age. The physical findings in these boys' P/ ^) J* ?" D& y& [
with this disorder are full pubertal development,
/ {2 C2 m! q* J$ Nincluding bilateral testicular growth, similar to boys
: ?4 Q8 r1 ?3 }; _! Ywith CPP. The gonadotropin levels in this disorder
  o5 G' P% U  n. y9 Z- @! G2 eare suppressed to prepubertal levels and do not show  i3 ~6 S' q5 ^& ~5 W: j' q3 b
pubertal response of gonadotropin after gonadotropin-$ y. O$ m0 `  A& _
releasing hormone stimulation. This is a sex-linked! I. T, }* p" o
autosomal dominant disorder that affects only
5 W0 D) d. y& i& X4 lmales; therefore, other male members of the family
) N! |) t# c2 a; Y) l3 t# K1 Z0 Xmay have similar precocious puberty.35 i- R0 o" x, W) q! c) K
In our patient, physical examination was incon-
4 r; E* x1 t* X) h$ w! D- Asistent with true precocious puberty since his testi-& b- g- f3 k1 [; v0 D; `
cles were prepubertal in size. However, testotoxicosis
9 N; v: f: b1 W4 mwas in the differential diagnosis because his father, @. Y8 r, M* A% c4 P
started puberty somewhat early, and occasionally,
: R  ^9 Y0 I5 |; c. \testicular enlargement is not that evident in the
( ^1 j9 ?- f9 ^4 F. \1 |" n) Q* V# Obeginning of this process.1 In the absence of a neg-
( H; g4 U( D9 v' F# N) N  Iative initial history of androgen exposure, our# y& v$ y1 `+ |0 A/ d/ c- x( S, c: Z$ \
biggest concern was virilizing adrenal hyperplasia,
, ?% j0 {9 i. F- z4 j4 c, {either 21-hydroxylase deficiency or 11-β hydroxylase
6 l% d- v9 X+ ^4 E1 V1 Kdeficiency. Those diagnoses were excluded by find-! R* D% b3 h, n" x8 m' p9 A: c2 A
ing the normal level of adrenal steroids./ Y; C: E8 V" n, ~) J7 M
The diagnosis of exogenous androgens was strongly2 ?  p4 P6 G/ f0 _3 M1 h
suspected in a follow-up visit after 4 months because
; a8 V9 A& p1 Ethe physical examination revealed the complete disap-* y' x$ k+ d8 W) s0 K# {# C
pearance of pubic hair, normal growth velocity, and4 s' S. o5 S+ A+ E$ a
decreased erections. The father admitted using a testos-
6 M: W9 O9 c  p2 E5 A1 jterone gel, which he concealed at first visit. He was
4 q+ M2 G& ?5 k: h. Yusing it rather frequently, twice a day. The Physicians’6 n2 x. {7 j! v2 `3 V! Y2 S
Desk Reference, or package insert of this product, gel or
' R( x$ }* i- D8 k1 ]. e8 Ncream, cautions about dermal testosterone transfer to
# V4 X0 B& k. c4 B& l' u# A2 B; Munprotected females through direct skin exposure./ E7 n1 P" Q+ z4 [# z9 G
Serum testosterone level was found to be 2 times the
, i; e" x- N8 ?4 ?1 j# r! A4 O8 zbaseline value in those females who were exposed to9 P1 T7 A  v, M! X( c3 e) U; T9 d. G
even 15 minutes of direct skin contact with their male; j" z, D- P' B) G+ N: Q$ ^
partners.6 However, when a shirt covered the applica-' G; V3 h3 U7 y# _$ Q5 G7 I
tion site, this testosterone transfer was prevented.
. m$ ], h$ M+ DOur patient’s testosterone level was 60 ng/mL,
$ I+ ]0 o$ I0 G3 u* a) r. jwhich was clearly high. Some studies suggest that& u* P" R. U- u
dermal conversion of testosterone to dihydrotestos-
( e; Y6 q7 C; j7 s+ r4 B) Lterone, which is a more potent metabolite, is more& E9 V6 d+ W3 y0 s) p: q: K
active in young children exposed to testosterone
7 `/ N& f1 T0 G+ Gexogenously7; however, we did not measure a dihy-
7 N; V4 G* V1 k- Ydrotestosterone level in our patient. In addition to
8 H: n4 s2 x7 k6 I( Tvirilization, exposure to exogenous testosterone in" ?: E9 c, [7 x: q
children results in an increase in growth velocity and
- ]* W5 p7 s' M; ]0 Wadvanced bone age, as seen in our patient.2 T5 r' `4 T% ?7 v1 ^
The long-term effect of androgen exposure during
$ f8 }1 @: `+ a$ m0 \( P4 Tearly childhood on pubertal development and final2 a4 S% ^4 p! b& @0 f
adult height are not fully known and always remain/ F; [0 r. z, o3 e) t: ?5 v. w
a concern. Children treated with short-term testos-
. M% V7 f4 ~" a" Tterone injection or topical androgen may exhibit some
- s& B$ u6 m$ f% S* _* E( _acceleration of the skeletal maturation; however, after+ j& n/ S+ i8 a
cessation of treatment, the rate of bone maturation
5 @; y! {  F# z$ D/ idecelerates and gradually returns to normal.8,9
0 q0 f/ t) Z, r5 ]4 K$ ?9 Z1 @There are conflicting reports and controversy
) |8 C$ B1 T$ A3 a: Dover the effect of early androgen exposure on adult
7 i9 a3 ]  ~- Xpenile length.10,11 Some reports suggest subnormal) l  M* w" ?  B7 N8 F. ]* T
adult penile length, apparently because of downreg-
1 b( I( n# h' a1 Fulation of androgen receptor number.10,12 However,/ o5 i3 j7 v' q9 o9 k+ ^
Sutherland et al13 did not find a correlation between/ n$ D/ Z# F% `2 f- e( K+ c
childhood testosterone exposure and reduced adult9 m; i8 ~: D% g" C$ m
penile length in clinical studies.9 ~* A% I8 @  w: S
Nonetheless, we do not believe our patient is* X. z6 P  ?% [3 R
going to experience any of the untoward effects from- W& p" A$ s2 ?% G5 U
testosterone exposure as mentioned earlier because. i0 X5 I5 Q+ U+ }! o2 m
the exposure was not for a prolonged period of time.. y  p: ?3 ?: O: a7 F% Q" H( ]
Although the bone age was advanced at the time of+ _+ Z0 {" E6 ~$ z( D
diagnosis, the child had a normal growth velocity at
: V( F' x4 C& c9 g; _9 D5 P' mthe follow-up visit. It is hoped that his final adult
) l  M' I  }" b) u; A) bheight will not be affected.
. \/ M  Y! p4 E& ~Although rarely reported, the widespread avail-
" u. Y4 P1 {" V7 A0 a7 iability of androgen products in our society may/ l( w0 ]  d& k. D
indeed cause more virilization in male or female
2 K$ A, Y/ D; D7 s' j/ ychildren than one would realize. Exposure to andro-
4 n* t* U3 p5 H6 Jgen products must be considered and specific ques-
, l: v) e) N/ ]/ }  dtioning about the use of a testosterone product or
2 ]4 V  o# T8 V$ w3 f0 l% c7 }gel should be asked of the family members during
0 C; s* E2 _& A1 ?& k# L; Qthe evaluation of any children who present with vir-1 x% k+ ~- B! S1 @8 L
ilization or peripheral precocious puberty. The diag-
3 X7 j+ S6 u% q2 `, L6 Vnosis can be established by just a few tests and by
9 G. B1 U2 d7 E& G8 xappropriate history. The inability to obtain such a) \4 f8 t5 i$ D) Y
history, or failure to ask the specific questions, may
3 u, f  j- G5 h( Z8 t7 Q! N" a* A4 jresult in extensive, unnecessary, and expensive6 W& W* m# c& w( B1 j
investigation. The primary care physician should be% Y! c' B( k; [* Q5 K
aware of this fact, because most of these children2 A& {; W) e- B/ X! N
may initially present in their practice. The Physicians’
  N8 G7 G/ k8 X9 @9 f; Y: ^) t5 mDesk Reference and package insert should also put a
8 Q" ^1 J1 [% e7 V8 R' Kwarning about the virilizing effect on a male or% E0 P& c( N  j' p' {
female child who might come in contact with some-
2 J% d( S3 c% none using any of these products.
4 D: j% x# X' I5 b, t9 H" }+ v; oReferences
3 `: z3 c, N, L$ l4 b) ^1. Styne DM. The testes: disorder of sexual differentiation# Z7 R' o6 A0 k; Y& b, k" Z
and puberty in the male. In: Sperling MA, ed. Pediatric
8 R7 I% G! b! \$ iEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
! e6 |: L. e2 G  [; K2002: 565-628.
* t6 L# D8 G+ E2 ~2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious1 b$ Y! l& Y7 A  S4 p; w
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
6 `# b8 c# g( C. K( Q/ NBoy Induced by Indirect Topical+ _$ Z3 ]0 q  b3 Z; o
Exposure to Testosterone! T2 X- Z6 {) F/ L6 B- U% h  i, t
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2# s4 A) R& t9 N% J* y
and Kenneth R. Rettig, MD1
  m, B" w- Y" X/ C! M+ |  mClinical Pediatrics0 [& ]4 L( y1 k
Volume 46 Number 6
$ L$ Q! d/ E: t! R, rJuly 2007 540-543% B% z! e, b- W; r6 N' b' _
© 2007 Sage Publications# }+ p- G% N6 s7 C0 e% T4 G3 k- A: V
10.1177/0009922806296651' {) W. ^3 F: a* c
http://clp.sagepub.com
9 u1 A( |7 C9 Zhosted at
5 ?9 s& d- d! k, v) }/ |# rhttp://online.sagepub.com: o& k1 ?( M# V& n$ ~
Precocious puberty in boys, central or peripheral,$ _9 K2 J8 W1 v' W" g: i
is a significant concern for physicians. Central) R6 a" V& K1 U3 b* C
precocious puberty (CPP), which is mediated
9 I! ^2 Z: w4 V  uthrough the hypothalamic pituitary gonadal axis, has
" B; b6 V5 N2 D$ y$ B( Ua higher incidence of organic central nervous system% ~* }( j  O4 g# y* [7 ^
lesions in boys.1,2 Virilization in boys, as manifested
0 w3 Q' s' ?6 Hby enlargement of the penis, development of pubic2 E% F) m4 P5 v2 _6 N: ~
hair, and facial acne without enlargement of testi-: i; h+ _+ n6 _
cles, suggests peripheral or pseudopuberty.1-3 We) z5 _: m4 |5 K# V8 w
report a 16-month-old boy who presented with the+ R- r! f" R& c: d
enlargement of the phallus and pubic hair develop-
2 [1 z/ x& y' @# t& S! Gment without testicular enlargement, which was due
. T' G! a! X+ Z3 K+ i4 r1 I! I* qto the unintentional exposure to androgen gel used by
+ N# ~. i$ Y: L3 jthe father. The family initially concealed this infor-  d! s% o. x' q7 x3 ^. w! D' j
mation, resulting in an extensive work-up for this
2 v! I/ l! k; [+ x* q/ P8 [child. Given the widespread and easy availability of9 I0 s6 Q! Q3 ~. Q9 z- t$ Q: ]
testosterone gel and cream, we believe this is proba-
/ h/ t6 e# |+ T4 ~3 a  Jbly more common than the rare case report in the, H* J7 y$ b% r6 J. w
literature.48 `- W, x% ^5 P' R# U$ P8 {
Patient Report% u/ j( {9 U" L0 n7 B6 u
A 16-month-old white child was referred to the; S; K; {: Y' W! j7 W6 c2 r
endocrine clinic by his pediatrician with the concern
% j: ~1 L( Z: Q; g& K4 l/ Nof early sexual development. His mother noticed
) p% C# d/ A* C% h& c! W3 |) `light colored pubic hair development when he was
! G; _7 T3 x; |! u3 }; dFrom the 1Division of Pediatric Endocrinology, 2University of
' x9 i: r& O) O& USouth Alabama Medical Center, Mobile, Alabama.
4 I8 Z' }$ q8 i" Z6 }; tAddress correspondence to: Samar K. Bhowmick, MD, FACE,
& j: C+ s( o5 T( pProfessor of Pediatrics, University of South Alabama, College of
- _0 F6 F5 ]  M+ G2 @Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
& T3 c& ?7 _) J9 v# be-mail: [email protected].
  `# t+ I, ?+ _+ V4 r3 Labout 6 to 7 months old, which progressively became
6 ?4 ^5 ~: ]/ D: L- rdarker. She was also concerned about the enlarge-
$ _+ `$ U- o. r$ M& c, l" wment of his penis and frequent erections. The child
# u4 c" ?6 u  [5 ?% a- ]0 Fwas the product of a full-term normal delivery, with" e: J* S7 O+ J; Q3 ?# G$ ~
a birth weight of 7 lb 14 oz, and birth length of
9 b5 E# R; ?4 E4 Z20 inches. He was breast-fed throughout the first year# f+ |0 q. |; m6 `2 Z( t
of life and was still receiving breast milk along with7 |8 M) I3 h/ w7 j
solid food. He had no hospitalizations or surgery,- h; p# J' A, R! I: ~
and his psychosocial and psychomotor development
$ U6 q6 s* }2 w/ ]+ X) K) Z) {was age appropriate.6 S5 M: o$ i* X0 m3 x; F+ R
The family history was remarkable for the father,% u- a  ]3 k8 w5 }; T
who was diagnosed with hypothyroidism at age 16,
# z( T9 ]; |8 o$ r5 swhich was treated with thyroxine. The father’s
+ A& Q( p" T* i. d4 X  oheight was 6 feet, and he went through a somewhat/ I: ?9 Q7 |: T, Q! `' z4 o9 B
early puberty and had stopped growing by age 14.
7 i( D! \& S' w; B) V# [The father denied taking any other medication. The, ~2 ?& }3 I" b. F
child’s mother was in good health. Her menarche, b. m! U' S7 w( ^$ F) D
was at 11 years of age, and her height was at 5 feet5 z2 m+ ?- Y- o, ^
5 inches. There was no other family history of pre-7 T/ S  S: ~. O: {4 F
cocious sexual development in the first-degree rela-
5 G+ F: e; {- |8 I  @5 jtives. There were no siblings.4 h" b: V# [8 D" F4 ?- p3 y
Physical Examination
) G) @+ e5 x1 C2 v3 @The physical examination revealed a very active,
2 D$ f/ Z0 H+ O4 Cplayful, and healthy boy. The vital signs documented2 V# e% P3 P& k
a blood pressure of 85/50 mm Hg, his length was! s* e# s* v' i1 g4 h0 U  {8 @) Q7 X& w4 b
90 cm (>97th percentile), and his weight was 14.4 kg
. K' {% z) K7 q' b! ^; O(also >97th percentile). The observed yearly growth9 L* t3 f2 _! x
velocity was 30 cm (12 inches). The examination of
% Z. j% S- M2 s3 _the neck revealed no thyroid enlargement.
- H. z: ?$ U+ O, O- f* \8 X7 e# p6 dThe genitourinary examination was remarkable for% X1 ]: x! h' G. ]0 A5 g$ A7 F
enlargement of the penis, with a stretched length of
' U1 d; `# d, g) J- L* D8 cm and a width of 2 cm. The glans penis was very well7 [0 v8 ?0 [, t7 ~+ ^: m! B8 h
developed. The pubic hair was Tanner II, mostly around+ S5 a0 ^  A: x6 z8 k2 ]8 ?
540
; P* C9 r, }: o0 ]! u  gat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
; b0 z6 @5 p5 K; t4 O; Ithe base of the phallus and was dark and curled. The
* k0 C7 _6 U  }+ o4 ~testicular volume was prepubertal at 2 mL each.
, F) m( w, n( [8 cThe skin was moist and smooth and somewhat: N) F5 \3 H* a0 @4 Q5 ^, j7 ?
oily. No axillary hair was noted. There were no
6 L6 I6 c  ?. M7 Cabnormal skin pigmentations or café-au-lait spots.8 P' P  m4 s1 A: M+ I. @" ^: d
Neurologic evaluation showed deep tendon reflex 2++ ]. I/ u% Z- g  |5 h
bilateral and symmetrical. There was no suggestion6 X2 B& r8 Q4 E0 R% a; H% f1 v
of papilledema.% v! H# D5 D1 @4 t  |6 [. w
Laboratory Evaluation
# d: s( k) ^7 n7 `. a) `9 q6 `1 u8 _The bone age was consistent with 28 months by( n. W7 h" @1 K' l; \" A
using the standard of Greulich and Pyle at a chrono-
) X1 R# t1 R0 |! E' V" {* N- j) hlogic age of 16 months (advanced).5 Chromosomal" A* @* }$ V' K% Q
karyotype was 46XY. The thyroid function test
( N+ a( h( {2 s% Ushowed a free T4 of 1.69 ng/dL, and thyroid stimu-
0 X- X/ k6 H: @6 |- \. x) x, F7 v% zlating hormone level was 1.3 µIU/mL (both normal).
; {* K( y( j% x0 o1 @" k0 wThe concentrations of serum electrolytes, blood
3 N- b! N5 ~$ M# I  lurea nitrogen, creatinine, and calcium all were
0 O' w6 _2 F* e# `5 s' c# ]within normal range for his age. The concentration
" l& C- O# y/ @& T5 ?; D; Vof serum 17-hydroxyprogesterone was 16 ng/dL
* C0 k, J6 w( M- A(normal, 3 to 90 ng/dL), androstenedione was 20
( V5 D; ]7 l9 @5 G8 \ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
, D' o4 E0 k" x4 q+ O9 {6 hterone was 38 ng/dL (normal, 50 to 760 ng/dL),9 m0 e2 q5 x1 E$ b4 a, |% `
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
6 z' t7 }& N: R# Q1 I! u; }  i: b49ng/dL), 11-desoxycortisol (specific compound S)
4 N% i% [% D( d0 N+ fwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-6 F/ P& g  ]& f/ n" H! O0 y' K
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total' W% Z3 K- h# t. X: C* f
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
/ N' G! i5 Y5 k2 u& C+ S0 jand β-human chorionic gonadotropin was less than/ @: ?& S$ k8 Y6 j
5 mIU/mL (normal <5 mIU/mL). Serum follicular
: o* M7 g5 |* T8 Wstimulating hormone and leuteinizing hormone
# l' y6 X9 v% J6 c2 B+ l* N7 S3 mconcentrations were less than 0.05 mIU/mL
; K2 A, L: j9 V8 Z) O0 _! f' s8 D(prepubertal).% v0 m0 b& n) Z& ^  u$ a7 s
The parents were notified about the laboratory  F$ p4 ^; s) V( C
results and were informed that all of the tests were$ C- @1 D' i. z% n
normal except the testosterone level was high. The: _4 \4 N" d# ?4 |+ _$ ~8 Q, V; X
follow-up visit was arranged within a few weeks to
4 S9 S# ^# X7 I3 B8 k6 k& Wobtain testicular and abdominal sonograms; how-
5 u8 z1 B  _7 [) ~/ }, m7 Mever, the family did not return for 4 months.
% W3 `. q. f' Q: p& LPhysical examination at this time revealed that the* y$ {- @% V3 }9 K/ [
child had grown 2.5 cm in 4 months and had gained% \  [! A8 F  Q
2 kg of weight. Physical examination remained( Z" x% b4 `% A: K* s) k
unchanged. Surprisingly, the pubic hair almost com-
* [! h" H+ f& |( R* hpletely disappeared except for a few vellous hairs at
/ J6 x$ M1 t% r: e% Z; |the base of the phallus. Testicular volume was still 2
8 G/ ~2 B* U! f5 t9 ], EmL, and the size of the penis remained unchanged.2 ?8 n2 O4 ]+ X4 h* r% z: N) e
The mother also said that the boy was no longer hav-5 d5 D% s! E3 n- e) |1 L5 i8 b+ t
ing frequent erections.
$ f7 z) E. S; S+ m3 c2 gBoth parents were again questioned about use of
* x% V) e' H4 O  \: ^6 H" eany ointment/creams that they may have applied to+ N# P  J5 s. a( D" H, |) W6 d" Q+ S8 O, a
the child’s skin. This time the father admitted the
0 i1 A! t- Q1 GTopical Testosterone Exposure / Bhowmick et al 541
' _; ^# i6 x4 h7 Z8 Y& ]use of testosterone gel twice daily that he was apply-
. |" q) D! T* B' Sing over his own shoulders, chest, and back area for, ^# n7 ?) a+ j! Q5 R) q: K! b
a year. The father also revealed he was embarrassed
, C: y( c* y# k2 C5 \+ qto disclose that he was using a testosterone gel pre-6 [" ?: g7 w: q, r6 K
scribed by his family physician for decreased libido- \" }5 d0 _0 v# B- V5 |/ l
secondary to depression.# G* W$ V: J$ k; H: f  K
The child slept in the same bed with parents.
6 o% `" h5 ^0 N4 U, g# W2 {The father would hug the baby and hold him on his- K( K- g2 ], u7 G* r5 d4 g9 `* o4 K
chest for a considerable period of time, causing sig-
6 z+ V8 B9 C; m+ E6 x, g! \nificant bare skin contact between baby and father.$ |7 K& j, l" }  K, f
The father also admitted that after the phone call,0 X0 c: Y" Z4 V: B+ q
when he learned the testosterone level in the baby
( [! |5 h, {$ s6 ^was high, he then read the product information
2 I& ^' g, p' H! T+ Wpacket and concluded that it was most likely the rea-1 @7 I' d9 n, j# b5 _2 S6 \3 e4 C
son for the child’s virilization. At that time, they  H; m! o& k5 s5 ~! }+ j( T
decided to put the baby in a separate bed, and the
9 U! ^5 k) J1 z+ b: d8 B: Cfather was not hugging him with bare skin and had0 D7 \' d3 e' e+ Q; e
been using protective clothing. A repeat testosterone' c- _  R& s0 P* i5 D
test was ordered, but the family did not go to the5 d3 [* E' |! @4 B  _1 Y$ B2 y* w
laboratory to obtain the test.
" e, B& [/ Q& A, B( F' uDiscussion
0 h- R! i. R3 b) M* E3 OPrecocious puberty in boys is defined as secondary
2 G- m) d& a8 m0 n. ~& x0 h; ysexual development before 9 years of age.1,4
* L+ q" M* X* m" a7 j, A5 sPrecocious puberty is termed as central (true) when' @3 W8 s/ h- M4 K8 e! ^) w
it is caused by the premature activation of hypo-9 Q; Y$ Q- ]) U0 v7 o+ E
thalamic pituitary gonadal axis. CPP is more com-
, v( _) W3 [" \( e6 }7 nmon in girls than in boys.1,3 Most boys with CPP" {( ]: M' W, G. M6 I9 K# l( Y
may have a central nervous system lesion that is
, @; B/ r+ D/ b1 Aresponsible for the early activation of the hypothal-
' W7 m" [5 W$ @% w! p1 Z+ S5 [0 lamic pituitary gonadal axis.1-3 Thus, greater empha-' D8 J4 d6 e! @! E) r6 Z5 q8 u
sis has been given to neuroradiologic imaging in
! _% Q; e1 O3 f3 k/ S- G1 Rboys with precocious puberty. In addition to viril-: S* ~5 l6 y0 T7 _% j8 U& C2 ^: b
ization, the clinical hallmark of CPP is the symmet-
4 s! m( t" N# Jrical testicular growth secondary to stimulation by
# H& ?8 Q. k9 j& @& @8 }gonadotropins.1,37 K4 m) }2 j2 [5 y8 s# M# `) N
Gonadotropin-independent peripheral preco-$ c; W: O' d5 W  g& P* h
cious puberty in boys also results from inappropriate" D+ U/ ~% I8 ?$ O! P; j: b
androgenic stimulation from either endogenous or
+ A# Q" K6 I" k, B$ ~exogenous sources, nonpituitary gonadotropin stim-1 p* d  X. a# c4 O4 p6 r# ~
ulation, and rare activating mutations.3 Virilizing
! V3 ?# p4 S4 v+ i8 z; s. Scongenital adrenal hyperplasia producing excessive. f0 T6 w; w: e; b/ j2 W9 v8 Q8 o0 }
adrenal androgens is a common cause of precocious' u8 D% {5 m9 E6 v/ g+ l
puberty in boys.3,41 G) C3 ?* U" y8 E4 j
The most common form of congenital adrenal8 R: o( c: n2 f$ r
hyperplasia is the 21-hydroxylase enzyme deficiency.% d( b, o  Y' h( _& H) K
The 11-β hydroxylase deficiency may also result in5 v9 [. e& z5 r- v8 V! a
excessive adrenal androgen production, and rarely,
& a& Y6 S* f  b$ p$ `! tan adrenal tumor may also cause adrenal androgen
; W+ ^) w. `7 \& fexcess.1,3
: ]# b& q) P# Oat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from8 }/ r/ Z* b% I' E( i
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007; S) c) Q4 g9 |' u1 P( h7 E9 {6 L) R( E5 k
A unique entity of male-limited gonadotropin-% z, [, H# t" m1 h4 T
independent precocious puberty, which is also known! S* b& \8 j; B. }5 p
as testotoxicosis, may cause precocious puberty at a2 H# z/ y% l5 ^1 n( Q! L3 g
very young age. The physical findings in these boys
* N4 l; V. t& z2 x( H6 v7 awith this disorder are full pubertal development,
2 `. q! S' n3 b8 I/ \1 Y# Xincluding bilateral testicular growth, similar to boys; z1 o/ K# G9 l9 p, I
with CPP. The gonadotropin levels in this disorder
8 ?/ s2 j5 J6 B$ E! R8 k! nare suppressed to prepubertal levels and do not show
2 R% B/ j) @$ |, K7 n& Dpubertal response of gonadotropin after gonadotropin-
4 m8 e$ P$ N' s$ Vreleasing hormone stimulation. This is a sex-linked
# D/ c. u% T# V8 n3 a: h8 ?+ i" l3 uautosomal dominant disorder that affects only
* L9 O/ [, \  `) |5 wmales; therefore, other male members of the family! i( ]& r- p7 e! F5 ^. E; p$ \$ ]
may have similar precocious puberty.30 Y; ]; _7 t# Q5 x- F
In our patient, physical examination was incon-7 P3 x1 Z1 \; Q
sistent with true precocious puberty since his testi-
, n5 p$ ~) W. B4 J3 d; H6 N( z: ~) |8 ^cles were prepubertal in size. However, testotoxicosis, Y6 T! V- E4 p8 U. q; U+ `
was in the differential diagnosis because his father* N; [/ c' d- k: t
started puberty somewhat early, and occasionally,
$ W9 |+ A9 ~# x0 G9 b' @testicular enlargement is not that evident in the
4 Z* X: V1 Y: ~1 Lbeginning of this process.1 In the absence of a neg-
4 Z8 D0 f2 R/ c8 D# J2 Aative initial history of androgen exposure, our3 k4 k5 B9 v) |9 g
biggest concern was virilizing adrenal hyperplasia,4 C3 m8 b7 Z6 [. y
either 21-hydroxylase deficiency or 11-β hydroxylase
+ V% [2 K8 J* Y4 V0 ?/ ^$ J3 Sdeficiency. Those diagnoses were excluded by find-6 m6 }+ g: n0 v" e+ G. F1 Z# J
ing the normal level of adrenal steroids.4 \2 m9 B- K( H0 _9 c3 g: _' y
The diagnosis of exogenous androgens was strongly
6 w; P( c  s5 r/ c3 Zsuspected in a follow-up visit after 4 months because
( f9 p( s1 y" ]) y( f" |8 z8 cthe physical examination revealed the complete disap-/ b7 g* H' q1 O# ~7 R# c4 u! ^
pearance of pubic hair, normal growth velocity, and+ F, [4 g3 q% m& E! K) Z4 C8 I
decreased erections. The father admitted using a testos-
9 z) }* ^- w- F" Z7 Z2 r( c4 Jterone gel, which he concealed at first visit. He was* e9 B* Y1 v" d/ c5 p; _
using it rather frequently, twice a day. The Physicians’
1 q4 u& D1 |  v% PDesk Reference, or package insert of this product, gel or7 y2 \% Y; g; c9 B
cream, cautions about dermal testosterone transfer to& K* ?' h7 x8 [- e, [8 t# |
unprotected females through direct skin exposure.+ ~) Z! i! P7 H3 i4 t8 A0 w
Serum testosterone level was found to be 2 times the, x5 S. G9 u1 G
baseline value in those females who were exposed to3 Q4 W. D9 F" F+ E1 V
even 15 minutes of direct skin contact with their male
, U. W; R$ h: E. W$ g( }! e1 `partners.6 However, when a shirt covered the applica-
. N% x- y) A7 E* qtion site, this testosterone transfer was prevented.  r: G& N2 i1 B  h, x0 _- K* s
Our patient’s testosterone level was 60 ng/mL,! o- ^/ K( w$ ]% ]. [
which was clearly high. Some studies suggest that, N; y1 X  z( T, H2 D3 H# {' m, c8 j
dermal conversion of testosterone to dihydrotestos-
+ T8 o4 D' `+ i; y. _terone, which is a more potent metabolite, is more9 \5 Z2 M; z1 S2 m# k
active in young children exposed to testosterone
7 }2 N  v+ R7 k1 texogenously7; however, we did not measure a dihy-
6 O2 }% t! C) R& {# C- odrotestosterone level in our patient. In addition to
: k8 w5 y0 m( ]# \; @9 T9 }" [virilization, exposure to exogenous testosterone in. q1 [' p5 `# v" x
children results in an increase in growth velocity and
4 [# J, k. A. p% G. J9 f+ A; ^advanced bone age, as seen in our patient.
: s; q+ Z- ?7 T9 LThe long-term effect of androgen exposure during
! e- B8 e- x: Q8 o5 bearly childhood on pubertal development and final9 D/ i1 a; [& ~8 K% I) g4 G5 [
adult height are not fully known and always remain
; ?& G& n( N3 y4 j  U, y# P6 Fa concern. Children treated with short-term testos-7 `" X- `" Q/ v# N5 U+ N9 f7 C7 t
terone injection or topical androgen may exhibit some
0 |6 B' Z. \& ]acceleration of the skeletal maturation; however, after
% d  @( J3 o4 T. N( A: ^& T: ycessation of treatment, the rate of bone maturation, G% ^  z. Z9 i3 H3 Q
decelerates and gradually returns to normal.8,9
5 H2 A4 e& l. ]# c3 J4 {There are conflicting reports and controversy$ [, A# L' k( F: \
over the effect of early androgen exposure on adult
+ ?% J( Y) N3 J& ^2 cpenile length.10,11 Some reports suggest subnormal
8 @$ c  K- O: J# eadult penile length, apparently because of downreg-
% P- j1 _8 I9 ~+ t+ K" S# xulation of androgen receptor number.10,12 However,1 E+ L1 F9 L. }0 r
Sutherland et al13 did not find a correlation between+ T* A& ^6 a$ P8 N
childhood testosterone exposure and reduced adult
9 P; n' `, r0 ]& x" A8 spenile length in clinical studies.+ L, G) L  k3 E/ ]1 M
Nonetheless, we do not believe our patient is
/ j$ @( e& S( ]. X6 b/ y, s2 cgoing to experience any of the untoward effects from
3 }% T( D2 w/ _, P" v; Rtestosterone exposure as mentioned earlier because& C. l$ I: o% _/ A+ s0 {
the exposure was not for a prolonged period of time.7 y; }# V4 ]! K' k3 X8 m
Although the bone age was advanced at the time of4 \* J5 }5 w; D) s; w) e# |! n: F9 G
diagnosis, the child had a normal growth velocity at
( [4 z) O- w: `5 u7 [the follow-up visit. It is hoped that his final adult' Y2 E! ?/ ?: Q& Z2 R
height will not be affected.
0 Z9 O. t( n0 Q) d# V0 v0 vAlthough rarely reported, the widespread avail-# J% [4 V3 e- `; x( f1 _" L
ability of androgen products in our society may+ T5 Z8 Q6 `1 h! I4 B& c
indeed cause more virilization in male or female) k. v; V) j6 t) ^( x
children than one would realize. Exposure to andro-. n+ O: l! X9 ~' U1 N' u8 |  v8 i
gen products must be considered and specific ques-9 E/ [' X, X! x
tioning about the use of a testosterone product or
% Z5 B9 G. M& Z) ~" X0 egel should be asked of the family members during
1 E: ?  G: s* ?- R! xthe evaluation of any children who present with vir-5 V, S0 {$ z6 F+ m
ilization or peripheral precocious puberty. The diag-% M" w  |$ ^0 J/ R* V
nosis can be established by just a few tests and by( V! b: X1 e) Q( h: U2 j2 {
appropriate history. The inability to obtain such a- m( c+ S$ x9 H( I1 `0 `9 a  t) h" M
history, or failure to ask the specific questions, may
2 ?  r, E& ?/ z5 d- p$ t8 Eresult in extensive, unnecessary, and expensive3 p! Q9 P1 w* p" A+ D
investigation. The primary care physician should be
8 \  A# d8 C% vaware of this fact, because most of these children
; w& H4 |& ~3 Xmay initially present in their practice. The Physicians’
. I* b: G# L) u. \1 v/ IDesk Reference and package insert should also put a
( {0 Y) r, D/ `8 i- k# u$ swarning about the virilizing effect on a male or/ ~1 v2 A( q+ x7 r- @1 h
female child who might come in contact with some-
5 e1 J1 s' R7 B! L9 v  Rone using any of these products.
: V  {+ I7 ]" r4 ~References8 ]7 j1 B! w  Q' W, o8 d; l" d
1. Styne DM. The testes: disorder of sexual differentiation) P/ V3 Y8 M$ w5 y) p1 }# ?2 ]
and puberty in the male. In: Sperling MA, ed. Pediatric
% g, ?$ x6 z# H  z; v2 cEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
8 z1 h  n% s; w$ h4 s4 ~2002: 565-628.6 a& L& m2 }8 q' J3 Z4 |: N
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
3 c& t: J$ M6 x- m: A0 e; G. t$ xpuberty in children with tumours of the suprasellar pineal
發表於 2025-1-7 21:59:43 | 顯示全部樓層
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
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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
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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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