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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% t( z; P1 E! S# p# F& E
Boy Induced by Indirect Topical
6 M4 y' c- L/ G" C0 u/ u% ZExposure to Testosterone
$ ]; _7 T' z5 t# q2 E4 TSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
# v6 a' J+ i6 l2 z$ Rand Kenneth R. Rettig, MD1  N# A- q; B8 C1 R# a: P3 @; I
Clinical Pediatrics  r1 x- g8 V: L5 F9 E! M6 m* q
Volume 46 Number 62 \+ ?. L2 M+ v# I" H$ u& P
July 2007 540-5430 U+ z9 t: q0 d; E1 v5 |
© 2007 Sage Publications
% i2 t5 O5 H4 y- L0 l9 f10.1177/0009922806296651
, p& c4 v- `" Y1 v% dhttp://clp.sagepub.com. @$ F! W6 d+ z. Q
hosted at
0 {: |3 x+ |0 P; @  Chttp://online.sagepub.com9 z* }7 _1 O* O4 O) P! }
Precocious puberty in boys, central or peripheral,
# i5 Y4 I2 N! nis a significant concern for physicians. Central- H/ b7 _/ m, b; `# |/ E* g
precocious puberty (CPP), which is mediated
$ W& o) G0 v9 C  Z  w4 T* }through the hypothalamic pituitary gonadal axis, has
4 Q( {' I  ~) a- |a higher incidence of organic central nervous system  `& Y# N# }% D8 E2 Z# L. O' T
lesions in boys.1,2 Virilization in boys, as manifested
( k  y2 H6 M0 Q! t: ~/ D4 @0 H) H, Aby enlargement of the penis, development of pubic- F+ ]; r% l7 P- R6 j1 S
hair, and facial acne without enlargement of testi-) d" ]+ a* y$ }6 ^+ \  m; C
cles, suggests peripheral or pseudopuberty.1-3 We
& j4 j0 T/ v" lreport a 16-month-old boy who presented with the) _, r9 D8 i! {2 |( m% t
enlargement of the phallus and pubic hair develop-
! n4 K& b5 Z) u4 D$ ament without testicular enlargement, which was due
1 p# l, k* ~$ ?* Y1 jto the unintentional exposure to androgen gel used by& [& o* F! i! G: b3 `
the father. The family initially concealed this infor-
& g' y3 K- d2 W- w$ ~1 Vmation, resulting in an extensive work-up for this* ]' v; s# C# S; P
child. Given the widespread and easy availability of
+ Y7 V$ l9 V0 T) d( wtestosterone gel and cream, we believe this is proba-; b( t( V8 `. d, ~6 Z$ v; G! v
bly more common than the rare case report in the
* X8 w- r! @& N9 `2 M  f$ Y/ ]. V! W; qliterature.4: v4 ^6 @0 y: D; p9 G
Patient Report
8 j" f- N# B: PA 16-month-old white child was referred to the
6 T4 p% _7 \  \endocrine clinic by his pediatrician with the concern. y+ K( K7 \; P" z, y+ I& z% D3 Q
of early sexual development. His mother noticed
- T0 w- B5 T- z# S7 v6 hlight colored pubic hair development when he was3 x8 b! V) }% u( A) E6 n$ F- u( y
From the 1Division of Pediatric Endocrinology, 2University of6 J8 x5 o& h7 c: n) S
South Alabama Medical Center, Mobile, Alabama.3 d: r. g1 x/ w0 c2 ^9 ?% Z
Address correspondence to: Samar K. Bhowmick, MD, FACE,
7 M  P2 W/ {" uProfessor of Pediatrics, University of South Alabama, College of/ S, T* `# X. p& P1 i& [
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;  n. B5 ]8 S. |' r0 V) A, Z
e-mail: [email protected].0 W6 V( ]* @+ |5 B
about 6 to 7 months old, which progressively became
# W- Q3 ?6 w, X* C: q7 w' ddarker. She was also concerned about the enlarge-3 ]! N1 w& n* q* H/ E% N+ N3 P, t
ment of his penis and frequent erections. The child4 T2 ~% W! q* x. f
was the product of a full-term normal delivery, with5 Z) w) ^3 Y6 n4 Y7 W
a birth weight of 7 lb 14 oz, and birth length of
+ A1 E& t( \$ p4 O$ O* t20 inches. He was breast-fed throughout the first year3 Z/ Q+ X/ u5 b. |
of life and was still receiving breast milk along with* t. |* X9 {, c& \2 p! x8 `
solid food. He had no hospitalizations or surgery,
; a* W2 C# [2 h$ L( ]$ c9 C5 Aand his psychosocial and psychomotor development3 A. D- k+ J" }& b  ~  z
was age appropriate.$ Y- B# s, R5 J" e6 w" k
The family history was remarkable for the father,
$ ]' L( z' m$ T: |who was diagnosed with hypothyroidism at age 16,
; x) `* R- l. P0 V+ ]# Ewhich was treated with thyroxine. The father’s
4 I9 ]- ?5 s; B; y' l: f4 wheight was 6 feet, and he went through a somewhat9 P5 `) h" z$ n/ v( ?  M1 ?
early puberty and had stopped growing by age 14.
( b! `- _. K: I5 P/ s: EThe father denied taking any other medication. The
& G' P+ H1 i6 m; p) [* ]7 ?child’s mother was in good health. Her menarche8 _" l7 R( }1 F0 s3 Y5 o
was at 11 years of age, and her height was at 5 feet0 M4 c% f* _# U' V+ D3 |) T
5 inches. There was no other family history of pre-1 _6 w& [2 N7 k( ?6 H$ I! n
cocious sexual development in the first-degree rela-+ E8 s: H8 l2 L6 d- p/ M9 u$ g
tives. There were no siblings." x* k, u7 c9 ?; ?1 |7 ^* G; C
Physical Examination5 P& l. T0 V9 z' _
The physical examination revealed a very active,
5 B2 N+ U8 F8 [( k& `playful, and healthy boy. The vital signs documented& o# g  G4 _' {+ i7 L8 }
a blood pressure of 85/50 mm Hg, his length was
* {, c: B/ b  v4 i90 cm (>97th percentile), and his weight was 14.4 kg! _) i. \& W, V
(also >97th percentile). The observed yearly growth- d; n6 m- u& M( U$ R' J
velocity was 30 cm (12 inches). The examination of
2 `+ W0 Q/ f  @. V# |8 Nthe neck revealed no thyroid enlargement.1 J/ z  Q8 h+ v- P% m; a
The genitourinary examination was remarkable for9 [1 \: r) v  Q# J3 z% r
enlargement of the penis, with a stretched length of# u5 N) U, d3 C/ I2 n& p
8 cm and a width of 2 cm. The glans penis was very well
4 H+ r' O& r# x2 Ideveloped. The pubic hair was Tanner II, mostly around
- o9 n. T: s+ J6 [0 x5 y. R540$ S9 ~& z$ I1 O: T: p
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
. z) H/ j$ u# B, d) L) Tthe base of the phallus and was dark and curled. The5 j3 d- `* P9 U" D! }
testicular volume was prepubertal at 2 mL each.
9 A! \$ v3 p/ x9 _; nThe skin was moist and smooth and somewhat  h* v1 `3 w, M4 q6 {. N3 N
oily. No axillary hair was noted. There were no
( v7 y$ I; k( E' x2 habnormal skin pigmentations or café-au-lait spots.' G, u9 V! ~8 e# m: r4 H7 }+ A
Neurologic evaluation showed deep tendon reflex 2++ \  K! [, H( s8 T& ^+ b1 s
bilateral and symmetrical. There was no suggestion6 F) D4 {, U& R/ c. m. V
of papilledema.& |/ n1 b( f* ]" H% d" z% q. f" x
Laboratory Evaluation4 V) \( ^0 X! @: o' l
The bone age was consistent with 28 months by
1 z2 N) F7 ^# Jusing the standard of Greulich and Pyle at a chrono-
" F: b  U  c' V) ]( {6 q1 hlogic age of 16 months (advanced).5 Chromosomal
$ g; h( o% @- p* i! Z: P" _0 V4 ckaryotype was 46XY. The thyroid function test# u" v4 \$ a7 k2 M! f& s; K
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
! y$ r' v6 Y0 z  o# rlating hormone level was 1.3 µIU/mL (both normal)., K# a& s- Z3 u! e$ A+ I5 u
The concentrations of serum electrolytes, blood% a, V) N* v* ]
urea nitrogen, creatinine, and calcium all were
  U$ v' C  y# @4 F9 G9 k; ?within normal range for his age. The concentration
: I& Z" s' y$ C% r$ ~8 iof serum 17-hydroxyprogesterone was 16 ng/dL. X* A7 ]. H/ `2 `; G8 n5 P
(normal, 3 to 90 ng/dL), androstenedione was 20  B' h4 I! y+ f, w4 ]# x
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-) E  k- A# L* b% F3 x1 h: O& {# p
terone was 38 ng/dL (normal, 50 to 760 ng/dL),8 }$ \- B  H4 R) m. }4 e; S
desoxycorticosterone was 4.3 ng/dL (normal, 7 to- e1 T7 t( k! `6 w
49ng/dL), 11-desoxycortisol (specific compound S)
* T: ?$ B/ @6 U: i. F+ |' {was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-; f: Z4 ^% ~$ S) Z) o* Y7 m
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
# U# m$ e! v& K& D( _testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
" F) ^. A! _* ~8 G; \and β-human chorionic gonadotropin was less than- [5 q6 Z' M. K1 P3 J
5 mIU/mL (normal <5 mIU/mL). Serum follicular5 `+ @0 h4 L0 s5 k+ f/ A2 H$ m
stimulating hormone and leuteinizing hormone
: |6 u" m: m5 c6 {: Y7 ?concentrations were less than 0.05 mIU/mL/ d6 I" g& ]* F1 s
(prepubertal).' M; s" `: u$ w& A
The parents were notified about the laboratory* a3 e: x- B$ b7 @' f4 r/ K
results and were informed that all of the tests were
& E7 h# d0 B& R0 m9 Cnormal except the testosterone level was high. The1 J+ t: ]9 X  G: ^5 t
follow-up visit was arranged within a few weeks to3 Z5 w2 r5 E# H8 j; E& i
obtain testicular and abdominal sonograms; how-
$ y1 T+ [0 k; f* Z! x3 I! Fever, the family did not return for 4 months.6 N2 m% r: K& x3 O. C  ^
Physical examination at this time revealed that the0 q. |7 P4 M$ `# J
child had grown 2.5 cm in 4 months and had gained
3 F/ c# b1 y3 K, K2 kg of weight. Physical examination remained
2 f( ?3 S7 h) ]* `; M+ j$ I7 Zunchanged. Surprisingly, the pubic hair almost com-
1 N; `, `. {9 `# ]pletely disappeared except for a few vellous hairs at
: l' L" p3 c; F4 y1 d, `: a* _9 hthe base of the phallus. Testicular volume was still 2$ S5 B3 r$ k. X" W1 r, S
mL, and the size of the penis remained unchanged.) _- ^* v2 d1 c) E4 m
The mother also said that the boy was no longer hav-
0 \3 n' g1 C* w0 jing frequent erections.1 u9 h: R7 Z  E( |2 b3 J) F
Both parents were again questioned about use of
+ y' J) I0 P' w) J2 t& |7 |any ointment/creams that they may have applied to
* t  X# y7 R4 l: d+ x1 S0 y+ Z5 `$ c$ Kthe child’s skin. This time the father admitted the4 [7 r, h4 z4 {4 B
Topical Testosterone Exposure / Bhowmick et al 541
4 d0 b/ j0 ]. ~' H; G! nuse of testosterone gel twice daily that he was apply-. Z% Y- ~5 O1 D' `$ _+ Z
ing over his own shoulders, chest, and back area for/ G9 D0 T+ j5 W
a year. The father also revealed he was embarrassed
4 h+ v7 I% Z: P5 D& [to disclose that he was using a testosterone gel pre-( b' G3 k6 A( w0 O" z5 I# L
scribed by his family physician for decreased libido
7 l" M% x# W3 M0 `secondary to depression.
# x. {, y! Y/ P; q( p4 qThe child slept in the same bed with parents.+ X* q0 v& \4 p. Z( Y4 p
The father would hug the baby and hold him on his
" I( n. l& K8 r" e1 O. Kchest for a considerable period of time, causing sig-& j; ?. X1 p% L- ]" }
nificant bare skin contact between baby and father.
8 G5 g( y. Z/ D* X; ]The father also admitted that after the phone call,3 M0 }7 m( E3 j' Z
when he learned the testosterone level in the baby
& j( `- E) q( G7 \: B) r9 ^was high, he then read the product information4 p/ o" [8 K7 {
packet and concluded that it was most likely the rea-
) g' ^+ l& t1 N+ G4 m  ~son for the child’s virilization. At that time, they3 G5 u+ A$ {. A7 K- S2 [2 d( \4 l
decided to put the baby in a separate bed, and the8 y& x1 w1 x; R6 @5 P3 Z- V
father was not hugging him with bare skin and had* m2 ^) ]) Z0 A( o0 c; E
been using protective clothing. A repeat testosterone
: p' c" ?6 c( d1 E9 ctest was ordered, but the family did not go to the
' e! r0 ]' v6 ?- w( i, Xlaboratory to obtain the test.
6 A* R4 [0 m; yDiscussion
4 p6 ?" G) y% f# wPrecocious puberty in boys is defined as secondary" x' v5 T3 Y/ [5 Q$ M
sexual development before 9 years of age.1,4
! t5 `! s+ C% o6 RPrecocious puberty is termed as central (true) when
& o' `. X- b2 }it is caused by the premature activation of hypo-
6 O. {2 y5 t& L% f0 Bthalamic pituitary gonadal axis. CPP is more com-. b& J3 ~, h. G7 [
mon in girls than in boys.1,3 Most boys with CPP
; g' T+ g7 B% w) C4 xmay have a central nervous system lesion that is
' r1 s1 ]. V: t/ r: l2 vresponsible for the early activation of the hypothal-
/ Y9 e5 f; C2 T$ x' Q( \amic pituitary gonadal axis.1-3 Thus, greater empha-% s+ w& k6 L- i9 F- }
sis has been given to neuroradiologic imaging in: C6 |. ?& m+ a- F9 H" a% E5 H
boys with precocious puberty. In addition to viril-: x( @' ~& C. P2 L0 |1 O, n
ization, the clinical hallmark of CPP is the symmet-
1 E( [8 Z6 h4 V3 |. P5 q9 xrical testicular growth secondary to stimulation by) ~+ w% j' b; v, O/ m2 H8 w* M* V
gonadotropins.1,3* e' v2 m, a; W6 W! `
Gonadotropin-independent peripheral preco-8 ]5 h. y- _* r3 g* ^
cious puberty in boys also results from inappropriate
; o6 }0 t' W* r# V: W- {. w) d5 }! Aandrogenic stimulation from either endogenous or
' W9 ~. O1 X' Kexogenous sources, nonpituitary gonadotropin stim-
2 N9 }# x, a! i* T2 kulation, and rare activating mutations.3 Virilizing
9 N3 Q# k8 ^' E3 k  t/ @5 R  I0 qcongenital adrenal hyperplasia producing excessive
2 G8 u$ U$ q2 Iadrenal androgens is a common cause of precocious: P  m% i6 N6 U7 e% C: ]
puberty in boys.3,4
9 I5 v7 Q. E. U' iThe most common form of congenital adrenal
2 E( c' B* p, w5 i" whyperplasia is the 21-hydroxylase enzyme deficiency.
: G6 N. e$ _) l9 F% mThe 11-β hydroxylase deficiency may also result in
6 k. O+ \1 n; p1 X5 @excessive adrenal androgen production, and rarely,
5 k# J: t* u, zan adrenal tumor may also cause adrenal androgen" I# |  c8 d. h5 p: a4 J+ _
excess.1,3) @: F. O7 {9 @8 F
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from4 ~) X0 ~/ E, O( S  I
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
9 ^1 L) M3 ~7 W; eA unique entity of male-limited gonadotropin-
! t" w; D6 \, Q' k9 f+ |1 ~' ?independent precocious puberty, which is also known, V! u: P1 X& t4 o
as testotoxicosis, may cause precocious puberty at a
* U. A' ~9 {0 g: Hvery young age. The physical findings in these boys! J# ?' x. t2 M
with this disorder are full pubertal development,# J  e( l3 B/ i% T( q$ S
including bilateral testicular growth, similar to boys, E0 P# _& s. q
with CPP. The gonadotropin levels in this disorder0 a( S( g$ q" {
are suppressed to prepubertal levels and do not show6 k% f* \# p" i# g
pubertal response of gonadotropin after gonadotropin-3 l+ V% s# q  a8 y
releasing hormone stimulation. This is a sex-linked
5 D# D: _5 D% |% F- oautosomal dominant disorder that affects only  y) _# P$ q/ p5 d1 K9 D
males; therefore, other male members of the family" d- C, M+ J3 j4 L. g
may have similar precocious puberty.3- c$ B4 ]# _: G1 C
In our patient, physical examination was incon-( i: ]* F2 j! L. A2 r0 J  i/ U* u  [
sistent with true precocious puberty since his testi-
3 d3 V( l6 n# s) Jcles were prepubertal in size. However, testotoxicosis5 |1 t* G3 Q" g8 C1 N' j
was in the differential diagnosis because his father
2 S& x9 H' r/ V, g. U& U, hstarted puberty somewhat early, and occasionally,
% m: S6 v, L4 Rtesticular enlargement is not that evident in the
% {, ~* J$ |7 h4 I. xbeginning of this process.1 In the absence of a neg-9 k) I) M! I! \4 I+ m! s' h
ative initial history of androgen exposure, our6 Q4 s/ k$ T" a% M$ V1 I& V. c$ ]7 O
biggest concern was virilizing adrenal hyperplasia,- D! V7 y$ G* z' d% L
either 21-hydroxylase deficiency or 11-β hydroxylase" T, q  {( s8 ]; Y5 i
deficiency. Those diagnoses were excluded by find-
! F0 [- Z7 O9 }( S" bing the normal level of adrenal steroids./ g: q- b) s3 ?0 b5 [6 S
The diagnosis of exogenous androgens was strongly
2 h% |2 O2 T+ m* T6 D9 p  w8 Msuspected in a follow-up visit after 4 months because  \, t, _7 H1 |+ a: d: }2 b' r
the physical examination revealed the complete disap-/ [; I# I; m( c
pearance of pubic hair, normal growth velocity, and
8 R0 A( J1 @. q6 N2 o- B2 |& Kdecreased erections. The father admitted using a testos-7 n1 ~5 L# V. g* }
terone gel, which he concealed at first visit. He was& P8 t( Y: v7 V9 }' \& Y
using it rather frequently, twice a day. The Physicians’: O9 R, D; u4 L* D
Desk Reference, or package insert of this product, gel or
, O, y2 g5 ^& b! ycream, cautions about dermal testosterone transfer to% X& D) x, @* f3 D+ a% R
unprotected females through direct skin exposure.9 T, R  k4 U% p3 J' q" c
Serum testosterone level was found to be 2 times the* f$ V, d7 ^7 k3 W0 |% i: T
baseline value in those females who were exposed to
* m/ i( c' m- L3 d0 b8 ?% J2 V/ weven 15 minutes of direct skin contact with their male
9 o% d. c) z( `7 u% a7 cpartners.6 However, when a shirt covered the applica-
+ C# Z6 i, O& b0 ntion site, this testosterone transfer was prevented.8 y# ]0 [( J- ~* d( {1 A5 n, ^6 r
Our patient’s testosterone level was 60 ng/mL,
8 K7 {8 Y7 X- a) o! Lwhich was clearly high. Some studies suggest that
7 I* }$ F* [. z6 T* D  sdermal conversion of testosterone to dihydrotestos-
- Z3 y' s$ H, O- @: w8 Z* Wterone, which is a more potent metabolite, is more0 w2 a" X7 e/ {4 N+ S* k& ^0 ]3 L
active in young children exposed to testosterone
! q9 h6 w6 Q% A; v$ n) Fexogenously7; however, we did not measure a dihy-
  U& E4 P5 c3 rdrotestosterone level in our patient. In addition to2 ?+ @8 \, Z: _0 Y
virilization, exposure to exogenous testosterone in4 J% q6 L5 Z) R- B
children results in an increase in growth velocity and& Q$ ~5 m4 I2 @7 |# e, u  W% r
advanced bone age, as seen in our patient.9 W3 E2 d' k% ]# \7 n+ @
The long-term effect of androgen exposure during
2 L' M. J9 W5 @# j: F9 r* t: ^early childhood on pubertal development and final
  m, s+ D# Y" yadult height are not fully known and always remain3 X- L$ Y4 v1 {
a concern. Children treated with short-term testos-
( L% H3 v2 y) [5 y6 w7 o  tterone injection or topical androgen may exhibit some2 E9 p. J; j+ o; T9 i* w' E
acceleration of the skeletal maturation; however, after
; w/ t2 @2 k2 f! |  {% ?cessation of treatment, the rate of bone maturation* {* Q: M. ]/ D* n4 s8 v
decelerates and gradually returns to normal.8,9& g; q- ^) j# k
There are conflicting reports and controversy
9 m: p, l% Q4 d  u; v* k- eover the effect of early androgen exposure on adult
3 ]/ T/ L/ ]' w& g) V: m6 c% |* _8 \penile length.10,11 Some reports suggest subnormal
# ^" l0 d  i3 ]' xadult penile length, apparently because of downreg-+ ?+ U/ l& p$ S" G( z
ulation of androgen receptor number.10,12 However,
  ~, H4 w0 C2 P& M8 L- [Sutherland et al13 did not find a correlation between
& T' j7 s, u  l1 Nchildhood testosterone exposure and reduced adult4 z5 c' q0 a: I, i# \( f
penile length in clinical studies.
4 C" T, N! ~. D4 i3 ]5 S  v8 |4 a3 JNonetheless, we do not believe our patient is
! h% L2 s4 T* P3 y, V4 Dgoing to experience any of the untoward effects from+ ]6 s0 p0 q( c
testosterone exposure as mentioned earlier because5 {6 _# M, D" G7 D, P
the exposure was not for a prolonged period of time.6 V' N; e3 V5 d  u
Although the bone age was advanced at the time of
8 R& U) D9 z3 vdiagnosis, the child had a normal growth velocity at
/ r( r) r- K( V& G1 ]2 ythe follow-up visit. It is hoped that his final adult
* P7 M$ ?. i/ W" j! H; W. Jheight will not be affected.0 ]4 a  P; \5 k+ o. U
Although rarely reported, the widespread avail-) `) l1 X) q! b
ability of androgen products in our society may
0 J/ l' x! {: P1 C# Qindeed cause more virilization in male or female
6 o  j1 p& G4 `. p) ychildren than one would realize. Exposure to andro-1 W( i. \- z# B. g$ }9 g
gen products must be considered and specific ques-( E" j6 _2 w$ ?, \' \' f+ z' r
tioning about the use of a testosterone product or
+ t6 @) O8 r- E6 b( ~4 }) Wgel should be asked of the family members during% w. ?2 q  m2 }6 x7 F
the evaluation of any children who present with vir-. I) A# S! \* R3 X9 D
ilization or peripheral precocious puberty. The diag-# t4 y' H# L  U, P
nosis can be established by just a few tests and by
6 L' v" H, {( q: t( Uappropriate history. The inability to obtain such a. P1 @) K- T( h5 {7 [5 S4 t
history, or failure to ask the specific questions, may, s2 e2 ~5 [; h7 i' l" {0 ^
result in extensive, unnecessary, and expensive. \( Z3 d+ c- |
investigation. The primary care physician should be* l+ g: Y2 ?0 }: b, \! T" M( n) q
aware of this fact, because most of these children
+ k8 Z9 N( @. q2 {% Z/ G8 j1 nmay initially present in their practice. The Physicians’# |; G) |5 z) H- W
Desk Reference and package insert should also put a
+ W% K9 h9 h4 Uwarning about the virilizing effect on a male or4 |! S) z% z+ E" p- l# m; b, G6 E
female child who might come in contact with some-! O8 W1 P+ t3 j7 \" f8 Z
one using any of these products.
+ {4 S/ I& N; ~. Y# V  Q9 EReferences3 g* s, ~8 \2 @9 J6 `
1. Styne DM. The testes: disorder of sexual differentiation
3 {1 g, l4 ~2 }/ @and puberty in the male. In: Sperling MA, ed. Pediatric
+ t6 m& L; `( Y% NEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;+ e! p! ^. j1 E  ~1 s( b
2002: 565-628.
0 m2 O$ R' R! |' a( J% W2 O3 u2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
+ H" w5 u2 l$ `8 Jpuberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
5 e9 r* [! Q2 u1 R9 VBoy Induced by Indirect Topical* E- u; N- I2 O/ c' \3 i9 L
Exposure to Testosterone7 a/ V( F" {( `/ y/ _& o
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
+ M9 u1 {7 ~* P0 e. e6 t6 vand Kenneth R. Rettig, MD1
! `( m) ]' U" J/ u- x- k8 OClinical Pediatrics+ M1 I% m7 C+ y1 j. `! f. O* u
Volume 46 Number 6
, i/ T) y" Z  Y0 B7 P, }July 2007 540-543
" F/ ~. f3 j2 |& A© 2007 Sage Publications5 i7 R5 b! Y% f7 e+ [8 m
10.1177/0009922806296651% |: m9 [- G, u0 r# c" G
http://clp.sagepub.com
3 I  v( K* ?& w# \. mhosted at
0 W, m# f+ Z1 b- i8 ahttp://online.sagepub.com; D* w& W% q3 Y7 f% v  ]
Precocious puberty in boys, central or peripheral,
& S, g8 O' i; M+ i* S5 `# \is a significant concern for physicians. Central) I* P; z) W4 @% M7 T! u
precocious puberty (CPP), which is mediated
3 K' s$ W5 J( l  K& P' dthrough the hypothalamic pituitary gonadal axis, has
+ r' H: p# z4 e/ X3 `a higher incidence of organic central nervous system& X5 ?& `: ]! w- b' t- y
lesions in boys.1,2 Virilization in boys, as manifested
1 A% U- v: H- i2 e; G" fby enlargement of the penis, development of pubic" u& E. o' ^1 s( G! H- H# C
hair, and facial acne without enlargement of testi-
6 ~1 r3 K# x' k, T8 j( ^: u6 Hcles, suggests peripheral or pseudopuberty.1-3 We
1 b" C0 |6 Z) {- f4 K+ jreport a 16-month-old boy who presented with the
2 |* r6 i. v& }& I1 H' T3 Uenlargement of the phallus and pubic hair develop-6 j1 x, u# }9 G5 f! V7 V/ Y8 A" Y
ment without testicular enlargement, which was due
, @) T+ @6 D# A6 G) @  m9 p1 n' gto the unintentional exposure to androgen gel used by" R! m0 @; P# R2 R& t. A
the father. The family initially concealed this infor-' J) J! B5 L7 S5 L" p, v5 C
mation, resulting in an extensive work-up for this
) a6 `. ~8 Y7 ], c+ jchild. Given the widespread and easy availability of
- d2 _0 i& S, K3 W# D; Ctestosterone gel and cream, we believe this is proba-& x- T7 g8 v0 r# u' s6 O
bly more common than the rare case report in the
# R& E" [6 X' |9 i0 q. q' W. y0 Pliterature.4$ A+ Y7 I2 a+ e" ?0 _! R: t
Patient Report' K4 Q6 S2 {  h) M' y8 f
A 16-month-old white child was referred to the  e( V  a+ q- f. B
endocrine clinic by his pediatrician with the concern& H* v1 s8 ~; z: ~4 P5 O# F3 e5 s8 H
of early sexual development. His mother noticed% r$ P- {; U# p; J$ ~& s
light colored pubic hair development when he was
/ `! z6 H- p6 {/ p1 eFrom the 1Division of Pediatric Endocrinology, 2University of6 W7 m& ^( u) W' q4 O$ L
South Alabama Medical Center, Mobile, Alabama./ o! K" o  k" \# [/ c/ `
Address correspondence to: Samar K. Bhowmick, MD, FACE,; w& U; f3 I6 E3 D8 k6 z& E
Professor of Pediatrics, University of South Alabama, College of$ X9 u# Y3 g9 n& {/ B7 p
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
7 I. y! w9 {) w: me-mail: [email protected].+ w  C" I6 P8 ]: Z' Z- w
about 6 to 7 months old, which progressively became
" S1 U9 K9 C& n+ [4 z  @darker. She was also concerned about the enlarge-
% T; x; S3 V$ W' q) Z( gment of his penis and frequent erections. The child
/ N& M% D: A% b/ Z3 n  u/ owas the product of a full-term normal delivery, with
1 j8 e. L4 b# V# t6 ha birth weight of 7 lb 14 oz, and birth length of
, H0 P! V+ Y% }, [20 inches. He was breast-fed throughout the first year
; r8 Q) G7 k0 M! S& c9 K9 Aof life and was still receiving breast milk along with# a, Z% G7 ]' g$ L  N% A$ `. c; y/ O
solid food. He had no hospitalizations or surgery,6 ^$ A  l2 F# M$ F& g
and his psychosocial and psychomotor development1 u* V) ^2 j9 P$ L+ ?  e
was age appropriate.
3 S! y0 B# c3 S& T# EThe family history was remarkable for the father,
9 a0 Y  ~: W% K6 W# w9 s4 {who was diagnosed with hypothyroidism at age 16,
" L! q2 q' l' A% ~: M2 Uwhich was treated with thyroxine. The father’s5 G* ]: N0 j& K5 l6 j
height was 6 feet, and he went through a somewhat
+ _3 H* Q0 Z9 z1 n( D0 xearly puberty and had stopped growing by age 14.! G/ I- r* E2 b3 w
The father denied taking any other medication. The
- Y: f" \# W* U" ~child’s mother was in good health. Her menarche9 ^2 p! W" p4 R$ s$ q  I( K1 Z
was at 11 years of age, and her height was at 5 feet! ~* `! S8 t+ R  k! u6 d, j# }0 W, B
5 inches. There was no other family history of pre-
/ R% _5 T( d: B' q$ dcocious sexual development in the first-degree rela-
  M& k; ~, u( s3 a% itives. There were no siblings.
+ j  T/ s% T9 L- c: VPhysical Examination
" Y* t4 R6 [" a# t4 x) Q- {& l  X- R6 ?The physical examination revealed a very active,
. b# Y- y4 s; nplayful, and healthy boy. The vital signs documented- t* d" i* ~- c
a blood pressure of 85/50 mm Hg, his length was' u4 t: G# p5 `& z1 V
90 cm (>97th percentile), and his weight was 14.4 kg
8 _. A5 e. D' u. }(also >97th percentile). The observed yearly growth+ `6 D$ c  g6 g
velocity was 30 cm (12 inches). The examination of2 A, f, n% w5 @. Z" y
the neck revealed no thyroid enlargement.
+ g% a7 C9 E9 n: ~1 E) w* }The genitourinary examination was remarkable for
! T; z. Z9 m( \. Q: @enlargement of the penis, with a stretched length of4 c$ b1 {3 D. m! C' O
8 cm and a width of 2 cm. The glans penis was very well
+ r9 T8 |) S! @% s- {developed. The pubic hair was Tanner II, mostly around' b5 i# r1 c3 C7 p0 g$ U6 w
540
/ O) D  `7 ^( w( Y& q: o  C0 I9 gat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from( V+ n) s7 L! e4 O* M) v
the base of the phallus and was dark and curled. The
" p, M# J, m+ a* |testicular volume was prepubertal at 2 mL each.
2 i  S* S2 i  c: uThe skin was moist and smooth and somewhat6 \7 y. \& F, v* w/ Y* C
oily. No axillary hair was noted. There were no6 `8 {; n6 x' S8 i' F
abnormal skin pigmentations or café-au-lait spots.4 ?3 t0 p5 g+ d+ H$ A) o& a
Neurologic evaluation showed deep tendon reflex 2+
& v4 f: N) k! L) V& ubilateral and symmetrical. There was no suggestion; ?2 V8 O  r8 Q1 B  h
of papilledema.: _5 B3 Q- V* k5 F/ \, G
Laboratory Evaluation1 y2 E5 u5 J! Y4 z3 ~# K
The bone age was consistent with 28 months by
0 {: u4 ]- X6 q3 ?# D! yusing the standard of Greulich and Pyle at a chrono-+ Q" p, i- ?( e4 u
logic age of 16 months (advanced).5 Chromosomal
0 t/ `$ ]/ U" m! U' _) R7 Y/ ~1 Jkaryotype was 46XY. The thyroid function test
6 ^& X' B5 w* m' q3 l2 h. {showed a free T4 of 1.69 ng/dL, and thyroid stimu-8 ^! ]' v( }2 C
lating hormone level was 1.3 µIU/mL (both normal).; L8 Q0 _' R9 G$ J
The concentrations of serum electrolytes, blood6 n) V/ X( J9 k! D
urea nitrogen, creatinine, and calcium all were
# D4 Z" ~/ n4 O, d8 L% V/ lwithin normal range for his age. The concentration1 g( k" m- f! c, M. J1 Z
of serum 17-hydroxyprogesterone was 16 ng/dL
- r( B4 w: [7 u& N" ?- [- b(normal, 3 to 90 ng/dL), androstenedione was 20
6 E+ _8 u' E8 o; B' p1 Eng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
; x( K5 V, f6 ~1 C; N' d4 p0 Nterone was 38 ng/dL (normal, 50 to 760 ng/dL),
5 b. R/ _; ~/ v4 w8 kdesoxycorticosterone was 4.3 ng/dL (normal, 7 to
$ J) B3 ~3 b+ i3 g49ng/dL), 11-desoxycortisol (specific compound S)' J) n6 y/ j* u; x
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
( |; u1 z3 W  n# k: Y# otisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
" [, h' J4 I' Ntestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
. @! k: [" u0 c% xand β-human chorionic gonadotropin was less than
8 B  ~) Q! e* ]- a: [3 Y5 mIU/mL (normal <5 mIU/mL). Serum follicular
/ J* H( W" D% O, A( ^* o, U5 |# Qstimulating hormone and leuteinizing hormone
, F. v" f& W! r' Y3 [; }/ Q& L! Mconcentrations were less than 0.05 mIU/mL1 |. q" d. C9 i+ J: V. v1 F. [
(prepubertal)./ I- E0 v& _& X' c
The parents were notified about the laboratory
$ c3 {( P( Z3 n) c+ ?5 |results and were informed that all of the tests were7 M9 I4 E5 p0 K  B( H
normal except the testosterone level was high. The
* |/ B5 k: [3 |follow-up visit was arranged within a few weeks to# ?# P! @2 `. ]0 |$ ~/ ]( V9 D
obtain testicular and abdominal sonograms; how-- k/ ?5 K6 h6 K
ever, the family did not return for 4 months.
* \3 h" J3 J+ N  y: {$ KPhysical examination at this time revealed that the
9 B7 A, [3 ~/ X  W3 m0 K( Vchild had grown 2.5 cm in 4 months and had gained
8 H& b, l5 U  M) B6 i) u" _6 P8 m3 h, ^2 kg of weight. Physical examination remained
% [8 |& L1 T- W- R, G% Munchanged. Surprisingly, the pubic hair almost com-: b, O) o$ o. m+ u; d
pletely disappeared except for a few vellous hairs at$ `$ ]  ~2 h# R0 q  \
the base of the phallus. Testicular volume was still 24 w# S3 }. i9 V$ I- w9 X" T7 R3 f6 p
mL, and the size of the penis remained unchanged.5 @1 e5 M3 C1 Z+ C
The mother also said that the boy was no longer hav-
9 o1 i3 g, b1 X, f: Y; Z; `ing frequent erections.
( j' X2 A. H3 qBoth parents were again questioned about use of3 I9 k! d; B: u. J7 k
any ointment/creams that they may have applied to3 s9 d, E* c: @3 K  i- E+ m  g
the child’s skin. This time the father admitted the" t1 S  E- ~/ ?; x% I
Topical Testosterone Exposure / Bhowmick et al 541
8 q; w$ ?1 ^, w. r; \9 tuse of testosterone gel twice daily that he was apply-
1 A) w" Q! x0 E- I8 X! q; Xing over his own shoulders, chest, and back area for% k! A9 s: X: H: k, R+ k) G8 {
a year. The father also revealed he was embarrassed
8 I8 n# i% @; ?3 W- S- e6 r% {to disclose that he was using a testosterone gel pre-1 D  P. @8 x% }. l4 \5 q
scribed by his family physician for decreased libido
6 n+ i3 v+ a" T# Ssecondary to depression.
+ S$ z+ p+ i9 Q& I2 e* c" e7 [The child slept in the same bed with parents.7 R' A, O6 A% D4 D" }9 q7 }
The father would hug the baby and hold him on his
9 H; x7 x7 E) x1 O$ uchest for a considerable period of time, causing sig-
9 J1 g+ J$ [2 {  u3 {nificant bare skin contact between baby and father., v' h; [9 n/ A- D
The father also admitted that after the phone call,
+ h. T$ s6 J, K& Kwhen he learned the testosterone level in the baby% m$ ^7 f4 Y$ y/ J; G
was high, he then read the product information9 x; z+ I/ g2 I7 m1 q& j
packet and concluded that it was most likely the rea-2 z1 T: `3 h+ K' Q
son for the child’s virilization. At that time, they8 A: F$ o8 B- O
decided to put the baby in a separate bed, and the1 k; ?0 |& u5 y- i  p
father was not hugging him with bare skin and had
. R: o9 c6 f- U5 d1 G/ [# I7 Ybeen using protective clothing. A repeat testosterone
& T! F5 M% R& n/ y5 u2 ytest was ordered, but the family did not go to the
% L6 Q* e% H; T" m! alaboratory to obtain the test.: c6 V; _+ B3 ?$ k, j
Discussion/ @$ |. }4 b! G: r9 `4 @
Precocious puberty in boys is defined as secondary
# {( C; I) o6 {sexual development before 9 years of age.1,4+ ]# ^  c! R+ [; x/ E/ h  a
Precocious puberty is termed as central (true) when
8 @% C& J5 U1 |it is caused by the premature activation of hypo-, z: U) i% O6 D
thalamic pituitary gonadal axis. CPP is more com-
. ]" j0 ~* G5 G* |( f7 X7 imon in girls than in boys.1,3 Most boys with CPP% c# Y0 g6 s: |! x$ h! F
may have a central nervous system lesion that is& S8 N$ \9 |. ?! U" J
responsible for the early activation of the hypothal-
. D# x8 p% @- ~amic pituitary gonadal axis.1-3 Thus, greater empha-
/ A% n+ D1 o4 K: c# a0 T4 esis has been given to neuroradiologic imaging in. ?4 l. K1 t6 A' T; C
boys with precocious puberty. In addition to viril-
) {& A$ ~* v7 f1 q% M5 Uization, the clinical hallmark of CPP is the symmet-
3 f9 e3 z1 e& O5 drical testicular growth secondary to stimulation by9 c5 I3 h- i! E1 m! g% Z" T5 I( P% g
gonadotropins.1,38 U& ~7 L( I+ |& N2 z( U
Gonadotropin-independent peripheral preco-
  x7 o# U2 G2 [( w# N! Qcious puberty in boys also results from inappropriate
& h  S/ s! Q$ i9 \5 c5 G" k) c3 ]0 sandrogenic stimulation from either endogenous or
- g2 r0 o+ R+ I$ [8 z; Jexogenous sources, nonpituitary gonadotropin stim-, j; R! \: f# y0 g) C( c1 v
ulation, and rare activating mutations.3 Virilizing  B$ U: ^; G* _
congenital adrenal hyperplasia producing excessive: H9 W' x/ ~6 ^/ F! V
adrenal androgens is a common cause of precocious# x' z( h# f/ ]5 I9 M1 H
puberty in boys.3,4. [, C' Y( R' D$ ^$ \
The most common form of congenital adrenal
8 `+ i9 I0 {( j$ z0 @7 Whyperplasia is the 21-hydroxylase enzyme deficiency.
+ e9 c" B6 Z1 Q- H: KThe 11-β hydroxylase deficiency may also result in
9 @! S! e) G% T: \5 y0 e+ Z$ V4 Nexcessive adrenal androgen production, and rarely,8 _% F8 T  G, A: j7 v
an adrenal tumor may also cause adrenal androgen0 ^% b, ~" }3 {5 }( Y' e
excess.1,3
2 r2 \4 p! R" W8 W# c3 Xat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
# l& _. A2 u6 |! P: Z542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
, c* K+ @3 \3 Q) ^3 G1 U* q/ ]5 gA unique entity of male-limited gonadotropin-
+ f/ Q8 G( _4 C& c2 Q# l% Zindependent precocious puberty, which is also known" r! T: \( V9 m6 z
as testotoxicosis, may cause precocious puberty at a. ^% m. J" ~  d1 b) ^
very young age. The physical findings in these boys/ C. D. \8 U4 Q' ?) S0 ]* E
with this disorder are full pubertal development,  a5 f0 Z5 S* n, N( N
including bilateral testicular growth, similar to boys
8 c! y2 T, R( Z/ u" E- Mwith CPP. The gonadotropin levels in this disorder
) G8 s8 ^! R) L: s! ?9 D. v  T& sare suppressed to prepubertal levels and do not show
) h% d0 b; }) R0 apubertal response of gonadotropin after gonadotropin-
( g3 T% W: a! treleasing hormone stimulation. This is a sex-linked# F; P1 K& v% I. a* ~; v2 Q, D& V
autosomal dominant disorder that affects only
  i$ `/ n2 ^  cmales; therefore, other male members of the family
/ a3 W3 h" z2 o0 l3 L; G8 I0 ?may have similar precocious puberty.3
' x% M+ \9 p0 B* ]In our patient, physical examination was incon-* ^: ^) @# _7 t# G
sistent with true precocious puberty since his testi-) a: A1 N5 c( ]! l: A
cles were prepubertal in size. However, testotoxicosis
/ P+ H) v% R( k9 u* Y+ J' awas in the differential diagnosis because his father* Q: q( ~0 `8 J' E2 B* i- R
started puberty somewhat early, and occasionally,- Y: p! ^) X% ^% y
testicular enlargement is not that evident in the
8 h7 a/ q+ h: s( P( _beginning of this process.1 In the absence of a neg-
; b' S2 `1 v# a1 V* u6 T5 y# Cative initial history of androgen exposure, our
3 o6 s/ a8 [' x6 Pbiggest concern was virilizing adrenal hyperplasia,7 N7 C' {7 G( l% ?  A
either 21-hydroxylase deficiency or 11-β hydroxylase
* v; P- B2 ]9 H5 V/ Bdeficiency. Those diagnoses were excluded by find-
  S& K, I) S3 ?, Ding the normal level of adrenal steroids.$ ~' H( h7 m/ D" j9 h3 p# b
The diagnosis of exogenous androgens was strongly) P  h* Q. w/ q" I% O9 ~0 e1 F1 J* V
suspected in a follow-up visit after 4 months because
/ q9 P& R4 M( ^. p1 Wthe physical examination revealed the complete disap-# S+ g  v2 b# p8 w! ^; `, a: s6 H7 y
pearance of pubic hair, normal growth velocity, and
  y9 F; u; E8 i+ Rdecreased erections. The father admitted using a testos-0 E3 D: d4 t4 ^/ |+ O9 N3 q7 X& l% D
terone gel, which he concealed at first visit. He was
+ |4 Y6 Q, N8 f# C! a$ d/ Gusing it rather frequently, twice a day. The Physicians’% w& u- d6 S$ `5 ~1 u, j3 x" A
Desk Reference, or package insert of this product, gel or
9 }# d: m/ ]/ J4 Y& I/ R% `cream, cautions about dermal testosterone transfer to! v, P' z7 D; Z9 a0 @" s
unprotected females through direct skin exposure.
. E# T( D+ n' ^  T. J6 S! tSerum testosterone level was found to be 2 times the
6 F8 N2 h" g  V1 Q  d- p8 ^baseline value in those females who were exposed to# \# u, W3 E' H/ p8 B, |3 h4 {
even 15 minutes of direct skin contact with their male# F4 Z! ]9 o) Q8 p% n
partners.6 However, when a shirt covered the applica-
: f5 O8 v9 V/ Q/ Rtion site, this testosterone transfer was prevented.
) ]; R0 q2 E8 Y1 n* POur patient’s testosterone level was 60 ng/mL,5 v3 @( ]( D' ~" Y3 b
which was clearly high. Some studies suggest that+ @4 w" j7 r4 d$ @/ C
dermal conversion of testosterone to dihydrotestos-1 ?0 v4 q1 l6 ?0 g
terone, which is a more potent metabolite, is more
0 L7 D' s: C7 a7 z/ Sactive in young children exposed to testosterone! M5 t% z' P  O1 C' ?
exogenously7; however, we did not measure a dihy-6 j3 g) p0 I) z( |+ H  }$ O1 M
drotestosterone level in our patient. In addition to
5 ^, g9 n$ Z0 x: Tvirilization, exposure to exogenous testosterone in
5 V/ s3 l& Y- ~+ p! P, vchildren results in an increase in growth velocity and$ x( x" _' b5 T6 Q0 c  M' i
advanced bone age, as seen in our patient.
/ z* j' y9 a4 Z) W2 xThe long-term effect of androgen exposure during. n* }! l+ E, Z1 X& M- r
early childhood on pubertal development and final, G' v8 l$ S/ X! }2 X
adult height are not fully known and always remain8 h. v; f9 e& A/ E0 _
a concern. Children treated with short-term testos-3 }% @/ C. Z% I2 I2 P& x: C
terone injection or topical androgen may exhibit some
) ^3 k  K, r' n& p) H; lacceleration of the skeletal maturation; however, after# ]/ W8 }$ Y: |2 h( K
cessation of treatment, the rate of bone maturation
. k0 y2 R9 f+ b$ W1 F; `+ Xdecelerates and gradually returns to normal.8,99 ]/ ]* Z8 Y+ v$ ^
There are conflicting reports and controversy/ q+ ]. ?# Q9 H% z* }! a
over the effect of early androgen exposure on adult
3 x1 s3 Z! f& M8 X9 Tpenile length.10,11 Some reports suggest subnormal$ X, t* o) }4 u% G
adult penile length, apparently because of downreg-
# W4 H3 q- Z! ?' c! |  Qulation of androgen receptor number.10,12 However,' z: V+ ^  M' P& V# }: ^
Sutherland et al13 did not find a correlation between7 @6 X$ X1 K) `' R3 z7 s3 l, w- u
childhood testosterone exposure and reduced adult# ]9 H. w9 `; j4 A' s* @% u% G" c
penile length in clinical studies., r  v% X6 d6 X+ w
Nonetheless, we do not believe our patient is- _8 S" w3 Y5 U1 I8 n
going to experience any of the untoward effects from4 z! c/ r5 x/ T9 c: N* d4 d0 m3 n
testosterone exposure as mentioned earlier because; m; W7 r9 Z; H: M
the exposure was not for a prolonged period of time.
! t4 F: T' f4 [' i9 U  ~7 ZAlthough the bone age was advanced at the time of4 ]( T  R& R* H, J
diagnosis, the child had a normal growth velocity at+ F3 ?' g: m$ B" C& d) |4 |* b" y/ H
the follow-up visit. It is hoped that his final adult8 M" F( t/ p0 ^/ x1 }: M
height will not be affected.- K/ s4 N0 \! n7 t% N
Although rarely reported, the widespread avail-6 F' ^, O0 d( d  g2 T
ability of androgen products in our society may
9 t9 ~% K4 N2 C5 F0 o( pindeed cause more virilization in male or female
! N, t# _& Z; s5 gchildren than one would realize. Exposure to andro-: i1 f5 V- G  `+ k5 G! t
gen products must be considered and specific ques-
/ G* b2 Z6 ]6 A/ ]tioning about the use of a testosterone product or0 _" p2 G: |8 s* C
gel should be asked of the family members during. v0 |: I2 |+ X) t; u
the evaluation of any children who present with vir-& Q9 t6 i- L$ Z' `' g, }0 H  n" R
ilization or peripheral precocious puberty. The diag-
1 [3 P) V1 L* ^. G. `+ K0 Vnosis can be established by just a few tests and by2 \' d$ K+ o2 H" f6 x& J- @
appropriate history. The inability to obtain such a
: S" @' G  c, O/ I- x* M3 A6 J- V" jhistory, or failure to ask the specific questions, may( g) E) c& {$ \* i; b
result in extensive, unnecessary, and expensive
. m% U$ w4 |  H+ q9 B# _) iinvestigation. The primary care physician should be" F# A0 N% b5 H; D' c; S
aware of this fact, because most of these children
( u5 l5 m# G8 F0 n* qmay initially present in their practice. The Physicians’
- u' n' w# B. p; \& ~Desk Reference and package insert should also put a
$ r  U% V  c  O+ I- J+ ]6 G/ Q/ Wwarning about the virilizing effect on a male or. u; a% Q( [3 j& Y
female child who might come in contact with some-- g- G" T' M* p- i! c
one using any of these products.
* p3 t4 N! ?1 Y" b6 ?2 J/ xReferences0 \6 B4 P/ c( f+ V  v+ h6 n! }# y9 x
1. Styne DM. The testes: disorder of sexual differentiation
- D1 h8 h9 ]. w) [/ b  kand puberty in the male. In: Sperling MA, ed. Pediatric3 m2 _, U/ {7 b- B; t
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;5 k( U8 f/ ^* d4 f: ~
2002: 565-628.- A5 G1 U: w5 ]- k" Y
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious0 u( @( q% W5 {9 U2 Z( _3 s
puberty in children with tumours of the suprasellar pineal
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感謝大大的辛勞分享!我會繼續在WK關注大大的文章!
發表於 2025-1-11 22:18:01 | 顯示全部樓層
女厕偷拍辅导班主任尿尿老师的逼很嫩还有一点
發表於 2025-1-17 16:31:39 | 顯示全部樓層
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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

0 r' d8 J0 A3 y) m5 V# G' E4 m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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