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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  ], A; f5 [1 E% ?. X
Boy Induced by Indirect Topical# i* H& n+ v8 W. _( A3 f- k
Exposure to Testosterone- s4 w3 m2 V( W" W$ i% O. m
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
0 I) t2 k6 k/ [) x" K/ eand Kenneth R. Rettig, MD1
5 x1 _0 X8 x: L5 KClinical Pediatrics
7 R: ?/ m- L# H7 tVolume 46 Number 6
9 ?; E/ ^9 @$ W) }July 2007 540-543' ^. z: K3 A8 A9 H
© 2007 Sage Publications+ f+ V1 J" ?% i+ r: s2 _  Y$ b. P
10.1177/0009922806296651* m: Y# w7 C5 u" d: E
http://clp.sagepub.com
# Y! C6 O0 s* f; d& O# ]7 Ohosted at
3 w1 K$ l' I  t5 d/ M8 E; _# hhttp://online.sagepub.com
4 _, @8 d" C) @Precocious puberty in boys, central or peripheral,
) A. l, Z% e  s$ X7 ?* y# o- _- v# r% ~is a significant concern for physicians. Central
: z+ J# _+ G1 [; \precocious puberty (CPP), which is mediated
  q. z$ K2 Q. c( B! ]+ wthrough the hypothalamic pituitary gonadal axis, has
$ c9 v/ Y; M4 L& p* Ga higher incidence of organic central nervous system8 V& n% `- U" M" r, f
lesions in boys.1,2 Virilization in boys, as manifested
+ p" ]; ]0 z8 M) K: @! I4 Kby enlargement of the penis, development of pubic5 e2 }  s0 N! z# H% P
hair, and facial acne without enlargement of testi-) U: [( k2 \3 T% w" s* c3 S
cles, suggests peripheral or pseudopuberty.1-3 We3 P- }0 h0 t2 s+ o" I1 \
report a 16-month-old boy who presented with the2 `/ O; B. s3 x% K) G( d1 o/ U
enlargement of the phallus and pubic hair develop-
: A4 ]$ F' L6 u7 ?ment without testicular enlargement, which was due
: l! L( l0 M& S) d/ hto the unintentional exposure to androgen gel used by  n5 \$ m0 D' E( I0 ^
the father. The family initially concealed this infor-
% u: z0 @% Z, vmation, resulting in an extensive work-up for this$ B0 {7 l- R& T
child. Given the widespread and easy availability of
! C/ S! L/ K, {$ j5 y0 Mtestosterone gel and cream, we believe this is proba-, \) u2 e' w/ \9 U5 w
bly more common than the rare case report in the
1 B# H# {3 F, Zliterature.4. Q* P7 p/ L/ T' ]' Y- d
Patient Report6 D/ L5 ^$ |  U2 j
A 16-month-old white child was referred to the
( _$ ^3 b0 L; L- V) Cendocrine clinic by his pediatrician with the concern
0 Q# [; T# a; m5 Cof early sexual development. His mother noticed
" d1 I! Z. U) g5 h$ @# T0 `light colored pubic hair development when he was) w  X# Z/ q/ [' G, M- m, F
From the 1Division of Pediatric Endocrinology, 2University of
& L$ X4 I3 [3 qSouth Alabama Medical Center, Mobile, Alabama.
1 g! H' l5 _0 Q4 d- |6 W, x5 FAddress correspondence to: Samar K. Bhowmick, MD, FACE,
# s5 U" A. k7 |+ p. R4 }# rProfessor of Pediatrics, University of South Alabama, College of
: j9 p9 v- |+ [! ]Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;2 B, Q$ D& b! `! z
e-mail: [email protected].
  D0 F4 ^" f6 T" }! `- ~about 6 to 7 months old, which progressively became
7 b- x  M, a( N7 u1 Z0 Wdarker. She was also concerned about the enlarge-
: B# M8 F1 f. s, @" qment of his penis and frequent erections. The child  `7 r) T. ], Z% W; A$ `! }( ~/ y
was the product of a full-term normal delivery, with  B9 \+ c2 P' ~$ n$ ~6 k0 @
a birth weight of 7 lb 14 oz, and birth length of- Q% d( a3 X' o7 S0 G) u( p
20 inches. He was breast-fed throughout the first year& P1 s2 J9 t9 }. m
of life and was still receiving breast milk along with
1 v$ O  c0 H3 P1 ?0 d0 V, g# fsolid food. He had no hospitalizations or surgery,
9 m3 Z" M: B2 N; o6 ~and his psychosocial and psychomotor development
4 P" D2 G8 j7 h6 W+ x0 x+ Wwas age appropriate.5 m5 j3 e9 z2 |, q% d
The family history was remarkable for the father,
, W! c( ^2 ~7 x& j' v  ]who was diagnosed with hypothyroidism at age 16,
, C6 ]& E, C" a6 {1 o. x" s- vwhich was treated with thyroxine. The father’s1 `- o; v% h5 z+ J8 }" P
height was 6 feet, and he went through a somewhat
; X9 @3 U* l0 ]( b7 \4 searly puberty and had stopped growing by age 14.$ K. k* ^, O" Q+ k" E
The father denied taking any other medication. The
  L/ v# _1 o& Y# C- _8 ?- Xchild’s mother was in good health. Her menarche
1 P, ~9 v. E6 v1 }& c( kwas at 11 years of age, and her height was at 5 feet
9 H; E" Q3 |! z" Y5 inches. There was no other family history of pre-
5 C4 M$ {, Y1 W5 f+ w2 B. ~% Kcocious sexual development in the first-degree rela-) I0 i( m2 E% ^4 ]
tives. There were no siblings.
- M8 @6 V1 e4 M  BPhysical Examination: j8 P, {/ I5 S
The physical examination revealed a very active,
! W( T! r# L% ^/ T' fplayful, and healthy boy. The vital signs documented5 }# ^: @4 Q1 o  A* A' \3 d
a blood pressure of 85/50 mm Hg, his length was
$ f# u9 Z" Y/ b0 A1 x% b90 cm (>97th percentile), and his weight was 14.4 kg
0 N/ Y( u/ w1 Q8 E2 R$ y(also >97th percentile). The observed yearly growth8 K# }" @$ ~* h  G; K
velocity was 30 cm (12 inches). The examination of
  `- O: Z" I8 L, U( Athe neck revealed no thyroid enlargement.- [+ s/ ~  I2 R! _( |' `$ V- n9 K
The genitourinary examination was remarkable for
9 q! ~8 q: {. K$ b: E9 R/ penlargement of the penis, with a stretched length of1 w9 H; o# e9 m" [* ~
8 cm and a width of 2 cm. The glans penis was very well
9 o. @9 U. k7 }# ?5 k% Pdeveloped. The pubic hair was Tanner II, mostly around
! Y# z/ n8 @8 N540" u2 E+ S, k6 Y& J! u: O2 `
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
, k6 r7 G& \/ J0 d1 Nthe base of the phallus and was dark and curled. The
' t  J9 d7 G: d$ @2 @8 ]' Stesticular volume was prepubertal at 2 mL each.' m+ E, E6 v( W5 f" s, |* r
The skin was moist and smooth and somewhat
" T8 |5 U+ j' voily. No axillary hair was noted. There were no
3 O& e7 z/ e$ l% i& y4 C. }4 eabnormal skin pigmentations or café-au-lait spots.
9 r0 W4 I& Y: I. S$ ?3 e  |Neurologic evaluation showed deep tendon reflex 2+4 \8 |9 Y( K! M2 b! H. W; ^
bilateral and symmetrical. There was no suggestion
: q/ U, E+ g1 h" c8 R2 G# mof papilledema.
6 L1 W: }$ P! b- p1 sLaboratory Evaluation' z! @8 Q& o9 P, k" v, ]* U
The bone age was consistent with 28 months by; l* g" d. z* S6 n
using the standard of Greulich and Pyle at a chrono-2 V- B6 m" t* L2 }
logic age of 16 months (advanced).5 Chromosomal% d- H- M9 m, K5 v. e2 U9 _: U5 A
karyotype was 46XY. The thyroid function test4 W4 _* p: W+ O6 n
showed a free T4 of 1.69 ng/dL, and thyroid stimu-  x+ N4 e$ A, s0 a3 K
lating hormone level was 1.3 µIU/mL (both normal).3 r/ Z+ z! _' d; P# o4 Z1 h6 p6 |
The concentrations of serum electrolytes, blood: V  E, _9 H8 w$ }
urea nitrogen, creatinine, and calcium all were5 ?9 p# J* o8 _- a- R
within normal range for his age. The concentration
# G7 N! _9 t9 Q! pof serum 17-hydroxyprogesterone was 16 ng/dL% Y3 q0 `3 s" m  c  j
(normal, 3 to 90 ng/dL), androstenedione was 20/ f5 ]0 v, }/ n6 p
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
/ z7 `) j# ]; N1 r- y/ uterone was 38 ng/dL (normal, 50 to 760 ng/dL),4 o9 W+ S0 a5 m) y! z  D# A8 n, \
desoxycorticosterone was 4.3 ng/dL (normal, 7 to; C" p0 S/ @& ^1 ~
49ng/dL), 11-desoxycortisol (specific compound S)8 u! Z) M8 v4 J5 i
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-9 o% T6 W2 G" G& d
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total% V- J/ @. E: E7 L* P
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
7 ^; d" p6 @0 A  n0 U% nand β-human chorionic gonadotropin was less than/ Q" k$ k, T3 b
5 mIU/mL (normal <5 mIU/mL). Serum follicular2 k- o8 q. a+ L( O: [0 l" ?
stimulating hormone and leuteinizing hormone$ M# u9 y, B, a7 x4 m
concentrations were less than 0.05 mIU/mL. p$ `" G: w& a0 }
(prepubertal).: n6 m# a4 C& Y3 H2 w
The parents were notified about the laboratory
, w; x! {3 S- Sresults and were informed that all of the tests were5 U6 N4 T! F9 x6 L5 l
normal except the testosterone level was high. The9 c) x1 i) h5 f9 T( b
follow-up visit was arranged within a few weeks to% o7 h  i0 |9 y( x& R; O3 b& a
obtain testicular and abdominal sonograms; how-5 ?' F5 o/ E) @3 _- x
ever, the family did not return for 4 months.& R" Q" ?' y& |5 ~# V
Physical examination at this time revealed that the. Y# T" ?' Q' O
child had grown 2.5 cm in 4 months and had gained
% C* F6 g' [. w9 E4 A. ^2 kg of weight. Physical examination remained7 B0 w5 ?0 H# K# [' r2 C' V
unchanged. Surprisingly, the pubic hair almost com-
; P0 w+ c% X* n* y; r7 Kpletely disappeared except for a few vellous hairs at# o7 @# s* R2 L
the base of the phallus. Testicular volume was still 2/ O! N1 h4 e; K0 I
mL, and the size of the penis remained unchanged.% w3 ]8 n2 i% H" j) _6 y9 ?2 c
The mother also said that the boy was no longer hav-
( E$ ~/ _8 }6 D, r1 w& Eing frequent erections.
" T- F$ T& T) o2 e6 F( pBoth parents were again questioned about use of
% _$ N+ Y1 ?) @& U5 @0 ?; |' jany ointment/creams that they may have applied to: j& A* M7 @& f: d4 T  z
the child’s skin. This time the father admitted the
0 [/ j+ W6 C! }1 F: r0 [- Q. NTopical Testosterone Exposure / Bhowmick et al 541
/ ?6 W2 R7 E# E  Suse of testosterone gel twice daily that he was apply-- l0 D( V% E! Q# d5 V
ing over his own shoulders, chest, and back area for: N) F3 I- U9 C2 P8 A6 k2 w5 o; f
a year. The father also revealed he was embarrassed& u# n$ g2 E9 x7 G; [' o9 p3 a
to disclose that he was using a testosterone gel pre-
' J6 c9 s: R9 yscribed by his family physician for decreased libido5 ^, H( J( k/ G- g: e% ~, P% _
secondary to depression.
) l+ |8 d3 Q/ KThe child slept in the same bed with parents.7 ?9 j! K% t* h7 O3 v5 E1 Z' {
The father would hug the baby and hold him on his
5 g, [5 I9 ]. dchest for a considerable period of time, causing sig-# U5 X7 L; w! N" M. ^
nificant bare skin contact between baby and father.. s* M$ i  x& w: ?& k+ R
The father also admitted that after the phone call,; F8 c% q# x& ^, j
when he learned the testosterone level in the baby! g8 Z" }7 V- i9 e% M  h
was high, he then read the product information. q5 }1 o' d+ m6 W# _. d
packet and concluded that it was most likely the rea-& Q3 d$ E5 B/ ], M) l$ T* `4 h
son for the child’s virilization. At that time, they
5 @9 V; S& b8 a2 N. {; P( Ndecided to put the baby in a separate bed, and the
6 E% W3 M( `) j# _& p% q) }father was not hugging him with bare skin and had8 f* n0 l% _* n
been using protective clothing. A repeat testosterone- L" I* _3 f- a, u
test was ordered, but the family did not go to the
9 a. V3 C, O! Vlaboratory to obtain the test.4 m! E" ^5 c% W3 [" L
Discussion( t/ [' F. N; U1 W  i9 T* t* |
Precocious puberty in boys is defined as secondary0 n) ^1 j6 v8 E& _5 T2 x
sexual development before 9 years of age.1,4, l4 N4 R" a1 D# [; s
Precocious puberty is termed as central (true) when
6 z9 n! x% `& |5 W1 F+ Kit is caused by the premature activation of hypo-0 m+ ?9 W# s% }
thalamic pituitary gonadal axis. CPP is more com-8 I" D% n3 y3 Z/ F
mon in girls than in boys.1,3 Most boys with CPP% F9 M3 ]' G  w6 P+ X$ }
may have a central nervous system lesion that is( a+ G; k& Q3 s) R
responsible for the early activation of the hypothal-
2 x, |" v& c6 ^$ @% X7 r3 P7 damic pituitary gonadal axis.1-3 Thus, greater empha-! _* `( F) `( L! A) a2 c
sis has been given to neuroradiologic imaging in
4 B* h" I0 [( \boys with precocious puberty. In addition to viril-  N/ l4 F+ r1 E
ization, the clinical hallmark of CPP is the symmet-" R6 V; j1 {' T$ X! w8 P1 c
rical testicular growth secondary to stimulation by8 I4 K4 V$ z$ w
gonadotropins.1,3% M% P5 T5 P: t& I: H
Gonadotropin-independent peripheral preco-
( J- {! F- p" f0 M+ vcious puberty in boys also results from inappropriate( r, G$ P/ c" A
androgenic stimulation from either endogenous or! ^- J6 G( ~& Q# n- X2 E
exogenous sources, nonpituitary gonadotropin stim-0 Z" Y! z; t% t' s& [
ulation, and rare activating mutations.3 Virilizing
. F8 ^- ~2 L. I( J  ~. \/ d4 Ucongenital adrenal hyperplasia producing excessive
7 A, B' O& }- @9 |+ Sadrenal androgens is a common cause of precocious
9 I) i, I0 U0 W8 u2 mpuberty in boys.3,4, z3 F9 C  x/ N+ e4 g
The most common form of congenital adrenal
& T7 X# |% [& Z: x+ I1 bhyperplasia is the 21-hydroxylase enzyme deficiency.: W" Q3 x) V+ |9 H9 N; y5 P3 l
The 11-β hydroxylase deficiency may also result in, t. Y$ X& a! T7 O% c0 }
excessive adrenal androgen production, and rarely,
! Y6 [- L) d; ]7 L  \an adrenal tumor may also cause adrenal androgen2 J2 t: T0 C, B
excess.1,3
, A6 B4 z& g$ Iat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from- x+ e7 O1 A" \# ?% r6 g+ n* ?
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
5 a! `- ^! i0 DA unique entity of male-limited gonadotropin-3 y1 y* j% O" P1 Y% ?7 z" k4 Y
independent precocious puberty, which is also known+ A4 B# q0 Z1 L6 m# u" l; V+ A
as testotoxicosis, may cause precocious puberty at a, ?9 f; @! m2 M3 D
very young age. The physical findings in these boys. r/ z& F' s3 K+ d# e) P1 l+ }
with this disorder are full pubertal development,9 x* A7 ]. S* R. L$ \2 j
including bilateral testicular growth, similar to boys
6 A0 T( l) M& J* Y0 ]% uwith CPP. The gonadotropin levels in this disorder
, k- J; s6 \& k# \2 ^6 ]are suppressed to prepubertal levels and do not show" H  ^3 t* H2 h  k
pubertal response of gonadotropin after gonadotropin-) q# t9 C( `  Y0 s1 p; s
releasing hormone stimulation. This is a sex-linked) h2 E5 b6 x1 `1 V" T
autosomal dominant disorder that affects only1 l# C0 u4 l6 R& Q" c+ D% x
males; therefore, other male members of the family. f8 V8 N# Z% ^0 N& S3 l
may have similar precocious puberty.3$ l/ Z9 y" M: S9 R+ B6 ^5 Z
In our patient, physical examination was incon-
% o- i  {. z! d3 h: E/ \sistent with true precocious puberty since his testi-
9 p" I* ?7 _! h" Ocles were prepubertal in size. However, testotoxicosis
2 G8 Y$ \! j* X/ R" [3 C, uwas in the differential diagnosis because his father
, y! z9 E1 o, I: V6 V. s- r2 v8 zstarted puberty somewhat early, and occasionally,0 R7 c* y  l3 \+ z; v# D
testicular enlargement is not that evident in the
8 y8 U( d6 `7 Jbeginning of this process.1 In the absence of a neg-$ p5 G/ \( r5 Y4 f  x1 \
ative initial history of androgen exposure, our
5 Q5 Z& U# [3 Bbiggest concern was virilizing adrenal hyperplasia,
- V$ [& {6 H/ P; ?$ Yeither 21-hydroxylase deficiency or 11-β hydroxylase! N$ D" ~" N$ M4 |4 g1 h' N" _% a
deficiency. Those diagnoses were excluded by find-
9 F% |( g; b* ^+ g( {% Ling the normal level of adrenal steroids.* |2 d5 ]4 O2 Y) ?+ S9 n4 O
The diagnosis of exogenous androgens was strongly
* Z( S, ]5 ~4 R, b: B$ X' {8 Ksuspected in a follow-up visit after 4 months because. y) E5 C: a8 u1 G4 b! P
the physical examination revealed the complete disap-- K* D: H2 ^+ A- i
pearance of pubic hair, normal growth velocity, and# @. W+ V9 a# Z0 n* a' U, o/ _
decreased erections. The father admitted using a testos-
  S; t/ i( `, U8 Z7 u7 F, ~terone gel, which he concealed at first visit. He was( m% U, g, f* \# x1 n% Z' a
using it rather frequently, twice a day. The Physicians’+ N. P8 O  i5 |# h' ?
Desk Reference, or package insert of this product, gel or
" `, x7 z1 \5 ~) mcream, cautions about dermal testosterone transfer to( @; b* G) }/ v; D" o  w9 M1 \3 Z3 T
unprotected females through direct skin exposure.0 D/ }8 y; C8 t6 ^" n
Serum testosterone level was found to be 2 times the
/ s9 y" g$ {6 j) j% j, b* fbaseline value in those females who were exposed to7 h" Q& _; t  z& m; Q6 \' B
even 15 minutes of direct skin contact with their male
8 V, s; H0 O- P( ?6 _# F9 I# _partners.6 However, when a shirt covered the applica-
) f8 U+ d7 a! D: Otion site, this testosterone transfer was prevented.
: h+ ]: j8 _" O: Z  dOur patient’s testosterone level was 60 ng/mL,
  r0 `7 t+ }; X* vwhich was clearly high. Some studies suggest that
* I' A9 u; T, c8 ]; \9 ]dermal conversion of testosterone to dihydrotestos-
- l; M2 R1 d* Vterone, which is a more potent metabolite, is more
3 u- q9 r2 q5 F' cactive in young children exposed to testosterone
7 ^7 N0 p6 F0 L: aexogenously7; however, we did not measure a dihy-
6 W$ n) Q8 N) j8 q, P" v: adrotestosterone level in our patient. In addition to( a- F( u  f' t$ b) t
virilization, exposure to exogenous testosterone in
3 h# R5 B: h. Q: z3 l! f& Ochildren results in an increase in growth velocity and
! V8 F. g4 ?( F3 U+ p3 @advanced bone age, as seen in our patient.
; V# Z2 x; ?6 a: n( n' ]" S5 dThe long-term effect of androgen exposure during$ A. z( ?4 }* I( F
early childhood on pubertal development and final
# d3 D1 N6 J; r- w# \, x7 w9 N: _adult height are not fully known and always remain
# S! l/ G1 P) T% M4 {a concern. Children treated with short-term testos-
$ F, ?/ B  r7 ]% c0 Cterone injection or topical androgen may exhibit some  n# {4 y- `$ c# ^; X: P- U
acceleration of the skeletal maturation; however, after
2 B5 Y& ^% x5 O7 Q) @) Ycessation of treatment, the rate of bone maturation
# `4 F$ s1 m# z0 }5 ~! w$ g/ A# hdecelerates and gradually returns to normal.8,9. `8 s3 a6 T; v
There are conflicting reports and controversy
) Y2 \; {9 N! `% h8 X! _% ^' iover the effect of early androgen exposure on adult
6 K  |2 U, j+ g* G2 Z+ Vpenile length.10,11 Some reports suggest subnormal
( c% B5 T3 C8 X# Iadult penile length, apparently because of downreg-
; o5 O, W+ _3 W" x; ?& }! Zulation of androgen receptor number.10,12 However,
" c3 p% D' N) @0 ]Sutherland et al13 did not find a correlation between
1 k1 A% o, h7 Qchildhood testosterone exposure and reduced adult
4 V: G/ G: o1 p5 B7 z& R0 openile length in clinical studies.
' f# ~- g) q$ Z+ \Nonetheless, we do not believe our patient is0 l7 j. V" M& x1 u5 o3 B
going to experience any of the untoward effects from
3 P' ~- D* n0 `- L  m4 Jtestosterone exposure as mentioned earlier because" w9 l: e  M1 ^" A$ s& _: k
the exposure was not for a prolonged period of time.
2 S3 ~+ l" P- Q# ?! [0 O& IAlthough the bone age was advanced at the time of/ M7 t4 Q) m) `" ]% c1 J- ~
diagnosis, the child had a normal growth velocity at
$ T0 p2 v$ E$ Z% A( A- _( J+ j4 {the follow-up visit. It is hoped that his final adult
5 c; r8 v) @6 G% f: {height will not be affected.
0 R% @- ^- M9 z& w1 l3 KAlthough rarely reported, the widespread avail-: Y% r, n( }  T4 n  j
ability of androgen products in our society may
  S/ n6 X" W2 s' c" N! vindeed cause more virilization in male or female' `, j( j; J- f6 n3 ~
children than one would realize. Exposure to andro-  g* {) ~8 J- n* u: h9 b( x. j
gen products must be considered and specific ques-
: S5 r9 ^1 p  {4 u; Ationing about the use of a testosterone product or* y( P" \( [3 s5 B
gel should be asked of the family members during: T4 _" N( f  b
the evaluation of any children who present with vir-
5 k/ |  J7 O9 q% ~( N! lilization or peripheral precocious puberty. The diag-& w" |! X) @, k6 j
nosis can be established by just a few tests and by( t% C- c6 X/ a' n
appropriate history. The inability to obtain such a
/ C' C. Z2 i$ f& Ehistory, or failure to ask the specific questions, may
! i5 c4 I( J" n! N6 Vresult in extensive, unnecessary, and expensive
/ |- v' f9 U% t3 ?investigation. The primary care physician should be
" v- I0 ^6 A2 |aware of this fact, because most of these children' ?/ b& H4 N- L# S8 {
may initially present in their practice. The Physicians’# [) r% q3 _5 B, O9 g( _
Desk Reference and package insert should also put a: x5 H1 v4 n3 K; z: K. c. Z
warning about the virilizing effect on a male or9 ]5 K, s$ [4 R2 I- E
female child who might come in contact with some-
0 X% H" W7 p7 T, u. @% Xone using any of these products.
4 @3 }. M  C% A) z% ZReferences
/ W" U- v4 q6 u; ~( @3 D1. Styne DM. The testes: disorder of sexual differentiation
' J- P% j: @1 a# m( T* Pand puberty in the male. In: Sperling MA, ed. Pediatric: s$ c2 ?5 _0 }0 C2 \  F0 P8 a
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
6 m+ n$ g% m2 o' x  r, B0 N. R2002: 565-628.( F3 l9 Z9 V4 B- H" K9 y
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
' B$ a: i8 X$ J% P1 fpuberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old' K& q: Y7 B% \6 S
Boy Induced by Indirect Topical' A* Y+ G& p, h' l' J
Exposure to Testosterone
: ~) b3 F  E5 v/ LSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2* x- `+ S  C+ D2 R: }7 y. f/ m
and Kenneth R. Rettig, MD1) _& e9 @( B9 L
Clinical Pediatrics
6 h2 U5 o' f4 N& N5 ^& r) z& BVolume 46 Number 6
  q  J) M9 C2 I, [' R8 V. H' JJuly 2007 540-543; [% {' O% \4 r, ?' {# |
© 2007 Sage Publications
2 E0 |4 I* _- N) j  H/ `10.1177/0009922806296651- i2 e% c* P/ u2 r/ D% o8 d( j# S3 B
http://clp.sagepub.com
* {; u( V5 T; Ehosted at
7 p8 m1 X" S! B# t) h& ^http://online.sagepub.com
% i7 f6 c/ k: O- [3 x6 {5 _Precocious puberty in boys, central or peripheral,
* p. ?9 p! Z. a5 }is a significant concern for physicians. Central
$ W9 E& o8 X5 \  {" x/ o, Q# z8 {precocious puberty (CPP), which is mediated
' m5 Y0 D: i* \6 p& u, s( `through the hypothalamic pituitary gonadal axis, has
/ U% S* Y1 y+ |- S$ ^a higher incidence of organic central nervous system
' c& B( l& H9 H$ Z& h, wlesions in boys.1,2 Virilization in boys, as manifested
! t( {3 o/ @4 m4 e4 {9 |by enlargement of the penis, development of pubic
% t5 `5 a4 Z2 v+ h4 r) Ihair, and facial acne without enlargement of testi-
# \) ^' [, q. M" [) vcles, suggests peripheral or pseudopuberty.1-3 We
1 i0 B( K/ P- \( sreport a 16-month-old boy who presented with the1 l& h8 R" t( x8 c
enlargement of the phallus and pubic hair develop-" c+ e! J" f( u5 Y) O" N7 u6 N
ment without testicular enlargement, which was due- h! g* j1 R" t
to the unintentional exposure to androgen gel used by
, j) I2 j2 r; {9 {the father. The family initially concealed this infor-
' f& h$ d' Y' V. k$ |# {; Zmation, resulting in an extensive work-up for this
/ q: D7 x) w1 fchild. Given the widespread and easy availability of, t+ n8 W4 X* A9 {$ B
testosterone gel and cream, we believe this is proba-* ^4 |8 n% k) }: G/ ~+ I
bly more common than the rare case report in the
( I8 t0 \4 H5 F- Y2 ^literature.4
, `# D/ n& W7 L' U9 c6 Y) N6 rPatient Report, s# N6 }- `+ Y. t# Z: v& V( M
A 16-month-old white child was referred to the
) r' I9 \2 c) y& `endocrine clinic by his pediatrician with the concern
$ v' W2 z& J7 ^$ F3 B/ {+ q& Yof early sexual development. His mother noticed
) b1 _+ I. h' b6 clight colored pubic hair development when he was7 O" B* W0 D: O3 u* [* Z3 m
From the 1Division of Pediatric Endocrinology, 2University of: W9 S7 N" n0 x3 }  C+ f# n, [
South Alabama Medical Center, Mobile, Alabama.& Z" K5 q- _  x3 s0 y: E
Address correspondence to: Samar K. Bhowmick, MD, FACE,, b, ~. A" q8 B- V4 P& q( @# K: ]
Professor of Pediatrics, University of South Alabama, College of
& y) F" ~( o4 @6 z: w' aMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
5 e  F( `; N( S6 W! m* m) }$ b1 C: Be-mail: [email protected].3 @/ }& h$ V3 Z9 b, y0 [! g
about 6 to 7 months old, which progressively became
' U) v+ s* m7 H) S, ^! g2 Adarker. She was also concerned about the enlarge-9 i& G2 j* R& R. _  [9 {  W
ment of his penis and frequent erections. The child
% e7 h6 P& A) {" K4 T. F5 `' {was the product of a full-term normal delivery, with( C+ ?) M/ X) H& _* x% f
a birth weight of 7 lb 14 oz, and birth length of2 b! _8 i5 z- W+ C& C' L
20 inches. He was breast-fed throughout the first year
% ?( w9 h4 S) v/ n6 bof life and was still receiving breast milk along with2 ]$ k8 A' V/ F" r! j8 ^
solid food. He had no hospitalizations or surgery,* h/ ?3 i6 v1 Z/ N2 l
and his psychosocial and psychomotor development
' T2 r3 x  m& E% c& G9 Swas age appropriate.
2 b5 p! ]' ~# r9 g5 \( {The family history was remarkable for the father,4 b, t6 s( @9 D, |- Z
who was diagnosed with hypothyroidism at age 16,7 j6 f+ {9 d$ u7 }1 m9 {: ?9 _
which was treated with thyroxine. The father’s+ Y- }- J: S; g3 I, m( t+ o
height was 6 feet, and he went through a somewhat; }, A# E% ~5 J7 C( }0 _! g6 I5 H
early puberty and had stopped growing by age 14.
  w4 y7 |; K! K: p5 v; n! Q$ o9 PThe father denied taking any other medication. The
2 J9 b. l2 K, t* H2 V9 v' dchild’s mother was in good health. Her menarche
0 R1 _0 H; N: T) P: _was at 11 years of age, and her height was at 5 feet
  H! o1 F9 B; k1 f3 S# B5 inches. There was no other family history of pre-4 z9 z# J' {( k' x. e; B$ Q
cocious sexual development in the first-degree rela-
0 V* p; }, ]3 n) ]tives. There were no siblings.
! g* X# y1 q: A+ [7 fPhysical Examination- b, I, M+ {0 C
The physical examination revealed a very active,
' C8 ?/ x) Z+ {" ]. K0 Pplayful, and healthy boy. The vital signs documented
9 n+ f7 x/ G; \& y$ J9 K  ya blood pressure of 85/50 mm Hg, his length was  R7 {& C. }7 h# Y# r4 m
90 cm (>97th percentile), and his weight was 14.4 kg
" p3 n3 z( F; K2 c& P  G(also >97th percentile). The observed yearly growth
4 X  R+ u2 H% Avelocity was 30 cm (12 inches). The examination of) j' K/ o4 @1 h5 {' C. [" I
the neck revealed no thyroid enlargement.6 D; o/ u" E  N( X& e
The genitourinary examination was remarkable for2 Y! |& ~3 Y6 h9 M; |& k, X" v
enlargement of the penis, with a stretched length of
: k  v, G: G- p& ]$ ^( ?4 B- X8 cm and a width of 2 cm. The glans penis was very well
0 _" r) P% K6 J# C4 ?" I: vdeveloped. The pubic hair was Tanner II, mostly around
* c* ]* j; y- g0 A. g! `540' X; N& F7 |- F
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from7 y) i" W3 Z! F
the base of the phallus and was dark and curled. The
! m7 a6 Q2 C1 stesticular volume was prepubertal at 2 mL each.9 ]$ J0 H, S9 `/ ~5 }
The skin was moist and smooth and somewhat
) A) J, L3 T- ?) f5 poily. No axillary hair was noted. There were no( F4 u# [; o, Q% c" f0 v
abnormal skin pigmentations or café-au-lait spots.
& I8 W3 Y2 D! sNeurologic evaluation showed deep tendon reflex 2+9 |  |( @3 [) ?# L
bilateral and symmetrical. There was no suggestion6 H# `4 Z* \% J+ t4 r
of papilledema.8 G) Q7 H: g' t( I
Laboratory Evaluation0 i0 e7 w8 U) A- K
The bone age was consistent with 28 months by0 U5 z5 j# s8 J; d! {  q1 A2 l
using the standard of Greulich and Pyle at a chrono-
! n1 K, L. T: ^+ T1 Tlogic age of 16 months (advanced).5 Chromosomal
& O" Q9 D/ m5 tkaryotype was 46XY. The thyroid function test/ k8 \: [2 f' [' r; b1 W/ L
showed a free T4 of 1.69 ng/dL, and thyroid stimu-8 i8 u4 S4 _# C$ g5 C
lating hormone level was 1.3 µIU/mL (both normal).
# ?! a! B& m" R$ tThe concentrations of serum electrolytes, blood
) F5 b8 T" m; xurea nitrogen, creatinine, and calcium all were
0 z8 u5 w$ h" H1 Awithin normal range for his age. The concentration1 o0 ^; o8 _! _1 L- y; g* {
of serum 17-hydroxyprogesterone was 16 ng/dL; G5 ?* A2 Q4 u9 T
(normal, 3 to 90 ng/dL), androstenedione was 20/ C" I" G/ T3 ?9 O( F8 X! J
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-( J# }4 l. u  M* n6 S0 y& F! D
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
( M; R: K! a& v7 C; kdesoxycorticosterone was 4.3 ng/dL (normal, 7 to
5 e7 t  s6 ~; I, S( v49ng/dL), 11-desoxycortisol (specific compound S)( a& x' B1 }4 [
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-: {5 u! s& b: B" Y4 q: K7 P- N
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total9 h/ p- O8 @$ W
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
) J- Q5 i2 j' V. V. {and β-human chorionic gonadotropin was less than9 c% j8 a- I5 B  M
5 mIU/mL (normal <5 mIU/mL). Serum follicular
8 F5 r, W: L  u' v4 wstimulating hormone and leuteinizing hormone: k' j/ T' T$ W* R5 H
concentrations were less than 0.05 mIU/mL' c9 C3 E# F# Z7 N1 h  |+ z
(prepubertal).. w% E! x7 C  `8 x. ^
The parents were notified about the laboratory
1 F+ ~- a' @& M* W9 kresults and were informed that all of the tests were* K2 V. R' W! K; x+ M/ T" G; h* b; ~
normal except the testosterone level was high. The$ g2 M; O, h( T& c! Q, @
follow-up visit was arranged within a few weeks to' M* B3 c( L3 F" ]
obtain testicular and abdominal sonograms; how-4 V# a( y& h) U" ^, U* q6 }+ U( C
ever, the family did not return for 4 months.
" W6 ?, e' q3 @3 e* L- uPhysical examination at this time revealed that the
! R) m  t# u4 L9 \$ R4 G7 a' {: mchild had grown 2.5 cm in 4 months and had gained
( p0 }- j+ X# t0 [8 S2 kg of weight. Physical examination remained0 k  |1 i" E5 T8 T, t
unchanged. Surprisingly, the pubic hair almost com-
5 ]0 n3 [0 X/ s7 {- v9 S/ wpletely disappeared except for a few vellous hairs at' S: @! I7 K1 J: {- D
the base of the phallus. Testicular volume was still 2
# ~% t: q; e( OmL, and the size of the penis remained unchanged.
( e$ z8 S6 t8 R; F4 `5 w+ TThe mother also said that the boy was no longer hav-7 U1 ]% {7 t0 }" N5 C
ing frequent erections.
0 h4 N% \8 t. M! zBoth parents were again questioned about use of
9 \  @% n/ B7 c& Sany ointment/creams that they may have applied to/ ]- Z% E, F: K' l
the child’s skin. This time the father admitted the
1 N6 C& X  `6 z+ aTopical Testosterone Exposure / Bhowmick et al 541
8 {, ?8 O, e/ Y# u! B+ l' Guse of testosterone gel twice daily that he was apply-$ a; J" K+ \: m, s% A6 l5 s
ing over his own shoulders, chest, and back area for
' }$ i6 g" i( t. ]5 I# H5 c3 `a year. The father also revealed he was embarrassed( M, i% n  N* N2 ]( h8 p& S
to disclose that he was using a testosterone gel pre-
0 b( _7 B: M' X( J# t2 n% Yscribed by his family physician for decreased libido
' ?& H. ~! ?  _5 A( Zsecondary to depression.& y$ {' @5 Y8 ^. P
The child slept in the same bed with parents., u, ^) o7 q- M: t" Y* }9 J
The father would hug the baby and hold him on his
1 R" w6 S/ [2 c7 ~& B* m; s) z8 Kchest for a considerable period of time, causing sig-
& H$ i9 `3 e. E9 o6 bnificant bare skin contact between baby and father.
6 U; O$ e2 S# T8 ]# C; p! Y& A- JThe father also admitted that after the phone call,
& y" e: u% y  b2 J) dwhen he learned the testosterone level in the baby3 R% h" ?* ^8 A5 ]& S% O
was high, he then read the product information/ X* }8 p! F$ R1 k, m1 M
packet and concluded that it was most likely the rea-
1 h1 Z( z. y# M& _% [' H" Ason for the child’s virilization. At that time, they. u! h" ~1 Y; O  \& {( l3 j0 o
decided to put the baby in a separate bed, and the+ n5 i; E- ^1 c* Y
father was not hugging him with bare skin and had
; ~+ t; z$ G0 D0 ^/ K& nbeen using protective clothing. A repeat testosterone+ B# v. H% C9 a2 W/ `
test was ordered, but the family did not go to the/ s' ?8 {4 w* i0 L4 Q. t
laboratory to obtain the test.
, B. r, k& O# ~) @3 x+ pDiscussion
. j" J! W2 |( z- q% L7 b& j$ NPrecocious puberty in boys is defined as secondary
; ~, G- p! I8 p9 P0 G) l0 xsexual development before 9 years of age.1,4
) ?) R* M  ^0 W5 g+ iPrecocious puberty is termed as central (true) when
  ~, f/ s% M+ hit is caused by the premature activation of hypo-
. `/ K" ^1 [/ I6 q8 Zthalamic pituitary gonadal axis. CPP is more com-
# s8 I+ Y; V' B! |  Zmon in girls than in boys.1,3 Most boys with CPP' ^& S8 m  d& i- s
may have a central nervous system lesion that is9 w/ D5 G. C/ U" u7 K+ ^
responsible for the early activation of the hypothal-
* `7 Q- }/ O& y8 l3 Q" Samic pituitary gonadal axis.1-3 Thus, greater empha-) P5 f/ i% R7 R# f) i8 @4 a+ U1 c
sis has been given to neuroradiologic imaging in' f- u* Y! Q  Y& }6 u, W
boys with precocious puberty. In addition to viril-( i9 Z0 S! |$ ?' S8 q
ization, the clinical hallmark of CPP is the symmet-
& q( }* |! g1 @rical testicular growth secondary to stimulation by1 Z8 R. ^( p2 ]% C9 ^% c1 M
gonadotropins.1,3; \, }% E3 R- P6 l, [; @  K
Gonadotropin-independent peripheral preco-9 X0 g' ]& \. Y
cious puberty in boys also results from inappropriate  M, R6 Z" N( w. A; U. W( m
androgenic stimulation from either endogenous or( Q, l& M+ @0 g7 Y* l6 q" \
exogenous sources, nonpituitary gonadotropin stim-3 T0 m  n, y! H$ P$ m6 E
ulation, and rare activating mutations.3 Virilizing
2 Y7 N1 ], n1 T" u# Ucongenital adrenal hyperplasia producing excessive
8 y; ^, H0 `# W& Z% radrenal androgens is a common cause of precocious- ^8 C, f6 h* I  k& p' O
puberty in boys.3,4
7 \$ Q. {6 J( C/ Z. p: jThe most common form of congenital adrenal* s' |$ p4 g7 F* {9 M
hyperplasia is the 21-hydroxylase enzyme deficiency.
5 `% T4 i. a# w4 F0 a0 {3 FThe 11-β hydroxylase deficiency may also result in+ V  E4 E; U1 v
excessive adrenal androgen production, and rarely,; A" D4 _7 a6 W& m- d
an adrenal tumor may also cause adrenal androgen1 w; U  }7 ^6 b* S
excess.1,37 ]. T" {. h# M, f/ v" u  \& X$ X  ^
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
! U. \. {* V" Z* ]2 w1 g2 R& H5 O542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
8 H" z/ G6 K# j2 g/ V2 j) i5 a* [A unique entity of male-limited gonadotropin-3 [1 Q9 F2 Y$ O8 f3 [! f6 o
independent precocious puberty, which is also known
- }$ E  t1 s5 n9 zas testotoxicosis, may cause precocious puberty at a, Q- s/ \/ X' S: T5 u% k0 ?
very young age. The physical findings in these boys) H: ~# A, R$ r; a$ k5 C! m
with this disorder are full pubertal development,9 @, n1 }7 t( U! J- N
including bilateral testicular growth, similar to boys
/ H. G; X' ~- swith CPP. The gonadotropin levels in this disorder" e0 O) _3 d- ?) k6 H$ S: M
are suppressed to prepubertal levels and do not show# @3 \. Z* u4 \# R) O) W
pubertal response of gonadotropin after gonadotropin-
. f, c. r2 g! d% e7 |8 U' K' \releasing hormone stimulation. This is a sex-linked0 @; {4 t, Y+ ~' i+ G; d7 y" F% n
autosomal dominant disorder that affects only3 Y& p7 O$ ]3 x- `4 n8 P7 k
males; therefore, other male members of the family" L  G0 Z* ]& }8 i+ N( |  d& R
may have similar precocious puberty.32 L( h3 w/ G" [8 |
In our patient, physical examination was incon-3 E. W5 b6 [8 k# `4 g& T0 c6 V+ F
sistent with true precocious puberty since his testi-
5 d9 q/ X8 W" R3 S% Z- R4 ccles were prepubertal in size. However, testotoxicosis' B* q9 k8 O, |$ Y' _
was in the differential diagnosis because his father
4 [4 }2 h7 V, Y- e2 Zstarted puberty somewhat early, and occasionally,
4 @* Y8 }, e( G. E& O3 Z1 D, S' dtesticular enlargement is not that evident in the2 S. a- }8 T$ Y* L3 {. u
beginning of this process.1 In the absence of a neg-* m( E( k! l" ]0 C  @4 c2 m4 d
ative initial history of androgen exposure, our
( a$ d4 O. o  f! o2 B2 Tbiggest concern was virilizing adrenal hyperplasia,0 F7 w7 s$ F) t2 K9 R! U$ G3 X
either 21-hydroxylase deficiency or 11-β hydroxylase; I3 }" {( a* u4 D/ }4 t
deficiency. Those diagnoses were excluded by find-' R& d! z: G4 a
ing the normal level of adrenal steroids.7 q; Y  G6 A5 O
The diagnosis of exogenous androgens was strongly- ?7 J9 B+ x, t- H8 T2 m# p
suspected in a follow-up visit after 4 months because
  z0 @" M6 M% V2 ethe physical examination revealed the complete disap-
' O& D9 g- Q. H+ T' Jpearance of pubic hair, normal growth velocity, and
+ l5 M+ Z% _, }6 r  F0 Xdecreased erections. The father admitted using a testos-5 i: @! T% g  g0 v7 a$ W' l- n
terone gel, which he concealed at first visit. He was
; J6 r' I' K/ kusing it rather frequently, twice a day. The Physicians’; U0 [5 F' h( [! P+ c
Desk Reference, or package insert of this product, gel or# w. h6 v3 |/ O# j$ z
cream, cautions about dermal testosterone transfer to4 k2 }5 x$ z3 L7 L: ]
unprotected females through direct skin exposure.
( S# L4 s" t6 T& o1 u& mSerum testosterone level was found to be 2 times the% b% W% i! K# J# S. d; G
baseline value in those females who were exposed to$ U9 ]# G' M% y1 l- c9 }: S, r
even 15 minutes of direct skin contact with their male' k2 c) H9 [- d; [) p) S0 r
partners.6 However, when a shirt covered the applica-% T* g$ w- H  A5 l1 Z+ z9 S& _
tion site, this testosterone transfer was prevented.
1 K9 g1 n8 U, z5 |, P& n! x) JOur patient’s testosterone level was 60 ng/mL,
! k% W9 ^# d2 M$ |; W2 Owhich was clearly high. Some studies suggest that) b% H0 @1 M1 e. l
dermal conversion of testosterone to dihydrotestos-
6 o$ F* J  p; Lterone, which is a more potent metabolite, is more6 j4 f) G9 K% t
active in young children exposed to testosterone
3 X5 C* n& z6 i$ D- B" u- e6 Vexogenously7; however, we did not measure a dihy-1 C# @2 ]3 P7 i: O
drotestosterone level in our patient. In addition to
' D% q7 _" L- |virilization, exposure to exogenous testosterone in
1 f$ d# d  u9 O- S5 a4 b$ h2 `children results in an increase in growth velocity and, X" X- o" _  K% s- ]5 p
advanced bone age, as seen in our patient.
! S) U$ C/ J/ U) o" e& B8 f1 mThe long-term effect of androgen exposure during
/ E$ r0 p3 D2 v2 Mearly childhood on pubertal development and final
" L- F- A: P/ C% s6 [8 `: uadult height are not fully known and always remain; w5 u4 ?8 ^2 Q: x
a concern. Children treated with short-term testos-+ I1 H* R- ~8 z+ f3 Z/ V
terone injection or topical androgen may exhibit some* w  _" H; a9 |+ h
acceleration of the skeletal maturation; however, after
4 h4 \8 c0 Y) H) \% p& s4 bcessation of treatment, the rate of bone maturation
6 y# m: K% r6 ]2 R' }5 `# u! \' j+ bdecelerates and gradually returns to normal.8,95 c, O  [2 b! s& X
There are conflicting reports and controversy9 @$ p. _- J$ t+ k* p2 {; D' C
over the effect of early androgen exposure on adult
* V, d0 g. P- P3 K- }penile length.10,11 Some reports suggest subnormal
; _5 H1 N$ Y3 P3 B- H0 Nadult penile length, apparently because of downreg-
7 D. d) W) H* Z" E( w# V% Fulation of androgen receptor number.10,12 However,8 y$ \! F; T5 U1 c+ {) |/ }
Sutherland et al13 did not find a correlation between
8 F9 V! j1 v' R: n1 i1 N) D9 E- Gchildhood testosterone exposure and reduced adult
, B: K* d, J% F9 U/ H% r  o* l, V  |penile length in clinical studies.
# b$ N! v9 r' q7 u7 g5 u3 cNonetheless, we do not believe our patient is  B# C3 H8 c3 b* w3 F0 y- G
going to experience any of the untoward effects from
5 H6 S% M. B2 Itestosterone exposure as mentioned earlier because2 @7 u& C( m# D: `/ Y# A
the exposure was not for a prolonged period of time.. Q8 ?+ e. c' f* E/ v
Although the bone age was advanced at the time of
# q0 W; O% D8 E0 }/ S- ]diagnosis, the child had a normal growth velocity at# R" p( Z) k9 H3 e& V1 i9 ~$ m
the follow-up visit. It is hoped that his final adult" x, _: ]+ o: g+ W, D9 \
height will not be affected.
- l* }( x; P" P$ bAlthough rarely reported, the widespread avail-
' N, x# {: _# X; mability of androgen products in our society may0 f" O+ l0 |% t# Q1 Y+ s% Q
indeed cause more virilization in male or female
( l3 g7 }$ o  [+ f6 J- o9 U1 nchildren than one would realize. Exposure to andro-
6 \3 w. j3 v" `! ?0 ], pgen products must be considered and specific ques-' A5 h5 P3 B3 a/ B6 p3 O/ Y
tioning about the use of a testosterone product or
: ^6 n9 a* B, @8 I* `6 Ggel should be asked of the family members during
2 |: D1 d9 G4 q9 Ithe evaluation of any children who present with vir-
- a7 A: p  N1 a: p, Yilization or peripheral precocious puberty. The diag-
) r9 t& b. g! @% z; q. t0 z# A8 jnosis can be established by just a few tests and by
  H0 z6 R! C% U' j$ l0 Qappropriate history. The inability to obtain such a' K& v; B. R; O0 K* Q# J
history, or failure to ask the specific questions, may  ^( |4 r) L" x
result in extensive, unnecessary, and expensive
9 \+ A/ h* L- jinvestigation. The primary care physician should be
8 X/ t+ C% [8 f6 Y3 o3 T2 X) _6 _/ K- qaware of this fact, because most of these children* i1 T6 }8 d/ V: c; O# o4 `6 U
may initially present in their practice. The Physicians’
. K$ @6 N6 g) T+ hDesk Reference and package insert should also put a/ C, Y. \) n! V. ~9 L% W7 I+ q
warning about the virilizing effect on a male or
% p' y* Y. I( o; I3 qfemale child who might come in contact with some-6 u4 x1 ^, }, \. }( N" n/ g6 C
one using any of these products.
4 f1 G2 B/ k  bReferences
, i) _5 `7 u- g* O1. Styne DM. The testes: disorder of sexual differentiation3 w8 D( ?  N! Y( n2 \( k
and puberty in the male. In: Sperling MA, ed. Pediatric
1 j+ G' m' m1 x3 u$ BEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
  Q) Q  j- q0 ?8 A7 `. D2002: 565-628.
' P. O# ^6 Q- m! I8 ?- M+ u2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
/ {' P; x8 V. Y  Z( Opuberty in children with tumours of the suprasellar pineal
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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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VIP精品區,資源無限好賺金任務區,輕松賺金幣
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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

- B/ @( b* g! f4 a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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