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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-Old2 @5 N) P, W0 T
Boy Induced by Indirect Topical7 g/ r' }" _* t! u
Exposure to Testosterone( j4 a3 k4 b4 n$ ?' ~
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,20 g0 J& d3 p$ z, o" q" C6 X
and Kenneth R. Rettig, MD1
% [- |  X  Z" m6 w# `Clinical Pediatrics
( E+ l4 _. \8 p, k) ?Volume 46 Number 6
# b. q; Y' Y- d% E! s8 h2 |July 2007 540-543
3 v3 p; W# _! z8 D* z) k& A1 _© 2007 Sage Publications- Q+ `5 G. u3 V7 {
10.1177/0009922806296651
: I$ w! ?: M9 \1 Z6 p$ @# Vhttp://clp.sagepub.com
# c$ \  V0 U1 F2 Z1 \3 shosted at
+ c6 c& W: G! C' o, M! Uhttp://online.sagepub.com
) v, U0 t1 U; Q! f( o! ]% h7 qPrecocious puberty in boys, central or peripheral,0 T4 d. k" H: I+ L. }+ d
is a significant concern for physicians. Central8 u4 c! ~7 R0 I
precocious puberty (CPP), which is mediated
! k5 E& R% s' n2 Q) `) k# Othrough the hypothalamic pituitary gonadal axis, has/ E# I6 v/ S+ E9 c/ X7 j
a higher incidence of organic central nervous system9 w/ v0 v! E* N7 |' A$ F' w5 C2 N
lesions in boys.1,2 Virilization in boys, as manifested. n- M5 X6 C. n% o. H/ o: b; @7 M7 B8 n& H
by enlargement of the penis, development of pubic
6 x  v0 g1 N0 k/ z8 Y' bhair, and facial acne without enlargement of testi-
5 n  d: S' S" T4 `1 R# g* Y3 ~cles, suggests peripheral or pseudopuberty.1-3 We
; I1 ]' Z9 L. d5 t8 Y6 Ureport a 16-month-old boy who presented with the* e( P, E* D% w4 V
enlargement of the phallus and pubic hair develop-- f7 A/ O+ H# ?% ]$ b
ment without testicular enlargement, which was due
+ l+ ?3 g) R" y0 H$ \/ Fto the unintentional exposure to androgen gel used by
& k& ~( ~% D7 X2 V) w7 O' Tthe father. The family initially concealed this infor-
( R- w: s9 A- M& Jmation, resulting in an extensive work-up for this
% q: M/ d6 f) ]+ O# r" {child. Given the widespread and easy availability of
. r& ~5 I/ F, Stestosterone gel and cream, we believe this is proba-
. d3 p  c1 g& m7 mbly more common than the rare case report in the
# ~' G. I: k; G1 t5 f# _literature.4& D; i. F8 @5 _7 m7 |  i  d* C7 U
Patient Report
. x8 j* ]+ |1 P  u; U: ^- O% QA 16-month-old white child was referred to the
5 p( ?. f7 U# e# \( b, vendocrine clinic by his pediatrician with the concern
% `. T9 N; p9 V, \of early sexual development. His mother noticed$ p: D8 \2 j1 c( f, k& }) ?$ {
light colored pubic hair development when he was! Q( F; a7 {$ {
From the 1Division of Pediatric Endocrinology, 2University of) P1 i0 V+ ?. m; a- q
South Alabama Medical Center, Mobile, Alabama.! x+ j* e2 w$ W1 z
Address correspondence to: Samar K. Bhowmick, MD, FACE,
6 e! O" ~7 i' d0 u/ X- ~Professor of Pediatrics, University of South Alabama, College of. U4 K  A: X: C' h4 S/ D) k. i
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;- {( x. w5 p* R, L' m. n
e-mail: [email protected].
8 M0 A, I( K9 t/ }about 6 to 7 months old, which progressively became
& P1 }1 S7 Z) i3 d; `darker. She was also concerned about the enlarge-
: B6 z+ `* {2 e# M; j2 p8 vment of his penis and frequent erections. The child( @0 P. K$ H( `/ j& Q6 g
was the product of a full-term normal delivery, with' E1 A2 \' H+ E" h) X
a birth weight of 7 lb 14 oz, and birth length of/ C7 n0 @/ h5 K$ l6 R2 ]0 F
20 inches. He was breast-fed throughout the first year
1 z9 \) z0 ^6 v8 Y1 Aof life and was still receiving breast milk along with
# o7 T) S7 E7 I! f5 S4 Vsolid food. He had no hospitalizations or surgery,5 D5 A. Q! j, r9 N$ C4 k
and his psychosocial and psychomotor development
2 ]& q6 Y6 d0 j9 N( l  Q+ hwas age appropriate.
7 d: \( k& r' P. w# [+ ^9 R5 D7 zThe family history was remarkable for the father,
* {$ ^( Q- Q9 K6 C# Lwho was diagnosed with hypothyroidism at age 16,
$ X2 A% m' @- O+ U- b6 l6 c8 V5 Qwhich was treated with thyroxine. The father’s) ^% A( s+ H5 K' l: x+ g* [
height was 6 feet, and he went through a somewhat1 c; m$ c* d( s! i% {- L) x
early puberty and had stopped growing by age 14.; X* i6 M9 L9 F' e* g
The father denied taking any other medication. The
; e. j) I; l1 ^  pchild’s mother was in good health. Her menarche
/ n. E5 d9 D- h, @6 Gwas at 11 years of age, and her height was at 5 feet
' j! N1 N- \7 L) H$ ^5 inches. There was no other family history of pre-5 z: H& K$ M+ Q7 f0 Y5 W
cocious sexual development in the first-degree rela-: G( m0 g+ e: Q7 Z) t/ y
tives. There were no siblings.. H8 i( n2 k9 m* e0 [2 P
Physical Examination7 Z8 C! y$ y. U  p$ V2 t
The physical examination revealed a very active,6 [- X/ }% i7 p
playful, and healthy boy. The vital signs documented
0 j3 {$ G. ]- Ga blood pressure of 85/50 mm Hg, his length was( U9 R7 G$ J$ v  W5 o
90 cm (>97th percentile), and his weight was 14.4 kg) R" M. v: ~1 _3 B8 x4 `6 d+ q; ]
(also >97th percentile). The observed yearly growth
9 X0 X& I6 u  a3 ~velocity was 30 cm (12 inches). The examination of7 i" f: K) J; d
the neck revealed no thyroid enlargement./ M  ]2 m/ {0 d4 |1 j6 k
The genitourinary examination was remarkable for
  e, V3 p5 T" M7 E" p$ ienlargement of the penis, with a stretched length of
4 d+ @! P: K6 k1 E% s8 cm and a width of 2 cm. The glans penis was very well8 _8 v! |- @" ~! I7 ?
developed. The pubic hair was Tanner II, mostly around
/ Q$ b3 s+ X% S6 I% S/ z% ?540
' v% [1 P3 }  a% e3 c" Bat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from: L8 @, l& W6 |/ F# _) u
the base of the phallus and was dark and curled. The
! K. y+ \. `1 z( c! a6 N( k9 Ttesticular volume was prepubertal at 2 mL each.
5 Z" |! k2 f8 E& c) k1 E$ z/ F- \The skin was moist and smooth and somewhat6 U: i2 ]( n# O; N/ Q/ _
oily. No axillary hair was noted. There were no
5 Z1 b  {$ q0 K( n+ u" dabnormal skin pigmentations or café-au-lait spots.7 ?* s) N6 b! }# B8 i
Neurologic evaluation showed deep tendon reflex 2+
" g2 v3 {; L8 Q, c$ ]7 jbilateral and symmetrical. There was no suggestion% F  L, r3 |8 y
of papilledema.
  f$ {% G3 L3 ]* s- aLaboratory Evaluation" X7 ~0 r- r& J& V* r/ D" v8 p# [9 P
The bone age was consistent with 28 months by
9 U3 ?. E9 `9 T: fusing the standard of Greulich and Pyle at a chrono-9 P7 w" N3 }+ E
logic age of 16 months (advanced).5 Chromosomal& J% [/ ^6 \- O% G8 \( E2 [
karyotype was 46XY. The thyroid function test6 i% @% v6 m7 n8 U9 b
showed a free T4 of 1.69 ng/dL, and thyroid stimu-$ x6 P  Z' h- A7 w% }
lating hormone level was 1.3 µIU/mL (both normal).  j1 s# G, n1 I7 y$ {) j) J) b
The concentrations of serum electrolytes, blood: L# _, F$ g( |( w3 D& b; |- B2 M
urea nitrogen, creatinine, and calcium all were% r6 T' y; o7 e% e5 B
within normal range for his age. The concentration6 X) h+ B7 d+ j2 `; h
of serum 17-hydroxyprogesterone was 16 ng/dL  P2 y; u# t1 T8 C1 k- s' |
(normal, 3 to 90 ng/dL), androstenedione was 20; q' Q: v/ @7 z# Y# E$ b
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-6 [* @$ s% G8 V5 e. n6 Z! s
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
$ @& s2 v' G2 b  v5 b. p* g. Ldesoxycorticosterone was 4.3 ng/dL (normal, 7 to6 f% Z" m+ O- t! I& S
49ng/dL), 11-desoxycortisol (specific compound S)' K9 P$ F6 r9 O8 `
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
" D. H( s5 T- n7 Ztisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
% Y; y/ R; a: ^1 B; stestosterone was 60 ng/dL (normal <3 to 10 ng/dL),' J% n6 Q& X- }" X7 D$ t' E1 r
and β-human chorionic gonadotropin was less than" K0 A8 p) b/ p! j& m0 W
5 mIU/mL (normal <5 mIU/mL). Serum follicular& G! k0 _/ c) `6 {
stimulating hormone and leuteinizing hormone
, m) Z0 _0 P  R$ N$ Fconcentrations were less than 0.05 mIU/mL
! `0 j9 m+ Y) Y9 B3 J& m3 Q(prepubertal).
+ g' _7 J/ f( G7 NThe parents were notified about the laboratory! z2 F: B/ ^. d
results and were informed that all of the tests were
% f9 e+ W: p  Gnormal except the testosterone level was high. The
" N4 D! B$ F0 J; j' ~follow-up visit was arranged within a few weeks to
  m' R6 d, h: _8 eobtain testicular and abdominal sonograms; how-
! P4 A  f2 a! |4 p; i' n+ Zever, the family did not return for 4 months.( d# w( c( X0 l$ V
Physical examination at this time revealed that the4 h( j( @' x# g3 ]! W
child had grown 2.5 cm in 4 months and had gained: q( i2 v. S4 R1 z5 [6 P4 M- [
2 kg of weight. Physical examination remained% q9 p# X/ J: ~0 c+ @7 I7 M7 Z
unchanged. Surprisingly, the pubic hair almost com-
* ^! ~, [" h6 o1 I) I' Ppletely disappeared except for a few vellous hairs at
9 E6 A/ A9 f" e& b3 }0 X/ b, D( Kthe base of the phallus. Testicular volume was still 2
/ p. \+ t" P  M# v* |* i5 J3 q$ t' OmL, and the size of the penis remained unchanged.: ?/ T* M- u6 l' v8 R
The mother also said that the boy was no longer hav-
2 ?! N7 s1 n( h- L4 J( D; {: Ting frequent erections.
/ Y; }$ y4 A. y4 O( D% eBoth parents were again questioned about use of: V; f; l2 n; N/ _3 m
any ointment/creams that they may have applied to3 K/ o- `" `2 q$ A4 T
the child’s skin. This time the father admitted the- _' C. n  t+ ]1 L' d7 A
Topical Testosterone Exposure / Bhowmick et al 5413 t- G3 N& D" a) r' O: r
use of testosterone gel twice daily that he was apply-
, ?( a( z7 b. B' w. g  N3 Zing over his own shoulders, chest, and back area for
  t. S& O! `5 U! G& l+ I, Qa year. The father also revealed he was embarrassed
6 |& s% y6 @) ~) ~5 ~$ Nto disclose that he was using a testosterone gel pre-! c$ j1 U- Z/ t* h& g
scribed by his family physician for decreased libido
) F. W9 @1 z" V: [! I( p+ g  Nsecondary to depression.8 Q: C* S- a* T& J
The child slept in the same bed with parents.
' i+ `  x) |+ a9 j% ?8 p. NThe father would hug the baby and hold him on his
7 ?3 z" b% N$ [: kchest for a considerable period of time, causing sig-
7 D5 F1 \& W/ z8 r# rnificant bare skin contact between baby and father.
. W2 A6 c% p' ^, |. O1 W6 i/ r/ XThe father also admitted that after the phone call,
- X; A3 z8 D+ n4 g2 wwhen he learned the testosterone level in the baby6 e( U0 Y1 |: P9 \% g
was high, he then read the product information7 k, k6 c, x' g" }1 m& r: \
packet and concluded that it was most likely the rea-. g% \& [3 m+ K$ l4 p: G" ?
son for the child’s virilization. At that time, they
: i4 `/ x5 |; \8 X# pdecided to put the baby in a separate bed, and the: k. C* I& [- i) R
father was not hugging him with bare skin and had* x' X# G( ~4 @+ N* A
been using protective clothing. A repeat testosterone
# J1 t+ H; u9 z0 q4 h2 z, d% Ttest was ordered, but the family did not go to the8 U& W' {6 y8 ^, w
laboratory to obtain the test.- A' k. w% |- D2 p, o
Discussion
# a& j4 H/ p5 `8 ]# L* v& _( W8 yPrecocious puberty in boys is defined as secondary
# ]% Y% t8 [' ?# q% tsexual development before 9 years of age.1,4
, Z  Q8 a0 v! u& K  pPrecocious puberty is termed as central (true) when
% l; E; X* L: [. Rit is caused by the premature activation of hypo-# f% M0 N" m( ^( \
thalamic pituitary gonadal axis. CPP is more com-$ I" x6 O$ v3 t+ F
mon in girls than in boys.1,3 Most boys with CPP
% |8 K+ f5 _+ R) lmay have a central nervous system lesion that is  N, J7 D/ a3 u6 {/ o
responsible for the early activation of the hypothal-9 }! z  _0 x' [* b
amic pituitary gonadal axis.1-3 Thus, greater empha-
; G6 l+ p: e; h% Y1 z0 e; w0 L. Gsis has been given to neuroradiologic imaging in
0 ^" o( Q6 X- hboys with precocious puberty. In addition to viril-
( ~& D6 C6 [, F+ e; U" U; g1 Wization, the clinical hallmark of CPP is the symmet-* r" |# a3 n0 g3 e4 c
rical testicular growth secondary to stimulation by
" @! Y: H) j" f6 \/ x* n! Xgonadotropins.1,3# L. N8 b' L3 K' k
Gonadotropin-independent peripheral preco-
4 H2 p# \" D; bcious puberty in boys also results from inappropriate
7 G/ y' [% q. yandrogenic stimulation from either endogenous or6 Y1 V0 \+ `+ {& d
exogenous sources, nonpituitary gonadotropin stim-
0 B6 M% x- X  |1 f$ Q4 l) ^) {ulation, and rare activating mutations.3 Virilizing8 D5 c4 B, u4 w, j  c, C
congenital adrenal hyperplasia producing excessive
1 H4 S* E+ D! Sadrenal androgens is a common cause of precocious+ f# S# D- Z3 z7 A
puberty in boys.3,4- B' b4 o. Y2 E( k& J1 }
The most common form of congenital adrenal
* N; S  @0 i4 n) y1 N; ?. A. }' Qhyperplasia is the 21-hydroxylase enzyme deficiency.
1 f! ^% B" K! l1 _The 11-β hydroxylase deficiency may also result in9 F4 j+ y2 }3 R& z3 f2 j* K4 b
excessive adrenal androgen production, and rarely,1 c5 F$ \( L. ^4 K7 A$ y+ o/ f
an adrenal tumor may also cause adrenal androgen
, b# R1 Y1 x& B* y0 f2 zexcess.1,33 t8 ^6 o1 F" n* L; e
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
" m# ]2 u1 a7 r* v( T8 _542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
( ]; G$ C+ p4 C( C8 FA unique entity of male-limited gonadotropin-
0 N- _, m. e, W- J7 Xindependent precocious puberty, which is also known
# g: x7 E9 d; ^* L1 Ras testotoxicosis, may cause precocious puberty at a
: H& x% |5 \# }+ g& W, }' k0 z$ gvery young age. The physical findings in these boys
+ [( J5 ]5 G3 dwith this disorder are full pubertal development,. x( J% ^% N) E+ q! h
including bilateral testicular growth, similar to boys
: c# S/ i+ ~1 O( owith CPP. The gonadotropin levels in this disorder
* a' l1 L* Q/ {9 B0 V& f, f* aare suppressed to prepubertal levels and do not show
0 f$ b+ W) `# d: L+ R0 g1 ?3 [pubertal response of gonadotropin after gonadotropin-0 L* @9 `" t* a* i! G
releasing hormone stimulation. This is a sex-linked/ I5 E7 D! z/ V+ {
autosomal dominant disorder that affects only
" m' O: L9 V- R) fmales; therefore, other male members of the family# U: t2 S) ], _+ f# q
may have similar precocious puberty.3
% b+ M; {5 N8 m0 XIn our patient, physical examination was incon-
' i' T* w2 N0 Ksistent with true precocious puberty since his testi-4 Q* O, s; Z: E3 o
cles were prepubertal in size. However, testotoxicosis/ d9 r+ P" [" t8 f" `1 O
was in the differential diagnosis because his father
# }$ U/ M8 ]5 D, l* a; ustarted puberty somewhat early, and occasionally,* ]" s% ]/ O4 q
testicular enlargement is not that evident in the
7 M8 p% g/ _9 s" U1 {0 {, C4 f. kbeginning of this process.1 In the absence of a neg-
5 d5 y4 B) K3 b  ^4 @ative initial history of androgen exposure, our: s* G& ]9 a! G+ W" x
biggest concern was virilizing adrenal hyperplasia,- O  i9 X# _) b" |1 _$ D
either 21-hydroxylase deficiency or 11-β hydroxylase3 E) V  F  Y4 r8 B% h! E1 p
deficiency. Those diagnoses were excluded by find-
. Y. D& m6 D. ring the normal level of adrenal steroids.
: e, E1 i1 F6 o4 oThe diagnosis of exogenous androgens was strongly
% `3 T2 Y9 L3 dsuspected in a follow-up visit after 4 months because
5 V" Z, K1 d. M* d5 o8 g: gthe physical examination revealed the complete disap-
' J' V: l0 n& c1 B) v# [3 @pearance of pubic hair, normal growth velocity, and
4 d& Z# J7 k7 I( C' U5 adecreased erections. The father admitted using a testos-5 x; q( j! ~3 z
terone gel, which he concealed at first visit. He was
8 a& y, O, R! B4 _: ~6 Iusing it rather frequently, twice a day. The Physicians’0 L  L% h) D! _$ f* A7 K
Desk Reference, or package insert of this product, gel or9 `5 o5 x* Y5 n1 w
cream, cautions about dermal testosterone transfer to. f* ~* a; }. x, R. F
unprotected females through direct skin exposure.
0 w% k. \& y  BSerum testosterone level was found to be 2 times the9 O4 |, S# u/ t
baseline value in those females who were exposed to, j. [# |; }+ ^( |3 [
even 15 minutes of direct skin contact with their male
! L( `* _" u- C9 k  f" `7 Hpartners.6 However, when a shirt covered the applica-
1 B5 j4 k6 G) V! u* ~# Btion site, this testosterone transfer was prevented.5 }6 q1 m: {# |4 E
Our patient’s testosterone level was 60 ng/mL,. m! ?9 Z& u  _* n! S' n
which was clearly high. Some studies suggest that5 |; b0 s- ]. I  Q
dermal conversion of testosterone to dihydrotestos-
8 l( f3 w6 w: d* X; p9 U) t0 vterone, which is a more potent metabolite, is more( `$ O5 ]: c% l( e( s' v
active in young children exposed to testosterone
1 y4 ?; z( v& `4 Yexogenously7; however, we did not measure a dihy-4 D% S. F/ Y( c6 h8 q
drotestosterone level in our patient. In addition to3 z% I) S& M0 ?( m8 l+ s+ ?! f
virilization, exposure to exogenous testosterone in! v4 }5 v; s) I% I# G0 d
children results in an increase in growth velocity and& R/ m) p% Y; v$ v, u
advanced bone age, as seen in our patient.
& v' _; F9 Y6 W( K5 N" ~9 `) z" gThe long-term effect of androgen exposure during
' r4 K( d) @) F) ?early childhood on pubertal development and final
, C, C: E& Q3 s* J6 `9 D( Fadult height are not fully known and always remain8 }! `3 ~) Y( @) D
a concern. Children treated with short-term testos-
5 B$ t) A, w( K6 V4 a3 Wterone injection or topical androgen may exhibit some
7 u. T3 }9 l% m6 Facceleration of the skeletal maturation; however, after
! i/ a: c# I; b. `$ ]* Dcessation of treatment, the rate of bone maturation
2 H6 A! N( [  I; |$ Y# G) F) t5 d+ _decelerates and gradually returns to normal.8,9% J" o$ d' F0 |
There are conflicting reports and controversy
( ^- z7 X- d( [) ~5 q' S) cover the effect of early androgen exposure on adult
$ {+ E9 S2 [7 Y/ Epenile length.10,11 Some reports suggest subnormal
" G# H0 K) O! ~9 w$ Ladult penile length, apparently because of downreg-" G' S0 p5 m8 f( z& i1 R7 y3 c
ulation of androgen receptor number.10,12 However,# ^+ `  m8 b& I: ~. T
Sutherland et al13 did not find a correlation between$ H% n3 {; X6 ~: A8 [1 x
childhood testosterone exposure and reduced adult" e! Y$ I  O0 f3 n7 v
penile length in clinical studies.% T  v2 c) c3 y6 [$ @2 l* L2 o
Nonetheless, we do not believe our patient is* i1 V$ {$ D5 U* {
going to experience any of the untoward effects from4 p" R5 |  m. N) {  \$ X
testosterone exposure as mentioned earlier because
4 D; h1 C! s  c) ?8 C$ qthe exposure was not for a prolonged period of time.
8 f& w: N8 @+ ^3 V; ZAlthough the bone age was advanced at the time of4 i3 q9 O; `* {1 X7 Z. G  Q* F
diagnosis, the child had a normal growth velocity at' ]3 G% [+ K* J/ A8 E
the follow-up visit. It is hoped that his final adult
* w8 w3 z' T" n5 v3 ?height will not be affected.  q4 Z7 x2 X7 [, a+ g* b
Although rarely reported, the widespread avail-
$ r0 x/ z. C$ k# j, u  n9 }ability of androgen products in our society may
" W5 a# c- M' I, _+ s* R$ P9 o0 Dindeed cause more virilization in male or female
3 j  U, o1 ]# |' J# ^2 _" fchildren than one would realize. Exposure to andro-  ^7 Z* W5 F( z# E
gen products must be considered and specific ques-
2 }5 M+ [4 p5 z$ qtioning about the use of a testosterone product or. O8 w, P; F4 P0 Z. a3 `8 d3 B
gel should be asked of the family members during. E% c& r# P% m6 r" H
the evaluation of any children who present with vir-% F; o$ {: y- f9 v
ilization or peripheral precocious puberty. The diag-" \1 S: C& L; h3 \3 L, p- o
nosis can be established by just a few tests and by
" a3 N, c1 {$ Y6 @/ x" Kappropriate history. The inability to obtain such a, H! z- `# b& _; M
history, or failure to ask the specific questions, may
2 p# {: _3 G( O6 Q1 Z) X2 V$ Sresult in extensive, unnecessary, and expensive* Q2 e1 u% @7 e, [7 o" [
investigation. The primary care physician should be
# s+ R" X, j/ k. e. Y+ x3 baware of this fact, because most of these children) B, V8 G; I6 b6 h
may initially present in their practice. The Physicians’
, n5 \) n+ P' X! J( X0 D! l0 aDesk Reference and package insert should also put a! _5 L1 r* V% p* K7 o
warning about the virilizing effect on a male or) o1 H! H& x* N. A/ P( q
female child who might come in contact with some-
8 O9 I' Z% q7 D' Mone using any of these products.3 Z/ \' K! `8 Q6 b( ^
References' n0 q  Z1 Q' [/ v; y8 E+ u2 B* L
1. Styne DM. The testes: disorder of sexual differentiation, o2 Q/ ?( `0 D6 I
and puberty in the male. In: Sperling MA, ed. Pediatric
4 l, n# f" ^9 X4 e  D' BEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;6 a' V. y& t; [
2002: 565-628.( f4 H9 M: `& V2 i4 |
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
9 O% Q' _5 m7 }  E7 cpuberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old2 B& D1 j. C8 {, S: [7 ~$ N
Boy Induced by Indirect Topical% j# S: l5 {+ G, N0 [
Exposure to Testosterone
$ }. z! M$ j5 g* cSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2; s. H2 D3 U8 D
and Kenneth R. Rettig, MD1
3 n" L8 a( W/ _Clinical Pediatrics
% l7 I, `$ k" |! r' t" p1 g3 WVolume 46 Number 6
* @& R: u0 P  k) ?# }& n/ K( x" OJuly 2007 540-543" P7 f% }4 ?5 o: [/ `  ?
© 2007 Sage Publications
2 S% }& K6 P; Y- t3 c1 u0 |2 |! i10.1177/0009922806296651$ b% D0 a4 u! Y: O/ v6 L( o
http://clp.sagepub.com
5 t& A$ v3 `+ }3 O: h8 bhosted at
, R; _8 J/ [, G+ l; C/ t$ X, J2 Shttp://online.sagepub.com
4 e' E% j+ M) F: L! k$ aPrecocious puberty in boys, central or peripheral,5 @& O+ a0 e0 Q
is a significant concern for physicians. Central, N6 \' t5 K9 ], P2 ^' b! b1 C
precocious puberty (CPP), which is mediated
$ E5 K, k! \* B6 u% y, wthrough the hypothalamic pituitary gonadal axis, has
; S3 X' m, @  \a higher incidence of organic central nervous system( n7 c0 f9 O$ x' }+ z, N, h; @' W1 G( u
lesions in boys.1,2 Virilization in boys, as manifested) W6 `7 X) C  G4 X5 h2 W3 O
by enlargement of the penis, development of pubic
5 ]5 B' w0 {' N& w" b5 D( M5 X) khair, and facial acne without enlargement of testi-  i9 V8 A3 B" d# B/ [+ g
cles, suggests peripheral or pseudopuberty.1-3 We
9 W) O5 e3 O5 [  U- g' R" V6 u: q. q% ]report a 16-month-old boy who presented with the+ D7 S. ^8 R$ q- l4 N. U
enlargement of the phallus and pubic hair develop-
3 N( f! v0 S0 c; V6 z' T" F( rment without testicular enlargement, which was due
6 f4 ]7 o, r0 f9 G) O( bto the unintentional exposure to androgen gel used by) X: J8 v% K6 d; R
the father. The family initially concealed this infor-, f% S- z$ `) t5 p4 O/ f. l2 ?
mation, resulting in an extensive work-up for this
2 V- w# O+ q  w  uchild. Given the widespread and easy availability of
$ Z$ }) @; c4 o! w4 V# @testosterone gel and cream, we believe this is proba-
9 {& V5 `4 i$ o0 K" g/ g8 }" nbly more common than the rare case report in the
$ E/ P* W& i9 Wliterature.4
; p4 u: O1 q& T7 \Patient Report
' M8 ]* r; K& fA 16-month-old white child was referred to the+ s0 A  _) L7 d* j! `" ^, P
endocrine clinic by his pediatrician with the concern
: n+ F/ D& {1 Gof early sexual development. His mother noticed
3 J, ^& i5 _$ `0 Jlight colored pubic hair development when he was5 H  \+ d  t" m0 X) r
From the 1Division of Pediatric Endocrinology, 2University of
; o! L' }( _) ISouth Alabama Medical Center, Mobile, Alabama.
+ u2 e0 e; |% ]7 q0 O7 k3 CAddress correspondence to: Samar K. Bhowmick, MD, FACE,( y( E, f0 B1 A0 Z
Professor of Pediatrics, University of South Alabama, College of
1 B) @* ]" @/ o+ R$ b) E( {( EMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
) O# i3 b' S3 x: ue-mail: [email protected].% y9 ^# W1 f- b' z
about 6 to 7 months old, which progressively became
9 n( ~# x/ _: I3 O( adarker. She was also concerned about the enlarge-) x* q' p4 w# G' _" W
ment of his penis and frequent erections. The child
9 i  E: U4 ]& Iwas the product of a full-term normal delivery, with' b8 ^6 m$ P: \& k- h
a birth weight of 7 lb 14 oz, and birth length of) h% `* D, y" l+ q" I9 L
20 inches. He was breast-fed throughout the first year7 b% B0 i+ n+ k- F8 W+ V
of life and was still receiving breast milk along with- e3 S5 R+ T5 ?% B' p7 u
solid food. He had no hospitalizations or surgery,
; ?6 q) X( e: Z- ^" R& u# zand his psychosocial and psychomotor development
* {$ \6 S$ [" Z. S; jwas age appropriate.% Q; f; c, v/ R9 V
The family history was remarkable for the father,
1 y2 J, v( }$ ]2 n; K6 M& i2 Vwho was diagnosed with hypothyroidism at age 16,* J9 W4 L9 L$ `! l( n% t9 T
which was treated with thyroxine. The father’s
) E# n5 \9 ?; i* Jheight was 6 feet, and he went through a somewhat
. P7 w4 a: ]7 [- l6 L; I. h/ K# yearly puberty and had stopped growing by age 14.
) o; `4 a; N9 A: YThe father denied taking any other medication. The
5 c9 {. Q4 R' v0 ], u+ _: rchild’s mother was in good health. Her menarche9 V& t9 h5 W2 H4 I/ Q/ j0 [
was at 11 years of age, and her height was at 5 feet+ c1 d4 o: }/ N( X0 Y# R
5 inches. There was no other family history of pre-
9 w+ Y5 _6 k& U) @/ s  ?4 Hcocious sexual development in the first-degree rela-
5 B+ i1 {6 E1 P: u+ e' |tives. There were no siblings.2 ~0 o: h& l) {2 Q: }
Physical Examination6 g/ S) _/ v; z
The physical examination revealed a very active,; c1 D4 i) V( M
playful, and healthy boy. The vital signs documented& ]. K1 @' ~# \" t
a blood pressure of 85/50 mm Hg, his length was. p5 s: r! C' G4 _: X3 r. x
90 cm (>97th percentile), and his weight was 14.4 kg
  K) ?2 K" t$ c6 h  o- s1 }8 h(also >97th percentile). The observed yearly growth7 z1 _9 L% b; h9 J
velocity was 30 cm (12 inches). The examination of
3 T  S' W' d4 rthe neck revealed no thyroid enlargement.. }" {0 ^0 [0 v
The genitourinary examination was remarkable for+ Q6 ]) ~* w0 i7 A' M/ e
enlargement of the penis, with a stretched length of2 |- T3 U" ]: a& X( C8 x) w' ]
8 cm and a width of 2 cm. The glans penis was very well9 K' C! }% W; L+ T7 C1 Q3 \
developed. The pubic hair was Tanner II, mostly around
4 k; d; L  C  s1 j5 x# q5408 t8 \4 z8 @8 o- w% m1 Q1 i
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from/ r" K- K: ~3 }% C5 l1 `7 Q
the base of the phallus and was dark and curled. The
6 {$ J* p  ~# H3 T, ?testicular volume was prepubertal at 2 mL each.
0 t0 [4 ]. G- f* pThe skin was moist and smooth and somewhat, W- [$ X7 Y! G
oily. No axillary hair was noted. There were no  v! Y0 Y5 y$ Z! e
abnormal skin pigmentations or café-au-lait spots.
: M+ Z" X3 b# INeurologic evaluation showed deep tendon reflex 2+
* g+ t- r& U5 _0 G3 W* ~& g, \bilateral and symmetrical. There was no suggestion
) r: V+ P0 v) f( S3 Dof papilledema.7 W; \/ j6 Y7 N& l
Laboratory Evaluation
  l6 r- E4 o3 ]1 XThe bone age was consistent with 28 months by
7 h2 i8 ?6 m) l% F) C1 Z& A8 Xusing the standard of Greulich and Pyle at a chrono-6 U; p2 O3 p6 I3 B) F4 O1 K% V4 q
logic age of 16 months (advanced).5 Chromosomal5 l( [' E; H2 H2 K6 `
karyotype was 46XY. The thyroid function test# g: Y7 P9 e6 J: h) [6 l) N. V
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
& g% [  J% j! f* m- ?lating hormone level was 1.3 µIU/mL (both normal).# ]% r) |8 d6 ?0 ?; m4 @
The concentrations of serum electrolytes, blood
' ~5 Q: _4 ?# xurea nitrogen, creatinine, and calcium all were
1 G" m. r8 C+ ~! }0 Gwithin normal range for his age. The concentration
& W3 C+ S6 ~4 N% H  \& X3 Z* xof serum 17-hydroxyprogesterone was 16 ng/dL
/ `2 N! J  c! {$ B, w2 g' a(normal, 3 to 90 ng/dL), androstenedione was 20
* \" q% \0 `/ Y# K# Yng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
/ K3 h4 v3 k6 m4 ^0 Yterone was 38 ng/dL (normal, 50 to 760 ng/dL),6 k; k/ t1 |9 B) X# _# X2 e! k$ a- [
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
+ a& a2 u+ S6 D% u49ng/dL), 11-desoxycortisol (specific compound S)0 q. O, j7 i& w6 N+ N  x. {
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-+ \& v" O, w6 N' b5 a
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total# C; T3 ^) ?/ H2 r7 h7 c
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),5 ~- Q) I" K1 P2 x7 `2 w: q3 P
and β-human chorionic gonadotropin was less than
% s( F% r, Y6 O- ~8 s7 H5 mIU/mL (normal <5 mIU/mL). Serum follicular
) x4 L9 w) f9 |stimulating hormone and leuteinizing hormone( S. Z' p7 K8 f
concentrations were less than 0.05 mIU/mL0 {; z1 P  O, \) V
(prepubertal).
" t3 R0 O% \: z' @" n0 }, ^4 }The parents were notified about the laboratory" X) {/ ~8 B. H$ c1 z
results and were informed that all of the tests were( U. k9 K/ W! Y! r0 Q; s
normal except the testosterone level was high. The1 }6 ?, N5 z# F1 ?4 Y' \7 j
follow-up visit was arranged within a few weeks to; h- Y1 R# ~+ s2 D( D. n6 g; _9 h
obtain testicular and abdominal sonograms; how-7 w- l; x4 _2 s; T
ever, the family did not return for 4 months.! U, s- N/ q6 b% I7 c
Physical examination at this time revealed that the
8 d' ]. r! o0 V" K. Pchild had grown 2.5 cm in 4 months and had gained
5 A4 r& r/ ^& u! t2 kg of weight. Physical examination remained( `) `, P( H. _2 i
unchanged. Surprisingly, the pubic hair almost com-6 _2 O3 f5 i! I" m4 ^$ o
pletely disappeared except for a few vellous hairs at
; I  G  B1 \1 |4 Z; t1 C% k% Dthe base of the phallus. Testicular volume was still 2
2 a% n! w6 z; r/ z: q  mmL, and the size of the penis remained unchanged.' {* d. Z0 P" @
The mother also said that the boy was no longer hav-/ b3 S9 Y* r" N4 l! B3 l: t; {
ing frequent erections.0 J. z9 n1 R9 A4 c3 _& _3 P1 l7 O
Both parents were again questioned about use of6 z/ {2 X7 R6 Z& E
any ointment/creams that they may have applied to# h8 \. S( J1 G, q
the child’s skin. This time the father admitted the
0 \+ n6 ?- ~1 wTopical Testosterone Exposure / Bhowmick et al 541) i% x/ |6 }2 G, R% g
use of testosterone gel twice daily that he was apply-) i  D$ l  f2 p, @
ing over his own shoulders, chest, and back area for4 ^6 s, t2 E$ J
a year. The father also revealed he was embarrassed" w, G* T' e% d6 H) v, I3 t& ^
to disclose that he was using a testosterone gel pre-# @% l" h/ w! I1 n: K! e
scribed by his family physician for decreased libido% }$ o& j% k0 z5 ], D( a
secondary to depression.* b. `' H/ h1 c2 _4 n
The child slept in the same bed with parents.
3 @+ ~! |9 G1 w& U! W3 |" o1 l/ ^The father would hug the baby and hold him on his
2 a+ V' q* Q3 n# L, y. ^+ achest for a considerable period of time, causing sig-
. a! e7 [1 _- W. f' W$ ^# enificant bare skin contact between baby and father.7 j; u% `. F, z  q! E# c$ u) O% x
The father also admitted that after the phone call,
0 G2 g4 d$ p( z+ e8 W" r) J) }when he learned the testosterone level in the baby
% N3 X: g: g  c6 |: I7 D8 f0 Vwas high, he then read the product information* U/ m# L0 x3 ~9 l
packet and concluded that it was most likely the rea-2 u/ V4 ^4 i/ Q, B& r
son for the child’s virilization. At that time, they
( o  `- N. H) Odecided to put the baby in a separate bed, and the
. g* f6 y- E4 Ifather was not hugging him with bare skin and had" n6 F6 |  j* y1 d8 X
been using protective clothing. A repeat testosterone! x$ I- {# o" X- }0 D
test was ordered, but the family did not go to the
  ?) N1 T; y) @' J6 f) Alaboratory to obtain the test.
. b0 f) R; r5 {  @Discussion
7 u$ d9 u0 x8 _7 p2 JPrecocious puberty in boys is defined as secondary' Z3 L& L# k' F2 e7 b
sexual development before 9 years of age.1,4
: G# n/ F7 g2 s7 oPrecocious puberty is termed as central (true) when# l1 ]& h! C- \
it is caused by the premature activation of hypo-
! P/ F* N" P- t3 I: vthalamic pituitary gonadal axis. CPP is more com-
) T2 i* V8 U+ \5 o3 _mon in girls than in boys.1,3 Most boys with CPP/ ~* ]5 T0 l, n1 p( r
may have a central nervous system lesion that is
6 Q* E) v& Q3 U) G$ Y  [" Y. _responsible for the early activation of the hypothal-1 G- K+ [, \. y5 }3 j$ U
amic pituitary gonadal axis.1-3 Thus, greater empha-
  v: O* f5 a, }; R" _. ]: u3 ^sis has been given to neuroradiologic imaging in. a6 x7 h4 y  G1 d
boys with precocious puberty. In addition to viril-8 A5 u/ v  _1 H# v4 h: d7 A
ization, the clinical hallmark of CPP is the symmet-
4 s2 z* I9 \9 q  Krical testicular growth secondary to stimulation by+ I( K# J/ [4 M
gonadotropins.1,3
1 f/ `+ o6 E' j1 |7 k: TGonadotropin-independent peripheral preco-
. |7 g  J. z, a2 \2 ^+ N5 hcious puberty in boys also results from inappropriate
  K, u1 B# M+ h" z3 |1 _androgenic stimulation from either endogenous or7 l7 p# t9 e& u: Y6 N; E# [9 |
exogenous sources, nonpituitary gonadotropin stim-
' m7 B! m& ]! W& a7 mulation, and rare activating mutations.3 Virilizing
" u2 E  ]+ K) |' N4 E$ Q( c' Scongenital adrenal hyperplasia producing excessive4 \7 F7 s! _5 ]; h* w
adrenal androgens is a common cause of precocious
( |! M. h. X% Opuberty in boys.3,4# L0 t6 ~0 W/ k# j9 t
The most common form of congenital adrenal
  D; U( y7 ^) w& x; V$ ^/ Y5 mhyperplasia is the 21-hydroxylase enzyme deficiency.$ b" X/ g& P' S. z+ _
The 11-β hydroxylase deficiency may also result in5 a3 M  X" J. F* x! Y
excessive adrenal androgen production, and rarely,. z; n6 o3 [) R
an adrenal tumor may also cause adrenal androgen2 {. c0 c' c, }+ {" U" v" o
excess.1,3; `+ d! n0 s" ]
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
+ c: X9 C0 u: k7 @: s542 Clinical Pediatrics / Vol. 46, No. 6, July 2007/ r1 [& Q% u+ a5 c) f' y
A unique entity of male-limited gonadotropin-  p: K- ^; g) J! c1 K$ f) Y3 Y* j
independent precocious puberty, which is also known
% h% _- D! R( Z) ~# Yas testotoxicosis, may cause precocious puberty at a
  M' W4 q/ e" v' k- g0 ~very young age. The physical findings in these boys  O5 L4 \* s$ d, f0 X
with this disorder are full pubertal development,
0 k9 |9 m( G$ \* v4 U" w  E- zincluding bilateral testicular growth, similar to boys
. }3 y+ `. ^% K1 O  Iwith CPP. The gonadotropin levels in this disorder8 h3 ^" p, M& G) s
are suppressed to prepubertal levels and do not show
; Q1 U0 ]7 A$ d3 Y' d8 `pubertal response of gonadotropin after gonadotropin-: a7 {7 f; [$ g; C: \# C
releasing hormone stimulation. This is a sex-linked# m0 y1 c# O# f; e& l2 x' G  Q
autosomal dominant disorder that affects only
% J  h  ?( u, E; Pmales; therefore, other male members of the family8 \9 \" u  B4 O' {# b
may have similar precocious puberty.3
1 W6 x% J. p( b$ S" ?In our patient, physical examination was incon-
% m+ \+ _0 r8 @( w( \sistent with true precocious puberty since his testi-
& s* O2 p( }1 ucles were prepubertal in size. However, testotoxicosis0 G) Q- q! a. C9 L1 E3 C3 ]+ `
was in the differential diagnosis because his father; v( O% U5 U6 w! F* ]- a
started puberty somewhat early, and occasionally,/ ~) n% M( w# x6 |( n
testicular enlargement is not that evident in the1 Y( _1 Y3 S, ?
beginning of this process.1 In the absence of a neg-' k% _3 e8 @* h
ative initial history of androgen exposure, our) `" P* e4 j% \
biggest concern was virilizing adrenal hyperplasia,
3 H' d3 D1 i& ^6 w! _: F" r7 i( ^2 Qeither 21-hydroxylase deficiency or 11-β hydroxylase% c4 h7 a' H+ w3 Q
deficiency. Those diagnoses were excluded by find-
. |2 p2 S! u5 S( x& S) c& @ing the normal level of adrenal steroids.
, F* n- {2 W: m9 q* L7 W! QThe diagnosis of exogenous androgens was strongly
" Y) E" c. L' E6 F" M  xsuspected in a follow-up visit after 4 months because- E  Y* v4 |; C2 ~6 D
the physical examination revealed the complete disap-' j4 F+ l7 ^) S3 m5 |+ v! C) V
pearance of pubic hair, normal growth velocity, and
* c* x% v( _8 o( ^# bdecreased erections. The father admitted using a testos-. s# `& j! B) p# n) c0 O7 K
terone gel, which he concealed at first visit. He was; E0 {/ I+ T) Y- |# @1 a7 T  l$ M. c
using it rather frequently, twice a day. The Physicians’3 q( W7 e; j$ ^" G5 B
Desk Reference, or package insert of this product, gel or0 M1 k* S' D- V' ]$ o/ i2 G
cream, cautions about dermal testosterone transfer to! R. k7 R7 A2 A8 w* r
unprotected females through direct skin exposure.
+ |) F# G$ p& e  fSerum testosterone level was found to be 2 times the6 ~, ~* M$ L  z. d
baseline value in those females who were exposed to
0 a- t  J+ q3 w; m" m- Jeven 15 minutes of direct skin contact with their male
' j% N9 @" [- ~) v3 Hpartners.6 However, when a shirt covered the applica-; N$ c& h, {4 D/ R
tion site, this testosterone transfer was prevented.. k- ~, j( s* Z
Our patient’s testosterone level was 60 ng/mL,
4 X/ g# k4 z6 ^which was clearly high. Some studies suggest that# Q# h# G! X- M2 u' @$ M
dermal conversion of testosterone to dihydrotestos-2 P! \; n- ~. m% `8 M) C$ e
terone, which is a more potent metabolite, is more
% `0 ?: |9 M/ C8 C) K/ {active in young children exposed to testosterone9 Y7 n5 S! A- d6 y/ W6 Q  l
exogenously7; however, we did not measure a dihy-, J; ~8 ], ]+ V. w" E' l+ x+ S7 h
drotestosterone level in our patient. In addition to" C* v$ |. v  `. f
virilization, exposure to exogenous testosterone in
; G8 O7 p2 O' M! P( |children results in an increase in growth velocity and
8 m" w0 \. M9 `- H0 Hadvanced bone age, as seen in our patient.
, v& s3 F( U4 O* \" aThe long-term effect of androgen exposure during+ m; C; x- O1 x3 r1 c- i
early childhood on pubertal development and final. e0 l) K- [1 l# _/ X
adult height are not fully known and always remain
) A: r# B& o/ o, Ka concern. Children treated with short-term testos-
' ~. j$ {3 Y' Mterone injection or topical androgen may exhibit some
. q, b+ r6 c/ k- X! z9 ]" m! Racceleration of the skeletal maturation; however, after4 {1 S& f) \6 i( D
cessation of treatment, the rate of bone maturation
" p! h6 h9 n! ]* r. J. b  p4 ^decelerates and gradually returns to normal.8,9
+ W$ n3 @$ h, Z; H0 R0 f9 O* L3 P! z, tThere are conflicting reports and controversy5 @: `* L) r: b( z" x0 \( c# Z
over the effect of early androgen exposure on adult; h* H# j$ t& i- Q, W) o
penile length.10,11 Some reports suggest subnormal& t" t, {: X$ g1 [
adult penile length, apparently because of downreg-
$ |) m2 F& f/ l7 r5 u1 ?+ R0 i$ z6 bulation of androgen receptor number.10,12 However,
/ r( y# g8 ]* }$ w' x, x* |8 CSutherland et al13 did not find a correlation between
$ J5 }- @4 g8 o% y6 {childhood testosterone exposure and reduced adult+ z8 [! u4 ?3 a% D" ^- E
penile length in clinical studies.
" g) n9 h; _$ k, l5 P  u' UNonetheless, we do not believe our patient is  }* k8 j( f- ?" K' K8 _. E; N
going to experience any of the untoward effects from
7 w+ \% \) L- d, Rtestosterone exposure as mentioned earlier because
+ Y7 r# y; Q( T1 o9 Z; P; s" s  [the exposure was not for a prolonged period of time.# r" D; o. q. p/ o- S# I5 C# w
Although the bone age was advanced at the time of% @5 Z  s+ b  r% i' |) I' Y& G  }5 T
diagnosis, the child had a normal growth velocity at
! F) q' A/ T* W2 ~/ J9 V, Kthe follow-up visit. It is hoped that his final adult
' ]0 j$ D+ Y8 g3 ~6 O1 R$ Mheight will not be affected.
  Q8 `+ \; h" J4 x: R2 DAlthough rarely reported, the widespread avail-
: B0 p* q+ N% g8 r& E. Qability of androgen products in our society may
) d/ M' U) a1 `# X& x5 L6 ?indeed cause more virilization in male or female+ m8 E4 d% B( p' v# S
children than one would realize. Exposure to andro-
, A5 x9 p3 Y0 G, qgen products must be considered and specific ques-
6 R7 S) I0 ^! R9 Y. z& n/ _( xtioning about the use of a testosterone product or
- E  V+ \; {4 F- T  ygel should be asked of the family members during  Y9 G/ _2 V$ Z5 k9 C
the evaluation of any children who present with vir-8 M8 L: V2 j# ^( X9 L
ilization or peripheral precocious puberty. The diag-
7 t# q. I- ~2 Inosis can be established by just a few tests and by
1 i2 i8 ]1 N" x, y& f; q7 ]: {appropriate history. The inability to obtain such a
/ g$ F" ~# W8 V3 G: V- h5 I8 \history, or failure to ask the specific questions, may( E5 f1 g$ g; [  Z
result in extensive, unnecessary, and expensive
% B( G( k+ ^) j. ]+ w; |investigation. The primary care physician should be4 d4 \! V9 a9 u/ o" H. x
aware of this fact, because most of these children
- T) S3 O8 A. l7 |may initially present in their practice. The Physicians’* S9 H, O2 T- s$ _. v" o6 U
Desk Reference and package insert should also put a) |. c3 ^5 e; i5 K) g8 a, u) }1 J4 g
warning about the virilizing effect on a male or$ Z- h" I1 i1 ?( [
female child who might come in contact with some-# H) s; w7 P9 V2 `$ R, v, r
one using any of these products.
. b. B7 H- F1 n" l* VReferences: d; \8 n4 {7 {* x9 d7 ~
1. Styne DM. The testes: disorder of sexual differentiation
, V) I/ D8 P5 j# t6 ]( r" \, Band puberty in the male. In: Sperling MA, ed. Pediatric
* w* w! s7 Q2 B' p% [$ @Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
6 H) |* S# T$ M/ w0 k2002: 565-628.1 Y5 O" y  o' x( t' b3 l
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious" C7 ^: `$ \  D% i7 V7 G; y* \
puberty in children with tumours of the suprasellar pineal
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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

9 u/ i3 W9 ?3 ^. l  G- \精妙絕倫的精品,感謝啊!期待你更多更好的創作哦!
發表於 2025-3-8 22:04:50 | 顯示全部樓層
絕對的好貼!謝謝啊!逐字逐圖地看完這個帖子以後,我的心久久不能平靜,感恩啊!
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