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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. L" J' A1 F3 z+ Z
Boy Induced by Indirect Topical
+ m* A" q3 V2 @8 z! ?- JExposure to Testosterone, B' E( V9 e& G  Q' ~5 O) ?- R
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
# b9 f" {1 o  ]" p, k( S$ wand Kenneth R. Rettig, MD1
5 U1 W& v- }9 ]6 ^" y4 D; q0 t! fClinical Pediatrics
$ K0 z. W6 g1 z& `3 t+ VVolume 46 Number 6' S6 h2 V9 P/ L& _
July 2007 540-543
- w" d2 m; M% |: \© 2007 Sage Publications* ~2 v/ L6 p, U) t
10.1177/00099228062966519 X' [1 a1 ^$ y& r
http://clp.sagepub.com
7 H4 W& Y" g. R0 e: phosted at
$ T7 e9 O% |- |3 m! K4 G! uhttp://online.sagepub.com
% j( b9 P+ S) W0 A( TPrecocious puberty in boys, central or peripheral,
$ B5 t8 A" n( e( `( bis a significant concern for physicians. Central
$ \: q' x9 J* L- h" u& l5 ?, Mprecocious puberty (CPP), which is mediated
2 k, F' |% @9 E. }( A0 X$ I9 Dthrough the hypothalamic pituitary gonadal axis, has5 u; t8 C+ B" p
a higher incidence of organic central nervous system
' ]( d6 f2 \' Y+ _3 h0 {lesions in boys.1,2 Virilization in boys, as manifested
1 H1 V- c5 e: l  Y) ^7 s% s- [0 C9 }by enlargement of the penis, development of pubic
4 N+ D2 r  n1 i$ q' L$ Jhair, and facial acne without enlargement of testi-
% p% P6 G4 ]' t7 `. j' k7 lcles, suggests peripheral or pseudopuberty.1-3 We
% d/ ?3 v7 ^3 k$ }/ _report a 16-month-old boy who presented with the4 L, U6 D3 F( V; U. g
enlargement of the phallus and pubic hair develop-, S. i" T/ ]* r; y3 L
ment without testicular enlargement, which was due
, R; {) P/ \$ i6 ]% ~to the unintentional exposure to androgen gel used by
7 K) y) a$ l+ W6 c" Othe father. The family initially concealed this infor-) J. s2 ?* d6 Z% u( F
mation, resulting in an extensive work-up for this) j& B) P/ C7 X+ t- S
child. Given the widespread and easy availability of; w9 X/ f5 F3 s+ |! ~! j1 J
testosterone gel and cream, we believe this is proba-
% P0 n% a- p0 obly more common than the rare case report in the: _8 O* |5 t  Q7 d
literature.42 `( S% y4 L- u% U$ I1 c
Patient Report( m- _$ q  e; S+ [0 y9 V& h& G; ^
A 16-month-old white child was referred to the2 V+ r9 G4 c* p9 t6 Z% T
endocrine clinic by his pediatrician with the concern- }! e7 \. e2 ?- h  K! {
of early sexual development. His mother noticed1 F* q6 [( H* x; x* o$ f3 |
light colored pubic hair development when he was. o/ ?7 n1 |% \' _
From the 1Division of Pediatric Endocrinology, 2University of& _  r* u+ V/ }0 S
South Alabama Medical Center, Mobile, Alabama.
" m$ E( [9 C, NAddress correspondence to: Samar K. Bhowmick, MD, FACE,1 @2 ]/ i( n# }7 s  m
Professor of Pediatrics, University of South Alabama, College of% E3 j. g" t8 M4 e0 e
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
+ C9 ?" t, Z8 I5 f: r$ l  ve-mail: [email protected].
% F3 T5 |, |8 D! l  h/ sabout 6 to 7 months old, which progressively became  M* u- p$ `- p9 p2 T8 a1 h+ z
darker. She was also concerned about the enlarge-4 q* `6 s7 i. b6 F, h
ment of his penis and frequent erections. The child+ S: y, E; n+ c* z
was the product of a full-term normal delivery, with
) i/ _! U7 n' Ga birth weight of 7 lb 14 oz, and birth length of
; s- Y5 B' k* N5 ~- O" e: n20 inches. He was breast-fed throughout the first year9 d* k1 l. v5 d7 O; n
of life and was still receiving breast milk along with( V9 \( q( X8 I( @3 _+ t
solid food. He had no hospitalizations or surgery,
4 l$ _$ [2 A5 E) P; m6 a# kand his psychosocial and psychomotor development
/ `  q  K- {, C1 o" n' Wwas age appropriate.
" _0 P: C# _8 [9 x0 w, UThe family history was remarkable for the father,, Y0 Y6 K. H" L! k  g, b* p; ?/ w
who was diagnosed with hypothyroidism at age 16,5 V6 ?$ m- c. g$ Q: w. \
which was treated with thyroxine. The father’s
& t5 }" I* T; P3 R- z9 Qheight was 6 feet, and he went through a somewhat
) q% n: w& }0 _1 P$ d4 dearly puberty and had stopped growing by age 14.
9 v0 h5 B' d5 W* u, I5 |" _The father denied taking any other medication. The( C  Y) _6 Z- x" Y0 L
child’s mother was in good health. Her menarche: s9 ^% C/ P) K8 d8 i
was at 11 years of age, and her height was at 5 feet
+ w) S# q5 f5 M' O; ~. p5 inches. There was no other family history of pre-; `' B( _6 ?% D2 m, }5 v2 c
cocious sexual development in the first-degree rela-9 F* J% y+ L* T  Z3 h% ?2 N1 b3 v2 Q- F
tives. There were no siblings.
% `0 m; O! q  _8 cPhysical Examination
6 L4 e1 r; J! {8 ]" g) X1 YThe physical examination revealed a very active,
; [3 g/ Z- O! d& F2 z) z& Z9 Mplayful, and healthy boy. The vital signs documented% }% c. a( o5 V' A7 a
a blood pressure of 85/50 mm Hg, his length was0 ~1 E7 T  d! k9 ]! N9 W
90 cm (>97th percentile), and his weight was 14.4 kg
  x& j. X# `  n. k0 r/ s(also >97th percentile). The observed yearly growth, i! `2 l6 }, |
velocity was 30 cm (12 inches). The examination of
  h! [9 J/ `, h, z2 a5 p1 i0 othe neck revealed no thyroid enlargement.+ l3 k& b! R: y/ Y: i+ ^
The genitourinary examination was remarkable for$ A1 v+ O2 {) D/ B& `
enlargement of the penis, with a stretched length of
2 H9 E% o# K5 h1 v! i8 }8 cm and a width of 2 cm. The glans penis was very well8 ~# [6 T1 S, V3 R- s) U2 ?
developed. The pubic hair was Tanner II, mostly around
- L/ G1 X& q  K- K/ D540/ h3 o- u8 z$ b" `& j% }) d$ v
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
: H: S: R; M( B& kthe base of the phallus and was dark and curled. The$ C4 u' R6 w/ b
testicular volume was prepubertal at 2 mL each.
& S$ w1 o* g9 n- Z' T# CThe skin was moist and smooth and somewhat
+ Q* E" t) u% x+ l  z( O& Moily. No axillary hair was noted. There were no
. ]! x+ X, k! }; ]/ }abnormal skin pigmentations or café-au-lait spots.0 ^# b+ M& h; h) Y0 G" y/ U
Neurologic evaluation showed deep tendon reflex 2+
7 C4 t$ s$ B/ |bilateral and symmetrical. There was no suggestion4 x5 c- c5 p( d! f/ |2 r7 P
of papilledema.
3 S+ s! h% e# b# BLaboratory Evaluation& g0 }$ p# Z8 R' ?
The bone age was consistent with 28 months by  ?8 l3 g4 h0 K- e
using the standard of Greulich and Pyle at a chrono-
. @; ^7 K+ ]& S, }" v8 N4 zlogic age of 16 months (advanced).5 Chromosomal2 ]5 O3 [9 Y- f# ~6 w* z! y
karyotype was 46XY. The thyroid function test( A' Y5 c3 }( ~( g4 F9 ]" ^' V
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
: ^- P; N2 `" o+ e* o% K% plating hormone level was 1.3 µIU/mL (both normal).
& K- |+ q3 t: ?; H6 F2 |7 R9 e, K5 vThe concentrations of serum electrolytes, blood
! f9 b' S: Y0 N" L2 @! r% curea nitrogen, creatinine, and calcium all were
2 m0 M1 y) t  q/ m! y: m2 zwithin normal range for his age. The concentration; b; y/ u% ]8 K& K  Q5 e4 E+ M0 h
of serum 17-hydroxyprogesterone was 16 ng/dL, I4 g" ^* L' r' |" J# E. U/ P2 ?
(normal, 3 to 90 ng/dL), androstenedione was 209 N; }2 V% T$ N4 L& E
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
4 O8 K; `3 V: ^5 [3 Dterone was 38 ng/dL (normal, 50 to 760 ng/dL),
) c  W" J( K5 M( {; rdesoxycorticosterone was 4.3 ng/dL (normal, 7 to
5 d) }' \; P6 X  U* B/ w49ng/dL), 11-desoxycortisol (specific compound S)
/ `# F" z/ V7 ~4 i9 b% C% `was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-& ~+ j. \" g0 U5 P3 |% `. e/ \
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total2 G: H* ^( M+ X) Q" U
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),! ^2 P8 }9 U. M, {
and β-human chorionic gonadotropin was less than/ f9 {& t7 w" d# {4 I
5 mIU/mL (normal <5 mIU/mL). Serum follicular
6 e7 ?, X& O$ ^* X& l) x6 Dstimulating hormone and leuteinizing hormone' z2 r- q  C  {' q8 y1 S3 J8 j
concentrations were less than 0.05 mIU/mL! t( t1 X, @5 |# Z8 \& r
(prepubertal).
0 m/ K( U( |& h( n. k7 i* H4 ?The parents were notified about the laboratory# Q# p8 _' p3 g5 W7 s
results and were informed that all of the tests were
5 s; S+ r5 c) V+ }normal except the testosterone level was high. The
6 W8 h/ M3 z" X3 _, \' Sfollow-up visit was arranged within a few weeks to) a+ l4 q7 w# |4 x4 q# m
obtain testicular and abdominal sonograms; how-
: ?! P# I2 b2 Z# Y' Z' tever, the family did not return for 4 months.
& P9 {! K! K2 f0 X; w5 @: J; VPhysical examination at this time revealed that the0 w. Z2 h: e* r: A3 {
child had grown 2.5 cm in 4 months and had gained
# r& m/ R, x4 i" S* J2 kg of weight. Physical examination remained
3 ^! m/ R* e- F2 Sunchanged. Surprisingly, the pubic hair almost com-
+ w0 u3 R# k3 @3 q4 c7 jpletely disappeared except for a few vellous hairs at* C4 b+ s. d) g1 v/ c
the base of the phallus. Testicular volume was still 2
5 I( r' i7 d) |) e! cmL, and the size of the penis remained unchanged.' r3 d4 Z; W; e" t! R. y6 @3 e1 T9 J
The mother also said that the boy was no longer hav-8 l- @; D, ]) H- H
ing frequent erections.( I* i3 ~& T$ K& N, {  S3 s4 C, M
Both parents were again questioned about use of
, {) z4 J8 |; Y5 D  `any ointment/creams that they may have applied to8 \4 M3 f; `  [2 `0 {3 r
the child’s skin. This time the father admitted the- e- _9 [6 _$ Y; k& E9 n) Q
Topical Testosterone Exposure / Bhowmick et al 541
. i, e$ a: d5 juse of testosterone gel twice daily that he was apply-
+ S) p! S7 w2 g5 ?7 @ing over his own shoulders, chest, and back area for8 \5 w5 w$ Y* v  R8 z: P5 i+ H7 K) d
a year. The father also revealed he was embarrassed
4 O/ N% [% W9 f* o) i4 Z. F3 z. {to disclose that he was using a testosterone gel pre-1 j' e9 y" C: }% V& b
scribed by his family physician for decreased libido7 x' j( ~4 R! Y. }! h. |
secondary to depression./ J8 ~% U( k/ L+ Q) a
The child slept in the same bed with parents.- q2 m6 {+ V5 q" o2 R4 s/ `7 ]
The father would hug the baby and hold him on his
$ K' X- B% G! E" I' [% N; Lchest for a considerable period of time, causing sig-
' P# |- |1 Y, e* Q6 Jnificant bare skin contact between baby and father.) Y; ^0 _# r# @, ^' ~2 X
The father also admitted that after the phone call,
- t0 C9 l* y6 Awhen he learned the testosterone level in the baby
6 _  O/ w% k% F- m5 R  Q, hwas high, he then read the product information
9 a/ G+ D  C" N- Q+ bpacket and concluded that it was most likely the rea-1 {. C% c  ?6 |3 s
son for the child’s virilization. At that time, they
& k9 P, _3 y- S$ P% Z  `decided to put the baby in a separate bed, and the
7 J. H5 k1 D* _7 ]father was not hugging him with bare skin and had; C; V, i; E. h, }
been using protective clothing. A repeat testosterone
4 Y5 i, {7 |* c" y+ K. \  ?test was ordered, but the family did not go to the
1 j( I3 u+ n9 f9 v6 j+ Vlaboratory to obtain the test.
5 {% K/ C2 m" f6 |# r% |" CDiscussion) R! a5 e/ }/ A' w
Precocious puberty in boys is defined as secondary
4 w" q' ?' {" C( psexual development before 9 years of age.1,4
) M; C* ]# T: R+ c8 o, P; YPrecocious puberty is termed as central (true) when
/ q6 V/ F; V4 C* C, ?9 h" X: xit is caused by the premature activation of hypo-
) x5 ~1 U5 |+ m$ F" I: W4 {thalamic pituitary gonadal axis. CPP is more com-
$ T: A- z; Z' b- Q' ?mon in girls than in boys.1,3 Most boys with CPP
  [" L2 H+ f5 o4 B& ymay have a central nervous system lesion that is9 s5 Q5 D9 W+ g) v1 ~
responsible for the early activation of the hypothal-9 R4 ?4 I! V9 ~- b3 C
amic pituitary gonadal axis.1-3 Thus, greater empha-$ d8 ^* L4 {, @# P" N  X% u$ O1 G
sis has been given to neuroradiologic imaging in: A# M0 Z  a! K
boys with precocious puberty. In addition to viril-$ {) Z. V% M2 z+ t
ization, the clinical hallmark of CPP is the symmet-* u0 T6 C8 o  q+ c+ W
rical testicular growth secondary to stimulation by
1 q$ S+ F, n3 c5 {" T, pgonadotropins.1,3
: l' v' R3 d& C  }# S+ LGonadotropin-independent peripheral preco-
- f1 g' }. O5 a5 f  }1 x; Acious puberty in boys also results from inappropriate
8 k. u( S5 ^$ G. Yandrogenic stimulation from either endogenous or
' `+ T' A9 N; h( h6 Kexogenous sources, nonpituitary gonadotropin stim-2 ?  d  t& {" ~
ulation, and rare activating mutations.3 Virilizing2 e/ U0 W2 k+ H0 u5 o9 S% t; m
congenital adrenal hyperplasia producing excessive
6 M0 |' f1 V7 q. U  I9 Dadrenal androgens is a common cause of precocious" ^" h/ m8 L2 E; Q/ M5 ^
puberty in boys.3,4
2 O, X6 w6 o, k0 U. u& v7 |The most common form of congenital adrenal
' @2 e/ z# D. c  e0 S1 F: G5 Z4 }hyperplasia is the 21-hydroxylase enzyme deficiency.0 |0 {: c% N/ m( E
The 11-β hydroxylase deficiency may also result in
; X& v" e7 S9 q: x# Zexcessive adrenal androgen production, and rarely,
" t- I! J2 C' W0 E1 Gan adrenal tumor may also cause adrenal androgen
2 }/ w7 z. P9 |1 fexcess.1,3+ B4 C5 g0 n: F1 ~! W# ]; A
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from4 i3 w$ b( @- |' v+ J2 k7 P8 B
542 Clinical Pediatrics / Vol. 46, No. 6, July 20075 l0 M8 ]) i: V* V4 u1 W6 U) ]
A unique entity of male-limited gonadotropin-. }, H$ _' @) C: N
independent precocious puberty, which is also known
& n, @  A5 m5 Eas testotoxicosis, may cause precocious puberty at a
/ k. [( ]! `4 Mvery young age. The physical findings in these boys6 S5 k3 o& L2 d6 g
with this disorder are full pubertal development,
' v7 j/ S+ \3 Zincluding bilateral testicular growth, similar to boys# Y$ X: n( {- x: }, Y8 d# E
with CPP. The gonadotropin levels in this disorder
! X5 T2 _; G  ]8 U' Eare suppressed to prepubertal levels and do not show
, R) W4 f! }* u, B7 u" gpubertal response of gonadotropin after gonadotropin-
& i- l( Y8 V* [) treleasing hormone stimulation. This is a sex-linked1 H7 u% B; Z. ^3 w9 I" o
autosomal dominant disorder that affects only& W2 b+ a# M4 d/ B* p4 E9 q
males; therefore, other male members of the family2 s9 |* d( \! }( S1 K
may have similar precocious puberty.3
" b/ e# k9 k, aIn our patient, physical examination was incon-
/ `( f( u% [3 ~' f+ Bsistent with true precocious puberty since his testi-9 O( g. W: C" Z
cles were prepubertal in size. However, testotoxicosis& d) T1 @1 w( x- J! D& y
was in the differential diagnosis because his father
2 a2 z6 l0 F6 Y: G* Q' xstarted puberty somewhat early, and occasionally," @4 d; r6 S. a
testicular enlargement is not that evident in the( \$ c  V) E: P
beginning of this process.1 In the absence of a neg-% }' l# S7 J' p3 L  ~+ Z
ative initial history of androgen exposure, our8 k. Q1 I" ]4 n- I
biggest concern was virilizing adrenal hyperplasia,: S& ]7 z- E, }' {- F% |
either 21-hydroxylase deficiency or 11-β hydroxylase& t2 r2 Q9 N9 w( s3 U7 p& k* G
deficiency. Those diagnoses were excluded by find-
" @9 K3 E6 Z: [2 n% o8 [ing the normal level of adrenal steroids.4 S) \2 ~) F6 D  O1 v0 b, r: B
The diagnosis of exogenous androgens was strongly5 k9 ?$ }9 x- l7 \. \: E8 \
suspected in a follow-up visit after 4 months because
. i. a  u, ?+ z1 m0 W7 K8 fthe physical examination revealed the complete disap-
2 C5 [- m7 E! [; l& npearance of pubic hair, normal growth velocity, and
) @8 C1 ?0 @6 x) i3 [decreased erections. The father admitted using a testos-
, D# w" J+ K# S1 S) j. w% iterone gel, which he concealed at first visit. He was, K% y6 A: }( R+ k+ f2 r( W) E
using it rather frequently, twice a day. The Physicians’
, g! ]% m2 _( |5 ]Desk Reference, or package insert of this product, gel or
! [$ D  o- p) X7 Q5 Gcream, cautions about dermal testosterone transfer to
9 |: u2 v% X& M' F( R2 G- g4 Punprotected females through direct skin exposure.
! {" h& k- b* B' t6 D# @0 NSerum testosterone level was found to be 2 times the0 ~$ d( S7 {0 G. i  w+ V  j
baseline value in those females who were exposed to7 B, ?6 f) r% ~" U  n5 W6 r/ B
even 15 minutes of direct skin contact with their male1 C0 ^* r+ W2 o7 U/ P
partners.6 However, when a shirt covered the applica-
9 K. U2 n2 P( S* E. t( P- O1 j! R. `tion site, this testosterone transfer was prevented./ C8 p' [: A5 w; ~. U( g6 F
Our patient’s testosterone level was 60 ng/mL,8 D$ f1 q7 e: H. ]6 K, [
which was clearly high. Some studies suggest that6 i7 a' [+ y: y9 f8 K3 X% a9 f
dermal conversion of testosterone to dihydrotestos-- \+ P! s2 [# x, h
terone, which is a more potent metabolite, is more
0 C  J2 ^3 G0 h, k& D  R' Q4 nactive in young children exposed to testosterone! b7 e& Y- c& C8 {) C& l
exogenously7; however, we did not measure a dihy-8 p4 t1 C! B: C
drotestosterone level in our patient. In addition to
. |3 |5 Q" }! ^1 M) t# Xvirilization, exposure to exogenous testosterone in& ?, z+ j) t6 t# O- N) c6 K3 ^
children results in an increase in growth velocity and3 E9 p4 |1 f: h6 @6 ?: n+ l" a
advanced bone age, as seen in our patient.4 X- r$ b8 N8 n- m: D
The long-term effect of androgen exposure during
  T! X* ^: L( ?& ^1 B' T, a4 dearly childhood on pubertal development and final0 e0 _+ r0 z( \: g; K4 k
adult height are not fully known and always remain1 K1 i0 }: b4 C* ~5 _  z* f* d1 C
a concern. Children treated with short-term testos-# u3 g  A* w- m# M0 I
terone injection or topical androgen may exhibit some
& e4 U( D) a( ^' Q# Sacceleration of the skeletal maturation; however, after" x: N0 f! d5 [
cessation of treatment, the rate of bone maturation
, q( [: n7 V2 E2 `8 `3 b9 rdecelerates and gradually returns to normal.8,9
. j7 l8 }' h, KThere are conflicting reports and controversy
4 b7 g. P( K/ j' L$ Nover the effect of early androgen exposure on adult2 y1 a# R1 U& R: I4 E9 G# M$ ?+ \0 X
penile length.10,11 Some reports suggest subnormal. a  l3 z* |$ j/ z
adult penile length, apparently because of downreg-8 S6 v" L: k" {. H# k& ?- J& [) B
ulation of androgen receptor number.10,12 However,
5 t) w2 R' o! iSutherland et al13 did not find a correlation between6 X6 G: p# k2 W. p) c5 ?( U& [
childhood testosterone exposure and reduced adult
3 D0 g$ ?; O! @: R  Upenile length in clinical studies.
- a0 B6 l& f5 `Nonetheless, we do not believe our patient is. r" f' J+ a# p2 _, _
going to experience any of the untoward effects from
/ R6 _! [, Q0 M$ Ttestosterone exposure as mentioned earlier because- h7 X( i% Y9 j. }
the exposure was not for a prolonged period of time.1 C$ b' J- |* l. p
Although the bone age was advanced at the time of
) \( ]: R' D* Ndiagnosis, the child had a normal growth velocity at8 Z2 E  P3 O. Q  n7 ]- Y& U/ \
the follow-up visit. It is hoped that his final adult$ I% Q' h+ g' p$ ~- l" k
height will not be affected.
" @. b  c4 r% S- f5 jAlthough rarely reported, the widespread avail-9 |5 i8 m% J9 V" Z, e
ability of androgen products in our society may$ r" S& n" Q5 M
indeed cause more virilization in male or female$ ^, D! M2 ^. r9 D+ F1 c
children than one would realize. Exposure to andro-+ ]" q/ I$ w2 w- x% n5 K* i: r
gen products must be considered and specific ques-2 k' a! \- j0 B1 \- T
tioning about the use of a testosterone product or. a4 j4 l4 \6 u3 K
gel should be asked of the family members during
/ b8 K9 Z( P) Z* ~) q. c3 I6 m- Mthe evaluation of any children who present with vir-
0 _3 |: y/ R  @- ]; ~ilization or peripheral precocious puberty. The diag-
! x: K# _( z- j1 {# onosis can be established by just a few tests and by7 X! M3 p" }: b# i$ m$ x! b
appropriate history. The inability to obtain such a! f, T. E0 e9 G. h
history, or failure to ask the specific questions, may
. D$ A7 Y0 T0 U2 S. Vresult in extensive, unnecessary, and expensive
0 ^- O# j2 P4 P0 Y0 Uinvestigation. The primary care physician should be
6 h; m7 V' F! m6 [/ |aware of this fact, because most of these children2 F/ j5 B( [2 y9 U# y
may initially present in their practice. The Physicians’/ }4 }& d2 W+ Q6 }8 n9 S+ E
Desk Reference and package insert should also put a
  v8 f, D, B9 R3 C/ p3 ~! }7 twarning about the virilizing effect on a male or
- V: C& W( w, V  }$ n# \7 G7 Tfemale child who might come in contact with some-
. P' O7 ]. V1 e5 I% C% gone using any of these products.
2 l% g: Q% Q! w+ \" |, y- gReferences% }: t9 k% r7 O9 r: [( Y
1. Styne DM. The testes: disorder of sexual differentiation: @* ~0 `- B! G4 c& ]  X" I; m. n
and puberty in the male. In: Sperling MA, ed. Pediatric
9 r4 e4 A7 I# i1 ?" b. [Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
2 n2 s( ]' P  b. P* p. W2002: 565-628.0 V4 h0 S+ L, c2 E0 \7 F0 y9 }1 _1 i
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious/ }4 A3 e& \* ?1 h/ q: G4 X
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old6 f+ j; @/ b( R
Boy Induced by Indirect Topical1 N2 j) ~5 ^) s+ J
Exposure to Testosterone& Z1 e' ^9 ?, @1 P& C6 D# t2 I4 b
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
/ L6 I% l) Q% iand Kenneth R. Rettig, MD1( K% Z4 C2 J8 x$ A5 r9 A, ?2 r2 w
Clinical Pediatrics
" X2 Z0 L! h3 ^6 Z2 u# q( lVolume 46 Number 64 L, X) |; ?: r; p- z) @9 ^- ^& R
July 2007 540-543
2 n. V# v6 q" R7 b. C! b© 2007 Sage Publications5 H5 @3 Y8 L5 a4 {
10.1177/0009922806296651
2 v1 g* f4 S* e" r! V  O5 bhttp://clp.sagepub.com2 B" Q* Y0 A0 ^8 d+ f% Q
hosted at9 S# a5 l2 F8 M% O1 O# [
http://online.sagepub.com
) s1 H+ h# z0 O2 _: lPrecocious puberty in boys, central or peripheral,) _4 @% w) N; b5 g
is a significant concern for physicians. Central3 e$ B( [0 F* ]1 x
precocious puberty (CPP), which is mediated) E4 T) L1 a8 j& K+ H. W" S9 j
through the hypothalamic pituitary gonadal axis, has2 J6 `4 K$ o& ~! P2 B$ X6 N
a higher incidence of organic central nervous system
, S; t+ O9 v- z$ K9 w3 W3 Glesions in boys.1,2 Virilization in boys, as manifested2 A' M  W0 [' h) R' o" c9 t$ i
by enlargement of the penis, development of pubic
  `7 I, r; r: b0 ^0 Jhair, and facial acne without enlargement of testi-
& D5 X7 ^6 w" \+ Kcles, suggests peripheral or pseudopuberty.1-3 We9 `" g" h; b9 a. g3 K
report a 16-month-old boy who presented with the
- T7 n/ |$ q, k( Menlargement of the phallus and pubic hair develop-, V$ _% A" M& e5 f% e
ment without testicular enlargement, which was due
/ h" s3 A1 j" `to the unintentional exposure to androgen gel used by
; _+ ~! c5 C+ [% j- F, f8 R6 b& }the father. The family initially concealed this infor-  C$ }" P  X6 I) z, E5 y8 b
mation, resulting in an extensive work-up for this
+ J( [# ^) X  l7 mchild. Given the widespread and easy availability of! H, Y$ b4 a4 B, Z$ j4 u) w4 l
testosterone gel and cream, we believe this is proba-- I# {* \$ H. Q9 O2 A
bly more common than the rare case report in the) L* F5 {- t. X5 Z: T
literature.4
* X2 P+ B3 L: b2 uPatient Report5 O/ w* i$ H2 x5 V; n) f' A1 y) k
A 16-month-old white child was referred to the; |, @0 W1 h  ~* |1 n. x+ t  M
endocrine clinic by his pediatrician with the concern) o: x- g( _  t1 g' p
of early sexual development. His mother noticed
$ c9 s( Q3 G8 jlight colored pubic hair development when he was; `0 b5 m. f# Y4 I% b0 o
From the 1Division of Pediatric Endocrinology, 2University of
! ^% Z4 X4 n& \  GSouth Alabama Medical Center, Mobile, Alabama.1 @! G3 `0 X7 }: e- \! ~0 U& f
Address correspondence to: Samar K. Bhowmick, MD, FACE,
" s# ]2 W! P4 g5 |5 g) ?Professor of Pediatrics, University of South Alabama, College of3 p" c3 O* G+ @: ~
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;* m& j# X1 C! h
e-mail: [email protected].
# ^  S; i$ x" J5 Eabout 6 to 7 months old, which progressively became
# d, \! C. M4 w1 T+ Z* k5 Qdarker. She was also concerned about the enlarge-
$ j9 q8 O& E/ a# y* o, X) h! A* lment of his penis and frequent erections. The child
; J. Y3 b9 |& ?, fwas the product of a full-term normal delivery, with, K  [6 r; }5 h) m( b
a birth weight of 7 lb 14 oz, and birth length of3 M+ \5 y2 p$ c8 y0 S
20 inches. He was breast-fed throughout the first year' E: H" L8 N8 @- u+ c6 |  w
of life and was still receiving breast milk along with* L1 K: l! m3 m  C
solid food. He had no hospitalizations or surgery,
, k8 N, {4 s$ G$ ?and his psychosocial and psychomotor development0 `) G1 b, M+ p- l" G$ k/ R
was age appropriate.  i+ y( M: K( v2 E" @8 U. p
The family history was remarkable for the father,
/ A, t8 v/ D+ o" H7 }' i7 h* u4 N/ gwho was diagnosed with hypothyroidism at age 16,
  N7 c& e+ O  K4 s% _3 S& V$ ywhich was treated with thyroxine. The father’s) c. R4 q# Z8 p) F) c. k5 ^# r
height was 6 feet, and he went through a somewhat# l1 l: d. [; ]' S  E! L' F
early puberty and had stopped growing by age 14.; \' P7 q& @( E4 N( s
The father denied taking any other medication. The- A( O4 h& |2 R" f
child’s mother was in good health. Her menarche. _0 H/ M. J: u+ P4 Q; _
was at 11 years of age, and her height was at 5 feet+ x% t. h# h: f9 L8 q, ?- I
5 inches. There was no other family history of pre-
, q9 Q: Y8 A, e8 g  Z) Qcocious sexual development in the first-degree rela-0 t% [; C# C8 C, D* A
tives. There were no siblings.3 F" W( q( I3 C. v
Physical Examination
& Q6 a5 k# {- k3 mThe physical examination revealed a very active,
/ h8 s8 _, O! N- Q# iplayful, and healthy boy. The vital signs documented
" r! Z. H7 r& j6 Q9 Ha blood pressure of 85/50 mm Hg, his length was0 X  {* G7 V! y- `/ ~
90 cm (>97th percentile), and his weight was 14.4 kg
& T7 o+ A  c! U7 y(also >97th percentile). The observed yearly growth
; D( i' E* B; R- k+ evelocity was 30 cm (12 inches). The examination of1 `; l+ F* r: A4 @
the neck revealed no thyroid enlargement.
7 _- L+ H, h9 h& x3 JThe genitourinary examination was remarkable for# t! U9 b8 z1 {' a9 _
enlargement of the penis, with a stretched length of
$ d- m: A' |: I8 Z2 T: p& q" k$ X8 cm and a width of 2 cm. The glans penis was very well( Q9 A3 I- \8 _" Q
developed. The pubic hair was Tanner II, mostly around
$ P) Z9 A" b; N8 c5 F540: B- ]1 T3 B9 l- ^
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
8 h; M- W8 h, n0 w: ?/ I5 fthe base of the phallus and was dark and curled. The! x7 }  }8 D2 r
testicular volume was prepubertal at 2 mL each.
" M  _4 d- e0 PThe skin was moist and smooth and somewhat
) O( o8 m4 }) q- D3 \6 Goily. No axillary hair was noted. There were no
! Q- p& U5 V( X0 u6 k9 {$ wabnormal skin pigmentations or café-au-lait spots.
( [6 w' k+ B0 Q$ _Neurologic evaluation showed deep tendon reflex 2+
# Q  c# T! K2 W3 p- X% Ibilateral and symmetrical. There was no suggestion  M6 }9 E8 T: V# y9 d" L5 z
of papilledema.% P6 [- P8 N& P' ^' q$ N, a
Laboratory Evaluation
& G0 W" Y  y; \7 S; ]6 Y; _The bone age was consistent with 28 months by' Q7 `( \* T8 m6 b" l
using the standard of Greulich and Pyle at a chrono-. @) {- d/ B" t7 [3 g$ F+ j
logic age of 16 months (advanced).5 Chromosomal0 U- Z9 D; Q+ N# F
karyotype was 46XY. The thyroid function test
+ m! m/ C  N1 n# ~- J( Pshowed a free T4 of 1.69 ng/dL, and thyroid stimu-+ y2 A, N/ D5 h" j. g! d
lating hormone level was 1.3 µIU/mL (both normal).' K& R: S" z- \2 X8 m! m5 J& L
The concentrations of serum electrolytes, blood
/ e) [6 `9 x- `& s" k' uurea nitrogen, creatinine, and calcium all were
0 q/ g- \+ e- B: ywithin normal range for his age. The concentration
6 u# O* y) m. Y; j: t) ~of serum 17-hydroxyprogesterone was 16 ng/dL& g% g- t8 y7 F; ^7 B
(normal, 3 to 90 ng/dL), androstenedione was 20
( X" R2 k( S2 Wng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
( ]" p  O% U0 G) S7 [7 v0 v0 aterone was 38 ng/dL (normal, 50 to 760 ng/dL),1 i3 V3 R& Q+ ?; j9 D
desoxycorticosterone was 4.3 ng/dL (normal, 7 to. I1 z  a  Z3 h- `9 c
49ng/dL), 11-desoxycortisol (specific compound S)
9 i, w" C7 I3 f! Lwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-# ]8 O; c9 x7 G6 C1 S% S: E" t
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total: N0 W! P1 k% s; n: c) w/ s# S
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
8 U/ z) G7 V. i- M! s( W0 C& G# @4 Band β-human chorionic gonadotropin was less than
. N" t- T  U! I% E  f5 mIU/mL (normal <5 mIU/mL). Serum follicular9 _+ q% J( v: R  R( E$ c' x5 G3 K
stimulating hormone and leuteinizing hormone7 l; S  j* Z( K: r* ~9 o: M
concentrations were less than 0.05 mIU/mL
1 N" j: G) G5 e+ d) k(prepubertal).
' F0 v) u* l$ B) [- {( b1 I+ zThe parents were notified about the laboratory4 i$ }9 z/ M( u$ y+ F! @& S# u
results and were informed that all of the tests were
7 y& [& \! k7 ~9 H3 b1 dnormal except the testosterone level was high. The
9 w5 x  l- V& S5 U. r, u: A: F( ^follow-up visit was arranged within a few weeks to
4 L5 ~" N- s3 w6 Nobtain testicular and abdominal sonograms; how-/ l8 M8 `6 }0 b% Z* A2 Y
ever, the family did not return for 4 months.. _; |4 {' [2 D& t; ]4 }
Physical examination at this time revealed that the- K* K- K0 t; ^8 m1 r
child had grown 2.5 cm in 4 months and had gained
, u% Y; V4 s  N$ O5 o/ K  {2 kg of weight. Physical examination remained! |; @4 ?& z) ]% d
unchanged. Surprisingly, the pubic hair almost com-* ]) u4 }8 J+ ]. X5 V
pletely disappeared except for a few vellous hairs at
' o4 }: V) R  P# C9 A: g2 c' N, Bthe base of the phallus. Testicular volume was still 29 k4 N. ~& S6 Z% G$ x3 u
mL, and the size of the penis remained unchanged.7 P, e; n( v' H  l4 @, ?
The mother also said that the boy was no longer hav-6 c+ A1 \. U; |/ ^  @- g( H
ing frequent erections.
2 {: W( f: A9 c4 |% t5 H  n' a. GBoth parents were again questioned about use of. @; d4 ?( f7 K/ k3 N5 C0 g
any ointment/creams that they may have applied to
% J# Q7 `! Z  Y. d+ _4 A+ \the child’s skin. This time the father admitted the
* A0 k! Z/ X$ }% J4 _) q$ lTopical Testosterone Exposure / Bhowmick et al 541
# K8 y) ]9 }# s$ H+ ]2 L. xuse of testosterone gel twice daily that he was apply-% c* y. `4 A) m: q8 u3 O# _' P
ing over his own shoulders, chest, and back area for
, Y- s) |4 Y% ]3 A* u) ga year. The father also revealed he was embarrassed1 p3 `6 g& d! d/ u$ X# U
to disclose that he was using a testosterone gel pre-2 B7 ?$ I3 [8 E: N! I2 w+ u
scribed by his family physician for decreased libido2 q- v6 }( b# X* n
secondary to depression.( H4 V+ e; r% _4 V3 C2 w- t( |* g
The child slept in the same bed with parents." t* W8 f# A' G8 s' J) C
The father would hug the baby and hold him on his; o2 A3 g* r# p6 N
chest for a considerable period of time, causing sig-
  c- r3 o( P3 L1 b3 g& Y' Cnificant bare skin contact between baby and father.0 t, h5 s5 i, o: z
The father also admitted that after the phone call,
' C: r- ~0 Z! P+ V8 s  i0 Z+ {& ~% jwhen he learned the testosterone level in the baby' t$ |$ i$ t6 `! e& r3 W; k
was high, he then read the product information
( b) t0 ]0 o$ Q7 i4 `packet and concluded that it was most likely the rea-
) f* O7 `( b9 d  oson for the child’s virilization. At that time, they' a, H: H9 I! m; L1 A
decided to put the baby in a separate bed, and the
8 A6 ?; D" K  @6 A; Ufather was not hugging him with bare skin and had
, c! y! D& U7 v+ y9 V3 c" v& }' `been using protective clothing. A repeat testosterone
. |' D. |! B7 jtest was ordered, but the family did not go to the
4 @6 v) P% v' hlaboratory to obtain the test.$ r: A9 O* J4 M. e8 S7 i( \
Discussion
) U4 _" ]# F- Z6 `( H' k5 kPrecocious puberty in boys is defined as secondary( c( N9 w! h" o1 ^6 M! r+ T: V+ ^
sexual development before 9 years of age.1,4
+ Y! T1 n! k* U- fPrecocious puberty is termed as central (true) when
. w: _( p0 b! {  Oit is caused by the premature activation of hypo-+ w! W0 o" y+ ^; g/ A% g" K
thalamic pituitary gonadal axis. CPP is more com-
" ~! ~# H; x$ u  R7 xmon in girls than in boys.1,3 Most boys with CPP+ p& {0 `& [2 z
may have a central nervous system lesion that is4 A9 H8 B7 ^8 d# n% [1 @
responsible for the early activation of the hypothal-* O5 n! M* j' A, B
amic pituitary gonadal axis.1-3 Thus, greater empha-
: w7 p3 M5 U$ asis has been given to neuroradiologic imaging in
7 J" g' l0 P* y; V0 P5 g; L6 pboys with precocious puberty. In addition to viril-
% W. F0 n* K6 J& C+ Sization, the clinical hallmark of CPP is the symmet-2 g; |! q5 |& A6 p/ z
rical testicular growth secondary to stimulation by
5 w9 {2 M' P# P7 y0 }: fgonadotropins.1,3+ Y' y" [" @) L& n9 X% q
Gonadotropin-independent peripheral preco-
1 k% w3 v+ U; j! Hcious puberty in boys also results from inappropriate0 E  o" {! |1 z: x/ m/ h* Q6 o
androgenic stimulation from either endogenous or
& }4 U. ?- W( `exogenous sources, nonpituitary gonadotropin stim-+ ]& i, i; y4 P# h/ @, E$ z, b
ulation, and rare activating mutations.3 Virilizing0 j6 I- @$ `, F# ]
congenital adrenal hyperplasia producing excessive
" ~3 ?4 ^) [! y- Cadrenal androgens is a common cause of precocious
) J3 F' w' g  Z0 P9 Y2 rpuberty in boys.3,4
1 n8 |' d& k, H( O) d; MThe most common form of congenital adrenal" b4 b. m/ c6 }: E6 C
hyperplasia is the 21-hydroxylase enzyme deficiency.( u* Z' D( K4 I: u  E% p4 p0 O. m
The 11-β hydroxylase deficiency may also result in# t6 j8 [$ ^# ?  W0 P5 g6 [
excessive adrenal androgen production, and rarely,
; ~9 H. U7 }1 |0 {2 n3 x4 oan adrenal tumor may also cause adrenal androgen
2 l7 U: C6 S7 n' Dexcess.1,35 B4 [! h, }1 q% O3 @5 @
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from0 H3 ?! {$ a5 A
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007, p& m5 G/ z9 M, ]  v' P: M& C
A unique entity of male-limited gonadotropin-
6 K  Z" `  R: q. N4 \independent precocious puberty, which is also known% c! @2 }  M$ r# u% [
as testotoxicosis, may cause precocious puberty at a5 m  R( R( I9 [" M; @  }; Q
very young age. The physical findings in these boys9 h, D$ w! {; h) k8 U: G
with this disorder are full pubertal development,* v1 ^6 e1 _) R( g  f
including bilateral testicular growth, similar to boys: V. ^  a/ w8 t2 j, b
with CPP. The gonadotropin levels in this disorder6 y+ l' o  p5 J" \* J" L( L
are suppressed to prepubertal levels and do not show
) g; H1 w; q. A  z3 \pubertal response of gonadotropin after gonadotropin-
; ]# x# y* Z/ y) V4 ~6 Zreleasing hormone stimulation. This is a sex-linked5 U! l+ F# O4 K5 L* o
autosomal dominant disorder that affects only, z* G. Y2 c# s" @7 l8 T. |' W
males; therefore, other male members of the family! S' U' Q2 R$ }( X7 G
may have similar precocious puberty.3
+ {5 n* l( W7 `3 MIn our patient, physical examination was incon-5 f+ ^& [2 Z9 ?4 k
sistent with true precocious puberty since his testi-
! [# |5 }0 _. R( ]- J" Pcles were prepubertal in size. However, testotoxicosis+ I* b7 V  _: I
was in the differential diagnosis because his father
& @' w( ^6 u2 t! G* z2 ustarted puberty somewhat early, and occasionally,
7 K5 B! l! L  ~: atesticular enlargement is not that evident in the% w7 s# G4 Q4 {2 T* F, q
beginning of this process.1 In the absence of a neg-
  y8 r% R0 s2 V! p' @* s/ tative initial history of androgen exposure, our
9 U8 f: b4 u- ~9 b- Hbiggest concern was virilizing adrenal hyperplasia,
8 `; X3 i3 E# J( ieither 21-hydroxylase deficiency or 11-β hydroxylase' a9 C* m3 v' r5 ?4 `
deficiency. Those diagnoses were excluded by find-
% Y( l" c7 s. j# V/ |ing the normal level of adrenal steroids.
- j' h5 _/ O" A2 W5 M5 oThe diagnosis of exogenous androgens was strongly
9 J, |( s' V2 u/ J) `- Y  psuspected in a follow-up visit after 4 months because: s/ s( @( G# n( @
the physical examination revealed the complete disap-4 `: z$ z  O  M- f7 m3 Z' K( y" i
pearance of pubic hair, normal growth velocity, and* J# {2 l' M; k* n; {5 ~+ x
decreased erections. The father admitted using a testos-5 Z" ], ^8 R* w% Q
terone gel, which he concealed at first visit. He was
% ?) Y9 N" o4 L3 g" G. V% Yusing it rather frequently, twice a day. The Physicians’
6 o$ M& q& r) g" zDesk Reference, or package insert of this product, gel or
5 F1 G; ^& v% \$ l! `cream, cautions about dermal testosterone transfer to! `& n- u1 D) @/ [- X$ D
unprotected females through direct skin exposure.) J+ P' c! G% D! u+ |: S
Serum testosterone level was found to be 2 times the9 J- Z5 |( P# \* M
baseline value in those females who were exposed to
" r0 {# Z8 z# ~$ neven 15 minutes of direct skin contact with their male
, g+ W: n3 T- d* M7 `2 |/ Fpartners.6 However, when a shirt covered the applica-
1 l3 K) o# r( s, Xtion site, this testosterone transfer was prevented.0 g* ~9 P0 Z0 F3 w
Our patient’s testosterone level was 60 ng/mL,
# p, ]  x3 {9 D" Twhich was clearly high. Some studies suggest that4 L' K4 p# B1 J) k! q/ s( R
dermal conversion of testosterone to dihydrotestos-
- Q# ?3 p0 U; B! J6 cterone, which is a more potent metabolite, is more+ V1 N! E+ K% P: Z
active in young children exposed to testosterone
2 \6 r1 m' @: K( lexogenously7; however, we did not measure a dihy-1 Z' H" ]( S5 p. i9 F, Q
drotestosterone level in our patient. In addition to! t6 x. u9 y) A7 F  F
virilization, exposure to exogenous testosterone in4 p+ i" I* t; v& x1 d' R
children results in an increase in growth velocity and2 i0 s( G. _4 x
advanced bone age, as seen in our patient.. a8 N* J7 v0 q2 Y
The long-term effect of androgen exposure during
  A5 g; ~( u+ _- ?! ?early childhood on pubertal development and final
( l9 _/ P: L1 Q6 P/ o9 ~- Eadult height are not fully known and always remain+ t* o3 X8 F2 [' [: W3 Y' ~
a concern. Children treated with short-term testos-3 M1 Z  ^, @$ C
terone injection or topical androgen may exhibit some
6 P& `$ c% ~# p: s$ c. v: i" Eacceleration of the skeletal maturation; however, after
2 B  \. a- o; u* Jcessation of treatment, the rate of bone maturation: E4 k8 d+ j& d; ]. H; Y% ?
decelerates and gradually returns to normal.8,9' m( N* `3 R1 C$ A
There are conflicting reports and controversy
$ z5 ?, B8 g* ?$ q. U# Cover the effect of early androgen exposure on adult) [7 Y! R6 N2 l# h) b3 O" N: R3 E
penile length.10,11 Some reports suggest subnormal, c% e  S, V' {7 H
adult penile length, apparently because of downreg-& b& d& h0 W: B  V% d
ulation of androgen receptor number.10,12 However,
; W) q; y$ Z6 c3 USutherland et al13 did not find a correlation between$ v, x8 o8 q( q/ g
childhood testosterone exposure and reduced adult
: H. c' |3 z! d+ R! rpenile length in clinical studies.
4 O) w/ g  j0 JNonetheless, we do not believe our patient is, V% z* Y- u4 s: _4 d0 p, p2 ~
going to experience any of the untoward effects from( g1 |# R( x4 u& ^5 x6 r
testosterone exposure as mentioned earlier because, h9 s( k% ~! d$ H# |
the exposure was not for a prolonged period of time.. c9 ?0 F6 Q6 I' F& F
Although the bone age was advanced at the time of4 _# p* t, X. r  s% @4 h
diagnosis, the child had a normal growth velocity at  @8 Z0 |9 N) {
the follow-up visit. It is hoped that his final adult& K/ N6 Y/ a, \8 M5 O
height will not be affected.
/ f3 N- `* @3 }7 ?% ~4 cAlthough rarely reported, the widespread avail-
2 g$ a# d  ]8 F% D* D3 g/ ~ability of androgen products in our society may4 r  w8 v( D) F; U: y  p
indeed cause more virilization in male or female, q$ `6 c9 W' n$ h6 @+ S
children than one would realize. Exposure to andro-
' y$ z0 U( ~* l5 g+ }gen products must be considered and specific ques-; O* i1 e3 A% x
tioning about the use of a testosterone product or( l. C! I# V* W
gel should be asked of the family members during% r/ q# M7 D! w( V+ W
the evaluation of any children who present with vir-
2 J/ \$ b' V6 m, S1 O, x$ ailization or peripheral precocious puberty. The diag-- E$ C5 X6 L, i" _; ?  e2 m/ q
nosis can be established by just a few tests and by/ ?1 g2 b& p, j- [( l5 U' I
appropriate history. The inability to obtain such a: M- |5 d& m7 D+ A" R9 u/ [: K$ W
history, or failure to ask the specific questions, may
. h% X+ g2 G: k9 p& {4 hresult in extensive, unnecessary, and expensive+ g; \9 U% f) }" D6 C3 E3 p
investigation. The primary care physician should be
9 u3 ]9 E+ R- ~( Q0 Paware of this fact, because most of these children: `7 ]% \3 m* C; a6 S# {
may initially present in their practice. The Physicians’
8 j0 t# U; R& \Desk Reference and package insert should also put a
' E: s3 D( U4 }. H! H' ewarning about the virilizing effect on a male or0 ?2 [1 x+ `  k9 c7 l8 e# r
female child who might come in contact with some-" l& ]* e6 ~/ A+ C( I4 q
one using any of these products.
$ q: U9 J- V5 |$ a* _! E5 ?References
, G" n$ t, m; n) i8 \1. Styne DM. The testes: disorder of sexual differentiation
, D; o: s8 v3 {; P7 F) l8 Cand puberty in the male. In: Sperling MA, ed. Pediatric4 ~2 R7 n/ h2 S9 `% w
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;9 l  Z. V! Y# |, Q3 O6 @( A: r
2002: 565-628.! ^7 z6 m3 T' \- c/ B
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious$ D+ C" F# l1 e$ b8 a0 _
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

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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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