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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
( g: B3 Z2 r7 k, o- FBoy Induced by Indirect Topical7 N) K9 e- r1 G- q- o
Exposure to Testosterone
' n3 M* I/ R3 N+ H0 r; ySamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
% W6 {7 u# o- j1 F( }- \' l. M7 Iand Kenneth R. Rettig, MD1
1 x" {6 ~; @4 s, ?& U: x7 SClinical Pediatrics/ k' S' P# |- ~' H" G
Volume 46 Number 61 I; b, Z1 j' R& |
July 2007 540-543
& }! x6 R/ a) R# z& p" L( u© 2007 Sage Publications, @$ `% M3 B- q1 ?# L: b1 ^
10.1177/0009922806296651, H0 T7 l8 s* q
http://clp.sagepub.com
* R7 `8 `% K! f# Y2 ]" n9 zhosted at
  G: c+ D; j+ r3 Z$ [. O! uhttp://online.sagepub.com
9 A6 y5 B4 D# f' e2 b9 SPrecocious puberty in boys, central or peripheral,
8 p+ e* j$ g4 I' W( G- D$ S7 @8 bis a significant concern for physicians. Central" H) B  J. e7 a) J
precocious puberty (CPP), which is mediated/ J* T) O" ^. m
through the hypothalamic pituitary gonadal axis, has
& B+ n' J6 I8 X) L, pa higher incidence of organic central nervous system
1 m6 I7 S+ c; h7 Y8 A  ^lesions in boys.1,2 Virilization in boys, as manifested. t. v% d$ l& m2 a  n
by enlargement of the penis, development of pubic3 t8 G4 s* y; K
hair, and facial acne without enlargement of testi-5 V; C4 f1 e$ L$ \
cles, suggests peripheral or pseudopuberty.1-3 We5 q7 N- q; U% e% _1 |% v
report a 16-month-old boy who presented with the' m5 h! L; |! y- E' j! c' V/ o
enlargement of the phallus and pubic hair develop-
, x, U) X4 `, ?9 T, }" a4 d  e" mment without testicular enlargement, which was due
/ I/ v) _" A" cto the unintentional exposure to androgen gel used by1 O" R& \; ^$ n$ p2 N3 h3 Y  w
the father. The family initially concealed this infor-0 M2 r. b1 j0 K
mation, resulting in an extensive work-up for this
" T1 j9 x. P9 N- achild. Given the widespread and easy availability of7 t; D6 F; u6 Y/ B5 z. @9 e: S
testosterone gel and cream, we believe this is proba-
  U+ i+ x" @; h) @9 c' p0 Fbly more common than the rare case report in the8 d! ]* s5 Z, h7 u. G  o
literature.4
/ f% `; {" n* |8 _+ F( hPatient Report
) J3 ^$ g3 _8 D  m  J3 jA 16-month-old white child was referred to the+ u% t0 h! R5 w4 Q5 M: d
endocrine clinic by his pediatrician with the concern
4 X# p3 f+ u8 w7 ]' U( @% J, Zof early sexual development. His mother noticed. H: L* O% z& a1 G# \
light colored pubic hair development when he was
5 y* s( M0 b' c% Q2 wFrom the 1Division of Pediatric Endocrinology, 2University of/ I* H0 w2 j& [$ g. X8 O
South Alabama Medical Center, Mobile, Alabama.
/ I! z4 r+ P0 iAddress correspondence to: Samar K. Bhowmick, MD, FACE,
6 \5 @6 Q. V/ J" ]) s8 ?1 ^Professor of Pediatrics, University of South Alabama, College of
: Y) V( Q% V- |; tMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
& K* b; ?6 L- j" d. P& N# {e-mail: [email protected].- p$ p6 F& F) Y# Q2 A
about 6 to 7 months old, which progressively became/ J! Q* V" m* P7 Z' a; y
darker. She was also concerned about the enlarge-: R# g  Z0 x% j- ]% ]. x& S
ment of his penis and frequent erections. The child
1 q( {' _6 B3 Q: hwas the product of a full-term normal delivery, with
- g3 n/ C. A# D! L/ b0 H/ n3 Va birth weight of 7 lb 14 oz, and birth length of
* N$ O% W, ]" ^, s20 inches. He was breast-fed throughout the first year% ]3 @6 R% t+ a* i4 f. d
of life and was still receiving breast milk along with$ M: _/ y# @- d, }8 b
solid food. He had no hospitalizations or surgery,
6 C2 Y  k$ b4 s' \/ x( A$ }% L1 Pand his psychosocial and psychomotor development3 {) R3 _7 p* ?" B5 G3 P
was age appropriate." x0 c  g: \7 j3 O
The family history was remarkable for the father,
) z1 P0 m+ i' Q/ u; C0 {( Rwho was diagnosed with hypothyroidism at age 16,
  H% ?: B3 `* }which was treated with thyroxine. The father’s0 k5 u1 N- d  w# W
height was 6 feet, and he went through a somewhat
2 \* H% ]  v9 f" ]' K5 V; a- Vearly puberty and had stopped growing by age 14.
# V1 U8 \: ^$ o, {7 r2 Z. d- N, nThe father denied taking any other medication. The
* g4 y6 O# i9 Q/ i/ Z9 ^% @child’s mother was in good health. Her menarche
4 u5 ~4 [! H3 v0 e5 E: {! Jwas at 11 years of age, and her height was at 5 feet
- e* K6 F. I7 c$ F+ E, t5 inches. There was no other family history of pre-1 m# \" l' g; R, `
cocious sexual development in the first-degree rela-5 T" |/ J* U; |( U- [, s2 a- Q
tives. There were no siblings.$ \8 U7 t) K( J3 e/ Z7 p
Physical Examination
) A6 D/ j. J2 x* H6 @& ^, @The physical examination revealed a very active,/ u1 m) w! d3 u: ^9 ^4 D0 a
playful, and healthy boy. The vital signs documented
5 d$ d9 S! ~/ G" x- p8 t$ Ba blood pressure of 85/50 mm Hg, his length was
# ^7 [7 j% T8 B90 cm (>97th percentile), and his weight was 14.4 kg5 O% n$ R: z" B$ c( K# z5 _: Z
(also >97th percentile). The observed yearly growth
, L9 J# n+ [0 L$ d0 |0 K; wvelocity was 30 cm (12 inches). The examination of) Y! m  M6 l+ d9 R7 U
the neck revealed no thyroid enlargement.% W2 s: e( u1 P0 `
The genitourinary examination was remarkable for
; j: O( T3 O6 Z  d$ B+ X2 S$ s; s# Penlargement of the penis, with a stretched length of1 R. i3 [  b8 r* L4 x0 d
8 cm and a width of 2 cm. The glans penis was very well
- ?0 [9 D0 Y$ X& A. f. c: Gdeveloped. The pubic hair was Tanner II, mostly around
# ~5 {# N+ L3 e+ ]. W& i% i- e% J$ X5400 f- N/ A* p- a% W% C! e7 f
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from+ h6 \. d" I# Y5 }
the base of the phallus and was dark and curled. The+ Y' w4 p$ l+ a
testicular volume was prepubertal at 2 mL each.
. B0 @2 n/ W& x( t; S; H7 jThe skin was moist and smooth and somewhat1 J  A" f8 n+ Q9 T: F1 X, U6 M7 m
oily. No axillary hair was noted. There were no5 N9 n! X% P" `- Y* R* |: B
abnormal skin pigmentations or café-au-lait spots.
) p0 z% n. G5 |/ R  xNeurologic evaluation showed deep tendon reflex 2+3 A1 u, G3 l6 l
bilateral and symmetrical. There was no suggestion* i( z: o& O9 H. ?2 D
of papilledema.
4 Y% i0 R7 }8 y8 fLaboratory Evaluation- a% m2 n8 Q' F7 ~9 x
The bone age was consistent with 28 months by
" i6 H; H9 c+ _* b  P( Eusing the standard of Greulich and Pyle at a chrono-" r/ j2 N8 P( f4 W' `! G" W
logic age of 16 months (advanced).5 Chromosomal* m, ~& W  ?6 b% c
karyotype was 46XY. The thyroid function test" M' v7 A" Q8 z2 |
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
! l$ \+ V( X! L4 B3 O+ plating hormone level was 1.3 µIU/mL (both normal).2 x! l2 Q( d7 }+ a/ t0 g
The concentrations of serum electrolytes, blood
: N9 ?1 `7 s% g7 {urea nitrogen, creatinine, and calcium all were
4 p* t! r# L' h3 Swithin normal range for his age. The concentration
; {7 [. g! F" c) j3 Y. c, @+ wof serum 17-hydroxyprogesterone was 16 ng/dL
& Q5 m$ w4 W; g3 d; H(normal, 3 to 90 ng/dL), androstenedione was 201 C! ^+ @/ @' |* b
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-, q% n' Q: {6 e
terone was 38 ng/dL (normal, 50 to 760 ng/dL),! S7 k3 H  J" ^4 V
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
# R9 E5 V& F! p! O' ?7 y49ng/dL), 11-desoxycortisol (specific compound S)
4 W- b' j( @, T" c' E: mwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-( s; ~: K& F2 c8 ]3 ^
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
5 |! {: O4 _" j* s! Ltestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
" T6 i" L* h+ x- C) Zand β-human chorionic gonadotropin was less than4 s+ d9 s; T) d' Y; a
5 mIU/mL (normal <5 mIU/mL). Serum follicular+ l) k) w6 w$ T8 Q
stimulating hormone and leuteinizing hormone( W9 ]# a  p2 ^  s9 T2 I* }# B
concentrations were less than 0.05 mIU/mL$ L' _7 U& m* ]' D5 K* j7 G
(prepubertal).
$ l5 S' \$ ?8 p# b6 o' x2 q* C( fThe parents were notified about the laboratory. w: Q  m5 X6 f2 v$ y& y+ ~
results and were informed that all of the tests were
  I3 R6 P3 G* w+ Q. \6 W' t: ]/ Enormal except the testosterone level was high. The/ ~& h. Q/ \6 b2 c, S" G/ N; R
follow-up visit was arranged within a few weeks to
+ b8 F* V# h  d6 hobtain testicular and abdominal sonograms; how-
* r0 g2 V4 f& ?% hever, the family did not return for 4 months.8 v2 R9 i2 }! p+ d" c
Physical examination at this time revealed that the, m$ w2 i( [. d6 q* H% _  w
child had grown 2.5 cm in 4 months and had gained
5 I! V: ~' A6 A0 y6 p1 N2 kg of weight. Physical examination remained0 K; h- n5 Q- V( M
unchanged. Surprisingly, the pubic hair almost com-0 T5 Z+ V' w* O0 O, }
pletely disappeared except for a few vellous hairs at
. {% n- P) x9 U. G5 cthe base of the phallus. Testicular volume was still 2  P2 `2 R: t  `$ Z# g% \+ e
mL, and the size of the penis remained unchanged.
& F' }( |' {. _7 AThe mother also said that the boy was no longer hav-: S1 r9 c7 K5 o$ U+ Y7 E- k  H
ing frequent erections.
' |9 D4 D4 m0 _$ q0 u8 w1 ^2 G/ eBoth parents were again questioned about use of
& O* a5 d1 @  }' g1 V3 Xany ointment/creams that they may have applied to* d) a) f3 m3 L2 m& ^1 V( u1 Y
the child’s skin. This time the father admitted the( v& }- r+ x4 _* s% `* b; @
Topical Testosterone Exposure / Bhowmick et al 5414 b" ?  K" e# Z
use of testosterone gel twice daily that he was apply-$ v8 S* s/ }% g  r
ing over his own shoulders, chest, and back area for- r) I$ r% |9 N( ]* u: t
a year. The father also revealed he was embarrassed* q4 j+ A9 S. e: }2 K
to disclose that he was using a testosterone gel pre-
' E' ^" A+ r7 s' W6 X7 B, P6 }; Lscribed by his family physician for decreased libido
  ~3 h2 L: f4 p- |# e( osecondary to depression.! f% C$ ^8 ?- b. O& f, x6 a
The child slept in the same bed with parents.9 c, R7 R8 V. S% V
The father would hug the baby and hold him on his
* H; g# R7 C5 @8 E/ C5 cchest for a considerable period of time, causing sig-1 [8 l- {: g# F! u
nificant bare skin contact between baby and father.
/ O4 c+ P, g7 e$ r5 x. j" d* _' {The father also admitted that after the phone call,
1 v0 e/ I- g! U$ c  \- g5 dwhen he learned the testosterone level in the baby
! }4 o! {+ G5 E- ^; `8 A) vwas high, he then read the product information
3 K9 n" j9 P% I  \2 Vpacket and concluded that it was most likely the rea-9 }5 {$ |$ D  g3 s2 f# }+ j
son for the child’s virilization. At that time, they
; g. {# w( ]7 J, q9 g& ?decided to put the baby in a separate bed, and the
( U: L3 C  A+ |father was not hugging him with bare skin and had" ?' C0 _' K  d4 |9 t
been using protective clothing. A repeat testosterone2 Q4 T( i8 N- D( |. b- X
test was ordered, but the family did not go to the
& o; \( q5 j7 O3 @0 p- A& ulaboratory to obtain the test.  |! U3 _* T+ M4 x' P$ X* b( U- x
Discussion. j* B+ K) u/ o
Precocious puberty in boys is defined as secondary" O. \) J  W0 u+ H+ A
sexual development before 9 years of age.1,4/ Y* w" {9 Q$ O  G# v' f
Precocious puberty is termed as central (true) when4 D/ N& K$ \. ~+ j4 c! g' {; x7 r
it is caused by the premature activation of hypo-) l1 x3 m% g% t' ?% O
thalamic pituitary gonadal axis. CPP is more com-
( w1 ]  G3 e" K/ n  Xmon in girls than in boys.1,3 Most boys with CPP
$ D" o& x) L$ G6 q( Gmay have a central nervous system lesion that is8 j6 Q% Q' }0 ~7 D( }* _6 X
responsible for the early activation of the hypothal-
, Q. }( l* }& N. samic pituitary gonadal axis.1-3 Thus, greater empha-
# U4 A9 b* Y; [# Zsis has been given to neuroradiologic imaging in
: g7 g: ^5 z& d' eboys with precocious puberty. In addition to viril-* Y5 F. @* n( w0 l+ Y7 ?
ization, the clinical hallmark of CPP is the symmet-
$ G: O5 V* r, K* u/ L/ orical testicular growth secondary to stimulation by) A  B, L8 A2 A" |& p. `
gonadotropins.1,3" B! I6 u4 x) \- w
Gonadotropin-independent peripheral preco-
5 Z' q3 E  Y, w6 j7 {( |cious puberty in boys also results from inappropriate
& C( H0 U# g2 u% qandrogenic stimulation from either endogenous or
" H3 t3 ~0 r- A, S) Kexogenous sources, nonpituitary gonadotropin stim-
8 U5 X4 S7 s6 b( j8 Culation, and rare activating mutations.3 Virilizing
* W( G& a9 a4 G- }0 D6 mcongenital adrenal hyperplasia producing excessive
! j7 s1 [$ l' q5 tadrenal androgens is a common cause of precocious9 _- C2 C# t! _
puberty in boys.3,4
; }4 F, ?, H9 M' d6 R- {4 HThe most common form of congenital adrenal
' g1 q) C9 @, r' `' e5 b+ y, e" ohyperplasia is the 21-hydroxylase enzyme deficiency.9 ?! `+ d% {/ L: R
The 11-β hydroxylase deficiency may also result in: Z( p- w1 g( `2 n+ v1 g
excessive adrenal androgen production, and rarely,
  ~+ Y6 j: ?5 x: A- `an adrenal tumor may also cause adrenal androgen/ e( I, l8 O! Y9 d7 t
excess.1,3# k5 K0 `: P7 w- u$ ~: [: ?) d1 z- q
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from5 Y3 O. O1 ?  s6 d0 `. T" W
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
1 ?- A. }9 K0 U: n5 ?A unique entity of male-limited gonadotropin-
* E0 W- m9 u: x5 E: R6 k/ m# Windependent precocious puberty, which is also known6 ]7 z7 y7 u# x1 D" q1 `" e
as testotoxicosis, may cause precocious puberty at a" h6 }6 D1 _! D7 w' B
very young age. The physical findings in these boys
0 v: _8 ^. x. t& Owith this disorder are full pubertal development,$ Q3 J7 D  E. ^' a7 d% F' X
including bilateral testicular growth, similar to boys5 G9 p2 N  O$ v. q- i5 Y5 ~
with CPP. The gonadotropin levels in this disorder: [# f$ t- s- \& K8 y
are suppressed to prepubertal levels and do not show& y7 q/ ?, g4 }' e$ |# Z4 N
pubertal response of gonadotropin after gonadotropin-
% P# e3 r# o4 Y0 H, @$ ~& e) w) n% ireleasing hormone stimulation. This is a sex-linked# j& \+ s  t% ?: q. O/ i1 p
autosomal dominant disorder that affects only
8 q6 w- k6 ^& {6 G. g- `males; therefore, other male members of the family
3 Q0 M6 A1 K. R  Y3 ]% kmay have similar precocious puberty.3  w1 X# m5 t8 h9 i) g! ?
In our patient, physical examination was incon-
4 V$ H: r# m' Z# `- E7 asistent with true precocious puberty since his testi-/ o1 J9 Z% O' _
cles were prepubertal in size. However, testotoxicosis6 b( X! }, n% r4 x
was in the differential diagnosis because his father( B% H) t' Q) x8 j7 I7 S
started puberty somewhat early, and occasionally,9 j7 G) R8 X3 j6 b
testicular enlargement is not that evident in the
  C8 ^" u' ~( V' L, y; P/ G: Zbeginning of this process.1 In the absence of a neg-, I% F8 ~! T$ K& e( |- h
ative initial history of androgen exposure, our
" m6 C" R* J( V8 `7 T& I% }biggest concern was virilizing adrenal hyperplasia,& D( |7 U) L' Y
either 21-hydroxylase deficiency or 11-β hydroxylase
: ^9 i7 h  C0 {deficiency. Those diagnoses were excluded by find-2 w) i0 Y0 O9 l' j0 S% x% v- a
ing the normal level of adrenal steroids.- B$ K5 J" s+ N6 V
The diagnosis of exogenous androgens was strongly$ V1 g/ s9 ?% w- B$ t
suspected in a follow-up visit after 4 months because
: R1 i4 b, d* o, fthe physical examination revealed the complete disap-/ c1 @: v8 B$ f& {7 @" u
pearance of pubic hair, normal growth velocity, and
2 R/ f6 u) w. ?* t9 W( s) Gdecreased erections. The father admitted using a testos-
% g" i# e; _  F% j$ i6 Vterone gel, which he concealed at first visit. He was7 S% }) a5 y& ]7 `" K/ t5 O% W
using it rather frequently, twice a day. The Physicians’+ w# A; l, V# y0 R$ g
Desk Reference, or package insert of this product, gel or
' }& L7 [. T. @4 A# J  D/ ~  Jcream, cautions about dermal testosterone transfer to' ]* p: R2 Q/ J+ u9 Y
unprotected females through direct skin exposure.
/ H$ n) |  l( i# mSerum testosterone level was found to be 2 times the: N% K/ e9 l4 Q8 W. Z1 X# u& f7 X
baseline value in those females who were exposed to
- e' ^6 |5 c- |! Ceven 15 minutes of direct skin contact with their male: D8 _$ P4 U1 E
partners.6 However, when a shirt covered the applica-
( H2 G! a7 F) A% U# Z9 D% _tion site, this testosterone transfer was prevented.
! U/ O2 Z4 Z6 W% _; xOur patient’s testosterone level was 60 ng/mL,
; A: M$ d5 f& q6 O6 \which was clearly high. Some studies suggest that
* g% L% m4 z3 z/ ldermal conversion of testosterone to dihydrotestos-2 T/ _* Z# ^8 ]/ {
terone, which is a more potent metabolite, is more2 J7 `. W* p5 ]
active in young children exposed to testosterone- a) b9 j" I- S# l* z
exogenously7; however, we did not measure a dihy-& ?' X* R# y7 H5 p; O) U+ t! T
drotestosterone level in our patient. In addition to, G/ e( ~2 Y- ?' i2 ^6 ]2 j
virilization, exposure to exogenous testosterone in+ G, N& _. A0 U3 N! H7 H
children results in an increase in growth velocity and5 ~" |& ]/ _- e' k# N
advanced bone age, as seen in our patient.
3 R% H: [/ M. G8 I- q3 zThe long-term effect of androgen exposure during7 `" w3 h% H) |# L0 C% M
early childhood on pubertal development and final
6 ^* H6 f  ~# `9 Kadult height are not fully known and always remain
+ G* h$ J8 x( C8 B/ H) g; Z. ja concern. Children treated with short-term testos-9 A& E! Z4 V6 ]7 A7 v+ B) ~
terone injection or topical androgen may exhibit some
4 k) X8 {4 J9 ]( T5 tacceleration of the skeletal maturation; however, after
! o2 ~4 O% T1 v. F4 Q$ b( vcessation of treatment, the rate of bone maturation- _2 r# @. k1 `5 _
decelerates and gradually returns to normal.8,9
* L' c2 A5 N: ]& dThere are conflicting reports and controversy8 [* Y" w1 U# t4 X: T
over the effect of early androgen exposure on adult( q# B  @/ q: q% P7 P; V
penile length.10,11 Some reports suggest subnormal- m8 k% Q3 l' A' J# A& I* d* Q
adult penile length, apparently because of downreg-
) W. W1 l2 d* v" j& Bulation of androgen receptor number.10,12 However,
* ?! C: _2 E. U" lSutherland et al13 did not find a correlation between4 w. p* [, Y! Q% Q
childhood testosterone exposure and reduced adult
+ H! i# q( r7 rpenile length in clinical studies.
7 m% a9 Z- r' _$ g  `Nonetheless, we do not believe our patient is9 C* V+ J0 ^+ ^; t- s
going to experience any of the untoward effects from' c7 j2 q. O% n5 P* {# B
testosterone exposure as mentioned earlier because
6 @: z  ^3 v7 |1 N2 B2 cthe exposure was not for a prolonged period of time.
- I" q, }5 ~7 g, ?  e* T) \Although the bone age was advanced at the time of
! ]3 k3 m. [1 O( j" H* i7 Xdiagnosis, the child had a normal growth velocity at
# Y0 s$ W; Y  z, Jthe follow-up visit. It is hoped that his final adult9 A- T2 C8 Y2 @  b0 u( ?
height will not be affected.
9 l3 u: `; Z5 J; ?Although rarely reported, the widespread avail-
$ z3 H7 r6 \- m; D( V) Jability of androgen products in our society may
0 b& T6 e! d  p! M) ~indeed cause more virilization in male or female( \. c& p, M& f2 S$ i1 f- e$ S
children than one would realize. Exposure to andro-
6 Y) s9 o1 d$ A- ~! ugen products must be considered and specific ques-
2 e4 R: @9 g5 u& O1 D( ptioning about the use of a testosterone product or
7 w, c5 b2 A5 j+ N4 M% Wgel should be asked of the family members during5 f$ N4 f' z- E& S( W0 [
the evaluation of any children who present with vir-! x: D4 G! M& b# J( A
ilization or peripheral precocious puberty. The diag-
8 a, D3 E# ?  h! k) D( Knosis can be established by just a few tests and by4 |& W; H, I) d) D
appropriate history. The inability to obtain such a
1 D! T$ L$ v  m% R/ h% u3 ]history, or failure to ask the specific questions, may8 U' ^1 L6 g9 z9 F4 X
result in extensive, unnecessary, and expensive1 n, g( n3 L+ d
investigation. The primary care physician should be
" Z7 M0 {9 K2 B8 g3 m; `aware of this fact, because most of these children/ ]& @3 p6 O, d
may initially present in their practice. The Physicians’+ n9 @4 q: V" ]. q
Desk Reference and package insert should also put a/ s" g5 e( i5 j% A$ }
warning about the virilizing effect on a male or
% [5 E9 ]+ _6 r: S4 mfemale child who might come in contact with some-
. J) g1 a5 L$ u) m+ ^one using any of these products.: w& c% M. I# P9 M  ~
References0 V/ W/ d! P9 P+ n% x! j* L6 h2 R
1. Styne DM. The testes: disorder of sexual differentiation. {9 ?) M4 c1 g2 b
and puberty in the male. In: Sperling MA, ed. Pediatric* r7 n0 R; p. C& S
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;* M4 n8 N+ b7 O7 |! X0 u5 G
2002: 565-628.
$ K1 H6 m; y9 a( q  h' D2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious1 q. n) h% h, K8 z: X
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old1 d" A3 }5 L; D! R: u
Boy Induced by Indirect Topical% b4 e3 ^5 R( ~) {9 f! L% S7 x
Exposure to Testosterone5 Z7 {$ N$ A$ f6 K( ]
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2# U- J; I; j# Z
and Kenneth R. Rettig, MD1
% ~8 J3 L% c( _' N1 Q( S  T  A/ |Clinical Pediatrics; M2 L4 X( X# |  Y3 D
Volume 46 Number 64 Y# w( \: c0 W& S, z, z- |
July 2007 540-543
; W! W6 C3 V0 S9 X© 2007 Sage Publications
3 |1 m8 g6 G9 F" h; {10.1177/0009922806296651
; S- Q* I! R) \http://clp.sagepub.com1 r* i+ G, Q! D4 }* U$ f
hosted at
& D) m9 q$ U$ L* D$ Dhttp://online.sagepub.com, m% J/ a  w3 Q
Precocious puberty in boys, central or peripheral,( A3 @) i* U& C0 h
is a significant concern for physicians. Central; h' A. \3 A% u
precocious puberty (CPP), which is mediated0 G. u5 H" D+ ?1 p8 b) u% d
through the hypothalamic pituitary gonadal axis, has
5 X& f, M0 I$ l- Ga higher incidence of organic central nervous system
% S7 C0 r6 g- u; Mlesions in boys.1,2 Virilization in boys, as manifested
/ w2 L( V0 w1 ?by enlargement of the penis, development of pubic1 K+ V7 n# d7 G0 R$ u9 z2 o1 g
hair, and facial acne without enlargement of testi-$ k) S" m; G) m$ k
cles, suggests peripheral or pseudopuberty.1-3 We
0 P: V! n: g: k) Z+ qreport a 16-month-old boy who presented with the; f" N5 t% Z4 w4 G2 E! N0 g1 z4 C
enlargement of the phallus and pubic hair develop-# ]2 \& s& O% u3 D# x  X% c# Z
ment without testicular enlargement, which was due. p: ^! a1 h1 x1 j
to the unintentional exposure to androgen gel used by6 V& @" t' A3 p5 @- N7 F1 X7 g2 ]
the father. The family initially concealed this infor-) |2 Z8 }. _% ^5 L  _& ]$ }
mation, resulting in an extensive work-up for this* K. I; L, n4 }+ W- j
child. Given the widespread and easy availability of! ?5 {& s- ?3 g9 Y7 j4 G; S
testosterone gel and cream, we believe this is proba-
* ]. E3 ?, I  y7 Ably more common than the rare case report in the9 }. W+ Z% w2 F* t+ ~) l
literature.4
+ P6 p1 k, \# m8 S6 U5 I6 jPatient Report
* z3 G4 ], J3 `& j( c5 OA 16-month-old white child was referred to the
3 j+ R0 T" t3 z. _, I4 c* iendocrine clinic by his pediatrician with the concern" P0 a& m, x* C% }8 P2 Y; U2 J) |: [
of early sexual development. His mother noticed3 G% D+ e) w& p. E5 F0 e
light colored pubic hair development when he was
7 Y8 b( x; Q5 f. W' x+ x! SFrom the 1Division of Pediatric Endocrinology, 2University of
5 ]- a' B" Q; ~" P3 nSouth Alabama Medical Center, Mobile, Alabama.
9 y' j' ^5 n% a4 a1 \Address correspondence to: Samar K. Bhowmick, MD, FACE,
$ L5 S  {4 p& s( p6 Y9 g' ?Professor of Pediatrics, University of South Alabama, College of
& W4 m: n# `9 {5 a- y' IMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
( N6 F* v5 _9 B: ie-mail: [email protected].3 E( s* c# F7 {: C; s9 n
about 6 to 7 months old, which progressively became3 O! z8 R1 x% `% O. j5 A
darker. She was also concerned about the enlarge-( R) J& V% J) }& k) t
ment of his penis and frequent erections. The child$ j# F% _' s1 x
was the product of a full-term normal delivery, with
8 H) ?- m$ l. m6 m' V- ka birth weight of 7 lb 14 oz, and birth length of
) I# }+ u0 x3 y20 inches. He was breast-fed throughout the first year
; v' A# _) j! c: [of life and was still receiving breast milk along with
& ~& h* p/ a1 P) Ksolid food. He had no hospitalizations or surgery,
, Y( B. b- G& xand his psychosocial and psychomotor development
; P% c5 [1 u1 U4 b8 Xwas age appropriate.
* k% l7 P- U# z9 Y* ~7 z% |The family history was remarkable for the father,
: c/ ^1 Y5 B1 g2 @1 jwho was diagnosed with hypothyroidism at age 16,/ k6 \: G& A; z: d( S, l3 e8 z
which was treated with thyroxine. The father’s% M% \' z9 h5 `( Z
height was 6 feet, and he went through a somewhat
) z( M9 G$ O2 k8 A" p# ?: n! U$ [early puberty and had stopped growing by age 14.' Y# @" C0 e; |" [* f. U# N& E$ v3 s
The father denied taking any other medication. The* _! e( h0 v5 j
child’s mother was in good health. Her menarche
9 i# C/ k/ o8 V7 ^6 Twas at 11 years of age, and her height was at 5 feet
  C4 g$ S! @/ Z: D9 J; E5 inches. There was no other family history of pre-
4 R+ H, D* O; }cocious sexual development in the first-degree rela-
' b; p/ W: m5 u& a5 e1 y8 {tives. There were no siblings.
7 Q8 ]# B/ F( K9 N+ `. APhysical Examination' A0 [9 d8 S1 C- I. a
The physical examination revealed a very active,
% d) b! T, U5 m7 \6 o' G/ wplayful, and healthy boy. The vital signs documented
- I" j5 V& [! J  na blood pressure of 85/50 mm Hg, his length was# v8 H4 |( V2 m# c& @: S; E
90 cm (>97th percentile), and his weight was 14.4 kg
) P  o  K/ I2 p/ v/ ?5 J( ?(also >97th percentile). The observed yearly growth( J- o8 i2 f. ]* I/ Y: v
velocity was 30 cm (12 inches). The examination of
- |4 F: V* }3 b  C, z" ]" Jthe neck revealed no thyroid enlargement.
: J9 j/ s$ D% QThe genitourinary examination was remarkable for
2 V+ W4 W2 g- c3 _enlargement of the penis, with a stretched length of- u% N! y6 l) Z- p8 e4 M7 ~
8 cm and a width of 2 cm. The glans penis was very well( C3 a: m0 B8 B  |8 N' @  ^
developed. The pubic hair was Tanner II, mostly around
* Q, T1 p* i/ Q$ k* t540) \" b& k, b! t. r: f
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from4 j' g+ g2 z& x2 L1 H
the base of the phallus and was dark and curled. The7 M( I4 h7 t5 P: O- P( Q* s6 F4 q, z
testicular volume was prepubertal at 2 mL each.7 I: W2 l9 j0 g. R
The skin was moist and smooth and somewhat
' H. g8 i! x3 V! b# roily. No axillary hair was noted. There were no
9 [1 h2 ]9 z+ j  [8 y' H  mabnormal skin pigmentations or café-au-lait spots." p+ c8 F" D1 @5 X% b& |9 r
Neurologic evaluation showed deep tendon reflex 2+
3 F. `. z, e, p) n- j6 h* h9 Gbilateral and symmetrical. There was no suggestion
. w8 K9 q4 V) H/ G0 B1 [of papilledema.
  [* y6 ~5 \3 g& q& h. {5 O" lLaboratory Evaluation
! t! Z% L+ _# V+ e$ X) ^+ ]The bone age was consistent with 28 months by: k9 ?* d. R2 R# h5 C; [
using the standard of Greulich and Pyle at a chrono-0 M9 c3 d8 O$ q/ g
logic age of 16 months (advanced).5 Chromosomal# R7 ^: F( t# E& g% P, R
karyotype was 46XY. The thyroid function test
6 O& m4 x# C5 a, b% z$ dshowed a free T4 of 1.69 ng/dL, and thyroid stimu-6 }9 g; }7 P; |: F! A/ i+ i1 H
lating hormone level was 1.3 µIU/mL (both normal).
" w7 t! e/ ^! V' ~( pThe concentrations of serum electrolytes, blood
* Q( j+ t' e/ \, rurea nitrogen, creatinine, and calcium all were/ T. Y+ P  a* p* a9 n& d
within normal range for his age. The concentration- y, i* {9 S5 q! l. S" p
of serum 17-hydroxyprogesterone was 16 ng/dL
8 d" t$ Y! R. {" H(normal, 3 to 90 ng/dL), androstenedione was 20
/ j& ]! R# F7 ?2 ?3 dng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-& u* U. @; Z! v7 {+ n
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
# Y+ H: e; a2 K7 ~! v% Xdesoxycorticosterone was 4.3 ng/dL (normal, 7 to9 S  @  G9 |2 @, A: Q* h
49ng/dL), 11-desoxycortisol (specific compound S)
/ C/ ^, E2 k' e) Q/ Mwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-. o% C4 h9 n, g6 \% q
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total4 T* n( d1 y3 X; E. c! `; i
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
' k0 W4 i' Q" w* u/ S2 ^and β-human chorionic gonadotropin was less than
6 P( t5 y( h) d8 L5 mIU/mL (normal <5 mIU/mL). Serum follicular
- V! h0 X4 L% Kstimulating hormone and leuteinizing hormone  g1 m- G+ _; o
concentrations were less than 0.05 mIU/mL4 F, Y9 O' Y( w) t6 `2 s$ G+ a
(prepubertal).
7 U) F' K$ U2 l: |1 aThe parents were notified about the laboratory
5 z$ S( v! {: yresults and were informed that all of the tests were$ T) r9 k$ V0 y' r% T" m
normal except the testosterone level was high. The# Q- `0 q. U% @4 w6 p4 t0 q/ Y
follow-up visit was arranged within a few weeks to
7 h! s/ w( |7 ^- ]0 @- wobtain testicular and abdominal sonograms; how-
" S4 u+ C4 [2 b9 I. r" m- Kever, the family did not return for 4 months.
" Y1 k( A# s: X" C' E2 }Physical examination at this time revealed that the6 r% y$ B2 L1 d+ C( J
child had grown 2.5 cm in 4 months and had gained
$ R+ Z9 v; s6 E4 I2 Y" ]" k- q2 F+ I7 K2 kg of weight. Physical examination remained
. b/ H, c7 \% R* Vunchanged. Surprisingly, the pubic hair almost com-
$ v$ v) L8 C6 g1 Q/ D* R4 ?pletely disappeared except for a few vellous hairs at
( V4 S1 W- {/ c; p  X1 Qthe base of the phallus. Testicular volume was still 2) _0 K$ k5 E' W% [* f- D
mL, and the size of the penis remained unchanged.( A/ O- P3 {& T- S: p4 W
The mother also said that the boy was no longer hav-
8 E" b4 ?/ M! |8 z& D' H  Ming frequent erections.1 _2 \  X1 i+ e5 q* |  f1 q
Both parents were again questioned about use of. J9 m8 B' ], K
any ointment/creams that they may have applied to5 j& ?3 y  f! p& ]9 a
the child’s skin. This time the father admitted the
4 k6 b- h' F3 m/ f* w' cTopical Testosterone Exposure / Bhowmick et al 541& c" Z# z9 K+ w% a
use of testosterone gel twice daily that he was apply-
5 o3 p9 f2 r$ ]1 ~8 p; jing over his own shoulders, chest, and back area for5 f# |) C2 Y+ t) @* i
a year. The father also revealed he was embarrassed
: q8 }& `8 M& p& D1 Mto disclose that he was using a testosterone gel pre-2 a5 M2 l3 D2 @/ V. y% o
scribed by his family physician for decreased libido
2 D3 f4 z' O9 F! i1 Msecondary to depression., w8 F# A7 P8 d9 c! N) J
The child slept in the same bed with parents.* I, |  T. ]6 u% }3 u* a
The father would hug the baby and hold him on his- ^. t6 d3 N/ t7 _9 I: M: y
chest for a considerable period of time, causing sig-5 u$ y* L" r( s. _; g8 H* b
nificant bare skin contact between baby and father.
3 h% l3 d% {) @5 CThe father also admitted that after the phone call,% p( p( [7 Z: L- X3 H* I' k
when he learned the testosterone level in the baby4 Q) b5 @1 r- o6 Y! L
was high, he then read the product information" h: b* Z8 n% m% q* k2 y" g
packet and concluded that it was most likely the rea-  e$ G1 t4 a6 i) r. Y7 T: N
son for the child’s virilization. At that time, they& y) c" |+ m! b4 h
decided to put the baby in a separate bed, and the
' ]$ U& f& B4 Q; n$ _5 A3 dfather was not hugging him with bare skin and had1 S% g0 m8 I; p2 v" Z. y1 X
been using protective clothing. A repeat testosterone
6 t% B5 D, j6 [* o. P: v, ~test was ordered, but the family did not go to the3 [& K6 P3 t8 _' R( o
laboratory to obtain the test.
3 i* V4 g6 d* E/ {4 @# J) ]Discussion$ _0 v8 _  \4 ~3 ]4 i6 T3 o
Precocious puberty in boys is defined as secondary
8 C2 d7 ~1 a) G1 ?3 y6 P% |1 Csexual development before 9 years of age.1,4' \; H7 L' f* F- Q4 Y1 T3 f
Precocious puberty is termed as central (true) when
% x. t7 |( |6 o  o' e, M  pit is caused by the premature activation of hypo-4 ]: F3 Q- t3 A1 f2 t4 N; {
thalamic pituitary gonadal axis. CPP is more com-
) ~0 z  u9 z" D: smon in girls than in boys.1,3 Most boys with CPP8 S7 q% J* R# p0 D
may have a central nervous system lesion that is
. v% u( a6 C8 H. [& B- M/ wresponsible for the early activation of the hypothal-" h0 ~& V; _/ i
amic pituitary gonadal axis.1-3 Thus, greater empha-. V- F' }" c$ d) e( Q9 i
sis has been given to neuroradiologic imaging in
" k4 C8 Z  `& ^: b, `1 Jboys with precocious puberty. In addition to viril-$ t& I/ a6 c2 W1 T
ization, the clinical hallmark of CPP is the symmet-
2 a8 p$ b6 @& ?9 s) l0 q: K( grical testicular growth secondary to stimulation by  D( O7 B7 T  s$ a; m# t# T3 F
gonadotropins.1,3
8 O6 T# F( v7 q) gGonadotropin-independent peripheral preco-
/ o$ }/ j0 ]$ p3 s' scious puberty in boys also results from inappropriate. n! N- C6 f* o
androgenic stimulation from either endogenous or
+ {8 D9 Z" U6 J8 bexogenous sources, nonpituitary gonadotropin stim-
/ Z) P' p& A$ nulation, and rare activating mutations.3 Virilizing$ ~& t, s7 E' l2 c% M
congenital adrenal hyperplasia producing excessive
; S6 p& x: I$ L; N( d0 ^! R7 [adrenal androgens is a common cause of precocious. R2 l0 p$ ?) p+ f) J. K
puberty in boys.3,4
- f0 X' j3 G3 N" h  F/ JThe most common form of congenital adrenal
% y. p8 |& ?) m! ~  thyperplasia is the 21-hydroxylase enzyme deficiency.' j& }9 Q1 P6 s! v9 O: O4 [
The 11-β hydroxylase deficiency may also result in4 D! Q( h! ^+ n2 [' O
excessive adrenal androgen production, and rarely,& P3 G9 n$ Y! \+ P9 z1 g# C+ ]
an adrenal tumor may also cause adrenal androgen
" `( T1 r+ B! f- Z' i5 e- Q. [excess.1,3- `1 f# X: O" j7 T& L, y: V
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
: W; g8 I- X! p' m+ M9 x8 _3 v542 Clinical Pediatrics / Vol. 46, No. 6, July 20076 j# j- L# j( j
A unique entity of male-limited gonadotropin-4 K  B8 a+ E+ l, h' x
independent precocious puberty, which is also known6 p' i. g* w( L7 A( V
as testotoxicosis, may cause precocious puberty at a
* v- }# F$ x, R. A2 p, v- c  lvery young age. The physical findings in these boys, b+ l! L2 r2 G- r8 o& J5 S- r
with this disorder are full pubertal development,7 E1 L- B" b& k, o8 j# ?
including bilateral testicular growth, similar to boys( k1 z- T+ ~) O" }
with CPP. The gonadotropin levels in this disorder
& [6 U6 K' ?2 V1 }4 xare suppressed to prepubertal levels and do not show+ M, u4 t  t( K
pubertal response of gonadotropin after gonadotropin-
( `- Q1 E3 R; i/ P. J! n5 Vreleasing hormone stimulation. This is a sex-linked
2 P4 h. K3 c1 |% w6 Q4 `1 F9 Gautosomal dominant disorder that affects only
4 m8 V. O  d/ c: T- Emales; therefore, other male members of the family6 `! v1 J, d: A% n  j& o; y
may have similar precocious puberty.3
. j# s, _" @: `6 L, ^  GIn our patient, physical examination was incon-$ _" i% s) |% s' j' C: H: c/ \
sistent with true precocious puberty since his testi-
' V% s; D  w+ tcles were prepubertal in size. However, testotoxicosis
7 @+ K2 ?1 @8 y3 R# qwas in the differential diagnosis because his father/ l* c5 `, c  V- w$ s7 I
started puberty somewhat early, and occasionally,% B) q0 f( x, u. q# Z  a7 w
testicular enlargement is not that evident in the
2 Z  I+ N+ n( V& Y  a. Z$ Ebeginning of this process.1 In the absence of a neg-+ ?$ Z3 L+ J. ]6 J# A
ative initial history of androgen exposure, our
' c0 R; G! _, F' T" {biggest concern was virilizing adrenal hyperplasia,  Z- L9 j" C7 p, X
either 21-hydroxylase deficiency or 11-β hydroxylase, z0 l/ z. j8 ?7 k
deficiency. Those diagnoses were excluded by find-: I' q/ p3 V* C- ]+ d
ing the normal level of adrenal steroids.
% R' {3 w  q. MThe diagnosis of exogenous androgens was strongly, m3 a7 ~: j- V4 r# o/ n
suspected in a follow-up visit after 4 months because
( ]7 u. |2 |$ ?$ i4 u% nthe physical examination revealed the complete disap-
  A' g9 u* L) z" {. I' upearance of pubic hair, normal growth velocity, and3 v$ x, ?" @' K8 X) V0 {) u
decreased erections. The father admitted using a testos-) {  t4 ^% Q! h3 u/ j
terone gel, which he concealed at first visit. He was
4 @1 g. K! h% t; g  Q( ^using it rather frequently, twice a day. The Physicians’- w  x& c8 I. b
Desk Reference, or package insert of this product, gel or
) U4 Q5 d4 s! L# g, Z3 ccream, cautions about dermal testosterone transfer to
, N5 E( E2 j3 y5 z; Xunprotected females through direct skin exposure.* T1 G$ V8 E9 {/ P( E, G5 X( q
Serum testosterone level was found to be 2 times the* f6 _' B1 B' v- n; C. q
baseline value in those females who were exposed to/ c; m+ {$ q, y' f. o
even 15 minutes of direct skin contact with their male
1 A8 T9 P# ?1 y& w9 R: K+ ?partners.6 However, when a shirt covered the applica-' B+ W. U0 s+ O: z- H0 \' X
tion site, this testosterone transfer was prevented.
" i0 e  X# n8 C( ]9 j% K2 _0 POur patient’s testosterone level was 60 ng/mL,5 m* K, A' g9 L5 q0 O4 Z$ {
which was clearly high. Some studies suggest that
, ]5 M8 N! P: ]/ \6 Gdermal conversion of testosterone to dihydrotestos-
& l  ^+ ~, ~& a9 G  V& z; H  mterone, which is a more potent metabolite, is more0 x5 @" Y$ a3 k) w  ?
active in young children exposed to testosterone4 U# v+ a! t9 Q2 g' k/ `
exogenously7; however, we did not measure a dihy-- ~+ T; C( v, i$ |
drotestosterone level in our patient. In addition to# n, Q7 w1 h# G; h
virilization, exposure to exogenous testosterone in6 a: |' t) V' f- e
children results in an increase in growth velocity and' a, }& h( C6 U1 \
advanced bone age, as seen in our patient.3 t' \& E. B: u9 d" h
The long-term effect of androgen exposure during9 X8 b) B& \. u0 e5 b) f: @
early childhood on pubertal development and final
, B* Q9 I1 U( B! fadult height are not fully known and always remain
5 f7 u) G8 k8 U; m  Qa concern. Children treated with short-term testos-0 ^6 J4 o! i  K) A& |* d0 H
terone injection or topical androgen may exhibit some6 H% a/ l8 T9 ^" ^- Y
acceleration of the skeletal maturation; however, after  }# D1 k% o3 q1 N( C; W8 O
cessation of treatment, the rate of bone maturation
0 v9 w! d" W7 A. F" |0 f6 h. Mdecelerates and gradually returns to normal.8,9
6 [; r) W3 E' `  |" H1 OThere are conflicting reports and controversy) c; f5 w7 C" J5 g$ c) M
over the effect of early androgen exposure on adult$ c% [0 t9 v# q; K
penile length.10,11 Some reports suggest subnormal+ G% i2 o& a1 d: q- i
adult penile length, apparently because of downreg-* A) G' B# I  G% }9 ]
ulation of androgen receptor number.10,12 However,( Q$ u( ~; g' Q7 d
Sutherland et al13 did not find a correlation between
' R2 H7 x. I3 B" Q: ^: d0 Tchildhood testosterone exposure and reduced adult& g* [- v/ S/ [+ r/ l4 y3 J
penile length in clinical studies.
7 x4 n  h  ~- t  rNonetheless, we do not believe our patient is$ |- P2 A4 P9 U) [
going to experience any of the untoward effects from
) S) [7 [9 I9 _5 x: e; btestosterone exposure as mentioned earlier because3 W: X' c( m* l$ Y' j3 u1 W
the exposure was not for a prolonged period of time.- U$ Y5 ^/ c- g) F
Although the bone age was advanced at the time of* A& ^. D4 i6 O
diagnosis, the child had a normal growth velocity at
* x  O1 a0 ^3 \' L" C, E) jthe follow-up visit. It is hoped that his final adult
1 Z2 m- j, P+ d" vheight will not be affected.7 k- b6 P4 j3 N
Although rarely reported, the widespread avail-6 k) t1 s) E& k$ h- u* h
ability of androgen products in our society may  c$ ^, y$ S  E: \
indeed cause more virilization in male or female3 p) Y* v4 K+ U! u
children than one would realize. Exposure to andro-
: K/ V) P3 }, Zgen products must be considered and specific ques-
" H4 P2 b9 b3 `- ^. w! R6 j! l: e" `tioning about the use of a testosterone product or
' k8 U9 d- P- Ggel should be asked of the family members during
' I* E3 B8 h4 A4 b' f& nthe evaluation of any children who present with vir-* C, S0 \! c0 y+ W
ilization or peripheral precocious puberty. The diag-
" x+ H2 X0 e- M1 s& |nosis can be established by just a few tests and by
5 ^% ]' @5 ?+ Z2 n9 mappropriate history. The inability to obtain such a2 m# H, j2 P2 }7 |
history, or failure to ask the specific questions, may6 b7 m" z& S- L% X
result in extensive, unnecessary, and expensive
9 ^. q$ M# F! D/ E% }investigation. The primary care physician should be! T; N+ Y; a7 m) r8 Q
aware of this fact, because most of these children
8 P4 r1 E, H# ]& `' L3 imay initially present in their practice. The Physicians’
$ ^, u0 `1 l: k7 J8 j2 vDesk Reference and package insert should also put a
1 z2 f. H8 m' b' dwarning about the virilizing effect on a male or
6 K7 N' i8 }8 ]2 S1 o0 ufemale child who might come in contact with some-: L! e% n9 f6 G  H, ^3 h$ u6 M
one using any of these products.0 R1 ]$ i4 w$ L
References
3 v9 f8 J2 `1 I# A% i1. Styne DM. The testes: disorder of sexual differentiation
/ D0 s, `3 Q& h5 F8 u7 Xand puberty in the male. In: Sperling MA, ed. Pediatric
" e) T8 D7 T# i8 C# r' }Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
7 J0 g2 s+ L6 V0 H) i+ k# H+ X2002: 565-628.
$ `) B$ [: Y7 E- H! i: m# ]0 E2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious; L" T' ]1 |0 {: s  ?* ~; b4 b
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!
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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

/ g2 D2 I4 |2 }8 c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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