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Sexual Precocity in a 16-Month-Old
6 Q" b, m- W  ]! [5 T8 TBoy Induced by Indirect Topical
1 e. Q3 K8 M, R2 t3 KExposure to Testosterone
% _2 U* S8 v! v  t% h, I7 uSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
4 B8 z5 d: x1 @, r# b% [4 Fand Kenneth R. Rettig, MD11 G* ~% o4 X/ D9 J# W- c
Clinical Pediatrics
5 A" b* [' }9 c8 c* hVolume 46 Number 63 `' c0 E0 b+ a' {# |( U8 N  X
July 2007 540-543) `$ i) Q/ s) i/ r3 _6 B8 ~& E- \
© 2007 Sage Publications0 P6 ~+ a1 m& Y6 S+ k- w
10.1177/0009922806296651
* ]  j) H0 K$ i; ]0 p" ohttp://clp.sagepub.com
8 I! [( t9 t5 E' Q1 l- {' A; @hosted at; Z4 s; V+ F5 n! V( |
http://online.sagepub.com9 q0 F" P; x* r
Precocious puberty in boys, central or peripheral,
: ?3 h, |$ q4 A( P$ M7 \% J$ O8 Qis a significant concern for physicians. Central
& T; f) H) P2 B% Hprecocious puberty (CPP), which is mediated
8 T% L( U5 z. u6 A8 ]/ _9 uthrough the hypothalamic pituitary gonadal axis, has8 _, X7 a0 r* o0 S! A2 {' B6 b" a
a higher incidence of organic central nervous system  P' r: }1 ^0 a( C$ s" C
lesions in boys.1,2 Virilization in boys, as manifested, c8 m7 B' p" r0 y7 ]# r: r1 s
by enlargement of the penis, development of pubic
( ]7 p* N2 F! Y: bhair, and facial acne without enlargement of testi-
3 p5 k5 ~# o; o, Ncles, suggests peripheral or pseudopuberty.1-3 We+ k3 _8 ~6 m& v. _/ H. k/ l
report a 16-month-old boy who presented with the, g4 x( |- r9 Q) W  f$ a0 B
enlargement of the phallus and pubic hair develop-
, ~: N/ }9 H( `1 _5 bment without testicular enlargement, which was due
8 Z1 e- D" M% M6 J! Nto the unintentional exposure to androgen gel used by  P9 d% N/ K# X  [6 D
the father. The family initially concealed this infor-
* D2 G2 Z7 u# S$ i& ~0 tmation, resulting in an extensive work-up for this# H* `, ~+ K+ ?
child. Given the widespread and easy availability of1 U8 l, b  z$ A: |- W
testosterone gel and cream, we believe this is proba-3 y" g7 i7 A) \4 r3 L3 y
bly more common than the rare case report in the
' J. g2 o# N& ^) N# J$ U, g; ^literature.4" g6 Q1 z! N3 m7 V4 u
Patient Report
3 g$ W8 V9 Y/ z+ ]6 z$ iA 16-month-old white child was referred to the
/ J1 T' \  R% P0 D$ ]/ z( Dendocrine clinic by his pediatrician with the concern3 u- t! l# ]0 a* p$ ~' M5 ?
of early sexual development. His mother noticed# p# o( y5 ], U) H
light colored pubic hair development when he was7 O0 |3 ]' P/ q3 S/ K
From the 1Division of Pediatric Endocrinology, 2University of
  v: z0 W. w8 u8 {South Alabama Medical Center, Mobile, Alabama.
* E! W# c7 p2 H1 KAddress correspondence to: Samar K. Bhowmick, MD, FACE,
( t* r; N; g" H6 mProfessor of Pediatrics, University of South Alabama, College of1 A/ B6 s8 N+ g( k* Z$ S& Z
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;+ B( @6 f. j  S* e& e* e% e$ I
e-mail: [email protected].
1 M) Q, O7 O3 Mabout 6 to 7 months old, which progressively became
- P/ D- U8 }, ?# ?+ udarker. She was also concerned about the enlarge-
1 n4 X2 z7 ~0 S6 d1 Mment of his penis and frequent erections. The child/ b+ a& }1 H5 ^2 c
was the product of a full-term normal delivery, with
; i; O- a0 _) ]9 \0 e& Wa birth weight of 7 lb 14 oz, and birth length of: Z" O7 W9 b+ I6 ]8 E1 @% g
20 inches. He was breast-fed throughout the first year3 x/ B8 S9 n8 I8 q1 F
of life and was still receiving breast milk along with  X2 @; X! @- O. e! J! G) \. o
solid food. He had no hospitalizations or surgery,  U+ a" v( _9 b8 y
and his psychosocial and psychomotor development; g; X5 G5 Z+ J. I; \8 i
was age appropriate.
" e- ^; V7 A1 q) I, z" rThe family history was remarkable for the father,7 Z6 `1 G$ M! r  p$ y4 @8 T
who was diagnosed with hypothyroidism at age 16,1 Q5 r2 a" H+ P3 B7 u
which was treated with thyroxine. The father’s
$ m# E" F5 G- [$ V$ l9 Fheight was 6 feet, and he went through a somewhat9 ?$ |3 R0 X8 e$ f  q
early puberty and had stopped growing by age 14.3 D( n4 @" S: E8 m8 q0 ]' H
The father denied taking any other medication. The" U! _* c  D; d- V+ F% W  @
child’s mother was in good health. Her menarche
2 d4 u; L+ ~  Mwas at 11 years of age, and her height was at 5 feet" h' ?- y; z- ?3 W9 b
5 inches. There was no other family history of pre-
) ]& g  T2 G# E0 Tcocious sexual development in the first-degree rela-1 y- D/ d* I2 n1 B# V
tives. There were no siblings.
, a( s$ m! ?# e& a" c+ yPhysical Examination& z) g: ^: }- K; w7 B8 u: m" d  j: \' k
The physical examination revealed a very active,
& ]6 c$ y* s# h+ aplayful, and healthy boy. The vital signs documented
6 \% W* o6 [4 Z5 h/ Wa blood pressure of 85/50 mm Hg, his length was9 H$ x% |0 m0 q7 b
90 cm (>97th percentile), and his weight was 14.4 kg
/ J, L, Z- l6 Z: h  i5 C& }(also >97th percentile). The observed yearly growth
9 N) a$ E* r) @1 D  [) a* d% {velocity was 30 cm (12 inches). The examination of- i2 K- |" E0 j6 K% P. }
the neck revealed no thyroid enlargement.  X8 a; ?2 w6 ]) ]% M  f
The genitourinary examination was remarkable for7 @# U$ l+ d; T: T/ [% j" f; V' A
enlargement of the penis, with a stretched length of
, R0 O1 {" ]5 t1 ?  b" ?8 cm and a width of 2 cm. The glans penis was very well
/ x  U  @5 T, D+ t6 {5 Zdeveloped. The pubic hair was Tanner II, mostly around
0 k  `" |  a+ `5403 _- C7 i' Z" c* ]
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
/ M( h& _  H. G9 n6 ]the base of the phallus and was dark and curled. The- e9 c! J7 V: H: K  }1 r$ e8 o; P
testicular volume was prepubertal at 2 mL each.
# @4 I4 ~! U9 F# B& `+ XThe skin was moist and smooth and somewhat
2 X: }3 S! r! [9 }oily. No axillary hair was noted. There were no
+ ?( A* Y/ M8 p$ n' sabnormal skin pigmentations or café-au-lait spots.( O, \& Y8 r6 @3 }" F% g1 l8 f' M
Neurologic evaluation showed deep tendon reflex 2++ v! Q: C6 f: t8 F* k0 X
bilateral and symmetrical. There was no suggestion
% F* L+ @/ k3 I3 ?# ^+ {( t) h. y; Nof papilledema.
" y0 [6 X- \9 c. iLaboratory Evaluation
$ g$ X  B. A, R# j# E: K. E) u+ mThe bone age was consistent with 28 months by
0 V0 q7 N( L3 M) `& p+ Wusing the standard of Greulich and Pyle at a chrono-
) K  V( d7 A  W  r8 n, ]% Zlogic age of 16 months (advanced).5 Chromosomal' i- C' J$ G% @: l. X, \& _3 [
karyotype was 46XY. The thyroid function test
& Z# ^% \( J3 r; E/ Q6 `) `# Yshowed a free T4 of 1.69 ng/dL, and thyroid stimu-9 ?0 ~6 v2 k4 e! E! P
lating hormone level was 1.3 µIU/mL (both normal).: ]+ b0 t1 {: e$ n% Y
The concentrations of serum electrolytes, blood  c% o6 }9 G9 S9 D% _: |
urea nitrogen, creatinine, and calcium all were
3 G& `5 ]2 C6 c# cwithin normal range for his age. The concentration
" }; D) ~6 C9 Q# Nof serum 17-hydroxyprogesterone was 16 ng/dL. j6 \: w7 u" u' X3 f8 h4 f+ K* a
(normal, 3 to 90 ng/dL), androstenedione was 20
, G5 ^) A( l1 rng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-" u9 z( U0 w1 B0 s) N* m& Z
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
1 @, M1 k; G/ I4 vdesoxycorticosterone was 4.3 ng/dL (normal, 7 to
$ P" `2 R" M  h& ]2 g/ w49ng/dL), 11-desoxycortisol (specific compound S)
9 M, @% O  y- j4 j9 @2 ~was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
) X  F, q- F7 x0 B$ ?tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
. O/ y# I& d* i$ H8 ^testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
- V. ~0 ]6 \) Rand β-human chorionic gonadotropin was less than
* ^, b& f- R- _% B) D% F5 mIU/mL (normal <5 mIU/mL). Serum follicular
2 B$ ~- K3 f0 V' k) R+ u, `stimulating hormone and leuteinizing hormone& Q' P$ E: W' C  A2 d3 f
concentrations were less than 0.05 mIU/mL
1 V2 I7 r3 Y; n& w! K( a(prepubertal).% Y* O& p5 ]! \
The parents were notified about the laboratory/ I. s4 D. f1 C5 a' k, K. m
results and were informed that all of the tests were* H% _4 P2 b6 @* ~$ A+ }- `# ~& h
normal except the testosterone level was high. The
7 M1 S5 \* q7 j9 c( ufollow-up visit was arranged within a few weeks to2 E3 E6 G% j$ x$ P
obtain testicular and abdominal sonograms; how-
$ E9 v/ a4 _" Y* Oever, the family did not return for 4 months.
# |1 V$ L3 o2 u: V" XPhysical examination at this time revealed that the( n7 i1 r7 A& V
child had grown 2.5 cm in 4 months and had gained; z) M% n# o- E! r! |, p) v
2 kg of weight. Physical examination remained
) f! M. s, [! R  v8 L1 X, W% M1 ]# qunchanged. Surprisingly, the pubic hair almost com-
2 S% K+ S* v) b% gpletely disappeared except for a few vellous hairs at( Z9 e. H: A" q" F, l% u- q$ d5 v
the base of the phallus. Testicular volume was still 2
! V5 V2 Z  `$ U2 Z2 ?mL, and the size of the penis remained unchanged.
8 n5 W: B8 e8 u( q: v: ~# V" mThe mother also said that the boy was no longer hav-
; a" ]1 E9 W+ s8 }, Oing frequent erections.- n3 H3 f; t% e8 d* J
Both parents were again questioned about use of
  m, G& m6 `9 n6 D& P( fany ointment/creams that they may have applied to
/ J' b0 M) P; ]' y. q; Z  }the child’s skin. This time the father admitted the8 I) M" F) o  q0 [2 a- {; B( D
Topical Testosterone Exposure / Bhowmick et al 541
7 c0 Y# m, ~7 Nuse of testosterone gel twice daily that he was apply-
1 h# p2 c2 C2 [9 D0 v* Ming over his own shoulders, chest, and back area for
/ p& i& v! m* ?: O* T' Na year. The father also revealed he was embarrassed
/ f% q3 W  U* d: _. }4 m% E2 oto disclose that he was using a testosterone gel pre-) U4 a" H- m! R" i7 X" k
scribed by his family physician for decreased libido
! Q! X0 V% B8 r0 p; Osecondary to depression.
# B* [6 K! G+ ^8 [8 F" s) [% U+ XThe child slept in the same bed with parents.
7 d! B( V$ g7 M: {  }The father would hug the baby and hold him on his
) Z4 t& L- ^4 ^9 q0 j' Achest for a considerable period of time, causing sig-
& c- P7 k; @; }$ ^3 Z7 ~nificant bare skin contact between baby and father.5 D2 r3 H' v7 }
The father also admitted that after the phone call,6 c% [: P; h* h* i+ s. V
when he learned the testosterone level in the baby
0 d% E) y6 g4 g: Hwas high, he then read the product information+ w. A9 X3 t6 K+ C& n2 E$ j
packet and concluded that it was most likely the rea-/ c, o+ |; p6 Q& O2 M! A" G* F
son for the child’s virilization. At that time, they% W7 d9 ]3 t  Y- Q; T
decided to put the baby in a separate bed, and the+ l2 K: A$ Z8 ~; T
father was not hugging him with bare skin and had
: ?) \4 ]3 p, f8 t8 d; Kbeen using protective clothing. A repeat testosterone: ~; N6 o4 u& z
test was ordered, but the family did not go to the/ K. V3 O0 c/ p6 U! D* n
laboratory to obtain the test.
  U( S" K" ]" T( ^4 LDiscussion" g" O% O4 y) n2 d
Precocious puberty in boys is defined as secondary7 D4 i) E8 t' M' Y* S
sexual development before 9 years of age.1,45 a1 g& l! w& _, W* ]4 U
Precocious puberty is termed as central (true) when" P; N: l: W; h, V
it is caused by the premature activation of hypo-9 h$ Q5 v- d% R
thalamic pituitary gonadal axis. CPP is more com-2 ~/ A2 ?: u# i7 G1 v5 [
mon in girls than in boys.1,3 Most boys with CPP
- A) c) @# w+ d* ]: f5 Qmay have a central nervous system lesion that is
6 a6 h+ Q% \6 V- y# s: C. zresponsible for the early activation of the hypothal-
% I/ p- ~0 Q7 [4 P! Jamic pituitary gonadal axis.1-3 Thus, greater empha-8 k5 ~& t" t/ }+ p: V$ Z
sis has been given to neuroradiologic imaging in. o2 V# d+ Q& W
boys with precocious puberty. In addition to viril-! _- u0 ~9 d) J; B( Q2 h/ N* _+ F
ization, the clinical hallmark of CPP is the symmet-4 s9 c" {5 K$ U6 g2 {, E5 H
rical testicular growth secondary to stimulation by
% J( R: G4 Y* t' |gonadotropins.1,3
4 U& b" c, a% q: rGonadotropin-independent peripheral preco-
& T9 T( k/ |/ v8 Acious puberty in boys also results from inappropriate) \" a7 `7 x) z# c8 ?, ?5 |
androgenic stimulation from either endogenous or
  d$ `/ A+ q8 O* P5 n# R( g& bexogenous sources, nonpituitary gonadotropin stim-8 K- G7 Y5 z6 R# [
ulation, and rare activating mutations.3 Virilizing
* ?3 r) |! o( S, x4 x5 {congenital adrenal hyperplasia producing excessive9 C, S8 B0 |: ~" X8 j) {
adrenal androgens is a common cause of precocious
5 R$ e3 I( ~% h. F' g# C" R: s* a& ppuberty in boys.3,4( x& s5 O5 j* K) B
The most common form of congenital adrenal
0 e( ~  ]5 d% `; O( A2 h; Qhyperplasia is the 21-hydroxylase enzyme deficiency.
' P0 a8 a& e3 X$ o5 T5 oThe 11-β hydroxylase deficiency may also result in
- K8 O+ H- L3 g+ Z: xexcessive adrenal androgen production, and rarely,9 _# G  N5 t8 _8 j! p! g
an adrenal tumor may also cause adrenal androgen* U6 J- ^8 B% L7 X" [! a
excess.1,3
1 F( `  c3 e$ `$ v/ b( K! ]* t6 gat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from, n: V# T/ ]) l2 b5 B5 G4 `2 p6 k
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
6 ~) s! Y; ^6 I# f- J; C; j4 k' [1 ZA unique entity of male-limited gonadotropin-# L( }# `3 S. }; l8 `8 k* d
independent precocious puberty, which is also known2 R9 o# P7 R9 P4 `0 p: `# X+ t  d
as testotoxicosis, may cause precocious puberty at a/ J& d% \) B* z3 c" I" k; M# B
very young age. The physical findings in these boys
: v" h. t# E) J. U+ m2 E/ ?with this disorder are full pubertal development,
! m. m0 ]# F2 l% kincluding bilateral testicular growth, similar to boys
. a  u& |) ~1 h. ?6 [6 R3 ^2 twith CPP. The gonadotropin levels in this disorder
8 w% Z  r* l' K6 n9 aare suppressed to prepubertal levels and do not show- n3 o. y. n3 C- G- N  n
pubertal response of gonadotropin after gonadotropin-2 {) `3 T  u  a1 e1 p; [: p% n
releasing hormone stimulation. This is a sex-linked
+ N/ R  u+ S2 }# h$ C/ M0 Gautosomal dominant disorder that affects only& @, c  O1 y" u( ^( B% I# A
males; therefore, other male members of the family1 E& V* I! F% d
may have similar precocious puberty.3
. w3 `* ^% v9 [+ h+ M& d# e; tIn our patient, physical examination was incon-; _/ u1 @$ E* I- k8 J/ v
sistent with true precocious puberty since his testi-! D! D' |/ N, H" o! U' ~
cles were prepubertal in size. However, testotoxicosis
. O8 s  h8 t9 t& c7 ~3 N! l# A8 D5 \was in the differential diagnosis because his father9 m' g- p6 D% R7 v/ |; {
started puberty somewhat early, and occasionally,% f: c& X9 t* j+ D
testicular enlargement is not that evident in the0 d# R4 N  L) Y6 u, K+ Q8 U
beginning of this process.1 In the absence of a neg-
" Q, ^- c* P( t* e4 z+ b9 r0 vative initial history of androgen exposure, our
; Q; @: P6 k0 q/ n8 T" }7 z8 Jbiggest concern was virilizing adrenal hyperplasia,7 c. Q% R' e9 f2 \- M- i/ q9 ~
either 21-hydroxylase deficiency or 11-β hydroxylase
: p; _% S7 F5 mdeficiency. Those diagnoses were excluded by find-; w5 C! [: E- H* z' W
ing the normal level of adrenal steroids.
9 r+ |6 M7 b  h; g; [% `The diagnosis of exogenous androgens was strongly% ]- l3 j3 z; x7 a5 H$ |
suspected in a follow-up visit after 4 months because/ [6 q2 P1 [$ t. M
the physical examination revealed the complete disap-, K  S- `) B8 D0 q9 D3 z$ d
pearance of pubic hair, normal growth velocity, and
4 U* Z; i, b: Q, D+ c8 `% gdecreased erections. The father admitted using a testos-/ o, k# [. D3 I( K( p
terone gel, which he concealed at first visit. He was2 i+ z( Y9 l0 r  f" N+ R% l& |9 {6 X
using it rather frequently, twice a day. The Physicians’
* `) }+ l6 d8 z8 mDesk Reference, or package insert of this product, gel or3 _6 I5 C9 a7 @7 y/ F: u8 e' C" \
cream, cautions about dermal testosterone transfer to6 b1 W$ t9 |5 u7 G: m
unprotected females through direct skin exposure.# q, z7 \; E4 Z( x0 A* ?) a% m
Serum testosterone level was found to be 2 times the
0 m! s" }+ i( N1 c( @baseline value in those females who were exposed to
$ m& t$ h7 y5 W9 A" Geven 15 minutes of direct skin contact with their male
2 @( ]. R( f+ Q- opartners.6 However, when a shirt covered the applica-
6 X7 Z5 L, ^9 rtion site, this testosterone transfer was prevented.+ d0 w4 Z( F* g8 P
Our patient’s testosterone level was 60 ng/mL,
1 g4 r/ V' B: a! Dwhich was clearly high. Some studies suggest that( R4 z/ S7 ?0 t0 L- ~
dermal conversion of testosterone to dihydrotestos-2 W' D/ U/ L: L! @
terone, which is a more potent metabolite, is more" c# B) j: x6 o# L6 ]) D# c9 h
active in young children exposed to testosterone
; @+ g; e' n5 B" o7 V% Zexogenously7; however, we did not measure a dihy-
( \4 T6 V( ]7 @( K$ l& udrotestosterone level in our patient. In addition to) G$ m6 x2 P- I+ J# O1 ^! f1 Q. ?: `8 r
virilization, exposure to exogenous testosterone in
; k  g  U2 i8 @) M: t8 @children results in an increase in growth velocity and! L1 U) e- V" b$ ?/ l  L
advanced bone age, as seen in our patient.1 b: N' Z' S$ d
The long-term effect of androgen exposure during0 v5 j1 E3 i& Q( y9 q! \; J
early childhood on pubertal development and final
3 f# a/ ^% x6 Z, {/ g4 q7 d2 wadult height are not fully known and always remain
6 z2 n/ V* _& @a concern. Children treated with short-term testos-( i/ N6 w, M$ R1 Y: y
terone injection or topical androgen may exhibit some
. ~- ]. {% {2 i) t0 O% Racceleration of the skeletal maturation; however, after2 \. w0 u1 b( l
cessation of treatment, the rate of bone maturation7 r  ~/ H# }2 e  E9 W" ]) T6 w
decelerates and gradually returns to normal.8,9; j3 O% b2 b8 S# X/ |4 |( F. `
There are conflicting reports and controversy. A& s( U8 Q  k
over the effect of early androgen exposure on adult
7 n) B- i( y, N; k3 p+ M) Xpenile length.10,11 Some reports suggest subnormal. \4 _$ L% d1 {# {3 R# M
adult penile length, apparently because of downreg-: x! f8 {$ F% `' F, U8 N: H
ulation of androgen receptor number.10,12 However,
- q& k1 F( N  g7 B& Z" {# ?Sutherland et al13 did not find a correlation between
$ I5 m& D! V0 X/ s1 }- ychildhood testosterone exposure and reduced adult7 v* q- f5 K' B4 n8 @
penile length in clinical studies.
0 v' C. q7 i8 k6 HNonetheless, we do not believe our patient is' A4 w+ {0 @0 X1 i" S
going to experience any of the untoward effects from
% x: a9 q/ Z) w- k; M" Dtestosterone exposure as mentioned earlier because
0 V- j5 C. f  n; I; X: mthe exposure was not for a prolonged period of time.
8 n) K* n  M8 \8 Z4 hAlthough the bone age was advanced at the time of: N9 g4 J2 I) I- H( V! \; f. W
diagnosis, the child had a normal growth velocity at
% ~- d- {) |" u  }, o1 P8 Tthe follow-up visit. It is hoped that his final adult- C9 G' J) H& x5 Y
height will not be affected.
# `5 w4 ]4 ?/ {8 ?/ \- OAlthough rarely reported, the widespread avail-- z4 _1 o. N/ q/ c! B- _
ability of androgen products in our society may5 i, o2 l+ E7 q) F) J" n2 K
indeed cause more virilization in male or female/ U9 o' }' k" ]* R  b
children than one would realize. Exposure to andro-6 Y/ B9 p; I3 A3 k9 s
gen products must be considered and specific ques-
3 r3 M$ y0 A! o+ h: K6 ~: htioning about the use of a testosterone product or
: S, H8 }1 N# U' y0 X& Jgel should be asked of the family members during
( h2 Q! w6 F, V: N3 @7 J4 l( j4 Dthe evaluation of any children who present with vir-4 n4 [( X8 A) A& e/ G9 b' [
ilization or peripheral precocious puberty. The diag-
# _/ r$ s5 n6 N9 ~% N+ N; Snosis can be established by just a few tests and by
+ x1 Y+ h$ ?% T6 eappropriate history. The inability to obtain such a5 |# G! Y- L; P& a
history, or failure to ask the specific questions, may/ z/ l) l) ]. o+ v
result in extensive, unnecessary, and expensive
; t& x7 a4 }  A9 g/ b  Einvestigation. The primary care physician should be( @2 O1 B( m0 f
aware of this fact, because most of these children
; ~+ q5 E4 w: I- ~may initially present in their practice. The Physicians’2 g# @' X( |6 m: _4 F- Q
Desk Reference and package insert should also put a
/ r1 S7 V6 W( Awarning about the virilizing effect on a male or8 A9 r5 U+ H$ Q, E+ W3 A
female child who might come in contact with some-
8 o/ A$ w' t4 a  a5 Uone using any of these products.
7 [8 P4 V- \: Y6 e, oReferences
- V3 R  r; y! n2 E1. Styne DM. The testes: disorder of sexual differentiation' L4 E/ f4 @2 m# b9 Q6 P( u4 \) Y
and puberty in the male. In: Sperling MA, ed. Pediatric
' y( |3 Y; e; `; r: C: dEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
$ b5 ^* V: H0 E2002: 565-628.3 x; ~' Q' D$ V6 m5 M- H
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious' j& S7 d3 D% z# x0 S
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
( Y$ b% m- b/ ~6 o3 GBoy Induced by Indirect Topical  k  x& F6 L9 k/ r: ]5 Z$ S$ k
Exposure to Testosterone
; k7 n9 h, b/ DSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
! o2 u" G& }4 L' ?7 yand Kenneth R. Rettig, MD1  J1 O" C3 O  e0 [; D# ]3 G% u
Clinical Pediatrics
  _2 n$ e0 u+ z. z# q1 z  V$ b) x9 TVolume 46 Number 6
1 x: E$ V/ b5 R2 V$ LJuly 2007 540-543, T( Y5 v( H- x" I+ X$ z& @
© 2007 Sage Publications: I/ h1 J) f& p6 F$ A, \4 U1 x5 @. A9 [
10.1177/0009922806296651
, f' C( Q% }! c( H, ^http://clp.sagepub.com6 F! ]+ h$ e# E; B5 A4 c
hosted at
, E* J( ^( Q- [/ a" d6 hhttp://online.sagepub.com( T; |7 r/ p2 x; ]. h4 W- K% V/ s
Precocious puberty in boys, central or peripheral,
# u* k5 w9 X: cis a significant concern for physicians. Central
& x1 C/ @( p7 w6 L. zprecocious puberty (CPP), which is mediated
  L" A* v5 ]4 K4 |% pthrough the hypothalamic pituitary gonadal axis, has4 m  N) @0 W. L1 O. I
a higher incidence of organic central nervous system- q) I3 k. O0 q6 u
lesions in boys.1,2 Virilization in boys, as manifested: p4 A1 q5 i3 G7 |
by enlargement of the penis, development of pubic  n3 d; {) @( y" a
hair, and facial acne without enlargement of testi-
. G7 X( p) E- X9 ~cles, suggests peripheral or pseudopuberty.1-3 We& B. `) B9 Z$ q5 J6 _1 \7 N% [, m1 _
report a 16-month-old boy who presented with the
3 Z4 m5 ~2 n. `: O, j( I. r7 oenlargement of the phallus and pubic hair develop-
% K3 ]& v* {6 }: ]$ t9 E& Y8 rment without testicular enlargement, which was due8 S5 k' e8 n: O, D, S) w5 G! v6 V
to the unintentional exposure to androgen gel used by/ y2 Q: S7 a7 C
the father. The family initially concealed this infor-% k2 v( A; e( O3 k$ E. h! _
mation, resulting in an extensive work-up for this
; c. F, i1 E$ M, G) l8 C9 }+ uchild. Given the widespread and easy availability of
* L& x4 p+ L5 k4 O8 j+ p1 Atestosterone gel and cream, we believe this is proba-/ X+ S4 W% \7 P0 t
bly more common than the rare case report in the0 Z1 b* `: Z4 N- U  G: p
literature.4
% @$ y' A' _7 yPatient Report
& L; A4 k' h& }$ [3 r! FA 16-month-old white child was referred to the+ P3 O1 c5 b+ k6 B3 _! x8 |0 Z
endocrine clinic by his pediatrician with the concern* ]. _- H% z& F3 e: s2 C8 k! K
of early sexual development. His mother noticed2 }6 c6 O1 k) J, G# ?
light colored pubic hair development when he was
  w5 J0 U# f4 z$ E4 oFrom the 1Division of Pediatric Endocrinology, 2University of
8 ?+ d* i' `" }5 u6 lSouth Alabama Medical Center, Mobile, Alabama.
2 b# Q1 D: @/ Q1 Q2 C% EAddress correspondence to: Samar K. Bhowmick, MD, FACE,1 n5 ~8 M2 m0 ~" F. Z
Professor of Pediatrics, University of South Alabama, College of
2 m5 b' K7 {% z. ?9 v- pMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
2 H, h) G7 R+ O( d; \2 Ye-mail: [email protected].
" Z+ ^  p* o* W: t$ {( }2 {8 kabout 6 to 7 months old, which progressively became
5 k3 k/ ?! j/ q5 d0 E. P1 Sdarker. She was also concerned about the enlarge-
. F, f5 U" y( i8 \( A* y, x1 Z8 z& Yment of his penis and frequent erections. The child
9 y6 J6 Z0 k2 R5 Twas the product of a full-term normal delivery, with
+ I+ a% Q/ _+ m; b+ Z$ na birth weight of 7 lb 14 oz, and birth length of
  _, T# G( m5 f# x0 \! |  k- b20 inches. He was breast-fed throughout the first year
5 C: _; R8 i' ?8 w  |of life and was still receiving breast milk along with& |& x) o* s3 ^2 v7 }
solid food. He had no hospitalizations or surgery,% c5 u, g6 d8 I6 T, o+ m9 o
and his psychosocial and psychomotor development
8 P; Q# Y4 m: H8 p. kwas age appropriate.5 o* y  T6 X- f2 X
The family history was remarkable for the father,
& ]* a% l& d* T3 {who was diagnosed with hypothyroidism at age 16,
) T! D' P3 ~0 Z& ]  Qwhich was treated with thyroxine. The father’s1 q# D( n# P1 A: K
height was 6 feet, and he went through a somewhat. ~8 S& m) v; b+ o* \4 E: V* V
early puberty and had stopped growing by age 14.$ B% W7 `2 ^6 L4 R* S7 }" R
The father denied taking any other medication. The! r7 @. |! r# J, u: {) ?. ^
child’s mother was in good health. Her menarche
$ r& H+ F" ~0 k0 T" k4 y9 t) Lwas at 11 years of age, and her height was at 5 feet% }# n- X! a) Z& S* p  y0 P
5 inches. There was no other family history of pre-
' \7 ~4 W: `2 Ccocious sexual development in the first-degree rela-( p; R, R$ D0 ?7 E6 T' u' A8 ^, _+ G  g
tives. There were no siblings.* A7 C4 \- b. F
Physical Examination
) P1 i' i9 B! {The physical examination revealed a very active,3 e2 ]& z0 ]& u! W+ ?
playful, and healthy boy. The vital signs documented8 ~5 p& o) S- T# B" r# p4 p
a blood pressure of 85/50 mm Hg, his length was
6 B6 {1 a' n# s90 cm (>97th percentile), and his weight was 14.4 kg
* Z) O* k- H$ K) E5 N7 }* L( k(also >97th percentile). The observed yearly growth
2 P* P9 I! b, q( Z% Ovelocity was 30 cm (12 inches). The examination of
. ^: i, m6 {9 h; Wthe neck revealed no thyroid enlargement." H0 t/ A3 ]; \
The genitourinary examination was remarkable for) h' ]$ Y5 g+ p' l
enlargement of the penis, with a stretched length of/ w" g0 j( r. U
8 cm and a width of 2 cm. The glans penis was very well
4 S0 u! q+ C) S' e1 ?, Ndeveloped. The pubic hair was Tanner II, mostly around
9 k* H6 p8 d. o) z7 O: P5405 N1 Q5 C+ P" D: Y  n
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0 I0 C* f4 j+ {0 m, y2 q$ i7 pthe base of the phallus and was dark and curled. The" @6 S4 [8 p5 E4 r
testicular volume was prepubertal at 2 mL each.1 q. R/ r+ q4 h: {9 o% q& L
The skin was moist and smooth and somewhat
* o) s% Q( Q& f5 r; poily. No axillary hair was noted. There were no
, U2 H5 v/ v: {) _! B3 yabnormal skin pigmentations or café-au-lait spots.$ j2 N4 X) d* s" n- R9 _
Neurologic evaluation showed deep tendon reflex 2+
9 X: L8 N/ {4 m9 q) F) \) h' y' gbilateral and symmetrical. There was no suggestion
+ J2 U7 C2 M/ t2 Q, vof papilledema./ ?6 _" z3 a: e; @8 F1 w
Laboratory Evaluation
. v9 b. d0 L' A, ?+ q. P4 }" QThe bone age was consistent with 28 months by$ M- g+ K" n) L. [" d
using the standard of Greulich and Pyle at a chrono-. z1 v+ w- w& e7 V3 e0 m, N
logic age of 16 months (advanced).5 Chromosomal5 Z* j2 @7 h% k; r- k( t# x
karyotype was 46XY. The thyroid function test( I/ T: l1 }8 ^- |
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
- c  M, T2 T1 @0 rlating hormone level was 1.3 µIU/mL (both normal).
6 N5 n' q9 F4 PThe concentrations of serum electrolytes, blood
4 w, n( V- G- S# purea nitrogen, creatinine, and calcium all were. s( i: r4 P4 V( ~- e  G& b
within normal range for his age. The concentration
7 @$ x. O6 Y6 |! z; ^/ \of serum 17-hydroxyprogesterone was 16 ng/dL$ h  ]" ], f, F* L1 n  J
(normal, 3 to 90 ng/dL), androstenedione was 20
, O7 ?+ l$ x1 k) y4 E, i8 X0 mng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-' e9 j; k1 x+ e; |2 w6 q
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
* m! F' h1 e" m) }9 udesoxycorticosterone was 4.3 ng/dL (normal, 7 to8 I% V0 H$ a% J' N! s5 a/ `, `
49ng/dL), 11-desoxycortisol (specific compound S)4 l/ V7 R7 @4 T9 g9 a6 u0 u
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-3 v: [" ^+ s8 e
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total7 t: |9 n- I& }
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),- b- T/ b1 f8 @5 B4 H" |3 G  B/ z' ?
and β-human chorionic gonadotropin was less than# M1 f, S: G; k2 c. [4 k
5 mIU/mL (normal <5 mIU/mL). Serum follicular
, ]1 y! y3 G7 b4 p2 ~/ T' V2 |! tstimulating hormone and leuteinizing hormone1 ~6 R, f5 G* [# m  @; p/ V# Q6 i; j5 J' G
concentrations were less than 0.05 mIU/mL
$ x$ H& ]1 n* d( A3 z4 k(prepubertal).. G# _1 F- z: q; r: Q
The parents were notified about the laboratory
5 a/ s. a+ Y+ D0 |( w' U2 Q. Oresults and were informed that all of the tests were& f$ r2 ?3 F4 _3 j& E
normal except the testosterone level was high. The
, ~. R1 ~! |+ N1 K3 s- C8 k1 M1 Xfollow-up visit was arranged within a few weeks to
/ J. x5 F, X# d+ hobtain testicular and abdominal sonograms; how-: `0 I  l+ M( _# `/ P6 O9 C
ever, the family did not return for 4 months.. y9 j5 Y# v2 {8 S" Y  I" E+ y
Physical examination at this time revealed that the
/ Y% A) B+ D. |' R4 ]0 Y* Lchild had grown 2.5 cm in 4 months and had gained: l+ o3 `8 Q& @7 Q  |8 Y
2 kg of weight. Physical examination remained! p2 p2 ?! _$ {! o1 ]
unchanged. Surprisingly, the pubic hair almost com-- a. ]9 R0 k( d  g! R' ^$ C
pletely disappeared except for a few vellous hairs at
0 n! ?8 Z( V1 r# u/ @& fthe base of the phallus. Testicular volume was still 2
$ p5 l  n4 U; MmL, and the size of the penis remained unchanged., f. L- k8 ?2 F6 j5 f
The mother also said that the boy was no longer hav-3 y% s7 x- {& m, j  H
ing frequent erections.
' l8 Y. l/ q" }" m* p9 m3 f7 o% _' `. }Both parents were again questioned about use of
0 H' X9 }/ J& x. x# V) xany ointment/creams that they may have applied to! m, e* G- `1 ]: w6 Q' _- H1 y; {
the child’s skin. This time the father admitted the
( N* T9 \' p; ~: cTopical Testosterone Exposure / Bhowmick et al 541
0 T- g" L& s4 G9 Q9 ~/ xuse of testosterone gel twice daily that he was apply-
, C# h( `+ }  W5 Ning over his own shoulders, chest, and back area for
- K4 \# K& l. Y% ^a year. The father also revealed he was embarrassed
& A7 a& I+ @3 gto disclose that he was using a testosterone gel pre-
! w5 {! r# E, R4 Xscribed by his family physician for decreased libido
& y( P* E# h1 y" Z3 x! O1 r* zsecondary to depression.  J0 y/ W7 J" C  K0 D2 C
The child slept in the same bed with parents.
" L! M  J" q; n" ZThe father would hug the baby and hold him on his
& q7 e8 l5 O1 u1 X/ ychest for a considerable period of time, causing sig-% d0 Q7 ~. [8 V0 v* C* k, T
nificant bare skin contact between baby and father.& X0 o4 H2 A& Q1 U$ `. b. R, ]3 B
The father also admitted that after the phone call,
8 M  ?* ~' k# _" T  qwhen he learned the testosterone level in the baby# o! K+ d5 [. c
was high, he then read the product information
4 x4 {# w1 n0 D8 h' Wpacket and concluded that it was most likely the rea-; I+ o# ]( R" G+ ]5 G2 |) N
son for the child’s virilization. At that time, they% @1 Y; D' H7 z
decided to put the baby in a separate bed, and the
' w( Z" \. h" E9 B8 P9 Bfather was not hugging him with bare skin and had
3 Y0 L' E3 ]- r: ebeen using protective clothing. A repeat testosterone. g( ?, \1 H% w; Q5 Y( J1 b  E
test was ordered, but the family did not go to the
6 e; D: t$ w* A% Flaboratory to obtain the test.+ w# N5 f* D9 \* a$ F
Discussion8 t" C' f8 F% s9 k# K
Precocious puberty in boys is defined as secondary& C$ _$ g" j% \+ l
sexual development before 9 years of age.1,4! F, I" K: f( }# {$ k& L
Precocious puberty is termed as central (true) when: H# v1 M# Q8 S; s5 j2 i& e
it is caused by the premature activation of hypo-5 `; c) [- X+ b  Z% N2 c
thalamic pituitary gonadal axis. CPP is more com-% D) x2 V! b, P- x  |2 q4 }$ G
mon in girls than in boys.1,3 Most boys with CPP
2 C$ r  `/ H" s- E& y8 Dmay have a central nervous system lesion that is3 D6 n" h5 r! o6 ~: S
responsible for the early activation of the hypothal-6 N  {5 B) F1 U0 o  `& h* d
amic pituitary gonadal axis.1-3 Thus, greater empha-
; G+ y' J& J8 D) P2 R' |& @& O7 u, Bsis has been given to neuroradiologic imaging in
- I% f4 j2 q& c* s( H% }+ Mboys with precocious puberty. In addition to viril-
+ k% a% v' V) d4 H& h9 wization, the clinical hallmark of CPP is the symmet-- v. ^5 a" l. @( s
rical testicular growth secondary to stimulation by% F0 D* w* C+ Z1 L, P
gonadotropins.1,3& ^! U! w  M! P; v* k' `* v
Gonadotropin-independent peripheral preco-# d' V1 ?; {4 ?3 p( U& r/ f
cious puberty in boys also results from inappropriate7 X. d# g' r* W" x$ l9 M9 G
androgenic stimulation from either endogenous or% g( V8 J, J1 G1 t
exogenous sources, nonpituitary gonadotropin stim-
, U3 F6 G2 D* m# {! qulation, and rare activating mutations.3 Virilizing1 L0 n' H6 L+ k, L, _0 n
congenital adrenal hyperplasia producing excessive# x/ ~7 v3 Y8 A
adrenal androgens is a common cause of precocious% I! u' C; L* k, s3 i, r6 d7 c7 d
puberty in boys.3,4; O$ w5 u1 X  T/ z. J
The most common form of congenital adrenal
: r4 i+ Z6 I( a$ j. W, Lhyperplasia is the 21-hydroxylase enzyme deficiency.
$ J: g: `" Q* Q( v% V& OThe 11-β hydroxylase deficiency may also result in+ W/ U/ W. O: S. f, d; }! j
excessive adrenal androgen production, and rarely,# ^" F; W6 i% m, t
an adrenal tumor may also cause adrenal androgen3 `1 L: T( j( G7 u
excess.1,3' k# M* t* \3 A, Z) P
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from0 t8 n) q3 T* P5 _  {
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007% `3 r0 Z0 n8 J( B( \" ]
A unique entity of male-limited gonadotropin-0 W* P! Z) }4 F8 s
independent precocious puberty, which is also known
9 `  d9 N0 W" n+ j. K$ z' u" _as testotoxicosis, may cause precocious puberty at a
8 @! K3 S7 w$ f/ e9 U! Z2 Vvery young age. The physical findings in these boys0 W7 c. q+ O2 f# U6 t4 v3 Y* w1 S$ |( ^
with this disorder are full pubertal development,
3 _) y) L! M( ~* t+ ^; Tincluding bilateral testicular growth, similar to boys
9 A1 \8 z' L6 {. V+ kwith CPP. The gonadotropin levels in this disorder
/ i# S# }3 {5 M) k3 Qare suppressed to prepubertal levels and do not show
' k: r, K! [& w# n, q- epubertal response of gonadotropin after gonadotropin-
7 ^0 m8 s6 X; l# ireleasing hormone stimulation. This is a sex-linked' ^9 k8 h% s* c  d, E& y9 _
autosomal dominant disorder that affects only
# I: W8 D8 z1 m2 k7 A5 }  ]males; therefore, other male members of the family
$ L; E) W1 }5 P; [, y& ~9 Z( {may have similar precocious puberty.3! l4 }: M' ]0 L9 c
In our patient, physical examination was incon-3 {" W) [: y/ S: D! `
sistent with true precocious puberty since his testi-- V7 c. r3 h5 r( Q/ w, u( Y
cles were prepubertal in size. However, testotoxicosis1 B1 N1 C% }$ w- g" s- i4 S
was in the differential diagnosis because his father0 H0 W& i; d" [$ \6 n
started puberty somewhat early, and occasionally,- L7 r9 o" i: @' e; b( }
testicular enlargement is not that evident in the
3 T1 w0 ~$ k( b& J$ d0 Tbeginning of this process.1 In the absence of a neg-
. Y7 b0 `  {+ p* Q+ Vative initial history of androgen exposure, our
/ Y( i; `' T1 ~% `% @9 C$ J# A; nbiggest concern was virilizing adrenal hyperplasia,7 D4 b5 a1 `/ e' P
either 21-hydroxylase deficiency or 11-β hydroxylase1 g+ R0 ^. h! `3 n7 \
deficiency. Those diagnoses were excluded by find-2 t; c, i- t; j! O% G
ing the normal level of adrenal steroids.( @: ^. C/ L) i0 |( l; F- l" j6 G
The diagnosis of exogenous androgens was strongly9 \1 z  n% H' t! v
suspected in a follow-up visit after 4 months because
, {  D) C* N' y. Q2 hthe physical examination revealed the complete disap-
/ ~1 P; [1 G% d, y% A+ jpearance of pubic hair, normal growth velocity, and
! n/ M$ E: k7 |' Cdecreased erections. The father admitted using a testos-
- o1 I9 m9 E! o/ s. Eterone gel, which he concealed at first visit. He was
' M5 |+ j9 X, k: b; O0 z- Kusing it rather frequently, twice a day. The Physicians’  f% y  u% d7 O# h
Desk Reference, or package insert of this product, gel or/ Q* G; Q2 m3 A% T8 J8 q4 T
cream, cautions about dermal testosterone transfer to( N# i* g6 w( W1 w5 L3 c+ x
unprotected females through direct skin exposure.
9 s( C7 `% Y  ]$ J8 sSerum testosterone level was found to be 2 times the
# l/ e8 M# x) n0 ^5 Dbaseline value in those females who were exposed to
# O' C; F6 c5 g3 g/ F4 u( d% z# reven 15 minutes of direct skin contact with their male
8 X! [; D# a3 w9 ]: _* [/ fpartners.6 However, when a shirt covered the applica-
" h/ H1 ?1 }% L' [% k8 Stion site, this testosterone transfer was prevented.' R# _% D0 }/ {
Our patient’s testosterone level was 60 ng/mL,2 w0 P' J9 Y& t, j! R
which was clearly high. Some studies suggest that% l; h# Y9 z- \; k% [, x% p
dermal conversion of testosterone to dihydrotestos-2 G: M$ u0 d# |" n$ c6 Z; @' c
terone, which is a more potent metabolite, is more0 W" I% l$ f; s" p4 x7 h: {" z
active in young children exposed to testosterone4 d* c6 f, J0 U6 A: I- W0 u$ ~
exogenously7; however, we did not measure a dihy-( c% D! h; B2 L) V/ F7 H
drotestosterone level in our patient. In addition to
, C7 J- X2 ~. L, kvirilization, exposure to exogenous testosterone in
+ i+ b4 |7 X6 {7 y6 Dchildren results in an increase in growth velocity and
, ]: M) N1 `* j  [advanced bone age, as seen in our patient.
. M* K7 d( r# d+ \+ o. jThe long-term effect of androgen exposure during
& f! f# O  w9 cearly childhood on pubertal development and final
/ L* V5 ?/ T2 g: u7 W. ~( madult height are not fully known and always remain( y  @+ @$ U2 s: v
a concern. Children treated with short-term testos-
+ _: k4 r! s4 |) a0 W4 Z" c" n1 ?terone injection or topical androgen may exhibit some
: Y7 `% R7 M5 J/ T7 xacceleration of the skeletal maturation; however, after
2 b8 g) @- n; P% B! d. Bcessation of treatment, the rate of bone maturation7 A* q1 R& @6 _: V+ J4 G  h/ |. w
decelerates and gradually returns to normal.8,9
5 t+ s1 F6 ^- n, x1 KThere are conflicting reports and controversy$ \* U6 K, K6 n5 ^/ q4 }, y
over the effect of early androgen exposure on adult
: Z$ j% D. d. {1 \/ @( Q. Mpenile length.10,11 Some reports suggest subnormal
  g0 u" w+ R. ~adult penile length, apparently because of downreg-
, d7 k+ a7 L# J+ Tulation of androgen receptor number.10,12 However,6 \5 o) Q) \/ n3 L0 O4 Y. q0 |
Sutherland et al13 did not find a correlation between9 o$ K& s" S$ T( h* A3 I: z! N% ^6 Z
childhood testosterone exposure and reduced adult1 `+ a7 T7 P5 W7 D& l5 K- v8 j+ `
penile length in clinical studies.
( q- |. z$ j2 _7 \Nonetheless, we do not believe our patient is  a0 J2 W  [! @+ {8 E
going to experience any of the untoward effects from7 C& a1 Y8 v: W: d2 W0 b/ O6 O
testosterone exposure as mentioned earlier because
  J$ W5 t) G$ {$ D% }- Vthe exposure was not for a prolonged period of time.4 d$ F+ a, e: L- T! q) Y: [
Although the bone age was advanced at the time of
4 \3 A% A+ w( F! H) t* vdiagnosis, the child had a normal growth velocity at
) i) Y+ e- x/ t" ithe follow-up visit. It is hoped that his final adult0 |4 P. m, X5 m; w; O
height will not be affected.% R  i& Z0 k8 h* M) N8 L
Although rarely reported, the widespread avail-
9 u# f* q% E* s5 ~/ Z) s( k6 cability of androgen products in our society may6 T; i. Z3 \5 y% f
indeed cause more virilization in male or female7 N' b/ U4 D" L; p
children than one would realize. Exposure to andro-
- o- z& |; X( ], ^8 [& ngen products must be considered and specific ques-! q9 O5 P$ j1 z
tioning about the use of a testosterone product or
. R8 R2 n. z% O' \  p5 e" mgel should be asked of the family members during
# S& L' K8 ]: G! b9 r# u. gthe evaluation of any children who present with vir-
' R7 W- n& I( u1 {% \# |0 jilization or peripheral precocious puberty. The diag-
9 r6 a7 n- N- G( ~/ y  \9 s" d% wnosis can be established by just a few tests and by
; S- r. g8 B% U& Qappropriate history. The inability to obtain such a! V2 l- A. X9 v# E6 E  X+ a
history, or failure to ask the specific questions, may
! c- E% z4 X% U2 ^8 g- |7 `result in extensive, unnecessary, and expensive5 X% ]6 |$ H& Z8 v& z5 N7 L
investigation. The primary care physician should be
8 `) e' Q# v+ E9 Aaware of this fact, because most of these children7 S7 d0 \. m% W$ M
may initially present in their practice. The Physicians’& p( X) X+ g" g0 j& L9 m
Desk Reference and package insert should also put a9 }, O: I0 r# H0 [, t$ w5 E1 {1 b! f# x3 \
warning about the virilizing effect on a male or
, |3 H  \! ~6 F2 C& I' @0 O0 t+ Jfemale child who might come in contact with some-
" v" B; S, l4 C# E* ?1 y7 Zone using any of these products.
1 L1 o+ C: y. Y  \; |/ lReferences/ \+ Z7 n/ n% w( H. i  S
1. Styne DM. The testes: disorder of sexual differentiation5 [6 k  z' }2 I
and puberty in the male. In: Sperling MA, ed. Pediatric& R- X2 Z* W0 Q  s) w9 E
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;" _' Z3 f; Z: l: |1 x, f2 W- e, W
2002: 565-628.
. n3 o# t; Q/ x. G2 S4 b$ O$ q2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
! X. t) r- W& r6 G/ Npuberty in children with tumours of the suprasellar pineal
發表於 2025-1-7 21:59:43 | 顯示全部樓層
這個我收藏了!謝謝分享!WK的資源越來越豐富,這少不了大大的辛勞!
發表於 2025-1-10 10:43:39 | 顯示全部樓層
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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
9 `, i( X) m( S5 v: X
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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