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Sexual Precocity in a 16-Month-Old
( `' v4 ^% A% ]3 o# Y' u5 fBoy Induced by Indirect Topical' r. B1 Q2 Y8 e/ E" p1 e$ M* H
Exposure to Testosterone9 i. o/ _& P9 O& z, G/ ?, Y
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,29 u, J) e5 ~7 h1 B4 [- Q
and Kenneth R. Rettig, MD1- T$ s  M3 x5 b! ]* ]
Clinical Pediatrics
1 I9 K; U+ e) f" Z+ n7 UVolume 46 Number 6
! j5 s& R7 S, ]) z& S! s' VJuly 2007 540-543
+ d1 {! H0 W3 l1 {0 J© 2007 Sage Publications) r) h$ p' D! L; q, W' \% \; B
10.1177/0009922806296651
+ W2 E' S5 K! K' p, `# Z' N" {http://clp.sagepub.com
. b2 Q( Y% j, U$ Yhosted at6 l: J  y- b" _: a, n
http://online.sagepub.com
8 u2 J% s: a' X0 s# k5 kPrecocious puberty in boys, central or peripheral,& e6 h2 ~$ ~1 R& e; M
is a significant concern for physicians. Central
2 P! M% J. L5 ]% ?) e2 K5 z/ Cprecocious puberty (CPP), which is mediated. o- m  I8 Q6 c
through the hypothalamic pituitary gonadal axis, has
- |+ E# x0 Y2 F4 `( o! B& Za higher incidence of organic central nervous system2 _( s/ ~! D/ u0 [
lesions in boys.1,2 Virilization in boys, as manifested# {9 ^0 w  t! U' V7 V! z
by enlargement of the penis, development of pubic
, r/ E. ]  `! \" P3 ~hair, and facial acne without enlargement of testi-9 P. U8 d" ^6 R- h/ c3 c4 x
cles, suggests peripheral or pseudopuberty.1-3 We
+ a, m  a& n! x. y- p! R6 |7 T- lreport a 16-month-old boy who presented with the: ]6 e: `- Z2 f0 T
enlargement of the phallus and pubic hair develop-
# ]* G# H  F8 T5 N. ament without testicular enlargement, which was due4 m( @& D# m) M/ ^
to the unintentional exposure to androgen gel used by5 V( Q1 O/ j/ c: i% e6 h* j
the father. The family initially concealed this infor-9 L+ p4 H" q1 i0 H' U9 t
mation, resulting in an extensive work-up for this3 D& i4 B& G  f& V+ }; h" y
child. Given the widespread and easy availability of! Z% Z  K0 A" p" a* A1 S
testosterone gel and cream, we believe this is proba-) R& I9 r% n) e5 U
bly more common than the rare case report in the
: g) o7 ~7 i7 m2 x5 o; ~: ^5 Vliterature.4
5 u, v+ T3 d4 J. _Patient Report
4 `/ x6 F7 f4 ^A 16-month-old white child was referred to the- U# o# j+ \  I2 D
endocrine clinic by his pediatrician with the concern0 c% z' D  B4 f( L9 w' A& d0 f
of early sexual development. His mother noticed
" t" e- h( {+ E6 f6 ]" ~3 E; flight colored pubic hair development when he was+ ^3 S: G0 E  V2 Y
From the 1Division of Pediatric Endocrinology, 2University of! i) Y- f9 A  G4 p$ N; _2 k3 Q6 q
South Alabama Medical Center, Mobile, Alabama.+ V* _9 Y& n+ B1 V0 C- W5 u
Address correspondence to: Samar K. Bhowmick, MD, FACE,
2 g" ]7 m4 k5 x: y& j- V" xProfessor of Pediatrics, University of South Alabama, College of) P, d3 R  K$ F( ~6 q0 l* W
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
  w, D! E2 ?' z% T% M# ~e-mail: [email protected].
- k, c" A2 O$ [2 [. O' e" L8 Vabout 6 to 7 months old, which progressively became4 a$ [3 l# x7 l3 {' t" O
darker. She was also concerned about the enlarge-" z0 O9 L2 ?# M1 N) J0 h; q
ment of his penis and frequent erections. The child, \! Z' o* ]0 I: B  J& Q" {6 `, P8 i
was the product of a full-term normal delivery, with0 E) F# D1 c6 N* M: l
a birth weight of 7 lb 14 oz, and birth length of
% {/ \* W# Q/ O  K' C20 inches. He was breast-fed throughout the first year* j  \) M6 ]# i. m
of life and was still receiving breast milk along with6 Q. z$ `1 K7 r  V, O: n+ F
solid food. He had no hospitalizations or surgery,
9 P$ c! ?/ g( n$ i9 p2 eand his psychosocial and psychomotor development
3 ^7 P( k% N2 _3 Pwas age appropriate.
6 D" A% Y( s. K. i" J5 ~( v0 QThe family history was remarkable for the father,
5 z, u6 V: B$ Q/ \who was diagnosed with hypothyroidism at age 16,
5 Z- h. g% @0 V+ [8 W% }which was treated with thyroxine. The father’s- u, q# Y8 i- T. i8 b
height was 6 feet, and he went through a somewhat
- }+ j4 x) H, y5 `' P' Y/ \early puberty and had stopped growing by age 14.
+ O$ Y! t# }) yThe father denied taking any other medication. The
" H$ q& c& I6 w% n) ~child’s mother was in good health. Her menarche
0 T: v9 K& X5 B) A  o1 Awas at 11 years of age, and her height was at 5 feet
% i- u+ m1 w- y! L% r! W) L5 inches. There was no other family history of pre-7 ?2 z: P+ n4 n, d- e" u0 N6 m
cocious sexual development in the first-degree rela-
. q" ?2 d0 z* F, E* `tives. There were no siblings.
* }# t9 R  g: @Physical Examination
$ S8 s0 ]2 A7 U$ N5 m( AThe physical examination revealed a very active,
. S( t7 A3 j8 r% L! f4 }  [3 g1 tplayful, and healthy boy. The vital signs documented
) }9 E' g4 V0 |' H7 C1 V* T# @1 X( la blood pressure of 85/50 mm Hg, his length was* B4 i+ ~& B1 w! C4 v0 E
90 cm (>97th percentile), and his weight was 14.4 kg3 Z7 j. H) p: f5 h; \) b
(also >97th percentile). The observed yearly growth
- v+ {) C3 k  d2 F* N- yvelocity was 30 cm (12 inches). The examination of
; W  }. G# ?" x$ a3 X4 nthe neck revealed no thyroid enlargement.
$ r& S! B  j/ ]$ W: BThe genitourinary examination was remarkable for: v- @9 Y. p, F8 x+ @" m
enlargement of the penis, with a stretched length of
3 s3 s$ u! ?" B1 F4 ^, o8 cm and a width of 2 cm. The glans penis was very well5 U* S+ p( e6 y/ B
developed. The pubic hair was Tanner II, mostly around: L* y3 @/ C2 o+ Z
5405 w8 W1 w  u7 w8 ?2 l# ]
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from" S, i  ?( x, {1 N. ~0 `! U
the base of the phallus and was dark and curled. The) B3 ~5 Y$ F1 U4 U
testicular volume was prepubertal at 2 mL each.+ s8 l7 A' P1 J9 e0 B0 Z5 O! h' P
The skin was moist and smooth and somewhat8 Z2 x# w. ~# c9 @$ e
oily. No axillary hair was noted. There were no
8 D6 f% s, [6 |4 E" {abnormal skin pigmentations or café-au-lait spots.9 Y4 j. Y6 ]- C0 ?
Neurologic evaluation showed deep tendon reflex 2+
! N3 f3 o/ t& }, Pbilateral and symmetrical. There was no suggestion) M, A9 ^  U( ~0 Q1 L  s6 ?
of papilledema.- z& r$ R* \4 P4 n2 p( L
Laboratory Evaluation
2 _$ s) K6 x( C* [+ R3 q) CThe bone age was consistent with 28 months by
$ p! c" g0 |% u: eusing the standard of Greulich and Pyle at a chrono-
2 }) M+ v2 W/ [" \1 Llogic age of 16 months (advanced).5 Chromosomal3 X- I$ c3 `# T0 D
karyotype was 46XY. The thyroid function test6 ~( L8 Z) x* d5 ?+ x' @& E* C
showed a free T4 of 1.69 ng/dL, and thyroid stimu-5 J5 F4 K, E/ e9 w
lating hormone level was 1.3 µIU/mL (both normal).
; c! R3 Q8 s+ j# Y9 M( o5 K, \1 ?; h$ s! xThe concentrations of serum electrolytes, blood
( G' G; j: W) g4 r! a5 [& \urea nitrogen, creatinine, and calcium all were4 t, j/ d& y. m5 `, o% u- t' O7 t
within normal range for his age. The concentration, G. m  j4 ]7 `4 f2 X
of serum 17-hydroxyprogesterone was 16 ng/dL
$ V9 y0 i4 @! g  x6 f! N(normal, 3 to 90 ng/dL), androstenedione was 20
5 h# |! e, x' H5 Q$ f6 `( Zng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-4 r8 z9 A$ M$ }2 d) m) }% x
terone was 38 ng/dL (normal, 50 to 760 ng/dL),- @/ J! s+ j& l& D3 ~+ O  n
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
! V% F( c6 T, g- i49ng/dL), 11-desoxycortisol (specific compound S): |4 x2 P/ k3 k! X- E
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
5 R9 @7 e" `! V* q; u+ Qtisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total: P* |# E( L2 ^& Q& T
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),% e8 s7 h0 z1 K
and β-human chorionic gonadotropin was less than
/ l9 P: h7 \/ c2 {5 mIU/mL (normal <5 mIU/mL). Serum follicular* V! t  i; ?$ ]9 a" i
stimulating hormone and leuteinizing hormone
6 R) q: B4 E- S- S3 Qconcentrations were less than 0.05 mIU/mL
( T* l+ d! O, o# w0 m(prepubertal).& q9 p2 h# s. S4 C' e3 k3 A0 v3 G
The parents were notified about the laboratory8 v. d7 U  u; h
results and were informed that all of the tests were1 t8 i0 M4 {5 w7 W
normal except the testosterone level was high. The' n8 j% b# a, u( ~
follow-up visit was arranged within a few weeks to% d7 ^* r* F, h' m. W$ B3 O
obtain testicular and abdominal sonograms; how-- B- E( i7 z6 G# g4 C; |% P
ever, the family did not return for 4 months.
5 I1 T! V" m! a3 v& GPhysical examination at this time revealed that the
. I+ K2 u* T, \child had grown 2.5 cm in 4 months and had gained/ x) R) y$ I/ D
2 kg of weight. Physical examination remained+ H, S* Q: \$ x+ g3 t3 B
unchanged. Surprisingly, the pubic hair almost com-& |4 v8 Z. `5 X
pletely disappeared except for a few vellous hairs at2 z$ k* D  e- |
the base of the phallus. Testicular volume was still 2
7 t2 ?; s5 Q8 H+ r$ Y: W  `1 amL, and the size of the penis remained unchanged.
5 T1 f( O0 f: v* a) ?6 U9 u) l# qThe mother also said that the boy was no longer hav-
5 M, w/ X2 d, |$ A5 Bing frequent erections.6 ~$ ]0 P8 X7 h/ i! ?
Both parents were again questioned about use of9 \- w( e% A( [7 ~8 l
any ointment/creams that they may have applied to0 E! M: E% f( h( l
the child’s skin. This time the father admitted the- x; Q; {9 ~- `4 O# r7 P7 H
Topical Testosterone Exposure / Bhowmick et al 541+ M+ m' `: \, S0 |/ N& m
use of testosterone gel twice daily that he was apply-
) A' X  A/ h; j: ]! V8 D; iing over his own shoulders, chest, and back area for* V9 p, m3 {7 ~* A7 P4 c8 n
a year. The father also revealed he was embarrassed4 \4 e# ~8 c: W$ C% O. o
to disclose that he was using a testosterone gel pre-
. Z. V; J- G6 s% b; Yscribed by his family physician for decreased libido
; w4 z% D% B; c& x! P0 P% E6 Msecondary to depression.
- F  O/ k1 r& t! a" L6 qThe child slept in the same bed with parents.5 y# \+ S& n# }; Z
The father would hug the baby and hold him on his# [3 f/ k: j% ~' b8 f- Y' `  v: c% ]1 |6 U
chest for a considerable period of time, causing sig-" e" \* {# L8 Q3 @# e
nificant bare skin contact between baby and father.
5 r9 |- D: d; t$ T/ `' p. j' O" eThe father also admitted that after the phone call,
& t; }8 n. _5 }- g' Lwhen he learned the testosterone level in the baby
, M- I0 A% c. l: `was high, he then read the product information
6 T* l8 a. k9 T$ O1 G: qpacket and concluded that it was most likely the rea-" R4 D; O& Y: o2 }
son for the child’s virilization. At that time, they
* Q& G( j: u: `! C& k) |decided to put the baby in a separate bed, and the
! ?: m) [7 E% I! W' {- {' afather was not hugging him with bare skin and had
' n, A. W4 J8 Y9 P# cbeen using protective clothing. A repeat testosterone
  {. q/ [, n  F; [) Ttest was ordered, but the family did not go to the
2 n6 k& }& l* o( ]& E' ?- slaboratory to obtain the test.
! X1 H8 |* y' E# zDiscussion8 T1 ^" Y1 T, x1 K* g. A7 u
Precocious puberty in boys is defined as secondary
* k  I& E1 Y( F5 s& z8 s# I* {) Asexual development before 9 years of age.1,4
% S) c4 ^' w4 r" @3 ~Precocious puberty is termed as central (true) when
% S/ O& C* w1 Oit is caused by the premature activation of hypo-* v* Z; _% j' W! L" Q4 p5 s
thalamic pituitary gonadal axis. CPP is more com-; t2 C8 u! s! T0 E2 V1 ?) M
mon in girls than in boys.1,3 Most boys with CPP0 B& F% k7 X" C9 p+ ~# M) H. t/ {7 Y
may have a central nervous system lesion that is$ \+ P6 }# m% I
responsible for the early activation of the hypothal-
& G) b9 d3 j1 S+ R( [( Zamic pituitary gonadal axis.1-3 Thus, greater empha-
: ^6 O* R( R3 ~4 q2 ysis has been given to neuroradiologic imaging in
, I! n; x7 \' K' K, m+ U# \1 Lboys with precocious puberty. In addition to viril-$ C, D* q! ?- U2 p- j2 c
ization, the clinical hallmark of CPP is the symmet-
8 {1 q  z+ i( crical testicular growth secondary to stimulation by
0 F+ l) x% Y, k: g6 A" Ugonadotropins.1,3
! u2 p3 B* A7 wGonadotropin-independent peripheral preco-
7 G( b3 G+ ~6 N$ P, vcious puberty in boys also results from inappropriate, O# T9 u9 G. [# k/ o
androgenic stimulation from either endogenous or$ r7 J' c& {+ `; v2 x& y+ @
exogenous sources, nonpituitary gonadotropin stim-7 E2 c5 H: q3 R, s% }6 \& @9 {" K1 G
ulation, and rare activating mutations.3 Virilizing
$ o2 b/ T6 \' ?& c* k, ^congenital adrenal hyperplasia producing excessive
8 z2 @' J* c. T  G/ oadrenal androgens is a common cause of precocious1 g7 `0 H- u7 f4 |3 t) [- g! {
puberty in boys.3,4
) k' U1 C. Q- A, c+ jThe most common form of congenital adrenal' y4 q4 N5 V* K+ n  r
hyperplasia is the 21-hydroxylase enzyme deficiency.. V( y/ x0 u% r) r) x5 g9 L
The 11-β hydroxylase deficiency may also result in
' v9 v, o$ u0 V- e$ W& ]- Rexcessive adrenal androgen production, and rarely,
3 I) h6 M4 M6 D8 Z, X4 U6 Q  R& Aan adrenal tumor may also cause adrenal androgen6 V# s+ B" e& @4 l. l) n3 p
excess.1,31 u! Q( A. O* c
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
8 X1 A* q+ ?9 o9 V# H$ P542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
+ [  E" K' F, o$ g* E. w' a5 `A unique entity of male-limited gonadotropin-0 F7 F; z2 V$ N. Z" |& |
independent precocious puberty, which is also known+ }9 A) \( t3 s' R6 Q& k
as testotoxicosis, may cause precocious puberty at a  H4 Q% o3 V9 [. O
very young age. The physical findings in these boys  l$ p  O- M& m. b4 D' N6 v
with this disorder are full pubertal development,
/ c$ z1 _2 |3 x' }4 t: S+ \including bilateral testicular growth, similar to boys3 _8 m# ~9 ^8 M: P2 ~
with CPP. The gonadotropin levels in this disorder
  l* i3 M5 y7 ~* K, p2 Yare suppressed to prepubertal levels and do not show
9 P- a  [7 d+ \pubertal response of gonadotropin after gonadotropin-
6 ?+ ]8 r# s: @% ?releasing hormone stimulation. This is a sex-linked
# d& }, z, M5 t8 x" T, fautosomal dominant disorder that affects only
; s  `/ j) E4 F% G& Dmales; therefore, other male members of the family, c% J' X) q9 z+ t
may have similar precocious puberty.33 ]) k' S9 b# T; K& O# Y
In our patient, physical examination was incon-
/ I  M8 D" j* }1 I9 rsistent with true precocious puberty since his testi-
. D/ U1 D4 h1 e: [; L* v  G# S( Vcles were prepubertal in size. However, testotoxicosis
, q3 f! K9 r$ y# M5 c: j6 Zwas in the differential diagnosis because his father
7 C( w/ t8 ^( w; a( {started puberty somewhat early, and occasionally,
8 y! y0 c1 \; _. y' R9 otesticular enlargement is not that evident in the
' k% i" G5 L2 G' F- y# sbeginning of this process.1 In the absence of a neg-
( ]7 n2 T) U: c, A1 }ative initial history of androgen exposure, our. E- |+ E  V0 X
biggest concern was virilizing adrenal hyperplasia,
" P( f) W2 |- yeither 21-hydroxylase deficiency or 11-β hydroxylase; v1 l) I3 \' J" L7 F
deficiency. Those diagnoses were excluded by find-
' a% S2 ~& ]: L( R% p+ }ing the normal level of adrenal steroids.& r$ K" ^, O1 K' L7 J
The diagnosis of exogenous androgens was strongly
  t' \9 k6 y& g7 _* P2 ?suspected in a follow-up visit after 4 months because
/ y7 H2 S7 L) f- O9 Z# K) m  h. F% I- Uthe physical examination revealed the complete disap-4 Z7 `2 R/ i2 A
pearance of pubic hair, normal growth velocity, and
: d2 ^& s5 e! c6 kdecreased erections. The father admitted using a testos-
) a6 p3 S  K" j# ~4 gterone gel, which he concealed at first visit. He was
; A( X% P# C8 a' ?! ?8 busing it rather frequently, twice a day. The Physicians’1 D+ |, Z/ n! S' Q) `. ?4 y
Desk Reference, or package insert of this product, gel or
6 M' K7 _& _' D( fcream, cautions about dermal testosterone transfer to, A* }6 S2 h- x1 T: g
unprotected females through direct skin exposure.! f( |- s# z3 [; ~* ?- @) R" z
Serum testosterone level was found to be 2 times the
: ?# x& ]+ O, E& M5 Kbaseline value in those females who were exposed to8 H/ x; K4 j' e# H# g  l" A1 {
even 15 minutes of direct skin contact with their male
) X" @: k- v% r5 ~+ P: G5 w, Z6 i$ W7 Gpartners.6 However, when a shirt covered the applica-$ Z. E7 f: [2 o: ^# w
tion site, this testosterone transfer was prevented.
+ z3 v# R3 \# D$ X& mOur patient’s testosterone level was 60 ng/mL,
3 P: |. T+ k; fwhich was clearly high. Some studies suggest that; r  d1 Q( k1 ]2 k5 T6 W
dermal conversion of testosterone to dihydrotestos-
5 b6 i+ |3 i' E6 r) w: a; Lterone, which is a more potent metabolite, is more
& l7 {* A) B9 J$ Mactive in young children exposed to testosterone
. g( O9 D( q! f( ?exogenously7; however, we did not measure a dihy-2 C: s8 Z" k) T( e0 R: k
drotestosterone level in our patient. In addition to4 _# ?, L) i- M% d" J9 m
virilization, exposure to exogenous testosterone in
. t8 ~- n4 E' bchildren results in an increase in growth velocity and
2 D- p% e3 W# ?& s' aadvanced bone age, as seen in our patient.& f7 I( n8 W6 n' O% |
The long-term effect of androgen exposure during
8 Z. r  M- S/ yearly childhood on pubertal development and final& D/ a* W9 ^1 p4 W1 y) ~$ u8 S* X
adult height are not fully known and always remain
! P+ _6 i4 B9 Q, o. B4 Ca concern. Children treated with short-term testos-
2 Y1 a7 S  W: y8 l8 ?( E0 ^terone injection or topical androgen may exhibit some
( n8 P- P* T0 b2 l9 a1 R3 Iacceleration of the skeletal maturation; however, after8 Z) F) D: T4 _! k. ^* g
cessation of treatment, the rate of bone maturation) B: g  G  a) V% P9 Z
decelerates and gradually returns to normal.8,9+ d9 I  u, Y% G: r- ~7 Y; Y2 j3 Y, B
There are conflicting reports and controversy2 w5 z) \$ z* x4 w6 X: t/ a
over the effect of early androgen exposure on adult7 ?9 ]% e) R! Z  }1 A
penile length.10,11 Some reports suggest subnormal
' k0 V. Q# v+ x$ \7 S- S2 e8 s* jadult penile length, apparently because of downreg-
! Q# G2 Y3 i+ J* vulation of androgen receptor number.10,12 However,! G. h1 t7 L- e% M
Sutherland et al13 did not find a correlation between
6 O7 q1 ?) W$ C! o: x% h7 xchildhood testosterone exposure and reduced adult7 R- g- H1 |. U- J3 P5 y) e  C
penile length in clinical studies.
& r8 g* R( R8 a  |0 SNonetheless, we do not believe our patient is2 }' V  O+ ~- ?8 M) Y8 X
going to experience any of the untoward effects from
' |' d) I  {! r$ x2 Dtestosterone exposure as mentioned earlier because3 d& K2 F, i4 u9 F( H
the exposure was not for a prolonged period of time.
' l4 j$ a( I% I& }  V# b; VAlthough the bone age was advanced at the time of8 b: B( n9 c- U& j# N
diagnosis, the child had a normal growth velocity at8 M1 l0 G7 b/ Q6 a# o( K1 f( g2 ~
the follow-up visit. It is hoped that his final adult
0 e! _; ~3 K1 M1 `height will not be affected.
- b1 d; M! f" j! ~Although rarely reported, the widespread avail-7 g( T( b# A" ]* X7 s  o. n2 G. p  @
ability of androgen products in our society may# B! m! _( o) a# r: {4 x# g
indeed cause more virilization in male or female
/ N" I2 e# J' I9 [* Ichildren than one would realize. Exposure to andro-
6 V6 {4 e* x! Y9 v; Y% R* Kgen products must be considered and specific ques-
+ K" R2 P1 Q  T' ~) {  p6 Itioning about the use of a testosterone product or
+ R+ h/ J8 W& U) Rgel should be asked of the family members during
5 \6 a" E' P; l9 b, R/ a0 F, r* Tthe evaluation of any children who present with vir-, @5 c' x, @2 b# t: P
ilization or peripheral precocious puberty. The diag-
* ^4 D+ @1 Z4 A. g- U& \& Fnosis can be established by just a few tests and by
1 b8 x/ I* i0 Happropriate history. The inability to obtain such a1 T1 `7 y' g$ ^! S- O8 p! z0 @" y) F
history, or failure to ask the specific questions, may
; P5 B( p5 F2 b% B/ m& |3 d  ]; F$ hresult in extensive, unnecessary, and expensive
( F! a& F4 q3 J- ginvestigation. The primary care physician should be3 [8 L4 m! G2 w" W( |8 S2 F
aware of this fact, because most of these children/ y# a; z. Y9 `8 B# f& f
may initially present in their practice. The Physicians’, r1 s' ~, k7 r, U) s! h
Desk Reference and package insert should also put a4 n. x( ]* B. p3 J( y
warning about the virilizing effect on a male or
; X$ d. g2 j( w2 ]- nfemale child who might come in contact with some-" N4 L, R4 T! c; n
one using any of these products.
2 p# C4 E$ H2 ~5 SReferences6 e# f% m/ b% D" l
1. Styne DM. The testes: disorder of sexual differentiation
8 `: {3 m) r6 x. m$ Z4 Eand puberty in the male. In: Sperling MA, ed. Pediatric
; y! H- ]; S$ g9 x& O0 a' H/ dEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
6 f) S! J$ L- y3 j2002: 565-628.
' a# ?4 A8 }4 b2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious  @* B2 g: b# o+ v! J7 d7 e5 ]9 Z$ G
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old" v  u/ x. d+ o
Boy Induced by Indirect Topical  U( k3 e( @# w. |9 i8 a7 h
Exposure to Testosterone5 r( Z& J7 l( Q$ M/ U
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,28 ]: c$ ^4 Q6 F/ a2 p
and Kenneth R. Rettig, MD1
" l/ O4 o# ], `! s& K5 ]5 pClinical Pediatrics# E3 L4 N" _5 a! t& e6 Q
Volume 46 Number 6
7 E' K7 E5 C9 l0 aJuly 2007 540-543
) A+ `% V+ r  _* Z( ~© 2007 Sage Publications. I, V' x- P/ j0 L3 [
10.1177/0009922806296651
/ s3 N8 V0 g2 E- T2 ohttp://clp.sagepub.com; X5 q& p; i0 Z+ Z1 w
hosted at4 K: g- @! p+ r$ C4 \
http://online.sagepub.com/ ]0 D+ H- A0 s9 N4 N4 y+ v3 j' o" M
Precocious puberty in boys, central or peripheral,
' l1 n* ?0 z2 f! l) Ais a significant concern for physicians. Central/ r- {' x" i8 o  @  i1 N, ~
precocious puberty (CPP), which is mediated) ?! B% Q* c9 y$ S0 h, c- o3 v7 m4 o
through the hypothalamic pituitary gonadal axis, has" P2 ~  W0 L; P6 M+ F$ F
a higher incidence of organic central nervous system, v: w, s3 H3 I! c
lesions in boys.1,2 Virilization in boys, as manifested
) `- q' g6 I% ^/ mby enlargement of the penis, development of pubic
$ Z: t, q2 a" V) Shair, and facial acne without enlargement of testi-
4 X4 H: k' k# ocles, suggests peripheral or pseudopuberty.1-3 We
5 X% q. D; C, wreport a 16-month-old boy who presented with the" E" w: Y, _7 h- R, Q
enlargement of the phallus and pubic hair develop-
$ A  S" \  p. ^9 D4 ]ment without testicular enlargement, which was due; x: `3 [7 t7 I( ~
to the unintentional exposure to androgen gel used by# B! f2 L8 }3 h/ N7 i5 L
the father. The family initially concealed this infor-
2 n. F4 g2 p" R* ]; R9 Amation, resulting in an extensive work-up for this+ m) M+ |& a! s" p7 O
child. Given the widespread and easy availability of
0 ^, Y; \4 R6 g. p) H5 @  U% ]testosterone gel and cream, we believe this is proba-
  O: \# K# I5 Z. p; ]6 lbly more common than the rare case report in the
& D8 _' }5 i" U+ J. a, ^literature.4/ P: l8 q2 p! Q5 Y+ F& W# m
Patient Report
9 Z# P2 y( s2 |& |. `9 q. w0 ZA 16-month-old white child was referred to the. Q  k' q% b" J* B
endocrine clinic by his pediatrician with the concern
+ T9 h3 q+ a/ C8 t4 m1 J* nof early sexual development. His mother noticed
6 J$ ^0 ?& y+ j! Y- glight colored pubic hair development when he was$ Z, f2 u; h, p; d# @8 f$ L7 B" e+ @
From the 1Division of Pediatric Endocrinology, 2University of
! ~& {! m9 p9 G: Q* ySouth Alabama Medical Center, Mobile, Alabama./ Y$ C8 A5 E* U+ p4 f/ n+ l/ ^
Address correspondence to: Samar K. Bhowmick, MD, FACE,, F. R2 G7 h# q" R6 d5 f5 o
Professor of Pediatrics, University of South Alabama, College of0 U% H) m; S% u' D, a
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;  E0 E4 z; p' S- M
e-mail: [email protected].0 u2 ~6 U. b2 e; Y
about 6 to 7 months old, which progressively became
( M4 V; \% _+ t; Rdarker. She was also concerned about the enlarge-& \8 R* D3 N" H- H
ment of his penis and frequent erections. The child
" F* R: q8 A' l0 \$ hwas the product of a full-term normal delivery, with$ E# M0 J1 N8 X5 w% s( k
a birth weight of 7 lb 14 oz, and birth length of# i- D+ U" t9 d: L8 y: V' f
20 inches. He was breast-fed throughout the first year
# y8 v2 x  J! Y; U" |6 `of life and was still receiving breast milk along with
8 K# n! Q9 x  p* u/ a8 U# csolid food. He had no hospitalizations or surgery,$ e$ a$ @- ]) |
and his psychosocial and psychomotor development
/ n! x" |2 R  }, g4 E) Y& I9 z6 E! Dwas age appropriate./ _! d/ b  e0 \  S: a$ F, M, p8 Q
The family history was remarkable for the father,
+ H9 @1 c- u3 e1 j) qwho was diagnosed with hypothyroidism at age 16,
; |5 a( c0 q$ Q- k) Dwhich was treated with thyroxine. The father’s- D+ f$ y" k3 g1 b" j
height was 6 feet, and he went through a somewhat
6 i) @# t" a3 _' g2 n7 w7 I6 vearly puberty and had stopped growing by age 14.3 |' t5 J+ r4 w+ u
The father denied taking any other medication. The1 X: v! K' @/ g( F
child’s mother was in good health. Her menarche
2 [4 h  `" N. S5 L: u# N6 g$ S+ swas at 11 years of age, and her height was at 5 feet  f: P" V5 K5 t  U: j
5 inches. There was no other family history of pre-
5 C' v5 s' a/ W' [( }cocious sexual development in the first-degree rela-8 A, w, L# B( c3 y/ Z+ `5 w6 I
tives. There were no siblings.
3 W. n% }9 k5 h# `/ M  aPhysical Examination" k1 u2 ?; T0 R6 g( x3 Q5 G. S3 m
The physical examination revealed a very active,
$ t. `# H: x4 m5 q: f. ^playful, and healthy boy. The vital signs documented
. R9 F5 J3 }5 P3 A- G. xa blood pressure of 85/50 mm Hg, his length was: y% q- V' }! t
90 cm (>97th percentile), and his weight was 14.4 kg
& o3 u6 Y! d1 c+ O. q(also >97th percentile). The observed yearly growth
# @; q$ m! B# h; [velocity was 30 cm (12 inches). The examination of; U" {3 T: s- k$ x
the neck revealed no thyroid enlargement.
2 f5 F. U4 |# `The genitourinary examination was remarkable for
8 n: h# S4 S: y, ?! w& E6 Renlargement of the penis, with a stretched length of6 C& ^$ U; O7 h* x
8 cm and a width of 2 cm. The glans penis was very well
6 B4 r: M% r# P7 ~- Hdeveloped. The pubic hair was Tanner II, mostly around
" S0 t# L; m' |540; O- [) D! R1 E' m$ }
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
0 O$ y' G; k# xthe base of the phallus and was dark and curled. The
" Y8 j# Q) E. Y3 X& k- M5 ftesticular volume was prepubertal at 2 mL each.
: i1 q4 X5 G2 g4 t$ }2 i& aThe skin was moist and smooth and somewhat
% [( d- l- o; i: e$ R5 B7 l$ C) b2 Toily. No axillary hair was noted. There were no
( m) P1 {: ?. H2 a8 u& A  F1 Tabnormal skin pigmentations or café-au-lait spots.; ]  @) b, y3 V# _6 t) Z% v0 D! L5 _. D
Neurologic evaluation showed deep tendon reflex 2++ L& C4 g4 ]/ Q; g1 Y
bilateral and symmetrical. There was no suggestion
( M0 i, ~( ]% g  J; I2 Sof papilledema.
+ y0 q& y: f0 V& XLaboratory Evaluation: ^- f- _0 e. y9 k' d* a! r" b) ]( D
The bone age was consistent with 28 months by
& l7 z+ ]( ?  \4 d7 pusing the standard of Greulich and Pyle at a chrono-
' I, `+ L8 u& l8 }; R  ologic age of 16 months (advanced).5 Chromosomal$ m1 v9 W* N5 O/ m( N) w# `
karyotype was 46XY. The thyroid function test. [1 ^) I) a) X2 X6 f* \, y! E
showed a free T4 of 1.69 ng/dL, and thyroid stimu-( o# F* S+ S+ S
lating hormone level was 1.3 µIU/mL (both normal).4 `) W/ I* Y& \; N' e
The concentrations of serum electrolytes, blood
+ |, D4 C# e/ x6 jurea nitrogen, creatinine, and calcium all were
: v+ W$ \1 \3 c) ]% q/ @; b/ r& `within normal range for his age. The concentration2 T  T- N$ R# h* l  S
of serum 17-hydroxyprogesterone was 16 ng/dL4 i7 e: h5 a+ J5 |
(normal, 3 to 90 ng/dL), androstenedione was 201 M% s, U: n+ K6 q
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
% m: B3 _0 m( Rterone was 38 ng/dL (normal, 50 to 760 ng/dL),
- A) J  j4 {1 l' E. Idesoxycorticosterone was 4.3 ng/dL (normal, 7 to
, c) M  L) G; q* B% u: N4 o49ng/dL), 11-desoxycortisol (specific compound S)4 D; ]0 m( N( Y: q5 g, R/ ^
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-" P/ A2 F5 m7 I/ Z, Y
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total; e- }+ Y4 z% I! i9 @) G
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
8 l7 l9 [: T0 s' gand β-human chorionic gonadotropin was less than
% B9 D6 A4 w3 Z5 o5 mIU/mL (normal <5 mIU/mL). Serum follicular
3 q5 {. d0 S2 E, C' K/ M! tstimulating hormone and leuteinizing hormone
! M9 o) Y% S, Z' x; i4 Vconcentrations were less than 0.05 mIU/mL
8 [6 ]3 L* E- Z  Y* b# F! F(prepubertal).
/ B" J) d# U  z" VThe parents were notified about the laboratory
0 C5 g  l  q7 `) h4 G: Tresults and were informed that all of the tests were. G, l, u& w5 V2 {) d+ ^
normal except the testosterone level was high. The
* p0 g, u, U$ a- P; K. Yfollow-up visit was arranged within a few weeks to
! E) T; A% A  k) Y/ u) y. L2 s; }obtain testicular and abdominal sonograms; how-
8 m- v( [. c3 Z; U9 tever, the family did not return for 4 months.
2 t7 C" {$ M4 p7 V! KPhysical examination at this time revealed that the
! a" j- V8 c: [: V9 }child had grown 2.5 cm in 4 months and had gained3 p1 K- U. C5 t; r% u
2 kg of weight. Physical examination remained* E0 ?0 J9 q7 Y3 t" C  y4 z
unchanged. Surprisingly, the pubic hair almost com-
5 M/ C4 K* n* h! ~6 ]$ |4 v) lpletely disappeared except for a few vellous hairs at8 C4 B" E+ |5 x& H
the base of the phallus. Testicular volume was still 2+ ^* }% Y5 l) G- J  j' t
mL, and the size of the penis remained unchanged.5 D5 d& y) t& D5 p" j+ L! A
The mother also said that the boy was no longer hav-
0 r  ^1 _+ V8 \- I9 r' Zing frequent erections.- E1 U, J) |3 J/ m8 ]" Z
Both parents were again questioned about use of) X4 U/ O' G4 o
any ointment/creams that they may have applied to
& f2 {* B* o7 q/ J  gthe child’s skin. This time the father admitted the
' B" Y# [! _- B. I, |$ D8 RTopical Testosterone Exposure / Bhowmick et al 541
8 `0 `8 w" s- l: @, R& h" \4 ouse of testosterone gel twice daily that he was apply-, s( c5 L* U! X* |* A9 W( P( Z
ing over his own shoulders, chest, and back area for
* e$ |/ a7 L8 b( k$ Qa year. The father also revealed he was embarrassed
* B1 i6 @' h+ b/ _to disclose that he was using a testosterone gel pre-0 Z" h1 {8 K9 L: p0 v; \
scribed by his family physician for decreased libido3 U& k# K, r' o$ f6 @
secondary to depression.
3 W; Q3 s5 t. |# U; m- `  F8 s; WThe child slept in the same bed with parents.7 A/ b/ c! \7 I, x
The father would hug the baby and hold him on his
% N( k" q3 C! o) i( \4 Xchest for a considerable period of time, causing sig-
9 X5 x0 ]1 a' _' `4 J2 Mnificant bare skin contact between baby and father.
7 _6 s+ C* d, y$ nThe father also admitted that after the phone call,
/ n& M3 t$ K' c. B  Gwhen he learned the testosterone level in the baby
4 j' J5 L- s+ d, J1 t6 D1 A/ U3 Bwas high, he then read the product information0 U1 f  [8 ]6 ?' g; a5 e0 Z
packet and concluded that it was most likely the rea-& h2 f! R" F  x  ?3 H0 e
son for the child’s virilization. At that time, they
; n: [" ~# D( w6 `5 @decided to put the baby in a separate bed, and the
& ~9 u$ t3 [7 K$ h1 h3 Gfather was not hugging him with bare skin and had
* g  D3 P7 [) O# f& d4 Ibeen using protective clothing. A repeat testosterone+ i# S5 b1 i, v, ~
test was ordered, but the family did not go to the; |9 Q2 L- k* R0 K
laboratory to obtain the test.
& k& Q  i* A' h$ |Discussion
$ w) S( |9 I2 m- @$ e' q) i7 \Precocious puberty in boys is defined as secondary2 X6 C! a0 b# h! @. p1 X
sexual development before 9 years of age.1,4
$ h, |4 S' D$ P' T0 \/ w+ SPrecocious puberty is termed as central (true) when
0 R! }2 z7 y+ T, ?6 _3 W. U) x: Sit is caused by the premature activation of hypo-
, C# |6 @% J( ythalamic pituitary gonadal axis. CPP is more com-  v# r! v$ s1 W- A
mon in girls than in boys.1,3 Most boys with CPP
+ y' A0 V( z' k3 W9 gmay have a central nervous system lesion that is
7 W2 o4 ?" y" b$ o+ q. o" G/ E! Dresponsible for the early activation of the hypothal-3 f1 s6 G' N$ E! X% M
amic pituitary gonadal axis.1-3 Thus, greater empha-- f+ x* m* B2 |5 v3 G; T
sis has been given to neuroradiologic imaging in6 d6 q8 ]' J+ S' |% T7 `: [
boys with precocious puberty. In addition to viril-% |3 H* x8 W% I6 y( `3 p
ization, the clinical hallmark of CPP is the symmet-
  x# X: f  ?  v# P# {( k  R& \rical testicular growth secondary to stimulation by
  b, `. G6 K% z) t: Wgonadotropins.1,34 @0 m8 A; p. o- K5 U1 ]6 x
Gonadotropin-independent peripheral preco-
  `8 ~$ ~2 T( t  Lcious puberty in boys also results from inappropriate0 Y1 c" w) v1 X, j, G
androgenic stimulation from either endogenous or. a( Z2 N" y% N
exogenous sources, nonpituitary gonadotropin stim-# q) e+ j! Z. H& l: p/ h, w/ @
ulation, and rare activating mutations.3 Virilizing8 g1 b# B! `2 H+ v! G2 y
congenital adrenal hyperplasia producing excessive4 n1 G" Y% i! b! b& O8 U
adrenal androgens is a common cause of precocious
) `* @8 K3 V3 Z' @1 Cpuberty in boys.3,44 M& \- c& r7 h: O, A' u- L
The most common form of congenital adrenal
2 D+ R+ U; Q  Y- |8 ~1 E& Qhyperplasia is the 21-hydroxylase enzyme deficiency.
3 U8 y2 ^4 R: g$ w) u" |5 h: oThe 11-β hydroxylase deficiency may also result in
: J% H4 G" }+ w. k# @/ Texcessive adrenal androgen production, and rarely,. E# i, t- ?8 c/ V% t8 @' X
an adrenal tumor may also cause adrenal androgen
! ^1 D" h" e3 k* uexcess.1,3) H0 d/ C1 g( F* ^. W% w
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
8 z1 ^# R5 e- {542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
0 Q0 x; n8 B6 yA unique entity of male-limited gonadotropin-
9 o7 U$ S' u0 t  S3 X9 e7 ~independent precocious puberty, which is also known
5 y4 `* G+ ^; h/ p$ M: `* V% das testotoxicosis, may cause precocious puberty at a; ?# t* i% ?% N: e7 ~" A2 X+ u
very young age. The physical findings in these boys
/ n+ ^' T% @8 nwith this disorder are full pubertal development,
4 a' T) V5 ?8 R; Z  c% b/ ^9 ]" wincluding bilateral testicular growth, similar to boys
- j8 o( \0 @+ B/ l( A1 i  Swith CPP. The gonadotropin levels in this disorder* o, e# D. o; m5 t# ~6 V
are suppressed to prepubertal levels and do not show. B, @8 f8 {* I6 M1 f2 {
pubertal response of gonadotropin after gonadotropin-
. z4 E2 `1 U# lreleasing hormone stimulation. This is a sex-linked
" o8 [  R+ Y2 [/ X0 M! T$ X/ I+ Hautosomal dominant disorder that affects only' f4 q; w3 s/ y0 [4 k0 V
males; therefore, other male members of the family# z# T+ [- o" y! Q2 P; A
may have similar precocious puberty.3
. X* N; S# w( C* z* q  a) s. tIn our patient, physical examination was incon-
5 h. Y# ?7 S! xsistent with true precocious puberty since his testi-
; T# Y) `' `& K! L2 |! Mcles were prepubertal in size. However, testotoxicosis
9 w, A( r2 |% v& ]$ r# l5 bwas in the differential diagnosis because his father4 }( Q9 p* d8 t
started puberty somewhat early, and occasionally,
1 P2 W9 V, g: Z4 S# Jtesticular enlargement is not that evident in the5 M- e: C. ~' Z6 f' z
beginning of this process.1 In the absence of a neg-' \4 }8 E% d: C7 m4 j) ?9 c
ative initial history of androgen exposure, our; k/ f5 v  k& R# W. {: o
biggest concern was virilizing adrenal hyperplasia,
5 C0 q/ V3 D8 f) y9 m, ^  teither 21-hydroxylase deficiency or 11-β hydroxylase
& T2 `& z9 b; Y) H6 _" qdeficiency. Those diagnoses were excluded by find-6 D  n: g( ^, q7 g# _
ing the normal level of adrenal steroids./ {2 C* h9 i$ E; w, D) U  x& K
The diagnosis of exogenous androgens was strongly
$ M: r" a8 Z. m9 o& z5 Csuspected in a follow-up visit after 4 months because
7 C# d* g, ]# s' X* {1 z3 Bthe physical examination revealed the complete disap-+ S# j7 j) G# ?% Y  Y
pearance of pubic hair, normal growth velocity, and) L1 \& f# b, B8 v0 R8 k3 Y. r; @
decreased erections. The father admitted using a testos-
1 {  }( J0 Q$ \) L1 ~terone gel, which he concealed at first visit. He was' {2 p( h- x9 w4 \5 `$ \0 @" L" L8 W# V' N
using it rather frequently, twice a day. The Physicians’
4 |! R7 F6 A# j7 A5 hDesk Reference, or package insert of this product, gel or
4 v( \  Q* p& ^( j+ ecream, cautions about dermal testosterone transfer to
: ?# q/ q1 G8 b3 Y8 @unprotected females through direct skin exposure.& n/ A/ R2 t! J6 X+ ~
Serum testosterone level was found to be 2 times the
' ?" L; e- v9 u# Z, k- l* Obaseline value in those females who were exposed to
6 e' W3 \" s( aeven 15 minutes of direct skin contact with their male4 j" \* j- I+ _- u2 V
partners.6 However, when a shirt covered the applica-
+ w2 X* i8 |6 T+ ytion site, this testosterone transfer was prevented.
) j0 k, O5 E' \- o* D9 yOur patient’s testosterone level was 60 ng/mL,$ {# m; e$ u3 d4 u  ^4 W8 l
which was clearly high. Some studies suggest that: I, I+ _+ s0 g
dermal conversion of testosterone to dihydrotestos-
7 m/ V# |. ]! Wterone, which is a more potent metabolite, is more
, A. q% d/ k/ W5 e! Sactive in young children exposed to testosterone
9 p, ]8 V" ]# F2 S" e  ^% Uexogenously7; however, we did not measure a dihy-* s5 V4 K0 v. n2 S' j
drotestosterone level in our patient. In addition to
! k+ C. `9 L' w+ Fvirilization, exposure to exogenous testosterone in0 m& l9 P' ^: D
children results in an increase in growth velocity and
  X! k0 t# E2 J+ Z9 z5 F) Tadvanced bone age, as seen in our patient.$ ^- l* V4 a( [: |- A. @% n' m
The long-term effect of androgen exposure during
7 f/ R+ g$ T5 v; ?6 ^* `3 X. q7 kearly childhood on pubertal development and final3 a/ i5 E& _& u
adult height are not fully known and always remain5 x% f3 j! W% s, H. o$ X7 A: k- `7 p4 X
a concern. Children treated with short-term testos-9 c. Z9 `* z. b- e6 W8 Q" ~# r
terone injection or topical androgen may exhibit some5 g2 x; y+ |7 {! a8 M2 ]' v
acceleration of the skeletal maturation; however, after$ W5 l2 t/ a3 v4 ?  M: l1 g& q
cessation of treatment, the rate of bone maturation! _2 `; N3 _; @3 K  u2 u
decelerates and gradually returns to normal.8,97 m( I& V1 K2 t+ ~
There are conflicting reports and controversy
& v8 b( n, r7 j/ n9 ?over the effect of early androgen exposure on adult# n: j( ?9 |, g9 n$ [4 N
penile length.10,11 Some reports suggest subnormal8 w3 j! o) o% e9 c' T
adult penile length, apparently because of downreg-( R  I6 ]+ @* J& s' m
ulation of androgen receptor number.10,12 However,6 Q: J4 M( f7 Q# D2 j
Sutherland et al13 did not find a correlation between6 a3 b* R9 X3 A% @
childhood testosterone exposure and reduced adult$ ?5 n& t0 H+ u6 ~% k" w: q2 J  a6 Y: L+ e
penile length in clinical studies.
7 m) s" {. U+ R# E& h* c  \; Y+ ]Nonetheless, we do not believe our patient is/ P1 T0 v" A7 u+ Y, X; {, t8 X1 T
going to experience any of the untoward effects from
2 M$ n: N1 ^8 i3 Ntestosterone exposure as mentioned earlier because+ b* J' ]$ E4 Y. N; V0 V
the exposure was not for a prolonged period of time.
  z# K# {1 A( K0 {9 Q( M4 L- E+ rAlthough the bone age was advanced at the time of1 _( X% d9 Q. F! b- p2 T
diagnosis, the child had a normal growth velocity at. b: w: ~( f8 |; n
the follow-up visit. It is hoped that his final adult
% z: z2 l- c) S5 `# A: [: vheight will not be affected.
6 G8 K2 x8 X4 g% s) J2 S! ^Although rarely reported, the widespread avail-3 @% V& n( A: @) b& W; ~
ability of androgen products in our society may9 E& z" L6 f7 N
indeed cause more virilization in male or female
8 k( t- `) u, y* }6 r! I! l7 lchildren than one would realize. Exposure to andro-& a% H/ D  o, t7 d$ [
gen products must be considered and specific ques-5 e3 C5 b# Y8 I8 n: g( `2 {
tioning about the use of a testosterone product or
! w  z3 c9 }3 {8 b% lgel should be asked of the family members during/ O; M$ T+ V3 n$ ^
the evaluation of any children who present with vir-4 k( ?9 q0 `3 @# u! T
ilization or peripheral precocious puberty. The diag-
# d7 m+ ~; Q% t* xnosis can be established by just a few tests and by* ?& l* @' H  g0 F. o' J
appropriate history. The inability to obtain such a
* R9 f* H4 O+ L+ O: U0 k2 Bhistory, or failure to ask the specific questions, may
7 u) R2 F4 [" |result in extensive, unnecessary, and expensive7 r8 n. A# ]# ~3 U3 Z& X5 h
investigation. The primary care physician should be, n* i6 X2 _3 c- K% V8 X
aware of this fact, because most of these children
  n! ]7 v4 D3 [, y& _) R& i) \may initially present in their practice. The Physicians’
* m  n  n) H" d) ?  yDesk Reference and package insert should also put a' q0 N* Z9 R$ Y
warning about the virilizing effect on a male or
- E8 F" i' o8 `1 k  Lfemale child who might come in contact with some-1 ]% q4 P  K* A
one using any of these products.
9 g( \) z2 C' e$ M' F% H& K) w$ j7 wReferences
) D- e% C* {! B, z7 d9 B8 y5 v4 k1. Styne DM. The testes: disorder of sexual differentiation2 l5 R% @3 [+ H
and puberty in the male. In: Sperling MA, ed. Pediatric
. h0 O3 ?& [5 a, R% _Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
8 k- ?! Z7 z- e+ D5 V( j2002: 565-628.
+ z8 P8 K! t" _. P1 a+ w9 e$ U2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
) L4 s+ f  G0 `, ~% y2 Mpuberty in children with tumours of the suprasellar pineal
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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
VIP精品區,資源無限好賺金任務區,輕松賺金幣
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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
VIP精品區,資源無限好賺金任務區,輕松賺金幣
加入VIP,享受高級特權宣傳賺金又升級,超級棒
4个什么样的?
發表於 2025-1-19 02:41:05 | 顯示全部樓層
. k0 H9 h, U1 V* `
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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