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Sexual Precocity in a 16-Month-Old  a: a, q  ^6 r- o, o* L# X* L7 o
Boy Induced by Indirect Topical
. S. w7 L. W0 z3 Q. I+ |5 dExposure to Testosterone
" a5 i! y! r, i, USamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
/ u1 Y+ ?/ |0 f4 V+ @) I2 Pand Kenneth R. Rettig, MD1% X$ n8 d" j. o& k( b; l, z
Clinical Pediatrics
! S0 B! x% Q1 e8 O1 SVolume 46 Number 6
6 q( }* J  o' X4 r2 l9 D! kJuly 2007 540-5432 W8 ^2 b, }& e) N* v& L( J8 z# Z
© 2007 Sage Publications  y5 `$ H8 u5 E- {
10.1177/0009922806296651
$ W9 q$ o! \& {4 y+ ]3 ahttp://clp.sagepub.com
  y, D$ T7 C+ t% J' g( M8 Q* Ehosted at. ?! Q2 l& g! A7 j: C5 h; k% F
http://online.sagepub.com7 c; \9 l. G6 F: F. |2 |
Precocious puberty in boys, central or peripheral,
2 C$ Q- g. q6 S! R# v) x( n+ y& y, Cis a significant concern for physicians. Central) \' u  n% V$ l8 A. B
precocious puberty (CPP), which is mediated$ c, _# h& y* H) Y
through the hypothalamic pituitary gonadal axis, has
5 e3 j- b- Z* g$ p7 c2 D$ `  `a higher incidence of organic central nervous system  \) ~) `  w1 D1 |
lesions in boys.1,2 Virilization in boys, as manifested
% F+ {. p  w7 H8 ~+ f; Mby enlargement of the penis, development of pubic+ s8 r/ w- m# v! r. m* r
hair, and facial acne without enlargement of testi-: o+ D- [) R& s7 ]% N! j
cles, suggests peripheral or pseudopuberty.1-3 We* q  I7 T, U) E4 p  F
report a 16-month-old boy who presented with the
0 I! a1 p5 p% Y' U9 denlargement of the phallus and pubic hair develop-" G( t- O. I4 X' I
ment without testicular enlargement, which was due$ |* K4 v4 p) B8 X
to the unintentional exposure to androgen gel used by) i& h' _4 {$ `6 ?5 W( V- e) J
the father. The family initially concealed this infor-+ x/ l) e: n5 R$ V
mation, resulting in an extensive work-up for this# b# N( v- b; b4 J
child. Given the widespread and easy availability of2 l+ u9 ~9 V: K+ z
testosterone gel and cream, we believe this is proba-
$ F3 ~! v9 }  U1 Gbly more common than the rare case report in the  y% f5 y3 B# g; ]2 @
literature.44 ?! o! W/ k( f$ h
Patient Report
6 R! C$ o9 j" M/ F  kA 16-month-old white child was referred to the, M2 t* E+ F' H- Y
endocrine clinic by his pediatrician with the concern6 Z; t+ E- n+ d. Q5 o+ w8 e2 Z6 J5 v8 f
of early sexual development. His mother noticed
+ O7 q- ?* c1 c7 L  s0 klight colored pubic hair development when he was$ ]6 A4 }: D$ K
From the 1Division of Pediatric Endocrinology, 2University of
1 U- y9 ?$ v- X( |) ySouth Alabama Medical Center, Mobile, Alabama.- B( [0 h0 A- h' }  h2 O
Address correspondence to: Samar K. Bhowmick, MD, FACE,
& c* K5 Z& H8 T$ [% a5 UProfessor of Pediatrics, University of South Alabama, College of; C& T6 F0 s( O9 T
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;  ^/ ~7 a% N% p8 H4 ]; Z- s
e-mail: [email protected].% }( q( i: H5 I' t: Z2 H; m
about 6 to 7 months old, which progressively became) _0 e: U1 z# l; l7 m
darker. She was also concerned about the enlarge-; A5 l0 r9 I# k2 t  N7 ~% g8 K1 ?
ment of his penis and frequent erections. The child
+ j' f5 K5 }7 P& r7 O9 z: c6 \- T6 qwas the product of a full-term normal delivery, with
" P. \4 ~) K. ^  \( @. F& aa birth weight of 7 lb 14 oz, and birth length of* i3 B4 X2 b- t* }
20 inches. He was breast-fed throughout the first year
) X& H5 H( [6 m4 g9 K) i% K5 Sof life and was still receiving breast milk along with
# E0 @( d$ p- e. i( Fsolid food. He had no hospitalizations or surgery,# u7 @% X& A6 s5 n6 i
and his psychosocial and psychomotor development% a: s& [, ^/ H& r$ \
was age appropriate.
" }+ |* T0 }0 A9 E% k. [The family history was remarkable for the father,: ?9 W: l+ S! W) |
who was diagnosed with hypothyroidism at age 16,# \5 [( e; U( p9 j" z9 a5 P
which was treated with thyroxine. The father’s
) P* s  y# Q4 v. i  Y" x% |  zheight was 6 feet, and he went through a somewhat
; A' Z/ I/ b  R. E$ D" jearly puberty and had stopped growing by age 14.
8 H( i1 H2 h, [3 b* ?The father denied taking any other medication. The. ]' r2 z8 i. U- \
child’s mother was in good health. Her menarche
! O2 L  l& R" ~( C% V1 \* {- Dwas at 11 years of age, and her height was at 5 feet
+ r+ F  c% E; [: F5 p5 inches. There was no other family history of pre-
8 I3 p) B6 Q( y+ Ycocious sexual development in the first-degree rela-
! ~& c  d; e% p7 ztives. There were no siblings./ ~# x$ @- S( x, N! j+ t; J# j
Physical Examination
& V$ r% S6 s4 q/ M" A+ E6 zThe physical examination revealed a very active,( ^5 [0 L3 X9 w4 ^/ }
playful, and healthy boy. The vital signs documented
+ V9 P+ [) ~4 A6 {; d' m2 S8 Wa blood pressure of 85/50 mm Hg, his length was
2 g5 {3 H- o8 Q4 f! b90 cm (>97th percentile), and his weight was 14.4 kg
  F) R/ \$ M. b+ ]2 g(also >97th percentile). The observed yearly growth
& |7 D! W$ e" U$ Wvelocity was 30 cm (12 inches). The examination of# D$ |6 q- U2 c( V/ N% e) r1 l
the neck revealed no thyroid enlargement.
# W' O+ H8 ~$ t7 VThe genitourinary examination was remarkable for, k. q( g& m  Y, ]% c" W8 u2 h9 m/ A
enlargement of the penis, with a stretched length of
+ d- t4 i' k' I, T: B8 cm and a width of 2 cm. The glans penis was very well
5 b: T5 {5 b% v, |$ Hdeveloped. The pubic hair was Tanner II, mostly around0 T; I/ T3 {: S
5401 b' Q5 M  ]" `0 e+ @
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from; T# ~4 m/ [7 ^' q
the base of the phallus and was dark and curled. The" c4 l# ?/ k2 u4 Y. `' P: j
testicular volume was prepubertal at 2 mL each.) s! B8 Z( n- p; v
The skin was moist and smooth and somewhat
; C) n: X' [# K9 v; j8 O. Xoily. No axillary hair was noted. There were no) f( Y5 w# g" }: l4 ~) u# D" ?7 h
abnormal skin pigmentations or café-au-lait spots.
. j, X, F/ r2 C/ F1 p) b- INeurologic evaluation showed deep tendon reflex 2+  {) f% _) g, H. L6 M, i
bilateral and symmetrical. There was no suggestion
# _# S% Y6 z/ _, q7 Jof papilledema.
6 `4 d( @, R2 Y2 D0 N2 F; p! PLaboratory Evaluation2 X$ P8 Q" U# M' \5 n
The bone age was consistent with 28 months by' f" w4 ^$ Q( ~) }8 T( f
using the standard of Greulich and Pyle at a chrono-
/ B2 A6 [  w  w4 ?+ Q; glogic age of 16 months (advanced).5 Chromosomal) D7 l: j7 d' ]0 A2 n0 u4 f
karyotype was 46XY. The thyroid function test5 ^& f6 w+ O& f
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
# T+ p# E; a) W, e& W  _' Dlating hormone level was 1.3 µIU/mL (both normal).
2 \( d8 [9 |9 a- |The concentrations of serum electrolytes, blood! ]: k+ E0 m& b* ?# x9 J$ ?) e
urea nitrogen, creatinine, and calcium all were
3 a1 \1 Z; u  Mwithin normal range for his age. The concentration8 M  u* _( r) C! c
of serum 17-hydroxyprogesterone was 16 ng/dL
) _/ _% o0 B3 H0 ~: E(normal, 3 to 90 ng/dL), androstenedione was 201 f7 j8 v  g) y7 ?1 l  y. w: ^" g
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
: N/ g' \; l9 W3 U& H2 _8 uterone was 38 ng/dL (normal, 50 to 760 ng/dL),' O% d9 v2 a6 }0 G7 }7 H6 r, H
desoxycorticosterone was 4.3 ng/dL (normal, 7 to4 P  k1 B0 z5 Y/ E5 Z% [  o
49ng/dL), 11-desoxycortisol (specific compound S)& q8 a: L( T7 b
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-- W1 r2 r1 y7 W/ v% h* c  R: S/ L5 \
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
% B: w2 P" ]. Ytestosterone was 60 ng/dL (normal <3 to 10 ng/dL),$ L' n- J; X4 ]/ _
and β-human chorionic gonadotropin was less than' r; K7 w, L+ {' G4 t
5 mIU/mL (normal <5 mIU/mL). Serum follicular. D( g6 s  N3 P2 O  a! e) m
stimulating hormone and leuteinizing hormone( K3 x- a. @4 R# k/ M6 U5 K, L3 O
concentrations were less than 0.05 mIU/mL
2 n. e5 ~: J% r* S$ @) z(prepubertal).
. K7 Y$ e  l! ^; Z; ~% x8 SThe parents were notified about the laboratory6 r4 y7 E# N  @" e! J. R
results and were informed that all of the tests were
- w* t+ K! ]3 Z( }+ unormal except the testosterone level was high. The9 W/ E  z6 M* |  y5 G. `
follow-up visit was arranged within a few weeks to  D9 m6 W  [# ~5 l8 ^/ p
obtain testicular and abdominal sonograms; how-% R8 {$ g2 o; ~% ]% q
ever, the family did not return for 4 months.
; j1 V# O* R8 `# ?. r7 T9 F8 IPhysical examination at this time revealed that the" i- m- o5 k5 A+ q4 [, E7 |) i
child had grown 2.5 cm in 4 months and had gained
  @; l) D5 L4 ]$ ]3 ?2 kg of weight. Physical examination remained
' i; v. _  J0 Y5 r( K' e! T8 Junchanged. Surprisingly, the pubic hair almost com-
/ Y. p6 U. K1 @7 q5 Y3 D  M8 Zpletely disappeared except for a few vellous hairs at
! x: X3 [1 W# k; f0 Cthe base of the phallus. Testicular volume was still 2( q: a: K$ x: j
mL, and the size of the penis remained unchanged.$ S$ |/ l9 O" n7 V  C
The mother also said that the boy was no longer hav-8 F7 Z) L# e# `  \) z0 D0 J% ]% D% b
ing frequent erections.1 G$ y6 k& r3 p/ M& O6 ~
Both parents were again questioned about use of
+ n" ?3 O0 r1 h# ^, v' ?& e6 m  ~& z9 {any ointment/creams that they may have applied to' ?) P- U9 c% K$ P
the child’s skin. This time the father admitted the: [$ v  @3 c( z' F3 T3 ^
Topical Testosterone Exposure / Bhowmick et al 541
% B  J7 Z6 {, Y' juse of testosterone gel twice daily that he was apply-
0 B; Z4 ]& w+ ~; ?& ting over his own shoulders, chest, and back area for
/ N3 e8 ^. o+ P6 L/ ha year. The father also revealed he was embarrassed
6 w- R" J+ |: }. t" s$ I; fto disclose that he was using a testosterone gel pre-
) f' c+ E/ c4 q' P/ _( |; }scribed by his family physician for decreased libido" Y! m+ i$ u$ h) |% }( B
secondary to depression.1 Y4 F6 _9 V" n! {1 R
The child slept in the same bed with parents.
9 ~9 f3 O+ c  h0 Z6 j# W( H5 QThe father would hug the baby and hold him on his. i0 }/ s) E( P8 ?4 F1 i
chest for a considerable period of time, causing sig-
; s0 G1 O) {; u! J4 V5 Anificant bare skin contact between baby and father.
3 n6 W* _# v1 V, O+ y. T& f7 x. EThe father also admitted that after the phone call,( F( \; a( Q: o$ r' C! N
when he learned the testosterone level in the baby
& q( e; e" b+ a6 t9 mwas high, he then read the product information
  f1 I" \3 s; `7 y- [3 Kpacket and concluded that it was most likely the rea-
; }, V; |& J3 f7 N; Ison for the child’s virilization. At that time, they
# }4 F: A* L% x( l3 \decided to put the baby in a separate bed, and the
  Z' m% d& z. J0 J: m7 Y) Rfather was not hugging him with bare skin and had; n2 K- m: D8 n) E9 M( P
been using protective clothing. A repeat testosterone  z1 Z5 t( j2 b( b' W8 U
test was ordered, but the family did not go to the) i0 R' ~  M7 F, ~4 m" h
laboratory to obtain the test.! @) Z( D. c' q  @; v
Discussion' U; j2 D# |( R3 I& E
Precocious puberty in boys is defined as secondary
0 @4 Y  e4 d6 Zsexual development before 9 years of age.1,42 O( w8 b  U" Q6 [" T
Precocious puberty is termed as central (true) when
# z$ _4 Z0 z$ P2 ^: g8 I8 r3 L/ Kit is caused by the premature activation of hypo-
, x/ S+ E; B! }% z8 n/ u4 zthalamic pituitary gonadal axis. CPP is more com-. [* i( S% q/ W+ z* x
mon in girls than in boys.1,3 Most boys with CPP, g0 K& X* g  g* s: ^9 o
may have a central nervous system lesion that is( h7 X; v6 J. y' _- k* Y" Q: C
responsible for the early activation of the hypothal-
$ Z' v/ C8 x6 ^amic pituitary gonadal axis.1-3 Thus, greater empha-
" z8 m- W, l' d- V# Csis has been given to neuroradiologic imaging in
# l8 G2 u9 |0 @, s  rboys with precocious puberty. In addition to viril-
+ G- j* r% b; K5 _" gization, the clinical hallmark of CPP is the symmet-
! N7 h3 [& ]' J( c+ J+ @/ xrical testicular growth secondary to stimulation by
& b; j. N+ v2 y0 f0 A7 d1 D# Bgonadotropins.1,3& K9 B$ B, x# u& d( F( M" y8 z+ L
Gonadotropin-independent peripheral preco-
( d/ w& G- `  i, m+ A( ecious puberty in boys also results from inappropriate4 U% M6 H( ]  |/ ]( o9 K
androgenic stimulation from either endogenous or
: d! B% W7 m! M: |+ Dexogenous sources, nonpituitary gonadotropin stim-4 {( Z& l& B- A( w6 J8 t
ulation, and rare activating mutations.3 Virilizing4 m- T+ @& ?9 {5 n+ C
congenital adrenal hyperplasia producing excessive2 h3 C9 g" B( x# u, E5 t& c; i
adrenal androgens is a common cause of precocious
3 t$ V: d' m( Y+ Wpuberty in boys.3,4
% t% P" t6 P* f# B8 e7 {( u1 SThe most common form of congenital adrenal) W" N/ w) K  R, A6 H0 l! l
hyperplasia is the 21-hydroxylase enzyme deficiency.
+ W$ i. @0 S% i2 l" C# v% y5 N. BThe 11-β hydroxylase deficiency may also result in1 k6 e8 w0 l- z3 E. Y; U# I6 @
excessive adrenal androgen production, and rarely,1 l! D0 D+ f# m0 C4 W# I
an adrenal tumor may also cause adrenal androgen; S8 G+ _4 n6 X7 L; ]
excess.1,3
, f' r) f$ b+ T: n$ `: ]9 Eat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from. ^$ j" `2 C) N# E! Q
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
! k' R/ x3 |3 \( `) ?! k- h2 Q0 u- U$ UA unique entity of male-limited gonadotropin-! I+ o3 Q6 b( z/ X  H
independent precocious puberty, which is also known
  S; p( }2 s: e. H1 {9 Fas testotoxicosis, may cause precocious puberty at a
( M; f* h- V4 @7 Z9 K) hvery young age. The physical findings in these boys5 P8 ^1 i& Z& r& Q% {  ?
with this disorder are full pubertal development,% e' q) o9 T3 ?! ?9 P" s
including bilateral testicular growth, similar to boys
7 H* ]7 @* \* k1 pwith CPP. The gonadotropin levels in this disorder/ S+ l7 m' U* Z% Q) v5 M
are suppressed to prepubertal levels and do not show
( u& [7 }, g$ I- \pubertal response of gonadotropin after gonadotropin-* g+ u' w- h# H4 _& M, c; s
releasing hormone stimulation. This is a sex-linked# q8 ?/ n2 A4 j0 [
autosomal dominant disorder that affects only
9 l2 {9 O, _% [" mmales; therefore, other male members of the family
0 a* {. k. C3 _may have similar precocious puberty.3
8 Z7 P, }1 j0 i5 S$ ZIn our patient, physical examination was incon-5 O; S6 |1 D& @( f/ f3 ~
sistent with true precocious puberty since his testi-& k9 e$ t8 U/ ]4 a
cles were prepubertal in size. However, testotoxicosis
0 K0 |% c+ h3 Fwas in the differential diagnosis because his father
1 P5 O5 F1 F) ^* lstarted puberty somewhat early, and occasionally,& U* I0 K; ~4 m5 f4 b4 U
testicular enlargement is not that evident in the
. U/ A8 k7 G3 @, vbeginning of this process.1 In the absence of a neg-* l: n2 P  w: w) c7 x4 G2 p
ative initial history of androgen exposure, our
& b1 T+ Q; W+ z4 y) [( y  b( Jbiggest concern was virilizing adrenal hyperplasia,0 Y+ i- [. Y% D
either 21-hydroxylase deficiency or 11-β hydroxylase2 ^7 }$ C) k; Q- j  S; S- p
deficiency. Those diagnoses were excluded by find-  V) B' d1 @' X! l1 o+ ?4 a& d
ing the normal level of adrenal steroids.1 p& I$ j1 r& U# r7 w
The diagnosis of exogenous androgens was strongly( Q" [# F+ V) @+ I3 _. W
suspected in a follow-up visit after 4 months because7 r# ]7 c! a' G; n. p
the physical examination revealed the complete disap-. @/ Y9 s6 ~- m9 E& c) p1 n
pearance of pubic hair, normal growth velocity, and
" q) Q2 T2 P" f& hdecreased erections. The father admitted using a testos-
8 Q" Z* r1 S7 u; O% q' a7 [) }terone gel, which he concealed at first visit. He was
( l& R# B& _% B: Kusing it rather frequently, twice a day. The Physicians’9 [& J: B. C  d& p$ `' x+ ?# }
Desk Reference, or package insert of this product, gel or
8 t) M1 m  d2 ucream, cautions about dermal testosterone transfer to
! S- c- u1 W7 b9 m* Junprotected females through direct skin exposure.  S7 d' R7 s6 g
Serum testosterone level was found to be 2 times the% y5 L3 i) Y. d! W2 [
baseline value in those females who were exposed to
- P4 u' ]7 Z7 ^, o2 Aeven 15 minutes of direct skin contact with their male
- [8 P0 q6 M2 C( F: apartners.6 However, when a shirt covered the applica-
5 M6 N' h5 v8 T( \1 N. }& ?tion site, this testosterone transfer was prevented.
; ~% I1 X* L# g, X; l- E  b6 n4 VOur patient’s testosterone level was 60 ng/mL,. X! }/ P  E$ Y
which was clearly high. Some studies suggest that6 o( n5 I( n9 O0 }# c
dermal conversion of testosterone to dihydrotestos-7 i: O5 p, T: Z- _" o) q1 u
terone, which is a more potent metabolite, is more
. c" C6 E) j2 h2 U& [& ~active in young children exposed to testosterone3 y! i$ q3 V. N0 S
exogenously7; however, we did not measure a dihy-
# E- \: ~: R0 N0 q7 j) Q! cdrotestosterone level in our patient. In addition to; f0 M$ f# B9 N# u1 P3 E
virilization, exposure to exogenous testosterone in3 u- {* b, w% g# h
children results in an increase in growth velocity and. A) O6 {8 T' Y. h/ z/ d
advanced bone age, as seen in our patient.
8 T5 P8 r* Y. ~The long-term effect of androgen exposure during
8 j! ~& M* Y3 n1 H) qearly childhood on pubertal development and final) v( \# V7 A( U% a1 U+ }
adult height are not fully known and always remain
6 a, @1 A* a. Na concern. Children treated with short-term testos-
+ q  I3 B" U( pterone injection or topical androgen may exhibit some3 u' G/ [! C6 N3 N' v
acceleration of the skeletal maturation; however, after
5 S6 M5 t0 Q+ r; G  F# Ucessation of treatment, the rate of bone maturation
, H; x1 n; ]& [4 T0 Ddecelerates and gradually returns to normal.8,9
' j: U8 K3 B$ Z$ hThere are conflicting reports and controversy
9 [; L& j5 N( X  Q* O5 bover the effect of early androgen exposure on adult$ p4 F* s- x/ I, j
penile length.10,11 Some reports suggest subnormal6 j& p* e# ^) |4 _$ k2 B
adult penile length, apparently because of downreg-2 u3 ~( ^( T' `7 |/ w
ulation of androgen receptor number.10,12 However,
$ r: l& N' L$ a0 XSutherland et al13 did not find a correlation between1 }# k6 A" G# S5 b$ [
childhood testosterone exposure and reduced adult( V. @4 L1 k$ R5 ^
penile length in clinical studies.: F' o; p$ T' T0 l
Nonetheless, we do not believe our patient is3 o7 Y/ ?7 O. |4 M. L. K* g
going to experience any of the untoward effects from
9 k* W  l4 P! O4 p$ w1 @% ~* ]testosterone exposure as mentioned earlier because2 \; w: ?& w7 e: o: m: D
the exposure was not for a prolonged period of time.0 G. l2 k- |! l0 ]! i
Although the bone age was advanced at the time of1 n( @; L/ ~, M6 {0 \
diagnosis, the child had a normal growth velocity at
% E) K) R- X6 a( r& a7 k( W0 I  ?/ S) pthe follow-up visit. It is hoped that his final adult
- F9 v/ E8 e/ a; F2 r7 yheight will not be affected.
) F4 D  F  n* G- p7 yAlthough rarely reported, the widespread avail-
/ K6 }: M2 p( f1 ]- ]ability of androgen products in our society may
6 p- l" |) }! {% _" i. k3 Bindeed cause more virilization in male or female- \! }8 w% j- I9 p1 A+ e9 T& J
children than one would realize. Exposure to andro-
' @! E: X% _( V+ p2 w; ~gen products must be considered and specific ques-
6 A; I8 a7 r7 x4 P' b' f0 g0 }tioning about the use of a testosterone product or! {: |) B: c! Z1 r( h9 l# g
gel should be asked of the family members during
- |* I( E' Q; h# u! O; Nthe evaluation of any children who present with vir-
  \" B& j( H+ b# _ilization or peripheral precocious puberty. The diag-2 j6 x6 s, Y# b! t6 }/ U# _+ b$ X; c
nosis can be established by just a few tests and by
. e+ G: G9 @1 T' D0 _6 happropriate history. The inability to obtain such a
  ]+ G( B! R$ G# I6 |* C) whistory, or failure to ask the specific questions, may# g2 s) k7 m' @6 p* M# l
result in extensive, unnecessary, and expensive9 m& D8 C- ?# ?. W  G  `
investigation. The primary care physician should be
( M- f9 g0 K+ X  o2 E) maware of this fact, because most of these children
3 t1 C! t/ z8 U1 u: i! z4 Q  pmay initially present in their practice. The Physicians’
' ~/ I" m* J8 y, U2 U; A6 f7 ODesk Reference and package insert should also put a
  h% p4 S% p) U9 P0 h3 V* g, }8 q2 ^1 Z# vwarning about the virilizing effect on a male or! P$ @- T2 x: e$ ?
female child who might come in contact with some-
0 Z  a: C2 f7 D- K, M4 {/ ^4 V5 vone using any of these products.# S, G' t. m1 j) b3 s3 ^& H" c
References
- m% ]5 @- ^. Z3 T6 n& J3 X1. Styne DM. The testes: disorder of sexual differentiation; R& i( @$ M( Z$ [$ q% M3 \7 X
and puberty in the male. In: Sperling MA, ed. Pediatric
- z, H0 f3 s, c, h' K9 U  cEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
: _4 S2 v2 D  c6 x6 r, d: i2002: 565-628.
5 t+ I! t& F9 Z+ m# _$ G1 v5 M4 a2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious" y* \6 W( Q: S+ a
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
, G4 v, i% e; V( hBoy Induced by Indirect Topical. K: N/ [) [; y  t3 _! i7 U
Exposure to Testosterone# D( S. W7 G: F' w+ h7 l
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2& U* l! e8 G+ @# Z8 V; k( M  o8 @8 r# L
and Kenneth R. Rettig, MD1
- S0 D- ?0 t' o, o: Q+ L# HClinical Pediatrics
5 f  D2 d% l$ I+ N. j( T% cVolume 46 Number 6
0 V: E6 p. ~- zJuly 2007 540-543
$ l; W1 D/ v) K: z© 2007 Sage Publications8 n. O) r+ @8 q$ f5 C! _( A
10.1177/00099228062966517 r; o1 v, [  j
http://clp.sagepub.com
* b5 h3 R' F+ `. n  e* n* ]hosted at( d4 I; F* W0 W. j
http://online.sagepub.com% m5 d' ^5 `* I( a9 V% |! H8 ?
Precocious puberty in boys, central or peripheral,# f* c0 G1 L  ~! J8 d
is a significant concern for physicians. Central
4 o/ _; A. }* T$ h# T0 V) D& ?precocious puberty (CPP), which is mediated0 R7 E, J0 U( B2 d9 D9 b
through the hypothalamic pituitary gonadal axis, has
$ `1 c! `9 N7 q; q2 W6 W# Ua higher incidence of organic central nervous system5 [6 L4 a& s, p3 F$ }
lesions in boys.1,2 Virilization in boys, as manifested
  W! G. t: X% ?6 C" L9 oby enlargement of the penis, development of pubic) r& a  ]+ R3 `* i' Y
hair, and facial acne without enlargement of testi-; I' x7 s. r4 l' k
cles, suggests peripheral or pseudopuberty.1-3 We
5 [0 }' K7 a/ Treport a 16-month-old boy who presented with the
' N" b2 y* A' j# H, N1 Lenlargement of the phallus and pubic hair develop-
+ b3 I7 [4 s, J4 L& @ment without testicular enlargement, which was due
2 N+ D2 `: y# Xto the unintentional exposure to androgen gel used by
4 C9 X0 u* S& l9 Y. `" }the father. The family initially concealed this infor-
( z9 k8 `8 U  C0 O+ b9 z: wmation, resulting in an extensive work-up for this& r) F& E! \8 c& H( g! f! V
child. Given the widespread and easy availability of% C" J+ ]9 a; }* T9 p2 V
testosterone gel and cream, we believe this is proba-# U: {) \* ?) M4 I- }. |) Y
bly more common than the rare case report in the: G. v) ^& _! x0 M7 Z" X6 v
literature.4
, j1 ~: B( t4 J9 f( @  T  @Patient Report
5 z8 ]& L* t( ^( t, i( fA 16-month-old white child was referred to the
! c+ [; S5 Y# _- N% _! Mendocrine clinic by his pediatrician with the concern
* m* G# ?" ?5 j) J4 X) Xof early sexual development. His mother noticed
4 r+ M- m- C) k1 a- D  Glight colored pubic hair development when he was# P+ X5 M+ V3 I& Z* p& a, u9 a+ o
From the 1Division of Pediatric Endocrinology, 2University of4 U1 }$ c2 z0 H; j# _# I
South Alabama Medical Center, Mobile, Alabama.4 w0 J1 e6 V( t% ^
Address correspondence to: Samar K. Bhowmick, MD, FACE,: F+ I2 m7 l: ?4 F* w; q# }/ w
Professor of Pediatrics, University of South Alabama, College of+ `& G/ E6 H. q- D1 d3 S, z
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
' o, G4 h8 g+ f% ~) g. se-mail: [email protected]./ K. t. ^& b; \! c1 E  u
about 6 to 7 months old, which progressively became  k8 g% X* L4 P, F/ U% e2 w8 {
darker. She was also concerned about the enlarge-
5 T" y" d# P, z% i: Zment of his penis and frequent erections. The child; t2 t$ w& J# _( C
was the product of a full-term normal delivery, with
: d4 w# M$ \& n5 ?; [2 }' Ka birth weight of 7 lb 14 oz, and birth length of
7 o1 G, L9 k2 j. r' M9 d20 inches. He was breast-fed throughout the first year) \! B5 V2 H$ U/ t/ v
of life and was still receiving breast milk along with, H  Z2 ~& Y! d  _; z
solid food. He had no hospitalizations or surgery,2 c# M& T( m$ b* [- M) ]
and his psychosocial and psychomotor development
, E1 d9 M% @) T5 }. z  F& zwas age appropriate.  ~9 ], S# a( b$ K
The family history was remarkable for the father,
5 h! i9 H# [4 H9 @% _: k1 xwho was diagnosed with hypothyroidism at age 16,
9 a1 n6 c- X. Q( qwhich was treated with thyroxine. The father’s" o# O+ H1 N4 p- q
height was 6 feet, and he went through a somewhat0 Q: h$ I) r" x: w) O: h6 p
early puberty and had stopped growing by age 14.
( u- X2 t/ |) r- U2 tThe father denied taking any other medication. The# k, S0 {( a& R- ?
child’s mother was in good health. Her menarche
+ t" [& T. k' B; m. H! U$ T! Mwas at 11 years of age, and her height was at 5 feet
8 M9 m7 h  b8 g: t+ L  ?) t5 inches. There was no other family history of pre-
% `8 H$ T7 c2 Xcocious sexual development in the first-degree rela-
& m. {# i3 j) X- ~tives. There were no siblings.
$ t  u% m  }# m# d( pPhysical Examination+ z! D- Z% T2 G& d0 l
The physical examination revealed a very active,4 g- J( @! B4 T, k9 _5 {$ m
playful, and healthy boy. The vital signs documented! p+ D& N( B* o9 U3 n
a blood pressure of 85/50 mm Hg, his length was
/ B' t) A0 ]/ A) m90 cm (>97th percentile), and his weight was 14.4 kg9 p  N8 G4 u1 `! K2 L) j1 y
(also >97th percentile). The observed yearly growth# D( o3 p, G1 G8 _, L. W) J
velocity was 30 cm (12 inches). The examination of5 ^* g1 ~3 b# c9 O1 M
the neck revealed no thyroid enlargement.
2 B' ^( X" L* Q, u: v3 _The genitourinary examination was remarkable for( N0 W, L# V' S
enlargement of the penis, with a stretched length of
  G6 m+ t) M( |7 ^2 A8 cm and a width of 2 cm. The glans penis was very well' N$ s8 l; L) U6 M$ E; v
developed. The pubic hair was Tanner II, mostly around
& K' z' {* \4 n% R/ Z9 m3 N540
$ D* z) b9 I/ u8 ]at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
+ x; L( ], D% N6 z: l% ethe base of the phallus and was dark and curled. The7 X/ y* J- h" s9 u' |* [
testicular volume was prepubertal at 2 mL each.# w' f3 o1 ~' J
The skin was moist and smooth and somewhat9 \! H+ E: I, ?. V* a8 C! e3 {0 E
oily. No axillary hair was noted. There were no
4 N8 G5 G' w& ]9 _% kabnormal skin pigmentations or café-au-lait spots.
2 X9 m' ?3 l/ ]Neurologic evaluation showed deep tendon reflex 2+
5 h' O2 \& p2 c$ o' Ubilateral and symmetrical. There was no suggestion1 x  Y8 H/ r4 S; K
of papilledema.
  i+ }4 i% M$ p8 h+ f3 s; BLaboratory Evaluation
" R4 z2 E/ T& B  a: l3 T+ N. D1 eThe bone age was consistent with 28 months by" ^, `% W& t3 ]& M! g. V
using the standard of Greulich and Pyle at a chrono-
* K+ r( F! s& T& alogic age of 16 months (advanced).5 Chromosomal
$ q# A& b5 W  o0 n. Ykaryotype was 46XY. The thyroid function test* F$ _$ q8 @1 |+ Z- ?
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
' K/ d4 q3 D" qlating hormone level was 1.3 µIU/mL (both normal).
' N/ Z! h1 W* n9 {5 a1 `The concentrations of serum electrolytes, blood3 ]7 O7 X/ m3 R$ {& ~7 R/ R
urea nitrogen, creatinine, and calcium all were
+ S3 `7 H6 o& }+ owithin normal range for his age. The concentration' S; v% H: ]( Y$ |
of serum 17-hydroxyprogesterone was 16 ng/dL' x  J; D, I: w$ m( i" L
(normal, 3 to 90 ng/dL), androstenedione was 20
+ L' `$ m' W& G6 `! ong/dL (normal, 18 to 80 ng/dL), dehydroepiandros-2 a$ X3 k  }) T! \4 t
terone was 38 ng/dL (normal, 50 to 760 ng/dL),- m* Y! r, B! E6 [
desoxycorticosterone was 4.3 ng/dL (normal, 7 to+ c* j: U5 N4 Q* }2 a* a1 |
49ng/dL), 11-desoxycortisol (specific compound S)
, B+ h% T( t* R8 h, O2 Mwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-0 T& q( g" ?' C: W  j4 ^9 C7 O
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
+ k2 z3 S% Y: i, k' ztestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
8 I( @+ X, m- i0 c+ p8 Z9 h- p8 p) dand β-human chorionic gonadotropin was less than
) C2 W' H3 J" L& O7 y/ d: l5 mIU/mL (normal <5 mIU/mL). Serum follicular
* V  C8 G8 e$ P# bstimulating hormone and leuteinizing hormone
2 u9 O2 A" @4 ?, V7 P- p* D8 ^concentrations were less than 0.05 mIU/mL
) ]! p; Q; q8 D" g" m* N7 Z(prepubertal).+ e4 k( @  J+ \9 h
The parents were notified about the laboratory: \6 R2 `6 P# W; Q$ C
results and were informed that all of the tests were
+ q& Q3 F( [% A0 \+ q+ nnormal except the testosterone level was high. The5 I5 T% ]! U2 Q! Z/ z) M! w8 t6 u) E
follow-up visit was arranged within a few weeks to
2 Q- d, T. W8 x" X; lobtain testicular and abdominal sonograms; how-
4 Y  S  o% T# d5 O( Tever, the family did not return for 4 months.
' w# l6 D) T  ~" @" D0 QPhysical examination at this time revealed that the' G. x# ~4 W9 E$ s
child had grown 2.5 cm in 4 months and had gained
% c" K  ^4 w  o/ D2 kg of weight. Physical examination remained) d$ z+ n( @8 B1 K0 N& y
unchanged. Surprisingly, the pubic hair almost com-9 _; N  @9 y( K8 V5 D( i8 d, q
pletely disappeared except for a few vellous hairs at& s; {( x& V! p, Y; j
the base of the phallus. Testicular volume was still 2; r* I1 s1 K, l! J" T6 A. a
mL, and the size of the penis remained unchanged.
6 u% l6 t' m5 j5 C( A2 M* ZThe mother also said that the boy was no longer hav-
6 X6 S: _: [( Q( V+ g; wing frequent erections.
0 @, B/ i( R/ v2 oBoth parents were again questioned about use of1 {) ~! t5 B9 F' I0 p( v
any ointment/creams that they may have applied to
1 ?0 W; o8 t7 C9 b. r  xthe child’s skin. This time the father admitted the
  v. J2 i8 \+ t# S% b" m$ LTopical Testosterone Exposure / Bhowmick et al 541% h+ @$ ~9 U3 x- K$ Y
use of testosterone gel twice daily that he was apply-
5 W/ ^+ \( f4 ^ing over his own shoulders, chest, and back area for" |, f, r: Z- I  ^0 N
a year. The father also revealed he was embarrassed
7 W) ]! w% N2 B- h8 C+ O$ J) ?9 }to disclose that he was using a testosterone gel pre-3 `2 x8 ]! b, _
scribed by his family physician for decreased libido; b* Q; t3 G* i- S8 W" G( w- k( E
secondary to depression.9 O$ U* Z3 j2 h/ w; G
The child slept in the same bed with parents.. r/ G( Q3 O9 G: ~  Y
The father would hug the baby and hold him on his
" [# O8 Y* ?6 y, F" T0 P$ y  Ochest for a considerable period of time, causing sig-/ X0 d( P" ]% E& g; x$ Q
nificant bare skin contact between baby and father.
' l% O: t: R" s! k( G+ B: \8 vThe father also admitted that after the phone call,% ~3 e4 F$ d) i' @. E
when he learned the testosterone level in the baby; W* v) Q# \8 N$ O* J* m2 v
was high, he then read the product information
8 Z; X) W3 n4 {: ?! U; H8 Qpacket and concluded that it was most likely the rea-/ s5 q3 C  M  V2 G( G$ D; L
son for the child’s virilization. At that time, they6 J" P  t6 [& p7 X$ O/ `
decided to put the baby in a separate bed, and the
% k6 L- v& t1 p3 rfather was not hugging him with bare skin and had6 H& Z/ l. D' J/ k
been using protective clothing. A repeat testosterone
+ F1 H: Y* N0 \9 I  J, E) J! j  ptest was ordered, but the family did not go to the9 O9 N2 l$ C  h5 R. z' q' a. X# k
laboratory to obtain the test.
% Z/ |6 i' f, v/ h3 EDiscussion% L+ B9 i# A& x7 P1 C# T, _
Precocious puberty in boys is defined as secondary
& r4 V. S/ u  ]* W( |4 nsexual development before 9 years of age.1,4
; [/ B7 Z! ]1 ~( O' ]Precocious puberty is termed as central (true) when
: v3 g9 B7 i* nit is caused by the premature activation of hypo-- R$ a! H0 Z- z, R$ `- Y4 c5 j
thalamic pituitary gonadal axis. CPP is more com-% ]5 p( h$ Q7 e7 u% @- V
mon in girls than in boys.1,3 Most boys with CPP+ B# N; ^4 b4 J+ h% j* w5 ]1 x
may have a central nervous system lesion that is/ V5 X! P$ V; j) j# j
responsible for the early activation of the hypothal-
1 W% p4 f  U% ^0 S( B) Gamic pituitary gonadal axis.1-3 Thus, greater empha-
* t+ W; z) R* G* Lsis has been given to neuroradiologic imaging in
: o1 \4 I3 X6 r: Dboys with precocious puberty. In addition to viril-/ K, V( J6 _; b* \1 v" |  f5 M2 n
ization, the clinical hallmark of CPP is the symmet-  K: [( p  d5 t9 B0 z' F
rical testicular growth secondary to stimulation by! N6 @$ z8 V: h7 d' X
gonadotropins.1,31 b% ]9 f/ X( i  D7 y% O: P
Gonadotropin-independent peripheral preco-
) @0 n  R2 r  @cious puberty in boys also results from inappropriate
3 g) ?6 S! I  tandrogenic stimulation from either endogenous or, t) U  q) e9 Z# c3 f& f( G8 y* a1 x
exogenous sources, nonpituitary gonadotropin stim-3 ]* s! b/ {" w' k
ulation, and rare activating mutations.3 Virilizing# }# v- r" T$ o) g
congenital adrenal hyperplasia producing excessive% u/ f7 r+ f7 T( j7 X; K
adrenal androgens is a common cause of precocious# S* D# W. n6 q6 h6 ]
puberty in boys.3,4
  w% Y. r& Z5 m/ `The most common form of congenital adrenal4 y0 \8 a" q& ~7 V( n/ L  ~
hyperplasia is the 21-hydroxylase enzyme deficiency.
4 Q$ g! {6 `# v2 s- ZThe 11-β hydroxylase deficiency may also result in
) z. ~, D. D3 F, t) E$ [excessive adrenal androgen production, and rarely,
* x) n0 |! j& C# ^3 ?; C4 Ean adrenal tumor may also cause adrenal androgen
8 W% u- v* X$ M- j4 @excess.1,37 v/ m) `$ X8 ]0 `4 J% k1 t7 S4 d# T
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from0 o+ y6 s  ~4 t7 J% W9 a
542 Clinical Pediatrics / Vol. 46, No. 6, July 20070 ^* h' P- b7 M/ J- ]/ K/ b
A unique entity of male-limited gonadotropin-( I. P5 g; J9 t/ N  q. C. Z
independent precocious puberty, which is also known
7 M$ Y/ ]5 K+ I+ R5 Vas testotoxicosis, may cause precocious puberty at a+ b( `6 L* ?7 ?
very young age. The physical findings in these boys
% m3 Y: B" m% v: |9 b2 N9 _/ B, ~with this disorder are full pubertal development,
$ G+ ^0 V- j+ U! C0 @( Gincluding bilateral testicular growth, similar to boys
* Y. v/ m% Y" z, Q% Qwith CPP. The gonadotropin levels in this disorder8 @1 y- @  H/ w$ y. c) {
are suppressed to prepubertal levels and do not show% Z: ^# }) Y( b. t7 o
pubertal response of gonadotropin after gonadotropin-+ A6 o% u/ a* n1 z( w5 H9 q1 F
releasing hormone stimulation. This is a sex-linked
' G+ w9 |/ t$ p5 iautosomal dominant disorder that affects only4 g1 Y+ d4 z" T0 k/ v) l9 a
males; therefore, other male members of the family$ u0 @2 d! ]7 Z% C: @1 S4 \
may have similar precocious puberty.3
( k" U" p5 N! L  aIn our patient, physical examination was incon-4 D8 z3 K# K0 `/ t, V% _; h- {
sistent with true precocious puberty since his testi-( ]; V, B5 X( k0 \& p7 q; d
cles were prepubertal in size. However, testotoxicosis
& Y/ n  F7 A7 `! kwas in the differential diagnosis because his father
- T7 N3 v& E3 }, a: s* @, z$ Rstarted puberty somewhat early, and occasionally,2 H) ^# D1 h, x8 e
testicular enlargement is not that evident in the% `8 Q: l* w: l+ M' ^+ r
beginning of this process.1 In the absence of a neg-$ f: t, B: M) I
ative initial history of androgen exposure, our6 _1 j" t1 m9 e1 T8 i8 n3 E( |
biggest concern was virilizing adrenal hyperplasia,
3 s4 T# _) Y. F9 M( G% neither 21-hydroxylase deficiency or 11-β hydroxylase( S4 R* c) n. @' h6 a- z, G& @
deficiency. Those diagnoses were excluded by find-
: s( G# i0 y, `2 i9 {2 W. ying the normal level of adrenal steroids.' Y' ]* S! }7 W7 W- M
The diagnosis of exogenous androgens was strongly
( B# C& ~  s. Asuspected in a follow-up visit after 4 months because
, m6 ^# q- R6 M7 I7 p% Lthe physical examination revealed the complete disap-  `8 p. I( k* S' }& M5 L
pearance of pubic hair, normal growth velocity, and, D4 l6 `5 W3 n+ k$ B) t! u
decreased erections. The father admitted using a testos-
& i* z" A! t, t/ U% D0 u0 ?; }terone gel, which he concealed at first visit. He was
2 b9 b, q. C2 m3 v" v% Nusing it rather frequently, twice a day. The Physicians’. S* @, u% `6 P2 U
Desk Reference, or package insert of this product, gel or& q  j& }, `' X' w; _; g* z0 W* O1 p
cream, cautions about dermal testosterone transfer to
- V8 O" C3 Q! T9 y  \. t- Lunprotected females through direct skin exposure.) ]' F0 P5 d: N3 K4 ?' j
Serum testosterone level was found to be 2 times the
( F% q* Q: `' [1 z9 vbaseline value in those females who were exposed to" n! ^3 `2 S" X3 {  J
even 15 minutes of direct skin contact with their male
1 s3 @* k4 q- x* ~1 wpartners.6 However, when a shirt covered the applica-
0 m% r% T% x8 x5 c5 ]$ O# e, k- B7 Htion site, this testosterone transfer was prevented.7 l# X6 O9 Z; V, w: d
Our patient’s testosterone level was 60 ng/mL,- h2 m9 s& h" N/ h- `' m
which was clearly high. Some studies suggest that
( \! e$ h. Q* ]& j% X4 gdermal conversion of testosterone to dihydrotestos-
0 z/ T" y' ~- b  P2 T6 j2 @terone, which is a more potent metabolite, is more- @% E. ]  |  d  ~, }
active in young children exposed to testosterone
  ^8 f# y3 f" P# Zexogenously7; however, we did not measure a dihy-
# q* @$ c' @9 e/ X& H: fdrotestosterone level in our patient. In addition to
$ h/ _2 D$ s' [0 @2 [9 c( d1 g: Tvirilization, exposure to exogenous testosterone in
) q8 t7 N0 y) i* b. d3 a. gchildren results in an increase in growth velocity and2 g4 S# O& A  F2 t7 ?. L9 _: b
advanced bone age, as seen in our patient.
" R( A: E( e( q! [# ~) ^The long-term effect of androgen exposure during% \; E" ^+ X# G6 V- V
early childhood on pubertal development and final
7 @$ F3 ~9 R! Q9 c* U' badult height are not fully known and always remain0 N1 Y+ y" I' n5 O* ]0 q
a concern. Children treated with short-term testos-) T, U$ A+ o' L- [- V
terone injection or topical androgen may exhibit some0 L  O% |. v' t( B' E8 y
acceleration of the skeletal maturation; however, after
( G5 K2 t' e. _  c, s* \' wcessation of treatment, the rate of bone maturation) {( \! M8 t* K' c" X
decelerates and gradually returns to normal.8,9
  n, R3 H) [- V0 T# ^& ?There are conflicting reports and controversy
- }; y6 X; x# h0 x6 x3 H3 `, hover the effect of early androgen exposure on adult# n( @) w: m' i! g6 X
penile length.10,11 Some reports suggest subnormal, K: D1 A& y$ P0 L9 S, E
adult penile length, apparently because of downreg-% s; _5 _, h: N$ m% V6 H( [
ulation of androgen receptor number.10,12 However,
* r7 J1 O' A+ HSutherland et al13 did not find a correlation between* g% g' R* p3 o4 |4 e- B% s* U
childhood testosterone exposure and reduced adult
6 y: O5 y' L7 c: Q  w! I) R* K( Xpenile length in clinical studies.
2 ~9 F9 d2 v3 T: ~Nonetheless, we do not believe our patient is
! E$ W' C# ?; z5 X  F# c/ O9 Zgoing to experience any of the untoward effects from7 `; j1 _9 g: o; }
testosterone exposure as mentioned earlier because; n1 {) p$ ]9 w2 Y
the exposure was not for a prolonged period of time.
" l1 A/ |; {3 s9 cAlthough the bone age was advanced at the time of( A- U+ p6 q9 Q  T8 G. a. a
diagnosis, the child had a normal growth velocity at
5 Z: K. r; C0 l5 ^the follow-up visit. It is hoped that his final adult, C+ Q" K( n& p' M) B/ t+ j; {
height will not be affected.& X: w1 j4 U7 s' v' p
Although rarely reported, the widespread avail-
$ v+ b' `$ j- d0 c4 Q  _ability of androgen products in our society may
$ O! m5 l9 j9 S$ jindeed cause more virilization in male or female
7 r$ s% X1 ^( w: U/ Achildren than one would realize. Exposure to andro-8 v7 O. T/ D8 x
gen products must be considered and specific ques-/ Z8 D4 q% g# j% f7 Z* s; u* n7 R
tioning about the use of a testosterone product or
: g8 |5 d" Z4 Z! E. j5 U0 T' tgel should be asked of the family members during
4 h! H3 g" V+ jthe evaluation of any children who present with vir-1 k' o0 k8 l0 l8 X
ilization or peripheral precocious puberty. The diag-
- y+ O/ j, j4 h. H* K3 Jnosis can be established by just a few tests and by$ P$ U! G  Q8 e/ n
appropriate history. The inability to obtain such a: J1 k/ `  z0 g5 f
history, or failure to ask the specific questions, may
, |7 c4 G" W* z8 Kresult in extensive, unnecessary, and expensive
. y! U5 K: ?5 Uinvestigation. The primary care physician should be/ O5 Y3 J; M& n: I' B4 x% e
aware of this fact, because most of these children2 S' j5 |% X' t
may initially present in their practice. The Physicians’) z1 L7 N: l, |6 \" W: G! [2 z" [
Desk Reference and package insert should also put a6 n# K5 u4 s6 E: \% s
warning about the virilizing effect on a male or
! Y: H) k3 ]  u' J. wfemale child who might come in contact with some-4 D$ f1 \2 ^6 @7 G; s9 z. a& d( y
one using any of these products.* l* i2 `) c1 Y! x5 T, F! w0 t2 H( ~
References$ F8 T) {, Z- H0 @! A' |- X+ B
1. Styne DM. The testes: disorder of sexual differentiation- g" h6 R+ S) @+ Y) M- N+ \. ]9 u
and puberty in the male. In: Sperling MA, ed. Pediatric
/ D: B" D& D: x0 i0 uEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;2 r% g* w, ?; H3 J$ x1 b
2002: 565-628.4 I  l* c( n$ g! e: I: \5 F1 @
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious7 u' m& C9 e6 ^& ]) H- J$ ~: V
puberty 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
1 h1 X* x0 k- P9 \8 |
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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