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Sexual Precocity in a 16-Month-Old" P# I3 r7 ^- J. W' }  O
Boy Induced by Indirect Topical- s- f7 Q; a8 D& K, R/ J
Exposure to Testosterone
5 f( k$ J$ ^" P4 o* ZSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
1 k; V5 S" n! r0 kand Kenneth R. Rettig, MD1
' |. @' e2 h: e# R" i( ~5 LClinical Pediatrics
+ a- n& m4 P, f9 N+ \2 w7 {  s( XVolume 46 Number 6! `& Z/ Y! y% l6 m3 y3 r
July 2007 540-543+ O" G- I) m8 ?5 X$ L1 z7 A
© 2007 Sage Publications8 ]0 n" q' K0 X+ v
10.1177/0009922806296651
9 \1 h% a- v/ ~2 j$ h* C! jhttp://clp.sagepub.com& k( Z; i" u. Q
hosted at
' p7 @* h# E3 [; }http://online.sagepub.com9 K6 Q; a) g4 u* f4 W( B* K
Precocious puberty in boys, central or peripheral,1 p! A( o- a& Q1 h: f! i- l
is a significant concern for physicians. Central$ w2 J5 {8 q2 O1 O' ^+ v% `3 Y( }
precocious puberty (CPP), which is mediated
  `5 k  O' a( F/ Uthrough the hypothalamic pituitary gonadal axis, has7 O3 E0 p, `7 n4 t8 |- M3 K
a higher incidence of organic central nervous system2 R% ~$ M3 c6 Q9 k+ G/ _  n2 v
lesions in boys.1,2 Virilization in boys, as manifested
7 g! Y" V- K* _4 Z7 L, A% ^' e$ \( hby enlargement of the penis, development of pubic
2 m) @( Q3 F! {* L- e7 Chair, and facial acne without enlargement of testi-' p6 T! R( D. i
cles, suggests peripheral or pseudopuberty.1-3 We
/ p# ?% r5 N5 G! Q6 z! C, nreport a 16-month-old boy who presented with the
" ]5 n$ _$ U% }+ ?% Venlargement of the phallus and pubic hair develop-  E) I" t2 X# p/ h7 s; k5 _. l# I  V
ment without testicular enlargement, which was due, r, G3 d7 V, A3 W% Y" p$ Y
to the unintentional exposure to androgen gel used by
- a% I4 u) s2 S* w# athe father. The family initially concealed this infor-/ f5 s6 w$ {. j  ]
mation, resulting in an extensive work-up for this8 Y! r, r# i3 a$ c7 _7 N9 ~
child. Given the widespread and easy availability of- g$ D9 l, Z6 h" U; Q
testosterone gel and cream, we believe this is proba-) ^$ g5 s% V0 m+ ?2 H" J5 g
bly more common than the rare case report in the3 p; X! h: _/ M" U/ y+ p0 p
literature.4
* e* E: n5 l( ]  RPatient Report
$ ]5 G, D% L6 t( I3 J9 r: z) bA 16-month-old white child was referred to the
/ ~1 d% d6 M4 E: Hendocrine clinic by his pediatrician with the concern' I' i: \- [- `& C- t  P
of early sexual development. His mother noticed( W  R, p: B9 |0 d% x7 s  Q- `" X
light colored pubic hair development when he was5 v% e9 d- W1 Z% r
From the 1Division of Pediatric Endocrinology, 2University of5 Y' W. A0 f6 U* X" G
South Alabama Medical Center, Mobile, Alabama.! c4 i$ W. j7 o6 o, T. A) a
Address correspondence to: Samar K. Bhowmick, MD, FACE,9 n% ^4 l; m8 U7 Q0 t
Professor of Pediatrics, University of South Alabama, College of
; d0 Y) W& s9 `5 |Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
5 s$ |% h( p6 m+ @! w/ {e-mail: [email protected].. p' N0 p" N* w( q5 w3 C! G
about 6 to 7 months old, which progressively became% H6 j/ D! D: G4 W- i) m4 v
darker. She was also concerned about the enlarge-) s# h' p2 L& V6 X- Z* B- G
ment of his penis and frequent erections. The child9 H& y, S0 l4 m; V! k* R7 D
was the product of a full-term normal delivery, with
; l1 I! `0 D$ Q7 P; |a birth weight of 7 lb 14 oz, and birth length of5 j% ^5 S' J5 {, M( k
20 inches. He was breast-fed throughout the first year6 R, I/ p5 U. i/ Q' [0 J+ u
of life and was still receiving breast milk along with8 D6 s/ C8 z) }1 X$ t
solid food. He had no hospitalizations or surgery,
: z' q2 k% X. v& ~( x2 ~0 m0 b" y: eand his psychosocial and psychomotor development
! F' A& {( B% W0 t2 Nwas age appropriate.2 \8 |, W5 ]% G* Q5 o0 |+ A
The family history was remarkable for the father,# V% Q( L/ d8 s) o- Q' x
who was diagnosed with hypothyroidism at age 16,9 V" x0 o4 A; k# K
which was treated with thyroxine. The father’s2 R! M/ N; m1 K6 f4 q
height was 6 feet, and he went through a somewhat
2 G8 o0 E: e4 Y& \% e* V& Y- l/ ]early puberty and had stopped growing by age 14.
! r8 N# d4 r. }! [+ F" p' d1 y, B* y1 uThe father denied taking any other medication. The$ y* k+ v5 a+ v; u' U- r' z8 s3 C; V8 p
child’s mother was in good health. Her menarche; i& j" w3 b# }& }' Q/ o9 |. b
was at 11 years of age, and her height was at 5 feet
% {# L3 Q; q! }7 w5 inches. There was no other family history of pre-
$ n; s! U! o/ V2 ]6 Scocious sexual development in the first-degree rela-) r9 D' m' f5 R- [1 b
tives. There were no siblings.
& q0 q* P& |& k) K/ XPhysical Examination
$ M( @3 u  Q( z& jThe physical examination revealed a very active,
2 I) W4 {- m, r$ Gplayful, and healthy boy. The vital signs documented
  q- i2 l/ R9 ga blood pressure of 85/50 mm Hg, his length was1 F0 L* l3 ^& M/ V: _' X
90 cm (>97th percentile), and his weight was 14.4 kg
- H1 a( \, g# ~  {5 S7 u7 t1 q(also >97th percentile). The observed yearly growth9 Z2 H% s2 U4 u5 s
velocity was 30 cm (12 inches). The examination of
: j) r, q# {3 W( n: X3 Nthe neck revealed no thyroid enlargement.# M5 u: c# V3 y6 x+ O4 B0 g$ Z
The genitourinary examination was remarkable for
8 Z6 d$ K3 e+ Z1 c9 ?; R$ u0 Renlargement of the penis, with a stretched length of
6 T7 F" L9 I5 b8 cm and a width of 2 cm. The glans penis was very well1 Z$ d! j8 [% _1 T6 q
developed. The pubic hair was Tanner II, mostly around( @5 z" l) K& E0 Q
540
' o9 n  a# f3 p+ q. ?4 ~at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
7 B- Q* i% @( E6 ~3 K1 ?* }the base of the phallus and was dark and curled. The) L2 Z: i# L$ A2 F
testicular volume was prepubertal at 2 mL each.5 N. s2 h0 g. V* B
The skin was moist and smooth and somewhat4 B1 c& q8 L$ _- s$ c2 U- }
oily. No axillary hair was noted. There were no
* M$ t9 s% P& o. }. {5 u' J: Iabnormal skin pigmentations or café-au-lait spots.
3 L: F' ]- I/ ]" x* T- RNeurologic evaluation showed deep tendon reflex 2+
; E) `  p8 P$ a" Xbilateral and symmetrical. There was no suggestion
* q5 |; ^2 q/ R& {5 dof papilledema.
5 z& \! I$ m* D/ f( \Laboratory Evaluation
1 P1 K1 a8 u2 {' B( PThe bone age was consistent with 28 months by& ?5 ^1 j- _. x0 ^, s6 k
using the standard of Greulich and Pyle at a chrono-
. N$ D+ ~& B5 W& s" l% Ylogic age of 16 months (advanced).5 Chromosomal
& N' X1 S& F6 kkaryotype was 46XY. The thyroid function test
7 R7 Z% f. |+ K, [) g; q% |) Rshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
' m% G6 a! y  c9 u7 }$ ]lating hormone level was 1.3 µIU/mL (both normal).7 ]0 I7 w* ^9 p
The concentrations of serum electrolytes, blood
! n3 _" X5 }- Q6 purea nitrogen, creatinine, and calcium all were
7 C0 w5 @$ x. y) {9 Awithin normal range for his age. The concentration; C6 [0 m" ^, c' T8 {) ^$ s
of serum 17-hydroxyprogesterone was 16 ng/dL
$ U2 |3 {! H; m% X2 C(normal, 3 to 90 ng/dL), androstenedione was 20
; s$ |' Y# u  y% ]9 dng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-4 P) |  U. S$ l2 u
terone was 38 ng/dL (normal, 50 to 760 ng/dL),1 j5 @2 ]9 e) X/ w
desoxycorticosterone was 4.3 ng/dL (normal, 7 to  n  V# j2 E+ @4 W7 t4 d3 r/ q
49ng/dL), 11-desoxycortisol (specific compound S)1 y1 u9 h* X6 b; B
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
. G9 v. a' c3 I0 f( Ktisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total3 [' F( _+ ]5 c6 ^, Z  u
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
" }. P6 g* O2 S+ R* W  o$ }4 ?and β-human chorionic gonadotropin was less than3 ~- M( S$ m* L/ d3 Y5 |
5 mIU/mL (normal <5 mIU/mL). Serum follicular
  [) h, _" `0 Xstimulating hormone and leuteinizing hormone
& V& v3 p5 E# pconcentrations were less than 0.05 mIU/mL2 m* A0 y' H8 H6 L
(prepubertal).% U4 y% \  W  P: ~
The parents were notified about the laboratory4 V7 m, U6 r1 r* y- T* u
results and were informed that all of the tests were
6 V; a; U# f) m  s3 onormal except the testosterone level was high. The" }& D* i/ |2 ]! C
follow-up visit was arranged within a few weeks to
- ~: D* `. j- o( m! O$ _# w  ]# _( iobtain testicular and abdominal sonograms; how-  U- c5 @3 o1 u' y! @/ {9 r
ever, the family did not return for 4 months.
/ \" p; g1 \  l6 b2 JPhysical examination at this time revealed that the9 a6 X8 q# Q. _, k
child had grown 2.5 cm in 4 months and had gained' _8 `. U0 B9 E* z2 w/ k6 ?$ Z; T
2 kg of weight. Physical examination remained
/ y8 Q( E* k  kunchanged. Surprisingly, the pubic hair almost com-; i' f" P! `' H
pletely disappeared except for a few vellous hairs at) v, _1 g. _) Y6 w/ E
the base of the phallus. Testicular volume was still 2
- ^  J% l# R" b6 ZmL, and the size of the penis remained unchanged.
9 o* H; J! s0 q! H" R' rThe mother also said that the boy was no longer hav-
/ s4 X: w% C7 s; r" \  h; Jing frequent erections.6 K1 F' C2 W" e0 o+ k
Both parents were again questioned about use of4 K3 z! B6 l, i) C
any ointment/creams that they may have applied to+ e, Y5 ^* }; k! L0 c. u
the child’s skin. This time the father admitted the
4 Q/ g9 q6 O' Z& a3 pTopical Testosterone Exposure / Bhowmick et al 541( Z& f& l, `; A5 B0 s. D# f+ ]9 j
use of testosterone gel twice daily that he was apply-
0 y( \' C+ s5 ying over his own shoulders, chest, and back area for: i7 P. p8 k! _$ ?/ n  _- y
a year. The father also revealed he was embarrassed
9 u- ~& ^/ v* `: B, u3 Q7 qto disclose that he was using a testosterone gel pre-% S1 K+ k# _) Y7 R% G, K; q
scribed by his family physician for decreased libido
0 Z! ^, P) K0 R* ]/ Ksecondary to depression.
) o" `7 G7 W) u7 m% h* n2 g: x& UThe child slept in the same bed with parents.
/ h6 m4 E1 `! ~3 T; a; ^' P, t7 gThe father would hug the baby and hold him on his6 w8 ^/ F8 S# v& ~
chest for a considerable period of time, causing sig-
* V1 Z( F4 }; D  }& N3 Hnificant bare skin contact between baby and father.; [$ X' ?" J4 G- q
The father also admitted that after the phone call,7 R2 f/ R2 `- C- A
when he learned the testosterone level in the baby
* B" }% F  v1 Q7 I2 X, Ywas high, he then read the product information
0 Y1 `( }6 `8 H- Hpacket and concluded that it was most likely the rea-- ?! s1 w) T, M% [( ]  w
son for the child’s virilization. At that time, they( e. V* F9 N1 f  t
decided to put the baby in a separate bed, and the
* \8 V9 F8 v  B% @* nfather was not hugging him with bare skin and had
3 b, L9 X# q. Y' L1 T& gbeen using protective clothing. A repeat testosterone! Y; c" u5 b$ P0 ~6 d  X& [
test was ordered, but the family did not go to the9 C; p* P, o4 o: G3 M4 M
laboratory to obtain the test.! O) ~; j  y% f! c
Discussion+ S# K* y8 h. `+ {0 L+ R# F8 ]% w
Precocious puberty in boys is defined as secondary1 m, r, G% c* U4 O' C0 u# ^/ F
sexual development before 9 years of age.1,43 h% D; U* k; y
Precocious puberty is termed as central (true) when# c0 e, @0 x2 e" e4 \  J0 M
it is caused by the premature activation of hypo-
) h2 p! S# E; j6 Y; Z( K7 Kthalamic pituitary gonadal axis. CPP is more com-
/ H" a2 N6 I& w) @! pmon in girls than in boys.1,3 Most boys with CPP5 c* s, _/ a3 S# P& \
may have a central nervous system lesion that is
* x5 z  \% L5 I: |! aresponsible for the early activation of the hypothal-
8 @! z6 J- N; \, d6 [! G6 Lamic pituitary gonadal axis.1-3 Thus, greater empha-* i9 U/ k4 E# a9 f6 o2 v
sis has been given to neuroradiologic imaging in
" |& d" _# a) c* x# S0 j6 Xboys with precocious puberty. In addition to viril-
: Q& `1 M; D8 a4 T& y! M! Yization, the clinical hallmark of CPP is the symmet-
& }* I  H/ D4 m( J' |rical testicular growth secondary to stimulation by
6 E. W/ M' }/ _' u2 U1 b) V$ Rgonadotropins.1,3
. j  W" |1 L) B2 BGonadotropin-independent peripheral preco-+ Y. M+ p; p# p' t9 b
cious puberty in boys also results from inappropriate, Q4 v. ^5 C6 X3 H) t8 g" m
androgenic stimulation from either endogenous or
# u2 S% l- C1 v" O' Vexogenous sources, nonpituitary gonadotropin stim-! |$ l! l4 L( v2 F4 T& l
ulation, and rare activating mutations.3 Virilizing0 T( a, s  X% X' L
congenital adrenal hyperplasia producing excessive- _! V% V8 S$ y% H$ S/ n8 Y( s
adrenal androgens is a common cause of precocious. A) L0 ~. r4 m; S% ^" f- S
puberty in boys.3,4
& Y& D: t. K8 V, BThe most common form of congenital adrenal/ a9 s: I) k+ g% h( T
hyperplasia is the 21-hydroxylase enzyme deficiency.) b5 }. e* h: M5 f4 S0 M5 D
The 11-β hydroxylase deficiency may also result in5 ~6 g5 N3 c* P8 y
excessive adrenal androgen production, and rarely,/ S5 k# m, d9 c7 g& o
an adrenal tumor may also cause adrenal androgen: Y8 o5 X1 W2 r  l( x2 v9 O! Y
excess.1,3# E9 x0 [6 h* K. M6 q9 B1 i0 N
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from9 m; t3 V% Z6 B
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007# f  I+ F9 o+ q4 E( |; J
A unique entity of male-limited gonadotropin-  N9 M7 T/ y/ ]; l7 q5 N1 T
independent precocious puberty, which is also known+ P0 S- B8 K5 Z8 L, g
as testotoxicosis, may cause precocious puberty at a
. t) p! @7 v6 r3 Xvery young age. The physical findings in these boys
9 I+ j6 c( l9 w+ S( Q, n/ W8 f, vwith this disorder are full pubertal development,. `' p+ c6 D* d/ @
including bilateral testicular growth, similar to boys# {6 d9 M6 ^% U: b' `' A
with CPP. The gonadotropin levels in this disorder
, y, ?" |; D4 gare suppressed to prepubertal levels and do not show! V) h4 f. s6 N) y
pubertal response of gonadotropin after gonadotropin-
1 M/ n# B/ k) q" ~- Q$ |/ Nreleasing hormone stimulation. This is a sex-linked' [2 [8 q& F: }2 }5 A& ?8 Y/ `
autosomal dominant disorder that affects only
3 d4 g$ W0 f/ rmales; therefore, other male members of the family+ O0 f- }) Z5 g' L  h
may have similar precocious puberty.3$ \3 }- r" o8 Z" U7 |& J
In our patient, physical examination was incon-
+ b2 w0 X3 E! j. U4 gsistent with true precocious puberty since his testi-
* i: g7 e5 U& y5 o+ \* A) E% i' ]7 qcles were prepubertal in size. However, testotoxicosis( D* B$ Y  Z9 {" H
was in the differential diagnosis because his father* W( K% T9 i+ Q
started puberty somewhat early, and occasionally,
6 F' w9 w% U9 stesticular enlargement is not that evident in the
( u1 r+ ~. W, V4 x+ H# j: G2 Z& Xbeginning of this process.1 In the absence of a neg-+ o1 y& [/ q" `% k3 @4 @
ative initial history of androgen exposure, our/ f: U% w: i* I1 v
biggest concern was virilizing adrenal hyperplasia,
( j$ d( ?0 n2 g. Q/ seither 21-hydroxylase deficiency or 11-β hydroxylase
- l  h) ?2 P  ddeficiency. Those diagnoses were excluded by find-
2 A6 k) x: {2 ~( |ing the normal level of adrenal steroids.
! b' p) [2 z4 }0 _' ^. u/ L8 B7 ?& u# HThe diagnosis of exogenous androgens was strongly
* Y$ U0 D3 z- ~+ \suspected in a follow-up visit after 4 months because+ ^: }' y% P/ [' S5 N
the physical examination revealed the complete disap-
$ A4 g5 k( s% X$ L6 g+ xpearance of pubic hair, normal growth velocity, and
, [+ ~* D# q" edecreased erections. The father admitted using a testos-
+ F6 U# P: _7 J4 U2 E/ v5 y* tterone gel, which he concealed at first visit. He was0 x8 p2 k& B! E, T
using it rather frequently, twice a day. The Physicians’
. Q5 z7 n3 o- r- yDesk Reference, or package insert of this product, gel or! a( ~4 h; ~* ^7 z8 Z4 \# D7 W
cream, cautions about dermal testosterone transfer to9 [4 d8 a/ N$ w% M. k
unprotected females through direct skin exposure.
) m" s( f4 K8 a* KSerum testosterone level was found to be 2 times the
: k3 J9 w! v, W0 G/ B6 B. i" I7 Wbaseline value in those females who were exposed to
; O, c0 U7 y7 X6 Oeven 15 minutes of direct skin contact with their male
, b& \0 j; t4 }; Bpartners.6 However, when a shirt covered the applica-
1 M/ _  u% {3 i6 \tion site, this testosterone transfer was prevented.
0 h( m- t8 m1 M1 COur patient’s testosterone level was 60 ng/mL,
% i/ j+ ?: A4 N3 n4 Hwhich was clearly high. Some studies suggest that. \, E9 N' l8 P% J
dermal conversion of testosterone to dihydrotestos-
- n6 x  [5 [& z+ {1 A! a! Xterone, which is a more potent metabolite, is more
& H( b7 \, c0 h/ Yactive in young children exposed to testosterone
" A- S8 I8 @& i$ P! Gexogenously7; however, we did not measure a dihy-! f8 t+ m9 G) U) |. r' Y: |$ G6 w
drotestosterone level in our patient. In addition to
+ K* w1 r5 ^* F6 L! ~1 U, M% Tvirilization, exposure to exogenous testosterone in
: l( I! a9 H5 I' v6 kchildren results in an increase in growth velocity and
0 D3 z7 \8 y0 R- u) }* Badvanced bone age, as seen in our patient./ k0 s0 W8 S8 p9 J+ G5 x
The long-term effect of androgen exposure during% i% R, H- G+ h& K- {2 {
early childhood on pubertal development and final
$ T. X  {/ |" D% B- z9 P+ |adult height are not fully known and always remain! l; o/ ?. A( B; Q+ |; a4 F
a concern. Children treated with short-term testos-
8 `! o8 Y3 L, |1 J, q9 pterone injection or topical androgen may exhibit some4 B, I, F; v2 H4 y' q+ X& l
acceleration of the skeletal maturation; however, after
) ^6 [- o7 T+ g, V* M/ A& Scessation of treatment, the rate of bone maturation) l/ S6 d: Q8 y. o- T
decelerates and gradually returns to normal.8,99 ?! E# J2 k  ^3 H+ W* D
There are conflicting reports and controversy. C( Y, k$ L5 Q- j2 B7 l- t
over the effect of early androgen exposure on adult
* _/ u% P* [* K% e. b% q# T& openile length.10,11 Some reports suggest subnormal
- G" B2 Y; }! e1 K- W& wadult penile length, apparently because of downreg-
* e, W4 z: k1 `9 I$ xulation of androgen receptor number.10,12 However,0 U; X3 t: G$ H4 S& [! b( x
Sutherland et al13 did not find a correlation between+ W) e( ~  H; e6 u; j) H# r( E
childhood testosterone exposure and reduced adult' E3 P6 d# ^% g7 _; k/ M
penile length in clinical studies.( v' F9 D4 x& n' l8 ~% G  a+ t
Nonetheless, we do not believe our patient is
3 k% h. N6 k) c! Y& s- |going to experience any of the untoward effects from' P2 H4 W! |$ L6 g% z
testosterone exposure as mentioned earlier because( y1 ~  W0 g) n; N( C
the exposure was not for a prolonged period of time.4 }: Y4 l  t/ N) X1 }6 J4 m
Although the bone age was advanced at the time of/ Q  r& ]: @- r% g
diagnosis, the child had a normal growth velocity at1 i- d. n6 d& g! w
the follow-up visit. It is hoped that his final adult) b. W, O- R! R, n& Q+ {
height will not be affected.2 ?7 i' S" C: ]
Although rarely reported, the widespread avail-
/ g, S1 S: n: U3 Aability of androgen products in our society may
" t) k, G+ j1 [! K+ n/ Gindeed cause more virilization in male or female- z4 _  S8 B# k. h) I0 c& U4 [
children than one would realize. Exposure to andro-. V; O, N! n1 ?; O" }! t- f
gen products must be considered and specific ques-$ b4 D7 k& b( _" O- E8 m1 o2 j
tioning about the use of a testosterone product or6 w1 D6 ~9 p. E2 y0 h7 G9 |
gel should be asked of the family members during
/ |5 W1 P% z- k) u3 Uthe evaluation of any children who present with vir-
, ~/ O0 g" D9 _  [+ `+ Yilization or peripheral precocious puberty. The diag-+ ?. x# O3 {1 \, r
nosis can be established by just a few tests and by  P6 u: K0 V' r: \, D8 |$ d
appropriate history. The inability to obtain such a
0 |' L: n; ?7 B: xhistory, or failure to ask the specific questions, may2 J( R0 t4 s+ S
result in extensive, unnecessary, and expensive
" \! E7 ~5 \- |1 d1 k+ O" finvestigation. The primary care physician should be- Y, I6 I* v( O& V: }7 {/ J' p0 c' t
aware of this fact, because most of these children
8 c, @, ~  i9 {2 W. }- |may initially present in their practice. The Physicians’1 _: `  i9 i3 p8 ?; J3 j1 k9 t
Desk Reference and package insert should also put a
% J; m" L* x% |& w) Q/ G" _warning about the virilizing effect on a male or5 {& \4 s" p2 _* V; H, s; B& u
female child who might come in contact with some-
1 ^) r9 ?) b, q- i: [) B9 done using any of these products.  O/ Z* f( a: i# _) s% T4 Q" v" {
References
. ^1 P( f( Y$ O5 o4 v" B6 u1. Styne DM. The testes: disorder of sexual differentiation. g8 \' ]7 v" \
and puberty in the male. In: Sperling MA, ed. Pediatric
, F+ r$ C8 e/ h  CEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;0 b; T* H; h- j5 X: s# ~' H' y
2002: 565-628.
. c: K; @& x9 T! F( z: [2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
' F# z( [4 v$ F! [8 opuberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
1 n' q5 t( G3 q8 i  ]6 N/ RBoy Induced by Indirect Topical
/ D& M- {) o" HExposure to Testosterone* G! m! r$ l& z: T
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,27 U% r# W/ U8 Q5 h* z: x+ j
and Kenneth R. Rettig, MD1
$ d% I2 N) |6 n- ?4 X0 MClinical Pediatrics+ S+ ?8 D2 Y/ P
Volume 46 Number 6# [! q+ z4 E6 k! E; w  B+ K% `( x
July 2007 540-543
8 d2 T+ z( y# [; g© 2007 Sage Publications
' {! j3 e7 }- z4 {8 V10.1177/0009922806296651
+ a, U- A5 I. G! L/ Yhttp://clp.sagepub.com
4 Z- P) ^" V1 N7 }% R( t8 Uhosted at
/ a9 r3 W- B. r0 ghttp://online.sagepub.com
9 D4 D( G; K$ v/ @. OPrecocious puberty in boys, central or peripheral,! E3 |+ ?6 Y2 b1 i) K1 l
is a significant concern for physicians. Central& f4 L  y4 r8 {* T- a/ b. }
precocious puberty (CPP), which is mediated
/ h/ e- g% T0 z/ L7 A. ythrough the hypothalamic pituitary gonadal axis, has/ f/ p, c6 D* O
a higher incidence of organic central nervous system' ~# L: M0 x3 s/ j+ _+ e( z5 i# Y
lesions in boys.1,2 Virilization in boys, as manifested' n8 G7 y/ ]9 E8 ?( |
by enlargement of the penis, development of pubic
4 ]" M+ l# T& B) A2 P5 uhair, and facial acne without enlargement of testi-2 c% N! ]% F8 S8 a, k, d+ a% }2 a! G
cles, suggests peripheral or pseudopuberty.1-3 We( I2 i# y. s/ V
report a 16-month-old boy who presented with the
% o2 t$ T; Y  Wenlargement of the phallus and pubic hair develop-: j9 o* T) `4 [/ \' y* x
ment without testicular enlargement, which was due9 c! t: Z/ _7 @) V" ]
to the unintentional exposure to androgen gel used by
) _0 A8 a$ @5 h; _the father. The family initially concealed this infor-- q4 ?" g/ r( |& j
mation, resulting in an extensive work-up for this
7 d2 ^: g: J& Echild. Given the widespread and easy availability of9 Y: @9 I4 _( o
testosterone gel and cream, we believe this is proba-
' M4 W8 m1 Y$ W2 kbly more common than the rare case report in the
- h8 p! _+ D! r% q4 J$ C- m! |literature.4
3 d2 h" t, P# G& N) F9 L7 g) K9 hPatient Report$ \4 a- J6 \& d* v" `& r3 T0 S! f1 J
A 16-month-old white child was referred to the5 V0 m7 \. z5 L9 l5 g! D9 x
endocrine clinic by his pediatrician with the concern# x7 g# m& F+ f# R9 d% {
of early sexual development. His mother noticed' ~0 ^& V: L' _
light colored pubic hair development when he was
; P' [  x+ e' K# I# y9 c& nFrom the 1Division of Pediatric Endocrinology, 2University of
% g. B) E4 ~$ L7 ]South Alabama Medical Center, Mobile, Alabama.
& Q' n$ U- Q0 I* ^Address correspondence to: Samar K. Bhowmick, MD, FACE,
' j% V+ ]3 d0 ?5 N+ b3 A1 i) hProfessor of Pediatrics, University of South Alabama, College of2 y, i1 j4 `, a! w6 c
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;& q* w: d1 b& S2 D( M3 m4 ~2 \: d
e-mail: [email protected].
' R. D1 F$ M. [7 @about 6 to 7 months old, which progressively became
1 V$ @0 D, Y! e1 Q1 j# Z: sdarker. She was also concerned about the enlarge-, r- W8 \: [( \. f7 U& t7 l
ment of his penis and frequent erections. The child% \1 b! |2 R8 L& i2 C
was the product of a full-term normal delivery, with. w7 x0 ~! b3 i6 z7 c$ A
a birth weight of 7 lb 14 oz, and birth length of8 T8 A5 }; ]2 L+ V; ^
20 inches. He was breast-fed throughout the first year# p: E1 L1 m# t) K$ o8 n( a* j6 [) _8 p
of life and was still receiving breast milk along with( u- U1 |- P, e8 i& W
solid food. He had no hospitalizations or surgery,
9 L1 Z5 p. f7 a) rand his psychosocial and psychomotor development
6 A' k. [# [! i# Z$ Iwas age appropriate.: e1 }4 n$ m5 W; b! k  `
The family history was remarkable for the father,/ G* B- }6 N9 R$ l9 x1 t
who was diagnosed with hypothyroidism at age 16,
; e6 X+ m3 [5 U! C2 A5 ywhich was treated with thyroxine. The father’s2 X; b4 h+ j0 @* u
height was 6 feet, and he went through a somewhat
6 o! n  f3 ~$ `% j$ H5 @: M$ Yearly puberty and had stopped growing by age 14.
) t9 j* Z. Y6 PThe father denied taking any other medication. The  I4 h$ k4 ^  f
child’s mother was in good health. Her menarche3 F! o; b) ^7 A) U2 U* X6 H, m0 T/ L
was at 11 years of age, and her height was at 5 feet
3 n! L% E& l$ D* Y3 T4 I% b+ B5 inches. There was no other family history of pre-) c6 {  d6 O; g1 H7 a# W. i  v9 _
cocious sexual development in the first-degree rela-
+ C+ ~8 I: S) a( stives. There were no siblings.
$ h4 ^# c7 V( D+ P8 HPhysical Examination
. O2 M1 p- v0 Q+ kThe physical examination revealed a very active,: R) U5 _  D: f( V) b9 L
playful, and healthy boy. The vital signs documented! x4 ]& x: t% K, F
a blood pressure of 85/50 mm Hg, his length was* v0 q& J& C9 |- L' W
90 cm (>97th percentile), and his weight was 14.4 kg
+ j! m& A8 _2 y7 {6 H+ I(also >97th percentile). The observed yearly growth
7 |1 }+ F: Q& q3 Lvelocity was 30 cm (12 inches). The examination of( E- V6 i% N6 {5 a0 A* i# }( u
the neck revealed no thyroid enlargement.0 O7 U& a1 D4 v1 t) x8 f# B8 y
The genitourinary examination was remarkable for( @6 b! n4 \& N9 v7 M1 c- X8 R
enlargement of the penis, with a stretched length of3 g1 b' q4 ^/ T$ o( _# l4 |
8 cm and a width of 2 cm. The glans penis was very well
( y1 ^$ n& W# v( {, w' Qdeveloped. The pubic hair was Tanner II, mostly around- `1 w2 ^! R$ D8 `
540
, s3 v! u: l" K! a  v9 ^at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
& [) p, I( ]$ K: U  zthe base of the phallus and was dark and curled. The
& s. v3 _4 C( ctesticular volume was prepubertal at 2 mL each.( E3 r# d: a5 p% P9 w
The skin was moist and smooth and somewhat5 U1 n. ~) H( [# q- R
oily. No axillary hair was noted. There were no* z; a5 p$ c, Z3 E
abnormal skin pigmentations or café-au-lait spots.
+ S% j0 D* P+ r6 q7 wNeurologic evaluation showed deep tendon reflex 2+3 G9 T/ |- O, P1 m  G7 e: D9 Y* ?
bilateral and symmetrical. There was no suggestion
/ l) ]& c- U  f, a9 @" f& tof papilledema.
" ^+ U6 x! U) Q" yLaboratory Evaluation6 q$ L0 O/ ~5 c* R
The bone age was consistent with 28 months by
; z$ n& u8 ^8 Rusing the standard of Greulich and Pyle at a chrono-
0 t9 j: k2 G6 n6 alogic age of 16 months (advanced).5 Chromosomal4 \3 U! t& n- S
karyotype was 46XY. The thyroid function test
* p1 z! V" a  k% d7 M! pshowed a free T4 of 1.69 ng/dL, and thyroid stimu-! j! O. D' z  V+ w; z
lating hormone level was 1.3 µIU/mL (both normal).
0 p7 i# [  \, V- r1 E) p) oThe concentrations of serum electrolytes, blood
. D! [6 l# d) aurea nitrogen, creatinine, and calcium all were
- s' L5 W7 a. iwithin normal range for his age. The concentration
: ~8 j" Y- E1 [3 V0 o2 Z7 Xof serum 17-hydroxyprogesterone was 16 ng/dL+ x0 \2 _8 l& R0 ~! y
(normal, 3 to 90 ng/dL), androstenedione was 20
2 G6 l1 c- t8 a. F# v5 ?: Xng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
* M1 u: L! S: `terone was 38 ng/dL (normal, 50 to 760 ng/dL),
3 `8 l' {5 m: G9 t2 \" ~desoxycorticosterone was 4.3 ng/dL (normal, 7 to: I8 S8 {$ q& A4 S& ~
49ng/dL), 11-desoxycortisol (specific compound S), k6 j! a2 ^9 z9 A$ o4 s; D, Z
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
) ?% S) o( M3 wtisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total% X6 h+ `* Q) M( L: Y* X
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),, {# J. a8 O+ N3 n3 R
and β-human chorionic gonadotropin was less than
2 G* K& K9 b+ T, ~3 E5 mIU/mL (normal <5 mIU/mL). Serum follicular
( S& j( b5 b( ~1 U$ K8 astimulating hormone and leuteinizing hormone4 b' R4 h& p- w' d) `' v$ u) Y
concentrations were less than 0.05 mIU/mL6 E$ H- ^6 [. S$ @# O( e
(prepubertal).6 m' E$ F+ K7 f) G& @( e
The parents were notified about the laboratory
2 E: M. v! [* t  U2 _3 }results and were informed that all of the tests were
6 C1 Y) ^. I+ U9 V/ C8 Y( e5 mnormal except the testosterone level was high. The
* E3 o1 t3 Y4 g3 n+ p  Z- o" Pfollow-up visit was arranged within a few weeks to/ X3 T: c9 o" R/ T, Z* H
obtain testicular and abdominal sonograms; how-
, y( Q8 N+ U4 f4 o8 D1 yever, the family did not return for 4 months.5 u% o& ]. d5 z9 N' B
Physical examination at this time revealed that the
/ u# w+ [+ l( v8 x" g" Dchild had grown 2.5 cm in 4 months and had gained
6 Z) K) P4 G9 `5 \- j; k5 V+ J2 kg of weight. Physical examination remained
( y( F2 x. ?0 v! n% Y+ C+ uunchanged. Surprisingly, the pubic hair almost com-
+ V, L9 N. @* g& g$ B- ppletely disappeared except for a few vellous hairs at
& F/ X* B' C4 `" w! H" c9 jthe base of the phallus. Testicular volume was still 2
* k1 x+ P" @# b8 YmL, and the size of the penis remained unchanged.
, s# s- E( m  [8 \The mother also said that the boy was no longer hav-: }: u8 b+ y& k% s. ^3 o
ing frequent erections.
* j1 `3 y) {3 z$ D7 |- M! u+ XBoth parents were again questioned about use of; N; {! o& ~  W+ l3 _6 O
any ointment/creams that they may have applied to9 n+ E, r+ C( W4 n
the child’s skin. This time the father admitted the# ]: t2 M9 o$ ^0 P! s$ Q
Topical Testosterone Exposure / Bhowmick et al 541  t* s. m: D9 e: Z- V: U( c. l
use of testosterone gel twice daily that he was apply-
; c  `& H( x+ \( Oing over his own shoulders, chest, and back area for
% s: s  W" \: A5 z3 o( `a year. The father also revealed he was embarrassed
0 }& p' L' N0 K4 @to disclose that he was using a testosterone gel pre-
$ J6 |# h9 I/ V; Zscribed by his family physician for decreased libido* [# L5 b2 K# T; v8 M
secondary to depression.+ b6 E9 D' Q9 n* T, H- g
The child slept in the same bed with parents.
' r/ a  }2 a  L/ D- S0 y6 n7 ]  QThe father would hug the baby and hold him on his. ~1 T6 I: X& o
chest for a considerable period of time, causing sig-
# J& B/ k# R+ _9 u0 Z% i) K* Nnificant bare skin contact between baby and father.% E6 v( K4 x0 e: C
The father also admitted that after the phone call,
, p, [2 \' R! U/ b6 Q8 @when he learned the testosterone level in the baby
/ B; O$ b: `. z4 f1 `8 {5 bwas high, he then read the product information. V. v9 M0 t! ?6 G4 k
packet and concluded that it was most likely the rea-
; x/ g  R2 i' L" Q" ^  E( dson for the child’s virilization. At that time, they( f& e3 ?' v$ Z4 H% a1 E6 @
decided to put the baby in a separate bed, and the
- q3 s  e* H' M$ V' N" Lfather was not hugging him with bare skin and had% o) q) Y6 j3 v2 s& I
been using protective clothing. A repeat testosterone
& j& q, \! d  ~# P4 ~5 ~test was ordered, but the family did not go to the
6 Z3 s- q$ |% K2 V4 O3 ?laboratory to obtain the test.: Z  f  E6 Z& A/ P) p
Discussion8 o0 D' p1 Z7 |0 X' }$ Y5 i
Precocious puberty in boys is defined as secondary
5 ~) R  y: F5 e0 h7 s. Csexual development before 9 years of age.1,4
( V: M# N9 H- I+ kPrecocious puberty is termed as central (true) when
4 g. u% e7 o& [/ x7 w* G8 ]9 ]it is caused by the premature activation of hypo-5 n7 P) d; e, L( y0 E& T) m
thalamic pituitary gonadal axis. CPP is more com-! Q% n# U, M5 |  [/ M
mon in girls than in boys.1,3 Most boys with CPP
! |; y! S6 i+ ~may have a central nervous system lesion that is
4 K1 `8 W+ a! m$ Jresponsible for the early activation of the hypothal-, t' L9 ~' H/ S9 @2 ^) h
amic pituitary gonadal axis.1-3 Thus, greater empha-
) V1 Q% p, {) o6 ?4 Q5 I1 P! D- @sis has been given to neuroradiologic imaging in, C1 A* S3 e, }1 b9 b% H
boys with precocious puberty. In addition to viril-0 g- a& p' ~7 Y/ n2 a) Y4 W
ization, the clinical hallmark of CPP is the symmet-+ p' N; u% y, V6 G
rical testicular growth secondary to stimulation by2 z: m! y) Q  O- ?( M. X2 r
gonadotropins.1,3
' k9 g) a6 O) K( zGonadotropin-independent peripheral preco-
8 X+ J3 Y  j* I* T8 g8 M3 Ecious puberty in boys also results from inappropriate$ O( E0 t/ `; }) E
androgenic stimulation from either endogenous or; V& @! @" ~0 H0 A5 t/ u
exogenous sources, nonpituitary gonadotropin stim-5 {- D% e$ e3 a0 f. ?% C
ulation, and rare activating mutations.3 Virilizing* a. P8 x1 T7 O9 B- i
congenital adrenal hyperplasia producing excessive5 Y' h1 o6 B$ @. F% R0 J
adrenal androgens is a common cause of precocious3 _# O' S8 \1 Z4 ?" F
puberty in boys.3,4
0 \2 C+ k" ]( [7 P  j7 lThe most common form of congenital adrenal& X7 z: T7 J$ b/ O
hyperplasia is the 21-hydroxylase enzyme deficiency.
; J+ Z3 O2 A  R! m3 \* i  aThe 11-β hydroxylase deficiency may also result in, k5 n5 E& I: h/ D5 O! t
excessive adrenal androgen production, and rarely,# I4 v! y* v  V+ m. O& x; n5 J/ B
an adrenal tumor may also cause adrenal androgen
" [+ w+ }, Q; S) p* {: z" Nexcess.1,3' I0 T  ]2 o$ V$ K3 \0 q* M
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
% d, D, v# [  l+ K5 k6 D542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
# P$ S/ t6 u: mA unique entity of male-limited gonadotropin-
$ A: b/ h* T3 R* V* [$ ]independent precocious puberty, which is also known
% ^5 O4 G0 p  y/ Aas testotoxicosis, may cause precocious puberty at a
0 h- ~! L; _2 A0 ]very young age. The physical findings in these boys
7 ?+ J5 B) o! P' ?6 z; d0 E2 Hwith this disorder are full pubertal development,
+ C/ U0 P+ W, D( O7 W! y* _including bilateral testicular growth, similar to boys( x4 i& \, G! \* A# }  {( p8 w
with CPP. The gonadotropin levels in this disorder
* [# A/ N; R; |8 M" jare suppressed to prepubertal levels and do not show
8 ?8 o; e* o: X; S  H. Epubertal response of gonadotropin after gonadotropin-1 a  J2 s, K8 |" p( d0 n6 N
releasing hormone stimulation. This is a sex-linked7 L  N1 v% L- J6 r2 s
autosomal dominant disorder that affects only0 C7 ~6 O" d, T% b
males; therefore, other male members of the family
% C$ I7 v% |; dmay have similar precocious puberty.3
% M) @# F9 s- K* SIn our patient, physical examination was incon-
$ N# t8 K" X+ @% ^; S+ r; ksistent with true precocious puberty since his testi-& w: [: T/ @  G0 O, G1 r: v% e4 S
cles were prepubertal in size. However, testotoxicosis
( z( p+ b; F5 N7 c8 L. k1 z4 dwas in the differential diagnosis because his father
3 n- J/ S9 V& k+ g/ T" e) g- R6 Bstarted puberty somewhat early, and occasionally,3 R. K; O; E) W( `
testicular enlargement is not that evident in the
, [9 Z/ u& x1 y+ A$ g; kbeginning of this process.1 In the absence of a neg-
" a. m4 o, s0 ^0 Wative initial history of androgen exposure, our+ L+ o) q( ?, Q# @
biggest concern was virilizing adrenal hyperplasia,! R& T, B% f. Y
either 21-hydroxylase deficiency or 11-β hydroxylase  H& f: p5 _( x
deficiency. Those diagnoses were excluded by find-
- h) W$ Z0 r2 Z3 U% U( r" }ing the normal level of adrenal steroids.% Y& K+ T6 r3 ~* b4 U
The diagnosis of exogenous androgens was strongly
0 m" ]5 O* Z7 |suspected in a follow-up visit after 4 months because7 D. x! y9 C4 X: B
the physical examination revealed the complete disap-
$ e! H' j4 A1 T! ?pearance of pubic hair, normal growth velocity, and$ X  d: Y' ~- M$ m
decreased erections. The father admitted using a testos-6 @) \3 q$ s3 c9 X3 |4 C5 _3 r
terone gel, which he concealed at first visit. He was
9 U" R7 F1 R6 }; musing it rather frequently, twice a day. The Physicians’9 M% n$ K- x# q& v
Desk Reference, or package insert of this product, gel or+ b  b4 {4 d# V4 Q4 X
cream, cautions about dermal testosterone transfer to
& x) T) K9 n$ G6 t3 L& sunprotected females through direct skin exposure./ M) ~$ n6 s/ U
Serum testosterone level was found to be 2 times the
/ t5 E' Q" O* w) M; ~baseline value in those females who were exposed to
$ T6 u* @9 I9 W- x$ C4 S3 Veven 15 minutes of direct skin contact with their male
0 O0 d  i* t- x6 a' `) p1 Zpartners.6 However, when a shirt covered the applica-
8 f+ }( h: _) K( htion site, this testosterone transfer was prevented.
4 r1 a' i! W7 Z$ [3 TOur patient’s testosterone level was 60 ng/mL,
* f8 d+ R6 e8 }  U* G2 Fwhich was clearly high. Some studies suggest that! B+ Q7 _. K  Q- j( a6 T
dermal conversion of testosterone to dihydrotestos-
' C" e8 `" g/ ]( K) ]. }terone, which is a more potent metabolite, is more2 [, K; ?9 Q' U  N! V
active in young children exposed to testosterone9 N# O. F# B* I# x3 |$ T% V
exogenously7; however, we did not measure a dihy-2 I. T& M7 ?7 X* d
drotestosterone level in our patient. In addition to* z7 R& _- ]0 ~- R8 o8 S. f
virilization, exposure to exogenous testosterone in
% s7 b8 F2 i9 T, u* g5 Rchildren results in an increase in growth velocity and3 o! y5 D; `, O9 v! d9 @
advanced bone age, as seen in our patient.
8 B: g/ i6 J) W2 WThe long-term effect of androgen exposure during8 K5 Q$ g) I" `4 E% j' n
early childhood on pubertal development and final
6 X* ]- \2 ^  G7 e* l( d% {  aadult height are not fully known and always remain
) i. s  y5 O, y1 @- ^4 l/ Za concern. Children treated with short-term testos-6 a2 b8 O  X* O7 Z: y4 \
terone injection or topical androgen may exhibit some
8 X' J/ |# \) L( bacceleration of the skeletal maturation; however, after
# x9 v3 T" j; ccessation of treatment, the rate of bone maturation$ f1 j7 ]1 k4 F' O7 _9 _
decelerates and gradually returns to normal.8,9
  ?2 c) I' R% p5 }There are conflicting reports and controversy" L8 y4 p8 Y  g
over the effect of early androgen exposure on adult/ A3 |4 X# j0 I2 ~
penile length.10,11 Some reports suggest subnormal
- I- P! {' |0 C7 eadult penile length, apparently because of downreg-
- c+ r$ p* g* I2 ]" n6 ~" Qulation of androgen receptor number.10,12 However,
0 ^! ~+ _' ^! `( |Sutherland et al13 did not find a correlation between- ?5 o# j* p( R  r+ g/ Y
childhood testosterone exposure and reduced adult' w5 s( y9 z' E% a' U2 \
penile length in clinical studies.
/ D7 O0 S, G( Q2 _5 uNonetheless, we do not believe our patient is- ]2 b) u* x0 Y
going to experience any of the untoward effects from0 g2 c9 Y. w9 }* m
testosterone exposure as mentioned earlier because& N: e/ b, E7 Q( V) b, |
the exposure was not for a prolonged period of time." ]$ a! K/ L$ E, o- d
Although the bone age was advanced at the time of, O2 Q/ Y  c/ P) }/ u+ P1 {
diagnosis, the child had a normal growth velocity at  U. O2 ]5 l, ]
the follow-up visit. It is hoped that his final adult
" I% u0 M2 {* E% U9 nheight will not be affected.2 e  u" ?1 s3 S% _1 z
Although rarely reported, the widespread avail-
% ?1 @! M1 D' ]* a" O5 ~4 R: Yability of androgen products in our society may
# \" a) b7 _) w. [indeed cause more virilization in male or female" ?9 L& [: h& Y+ Q$ M% y* F
children than one would realize. Exposure to andro-/ i/ X$ A: W4 Z" R& q
gen products must be considered and specific ques-
! D6 N+ p" I$ H! p5 e# W* ctioning about the use of a testosterone product or
% a) b% F! z4 |: H+ \3 mgel should be asked of the family members during
, w5 s$ D+ [4 R' H* B+ ~# fthe evaluation of any children who present with vir-, [% U7 B! l7 Y; O: U' i
ilization or peripheral precocious puberty. The diag-; U  S1 ?" f  |  n6 m* L# |
nosis can be established by just a few tests and by
# d4 }6 |! Q; [5 \, b" ]appropriate history. The inability to obtain such a
6 v( f- c. J$ H: Q" z1 Mhistory, or failure to ask the specific questions, may
9 x: q# ~: H) x" v! M& [4 s# ?: iresult in extensive, unnecessary, and expensive- c; _( j& V% E% I8 c* f
investigation. The primary care physician should be! l/ M) i0 b* c, Y( g$ `( f$ f- N1 s
aware of this fact, because most of these children7 s0 Z. V: X' G! N
may initially present in their practice. The Physicians’% B! J" y8 m8 s! O
Desk Reference and package insert should also put a
- p! D" i9 N1 r) D& f) @% N6 _warning about the virilizing effect on a male or
/ v& N" t" A( r: }/ G: lfemale child who might come in contact with some-
/ k( z( N' W$ C3 p( n8 none using any of these products.; u# Y1 Y/ w" P! F: [; ?/ o
References3 F0 o: z4 N( C8 E# T, A
1. Styne DM. The testes: disorder of sexual differentiation" A9 ?- U% Y, t2 ~- H4 ~! K) h
and puberty in the male. In: Sperling MA, ed. Pediatric
$ i0 L5 F2 Q2 ~0 V5 `0 T9 Q. VEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;- M0 D- z2 I. s
2002: 565-628.
0 A- f! ^" t/ \- A2 B3 L" ]2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious; s& q/ Y6 S! S" c# t3 {$ r5 c
puberty in children with tumours of the suprasellar pineal
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感謝大大的辛勞分享!我會繼續在WK關注大大的文章!
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女厕偷拍辅导班主任尿尿老师的逼很嫩还有一点
發表於 2025-1-17 16:31:39 | 顯示全部樓層
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4个什么样的?
發表於 2025-1-19 02:41:05 | 顯示全部樓層
3 g( |$ F2 T% z( \' J, }* x7 T
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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