WK綜合論壇, WK综合论坛

 找回密碼
 立即注册
樓主: wk007

鄉下的妹子太便宜,一次四個都要了[12P]

[複製鏈接]
發表於 2025-1-4 03:25:35 | 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
Sexual Precocity in a 16-Month-Old$ Y7 r( n1 o+ b8 v% S0 N) Q7 z
Boy Induced by Indirect Topical
& N, A  C( \; D- b. m) a7 y% A. x: y  DExposure to Testosterone
* c& y1 C/ u# `& hSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
% W5 \& g; R  p& ?, Nand Kenneth R. Rettig, MD1" u) ]# {6 D* a5 H0 l& t( E5 h; T
Clinical Pediatrics
3 C) `* Z/ a3 w; h) sVolume 46 Number 6
! I' }6 [2 J! E  U4 h* D! i* k' c! lJuly 2007 540-543
9 k3 s( R) T0 r0 H© 2007 Sage Publications
. H7 O" |1 z: ^8 K10.1177/0009922806296651* L! n5 C6 o/ t' g1 E
http://clp.sagepub.com6 n6 ]2 I) t! `9 f1 {
hosted at
4 W" o; m+ N+ G7 Y6 S9 |http://online.sagepub.com$ E% B% ]/ {9 j3 s' r
Precocious puberty in boys, central or peripheral,
" I  i7 B+ D& I+ C3 Ais a significant concern for physicians. Central( O& X+ C# }; q3 R$ }. S( ?( R6 V$ s% [* t
precocious puberty (CPP), which is mediated! o( ]7 j6 x6 l5 p% E# O
through the hypothalamic pituitary gonadal axis, has
  a, e+ r7 |; |) Z+ W9 Oa higher incidence of organic central nervous system0 `- O' b/ ~: a# M& K3 b- @
lesions in boys.1,2 Virilization in boys, as manifested+ J$ ]- _" C0 G
by enlargement of the penis, development of pubic: r2 q1 i6 n0 L' P
hair, and facial acne without enlargement of testi-
: ?* T& n  Z5 E# scles, suggests peripheral or pseudopuberty.1-3 We
1 o' ~: Y1 K" q  [! v" @6 _report a 16-month-old boy who presented with the$ ]/ s5 C8 k( U9 L5 b( A
enlargement of the phallus and pubic hair develop-- F% b3 x& i2 g8 t2 S0 V3 h! N
ment without testicular enlargement, which was due
4 D' `0 H8 o; J# M+ @: ?. X2 f2 xto the unintentional exposure to androgen gel used by
+ a' d* R3 d% |8 a: t! X/ Fthe father. The family initially concealed this infor-; v, r. T5 h9 ?# `, T" ^7 f4 q/ ^
mation, resulting in an extensive work-up for this
; {: U$ Y  i/ mchild. Given the widespread and easy availability of
% I" z% P6 O. j* B& Htestosterone gel and cream, we believe this is proba-
3 k  T5 c; \- Lbly more common than the rare case report in the3 `& L$ x4 C1 {- o( i- K
literature.4
( P  o7 H) M+ z7 GPatient Report
0 O4 W: N+ `8 H8 Z' XA 16-month-old white child was referred to the0 j6 T- r$ }1 `4 S2 \$ S- i) P
endocrine clinic by his pediatrician with the concern, S; ?& J) M  o. Y: O6 n2 c
of early sexual development. His mother noticed
  k  }4 a, e5 A- B/ y4 G, m. Elight colored pubic hair development when he was
7 i3 c/ Z& n/ L; LFrom the 1Division of Pediatric Endocrinology, 2University of
! R# z& W5 G7 T* A3 P+ _: ISouth Alabama Medical Center, Mobile, Alabama.2 q/ \4 Z% [* P2 a% B. f" M: ~
Address correspondence to: Samar K. Bhowmick, MD, FACE,
( n/ c$ w" V* V9 X9 T' q/ MProfessor of Pediatrics, University of South Alabama, College of
* z# s& h% N0 p" D; K% aMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
# X2 Y/ ~0 o) j* Re-mail: [email protected]., u: @2 Z0 k2 j/ j1 A
about 6 to 7 months old, which progressively became& P. m- I  }" g0 }9 D
darker. She was also concerned about the enlarge-+ N. M6 L- }, i" A6 h) e8 d/ G
ment of his penis and frequent erections. The child' \2 Y( {; L  s/ X6 {& f7 U- `
was the product of a full-term normal delivery, with
3 V4 K/ |$ G/ y& w! Ya birth weight of 7 lb 14 oz, and birth length of, a$ y# o4 Y, K: l& T  Q
20 inches. He was breast-fed throughout the first year0 Q3 q/ y' N- h5 f- w) p& [
of life and was still receiving breast milk along with
3 i/ h* M4 i% ?, f+ b' Zsolid food. He had no hospitalizations or surgery,) F: l1 U2 U4 b( f1 q
and his psychosocial and psychomotor development
8 t! j5 U/ k+ E- q/ M/ n: uwas age appropriate.4 s+ A6 L+ M2 }0 Y7 Y) u& j- H
The family history was remarkable for the father,5 R" o5 g' k- l3 P  u$ Q
who was diagnosed with hypothyroidism at age 16,; n* w- F; l4 T. D: o( Z/ l
which was treated with thyroxine. The father’s
  l8 n1 D( B+ P& B. L5 [. u$ ]height was 6 feet, and he went through a somewhat% Z1 t9 @/ e# K2 x; \1 N) |% E7 B# D
early puberty and had stopped growing by age 14.
' `8 ?4 g8 o! R5 B. @The father denied taking any other medication. The
/ C/ I% _% H) e6 `! [child’s mother was in good health. Her menarche
7 }: x1 Y% l, |! J' Iwas at 11 years of age, and her height was at 5 feet
9 `& r  C1 m+ S% D# V3 n- l3 j5 inches. There was no other family history of pre-
9 ~9 Z$ N* g8 I  F& Ccocious sexual development in the first-degree rela-1 z  P1 E% Y4 b0 S9 R
tives. There were no siblings.! ^/ A* y5 X! p3 c+ l3 `
Physical Examination
2 M/ w# Y7 O+ j) t& }- q5 m- Z$ OThe physical examination revealed a very active,4 p/ ^# {: m: T9 f4 |5 E8 P, O
playful, and healthy boy. The vital signs documented  o6 b( f3 j4 O- u
a blood pressure of 85/50 mm Hg, his length was
* h9 v+ V: U$ @/ h4 O5 t' C* a90 cm (>97th percentile), and his weight was 14.4 kg. ?7 l7 u5 u* ]4 n
(also >97th percentile). The observed yearly growth% s# Q+ R$ S6 Q+ N
velocity was 30 cm (12 inches). The examination of
' u9 v$ u; M. uthe neck revealed no thyroid enlargement.& H* ~; n- Z3 h6 g
The genitourinary examination was remarkable for
& l9 O/ v4 |/ s& W1 U+ d' f, ~- [enlargement of the penis, with a stretched length of3 @" G. E5 ?% E5 U) s; a: x
8 cm and a width of 2 cm. The glans penis was very well
: i  T7 g+ Y& c" L  C: sdeveloped. The pubic hair was Tanner II, mostly around: F5 e3 m  [' o
540
# T. P$ d' m) I: z/ M6 S( R" o  vat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from3 Z2 V8 G1 h) K9 ]5 Y( h! S5 B" P/ {% R% F
the base of the phallus and was dark and curled. The9 s* f5 f  b+ o( H- Z  L! q
testicular volume was prepubertal at 2 mL each.& z! R. v0 X) ?7 ?2 M5 J$ p
The skin was moist and smooth and somewhat
$ i6 d6 `. ~: U0 ~" q3 F1 Eoily. No axillary hair was noted. There were no. M8 ?% |3 W& X0 d
abnormal skin pigmentations or café-au-lait spots.
. S1 A# x% s& j# f4 ^5 ~( vNeurologic evaluation showed deep tendon reflex 2+& _+ J6 \1 ^+ m6 F/ f. u0 K
bilateral and symmetrical. There was no suggestion5 y$ S& D5 ]0 f0 B& E( R9 Q
of papilledema." `2 z% c. V+ l
Laboratory Evaluation; ?- j, b! \$ o+ q/ Z
The bone age was consistent with 28 months by
9 A0 u0 C: ^5 J* {8 k9 Susing the standard of Greulich and Pyle at a chrono-, i, c6 H5 [- Q& b
logic age of 16 months (advanced).5 Chromosomal( f* x9 k# h" g
karyotype was 46XY. The thyroid function test$ ?! b+ M# k0 `+ i. z0 R! t  U
showed a free T4 of 1.69 ng/dL, and thyroid stimu-- m- \1 ?, n1 v9 }; [
lating hormone level was 1.3 µIU/mL (both normal).
+ G# m9 B  D3 w, s2 ]The concentrations of serum electrolytes, blood
) {1 q/ B' p6 W6 u5 Burea nitrogen, creatinine, and calcium all were9 h5 J9 k6 D1 F, P8 ~+ O
within normal range for his age. The concentration
% _- A* ]. K: P  ~of serum 17-hydroxyprogesterone was 16 ng/dL5 }' e$ T/ c/ f: l' d+ M: d8 [
(normal, 3 to 90 ng/dL), androstenedione was 20
9 u0 u' s7 \# C& fng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-0 d& [  y7 P; h: S: X# `9 Q9 B) n
terone was 38 ng/dL (normal, 50 to 760 ng/dL),& d4 W  ^- G% X3 ?
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
" w; z+ j' J! ~# Z$ x. _49ng/dL), 11-desoxycortisol (specific compound S)
1 B7 g6 z9 X! V4 xwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-3 c3 o: S, W3 k( s+ T& k3 l
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total7 o" r( [' F! @! l% {
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),+ v- P6 V: \+ {
and β-human chorionic gonadotropin was less than
2 a9 X! y3 v' m( p! z* T% C$ w5 mIU/mL (normal <5 mIU/mL). Serum follicular
7 G4 U% b/ |7 Qstimulating hormone and leuteinizing hormone
3 G0 `( o9 a! O2 o$ g) g: T' L" yconcentrations were less than 0.05 mIU/mL* \% ]3 M* k  D: a. l
(prepubertal).
9 d, p6 B8 \0 H% b* d6 f) bThe parents were notified about the laboratory
3 I7 v4 |8 u: W7 n& m- p  _results and were informed that all of the tests were7 ^% Y/ i" t0 X! A1 V
normal except the testosterone level was high. The
, N7 y- a/ f8 Xfollow-up visit was arranged within a few weeks to
' H4 L* f; j6 p& K8 D' ^obtain testicular and abdominal sonograms; how-  o' P" Z4 z( M, f
ever, the family did not return for 4 months.- Y9 n3 N5 ~$ }5 U
Physical examination at this time revealed that the
' J3 I3 _1 R( cchild had grown 2.5 cm in 4 months and had gained
5 h; M$ z- g" k/ T. o2 kg of weight. Physical examination remained
4 l7 @4 u0 D. ^# |3 [/ }/ lunchanged. Surprisingly, the pubic hair almost com-
1 e* C4 u1 U! F$ Xpletely disappeared except for a few vellous hairs at
4 O1 v$ b- g/ ~3 Fthe base of the phallus. Testicular volume was still 2  a7 A( D0 X% s' }! C5 Z4 T* R3 e% b
mL, and the size of the penis remained unchanged.
; w! ?2 X0 B+ z& q( eThe mother also said that the boy was no longer hav-
* l) {! c: L7 n7 ~- Eing frequent erections.3 Q+ T, {0 m5 R% p/ K
Both parents were again questioned about use of
4 @# W- f, T  I6 gany ointment/creams that they may have applied to
: @2 x/ V& f" O1 Z' p: Q4 C: Zthe child’s skin. This time the father admitted the& `* `) G; [5 g1 h
Topical Testosterone Exposure / Bhowmick et al 541$ z6 G, b) \. C) n
use of testosterone gel twice daily that he was apply-
) P8 \& q- {$ V7 p5 `; S8 ning over his own shoulders, chest, and back area for# S+ }  G( `6 I$ Y' g( [
a year. The father also revealed he was embarrassed% W3 i( Q9 P, i0 h
to disclose that he was using a testosterone gel pre-
% R; Y7 D( n) I' Z% T  Nscribed by his family physician for decreased libido
. g# w" T- H8 j- b( @* z/ A5 Ysecondary to depression.3 L- c4 a* A2 W
The child slept in the same bed with parents.
  O+ R( V! d7 X( _  [3 oThe father would hug the baby and hold him on his) C! {" R$ w% S) E
chest for a considerable period of time, causing sig-% J% i  K, u  E6 Y4 w1 l% T
nificant bare skin contact between baby and father.
+ l% z/ F; W( [# u  @( a& uThe father also admitted that after the phone call,, T' w& A2 y6 f! p  T
when he learned the testosterone level in the baby
9 N0 D+ {6 k! z4 N" Y4 P& a4 ]was high, he then read the product information
( z9 [# f& y% l8 S( s$ ]7 ]" D' kpacket and concluded that it was most likely the rea-
# n% i+ l0 _5 C, X' R& q' Bson for the child’s virilization. At that time, they# D6 t- i, \; P3 J
decided to put the baby in a separate bed, and the
  F6 c+ G) S. @8 _father was not hugging him with bare skin and had+ H. N+ ^, f9 k4 Y5 w" {
been using protective clothing. A repeat testosterone' p9 K4 }( B# n* ^  N$ V5 v
test was ordered, but the family did not go to the
# e! P( O" v! Y6 G2 E0 Klaboratory to obtain the test.
6 v9 N( n2 a- y) }* H% Z0 aDiscussion$ T- t( r5 B% D, g( X
Precocious puberty in boys is defined as secondary
" x8 I9 B) [: osexual development before 9 years of age.1,4( C! Z( N4 j* t6 g
Precocious puberty is termed as central (true) when% N( ^; a' N5 P- w3 u% C3 o/ g. b- I
it is caused by the premature activation of hypo-
* h& g4 H0 v( _: `- q( B" O1 Y& Xthalamic pituitary gonadal axis. CPP is more com-
/ G4 Y+ A, }+ ?8 h7 Xmon in girls than in boys.1,3 Most boys with CPP
  j9 z$ E  F+ h  f' mmay have a central nervous system lesion that is
4 k- F7 I; M2 E& X% S: gresponsible for the early activation of the hypothal-$ r' M  ]# w6 q! L! a* p$ A7 A
amic pituitary gonadal axis.1-3 Thus, greater empha-
5 Q5 S+ W9 M; Y7 w% |sis has been given to neuroradiologic imaging in
( K* Q4 I& M3 Sboys with precocious puberty. In addition to viril-, ?7 Y2 e+ m7 `* m  I  M
ization, the clinical hallmark of CPP is the symmet-
7 _; t' [9 Q3 Y( G) k- }rical testicular growth secondary to stimulation by
# M6 S  ~) Y: Fgonadotropins.1,3* [& |' y2 g& Q' P" M5 x
Gonadotropin-independent peripheral preco-( X; ?1 X* L- m$ a! e
cious puberty in boys also results from inappropriate. k9 J& V; |6 v' ^4 e
androgenic stimulation from either endogenous or7 J, w4 P4 A3 h6 k' V& a
exogenous sources, nonpituitary gonadotropin stim-: b( ?+ b# R& J: z) _6 I
ulation, and rare activating mutations.3 Virilizing
. N: X6 s, p$ X( F0 Tcongenital adrenal hyperplasia producing excessive1 P/ s' K7 h) b4 D
adrenal androgens is a common cause of precocious
% I6 a8 @1 \7 }3 Kpuberty in boys.3,4
9 A; N, n8 G6 r7 lThe most common form of congenital adrenal, K: B' e+ L: z3 r
hyperplasia is the 21-hydroxylase enzyme deficiency.
3 C( `/ o6 C8 j$ n5 d# B# c  wThe 11-β hydroxylase deficiency may also result in0 c" l9 m  n, f
excessive adrenal androgen production, and rarely,7 I( l/ o7 v$ t- l" q
an adrenal tumor may also cause adrenal androgen
: o2 s) M! d' J0 M* p' \9 u" g, s$ Pexcess.1,3. H/ g/ A7 f8 }3 j
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
- c3 V% ~- C: e: p2 i( ^542 Clinical Pediatrics / Vol. 46, No. 6, July 2007: N& R2 N1 A% s* d3 v/ u
A unique entity of male-limited gonadotropin-; X8 N& Z9 ?7 B0 }
independent precocious puberty, which is also known1 h) E! G  W7 P. v/ U/ |% u
as testotoxicosis, may cause precocious puberty at a
( u3 z- j; ^! |/ {4 y0 overy young age. The physical findings in these boys' K0 m) h, E' ]# M  ]
with this disorder are full pubertal development,, i' n+ ], Z8 [' a, \, L% D, e& g
including bilateral testicular growth, similar to boys/ x4 A2 D6 K/ I" A2 o, _) ~  ^$ m
with CPP. The gonadotropin levels in this disorder
2 M  n/ P4 ~& a. J% W0 zare suppressed to prepubertal levels and do not show! [6 x9 F7 T5 p$ X, N8 }5 A8 n" s
pubertal response of gonadotropin after gonadotropin-
; v8 h& O' H! k% Greleasing hormone stimulation. This is a sex-linked! I% V% b# v$ k; J6 _/ M2 o, i
autosomal dominant disorder that affects only
3 H- v& Z2 g% C  Smales; therefore, other male members of the family
7 _) |: _5 w, j- |" Kmay have similar precocious puberty.3
, |/ q7 o; s; j8 B8 i! PIn our patient, physical examination was incon-
& m& o5 v  o0 f' i5 ~% _sistent with true precocious puberty since his testi-: L6 m& ]8 v! X" I4 F, |
cles were prepubertal in size. However, testotoxicosis
; G' [' `! W( t! w5 ?6 @was in the differential diagnosis because his father1 X4 a) f; e! z4 ^, E* ~: d$ r
started puberty somewhat early, and occasionally,
5 B+ W& `* ~  x3 ~( [testicular enlargement is not that evident in the3 T9 l+ A! \# B- O% Y! X4 b
beginning of this process.1 In the absence of a neg-! i. i3 Z. M" |2 P# {! e
ative initial history of androgen exposure, our
7 y2 V" @6 Q4 F- X4 s3 xbiggest concern was virilizing adrenal hyperplasia,' w2 g4 z! E" d3 Z- ?
either 21-hydroxylase deficiency or 11-β hydroxylase
0 c# W  s# |/ R, c) {: Ddeficiency. Those diagnoses were excluded by find-
+ `$ ~- h- |- W; j, ^ing the normal level of adrenal steroids.! u' p$ [+ b; Q5 q( G# S( k( [6 O
The diagnosis of exogenous androgens was strongly
. Y( h% g/ m: s. j/ Fsuspected in a follow-up visit after 4 months because: p$ g6 ~- c; m+ |7 V' Q% y
the physical examination revealed the complete disap-
0 d3 D$ d0 P( L1 a1 H# hpearance of pubic hair, normal growth velocity, and8 m2 P) s+ `$ M+ \# G2 _( X$ J$ J% F
decreased erections. The father admitted using a testos-
8 c5 V. J8 S/ {terone gel, which he concealed at first visit. He was
& j  w, W$ H6 J$ {+ Z7 b, U6 Susing it rather frequently, twice a day. The Physicians’" d& J% L* U, O' b
Desk Reference, or package insert of this product, gel or  ?8 u4 A3 E3 p* t
cream, cautions about dermal testosterone transfer to
" u+ r5 L, d( y" Kunprotected females through direct skin exposure.
% `- f/ ?- E1 }; R! Q0 @  |4 z& u) LSerum testosterone level was found to be 2 times the
- `: T  m( t2 {8 [) ?( u4 A8 T6 ~baseline value in those females who were exposed to
7 A/ q1 N9 }3 Y/ ]) U8 h9 T4 Xeven 15 minutes of direct skin contact with their male2 [# S+ _+ d2 d7 h: T0 \" {
partners.6 However, when a shirt covered the applica-
# @' P: L" C9 E3 y1 ]% Qtion site, this testosterone transfer was prevented.8 y. X2 j1 p  O- G! g; Q
Our patient’s testosterone level was 60 ng/mL,
% N: y+ B8 l" `9 |8 E/ swhich was clearly high. Some studies suggest that
- C8 p! q; [" F  Bdermal conversion of testosterone to dihydrotestos-% G' o, c# Q; a1 R  x+ m1 r
terone, which is a more potent metabolite, is more2 ?9 F5 [" I9 |4 |" @7 F
active in young children exposed to testosterone, r/ A% ?5 t1 A% Y  A6 O
exogenously7; however, we did not measure a dihy-  ]4 d6 C* B# l; O4 f6 h
drotestosterone level in our patient. In addition to
" B8 m2 J' G" f5 m9 y  xvirilization, exposure to exogenous testosterone in
; k" p0 {" d3 n: _& N5 G0 [children results in an increase in growth velocity and  y8 L# D; M- N2 B
advanced bone age, as seen in our patient.
% t# U3 ^7 ?' E2 A: {/ IThe long-term effect of androgen exposure during. m; J2 a; {2 x/ s' |
early childhood on pubertal development and final
2 L$ x( Z8 T0 Y% ~adult height are not fully known and always remain
' F' H+ l0 x7 V* Sa concern. Children treated with short-term testos-4 n  o/ ^  U+ l! ]! U
terone injection or topical androgen may exhibit some
( q" h) F3 O0 r  j1 `acceleration of the skeletal maturation; however, after
/ m, `# o# c" G7 jcessation of treatment, the rate of bone maturation) p; C6 g5 v" A$ O
decelerates and gradually returns to normal.8,9) X+ y7 x5 O. ?
There are conflicting reports and controversy
. C& U; M9 a3 m/ {' @! ~over the effect of early androgen exposure on adult% g# D6 v% h- e* S
penile length.10,11 Some reports suggest subnormal+ v7 Y* V! g3 W5 ?2 w8 I
adult penile length, apparently because of downreg-, S6 [1 C5 ]+ N1 L! j
ulation of androgen receptor number.10,12 However,
5 K0 \' S9 t& n: t% t! eSutherland et al13 did not find a correlation between
% o4 Y2 y$ E* ^3 k) }9 echildhood testosterone exposure and reduced adult) d: `: q& H8 E5 {) I
penile length in clinical studies.( p1 o0 C8 q5 P+ O
Nonetheless, we do not believe our patient is
; p4 R0 A6 m. p8 ?going to experience any of the untoward effects from& |. w, f9 F* z" {% S( ~1 W, {
testosterone exposure as mentioned earlier because0 i3 ~7 y! c: t1 n
the exposure was not for a prolonged period of time.7 x% P8 n0 x  r, P8 @
Although the bone age was advanced at the time of
8 B9 i6 `9 n- {8 z2 D; M9 Wdiagnosis, the child had a normal growth velocity at" ]6 r; g1 D: n+ Z# ]5 I! n* w
the follow-up visit. It is hoped that his final adult/ k$ G0 ?9 D+ F* N
height will not be affected.
/ b4 C9 s! B, m! d& v  bAlthough rarely reported, the widespread avail-2 T- \2 v4 p: R
ability of androgen products in our society may
. n5 y6 v: n! c: Dindeed cause more virilization in male or female+ P& {1 p& F. Z
children than one would realize. Exposure to andro-
4 }0 a- b* w. m8 m* Z/ B( W7 ?" Rgen products must be considered and specific ques-8 @+ ?7 ?1 F2 o( A+ V1 R4 a& o* t
tioning about the use of a testosterone product or
8 j# e; m1 S0 y8 A  w* `" f3 {/ Egel should be asked of the family members during8 j" E( N1 t" |/ A
the evaluation of any children who present with vir-
/ p8 E  B* g% W6 X  V; Bilization or peripheral precocious puberty. The diag-+ L" S: d( h" H* |, M# I- _3 {3 {
nosis can be established by just a few tests and by: i) |4 C; n0 h8 ]* K% ]9 i$ Q
appropriate history. The inability to obtain such a
& J1 e, V3 d& Q1 Ohistory, or failure to ask the specific questions, may
$ N% q$ z4 r4 T0 k' y* @/ O1 a' Fresult in extensive, unnecessary, and expensive5 s0 F- i( N- O( h6 e
investigation. The primary care physician should be+ }9 d1 y; c& T; e9 O( v& s
aware of this fact, because most of these children
- v9 T4 _. v  H6 t1 nmay initially present in their practice. The Physicians’
' k1 h% X4 C; Y; HDesk Reference and package insert should also put a
2 h" N* E. {4 Q/ V# A9 R0 p& bwarning about the virilizing effect on a male or# R0 B0 Q* J- k
female child who might come in contact with some-
* X. q' \% k7 Q( u5 W4 W7 u" i4 oone using any of these products.
5 g# D; Q% \+ b7 Z# Q7 v+ }5 DReferences+ ]2 }7 K" v) ]. R3 p
1. Styne DM. The testes: disorder of sexual differentiation7 F+ ~: a* g1 e/ \5 E  Z
and puberty in the male. In: Sperling MA, ed. Pediatric
% h5 D6 h7 ]+ y0 {9 ^; o" `7 {Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
. C) d/ T6 ^% D5 J1 l" o2002: 565-628.* S' j3 r; m- a9 f
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
0 ]8 K- \0 L% y  {1 T' }puberty in children with tumours of the suprasellar pineal
發表於 2025-1-4 03:27:02 | 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
Sexual Precocity in a 16-Month-Old
* j6 V4 j# X% g+ W4 XBoy Induced by Indirect Topical
: }1 B  R- {+ r6 i5 z9 OExposure to Testosterone
7 t9 \% ^' l# V* V+ X( }5 Y# bSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
8 R7 R7 E9 v; |and Kenneth R. Rettig, MD1) b0 |6 h4 T( g  r; A6 |- }0 r
Clinical Pediatrics
' C9 I& c! D0 C- YVolume 46 Number 6
0 E1 u4 ]9 w  \2 ?# P- [) m: ^July 2007 540-543
; j4 ]; E2 R3 I+ {8 L- ~© 2007 Sage Publications; L, z, b. N) |' p5 A( a
10.1177/0009922806296651
; T5 L$ {* {; H1 R) F, Q0 M! lhttp://clp.sagepub.com
6 L3 k& d4 ~* y/ X: z8 ahosted at
! j; e/ z* ~% z9 |/ Hhttp://online.sagepub.com
- Z. |9 ]! o0 ]# D. FPrecocious puberty in boys, central or peripheral,
( f9 V( ]6 t( o! y- Nis a significant concern for physicians. Central4 d6 w" A7 h  s  \3 q( b" B
precocious puberty (CPP), which is mediated
; q/ Y9 ]( h8 R" {/ {' V' sthrough the hypothalamic pituitary gonadal axis, has0 |0 [/ V* }, f0 l; t3 n1 i
a higher incidence of organic central nervous system
8 w( R4 [/ G) }+ `4 Ilesions in boys.1,2 Virilization in boys, as manifested* [! e1 x- L* l- E" V9 j; z
by enlargement of the penis, development of pubic1 C/ S1 p; l4 i7 z- G- s1 _8 O
hair, and facial acne without enlargement of testi-
* n# r. K3 g" ]; V9 i3 rcles, suggests peripheral or pseudopuberty.1-3 We
5 `& N: \$ z' k8 K( Y+ u) jreport a 16-month-old boy who presented with the$ A4 _! t4 i$ h2 ]
enlargement of the phallus and pubic hair develop-
* R' X5 t# v* X1 q* |9 w# T0 ument without testicular enlargement, which was due% L" _1 W; h# p6 I; f/ M4 l8 p
to the unintentional exposure to androgen gel used by. U( ]1 h' Q8 a- s
the father. The family initially concealed this infor-" b+ [5 o+ U. u7 I8 h4 t- p
mation, resulting in an extensive work-up for this
# W. @9 x. Q1 Q: h2 T& Schild. Given the widespread and easy availability of
& |2 U8 Q7 T( |: I* K. z& H, |testosterone gel and cream, we believe this is proba-- a& K' B( o2 ?1 j7 Q3 H% i
bly more common than the rare case report in the3 p) i3 t$ N, {, ~7 H6 u
literature.4
* Q% L+ n, r0 u+ Z# {( WPatient Report
! f+ d. e# P/ C$ P9 _( G' JA 16-month-old white child was referred to the4 W' k. M, x8 h- l) c; X2 p; ]
endocrine clinic by his pediatrician with the concern
; u# F1 b3 U# e5 ]of early sexual development. His mother noticed% @& C; A) [. Y; {2 Y
light colored pubic hair development when he was
4 r$ D( p' _. b  M# G, Q) ~From the 1Division of Pediatric Endocrinology, 2University of
- [% O' U( r/ |7 U% LSouth Alabama Medical Center, Mobile, Alabama.9 j5 l9 Z9 A! l1 l4 J
Address correspondence to: Samar K. Bhowmick, MD, FACE,9 Y! ]4 e* Q; R) F
Professor of Pediatrics, University of South Alabama, College of3 j/ ]+ B2 \! }# n" f3 o2 K
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;$ |: b1 I0 j' K# b, f
e-mail: [email protected].& Y, s$ K( \8 v! \8 V
about 6 to 7 months old, which progressively became# v/ C( |$ g3 f8 t
darker. She was also concerned about the enlarge-" g( ]! l& I# s# j  G
ment of his penis and frequent erections. The child
' v! @' l; x6 ^# v; k; V- Bwas the product of a full-term normal delivery, with
0 P% Z  \. G1 d; f# Ia birth weight of 7 lb 14 oz, and birth length of( Y6 _4 V0 c6 I1 b9 K
20 inches. He was breast-fed throughout the first year
: ?1 A& C  v3 Y+ f& g/ bof life and was still receiving breast milk along with
) L* q6 ^% ^' y' `1 |solid food. He had no hospitalizations or surgery,
( e9 Z, D7 k3 H" @) {! I" band his psychosocial and psychomotor development9 M( F3 v  M$ l" d) T+ }) d
was age appropriate.
; s: ?, \0 `# F8 ^( P& vThe family history was remarkable for the father,9 k& |. Z4 y9 W! ^8 P; u
who was diagnosed with hypothyroidism at age 16,3 q, [3 E' H: S6 b
which was treated with thyroxine. The father’s
4 f3 j  F* H' B1 Uheight was 6 feet, and he went through a somewhat9 C& n0 F+ S8 q$ r
early puberty and had stopped growing by age 14.
& O, \: [- {( {6 X) HThe father denied taking any other medication. The
) v8 B: l6 \- schild’s mother was in good health. Her menarche
! ]7 _: K; Y; O% l# g0 [; twas at 11 years of age, and her height was at 5 feet4 l: b2 S' g# x
5 inches. There was no other family history of pre-# ?/ q1 f! u. |- M
cocious sexual development in the first-degree rela-
8 Z( G# f  b4 Ttives. There were no siblings.5 |* a# b& C* s& l* A8 O
Physical Examination
! L. ~6 `- ?" y2 R0 L: ~& ZThe physical examination revealed a very active,
. J, W' U* Y/ j, Q. Iplayful, and healthy boy. The vital signs documented6 ]& ^: G) h" f  e% t5 I+ x- |
a blood pressure of 85/50 mm Hg, his length was! v, G/ E1 W# L5 a% Z
90 cm (>97th percentile), and his weight was 14.4 kg
) k7 ?1 L4 p7 q' Y. w(also >97th percentile). The observed yearly growth
- ~2 B4 H; Y/ p2 `4 C! I; tvelocity was 30 cm (12 inches). The examination of  K* V- d' B+ f( H
the neck revealed no thyroid enlargement.$ ?' t9 Q6 J, [3 f0 ~; E
The genitourinary examination was remarkable for
. }& O2 q# x1 }enlargement of the penis, with a stretched length of3 Q7 ]3 t/ H2 ^4 F  ~
8 cm and a width of 2 cm. The glans penis was very well
% q$ K* M9 U; I$ G! V4 y! Ddeveloped. The pubic hair was Tanner II, mostly around7 ]- j" y! K6 h* A7 c2 B1 e
540
- z% `2 a4 d3 x* O9 \at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
$ D/ Z  K# o+ |( qthe base of the phallus and was dark and curled. The
8 u, n5 z5 B! H5 N( X# D: V) Ytesticular volume was prepubertal at 2 mL each.
# w& ]+ D$ J1 w; R9 U. JThe skin was moist and smooth and somewhat
. W" z1 C& C* _* ?oily. No axillary hair was noted. There were no
4 j; `2 `; T9 e" S5 W1 fabnormal skin pigmentations or café-au-lait spots.8 x9 t7 D0 q$ {" c* R, h0 b
Neurologic evaluation showed deep tendon reflex 2+
2 @0 _- O3 \9 Sbilateral and symmetrical. There was no suggestion
" `) r5 I0 F  X6 u3 }4 [of papilledema.4 Z: S! O/ I5 ^; h, Q5 _8 @
Laboratory Evaluation
$ u) K! O1 W' UThe bone age was consistent with 28 months by
) j. l2 r) @& n/ h" |6 g6 y) Tusing the standard of Greulich and Pyle at a chrono-
. u; o( u5 M4 C% R* Z+ flogic age of 16 months (advanced).5 Chromosomal; K, m# s. |# e  y+ e) m6 e8 ]
karyotype was 46XY. The thyroid function test8 w& d/ q. h, a0 U* G+ f8 t
showed a free T4 of 1.69 ng/dL, and thyroid stimu-5 Q  f3 H3 _4 ~
lating hormone level was 1.3 µIU/mL (both normal).
7 {  J/ m6 ~$ t& T8 @* U, CThe concentrations of serum electrolytes, blood
6 Z, i+ ?3 q6 C! s' [urea nitrogen, creatinine, and calcium all were3 e# H3 q' I! ^
within normal range for his age. The concentration
/ m$ ]0 e9 ]+ Q3 d0 W8 @* j8 N+ e. R( d7 Rof serum 17-hydroxyprogesterone was 16 ng/dL
3 X; }, r  `. L! T! k. B& X/ [0 T(normal, 3 to 90 ng/dL), androstenedione was 20
# s$ q; `) \, @8 Yng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
$ O* A5 c5 `- \8 ?8 Xterone was 38 ng/dL (normal, 50 to 760 ng/dL),9 S5 G5 w* W( s% z1 X) t  |
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
- _8 |0 b4 g. V' T9 V/ z) f49ng/dL), 11-desoxycortisol (specific compound S)" V$ e! Q8 z, x! g) j* T
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
: v' h$ }" w. ^6 F( x+ x% m& D0 etisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total' y) T  p( I: P6 L& S' E
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
8 ^' f6 R: y3 _9 g: [/ ~: M; f4 |and β-human chorionic gonadotropin was less than  e3 }6 `  y1 }+ w7 G' F) z
5 mIU/mL (normal <5 mIU/mL). Serum follicular
! s6 g  b& J% @; n$ ?stimulating hormone and leuteinizing hormone& q+ q* c5 @7 q4 e
concentrations were less than 0.05 mIU/mL
" z! E0 f5 Q. S/ s, D2 V* n& z. Q(prepubertal).6 X, M4 N9 t( C, R* B+ [, P
The parents were notified about the laboratory
, l0 p  n& X5 }7 i  [# l: aresults and were informed that all of the tests were8 d2 `! G& H) [1 b
normal except the testosterone level was high. The  I# M% [7 t( O, O
follow-up visit was arranged within a few weeks to
: R; G% c7 L1 f4 o1 u2 [obtain testicular and abdominal sonograms; how-8 K! B0 n& r/ M' Z1 a& I. l
ever, the family did not return for 4 months.
% d  J7 h1 v7 dPhysical examination at this time revealed that the
3 i5 R% f0 H4 x/ Lchild had grown 2.5 cm in 4 months and had gained7 c! L) T" t3 P
2 kg of weight. Physical examination remained& O' E, n: b+ e9 T" c7 W8 m3 h! _
unchanged. Surprisingly, the pubic hair almost com-
* e) ~; Q6 _# B- `; wpletely disappeared except for a few vellous hairs at
  F) v" o; }% |3 [) F4 H3 h; Dthe base of the phallus. Testicular volume was still 29 u9 d; ?# }2 k0 e5 w
mL, and the size of the penis remained unchanged.3 Q7 W) C7 H; U5 E7 s) |
The mother also said that the boy was no longer hav-9 f" d( a9 a1 D. r1 _) C# ]
ing frequent erections.
; G3 _# `! k9 y; z9 N+ nBoth parents were again questioned about use of
, X+ ?* [: \) ^) w! G8 \# Pany ointment/creams that they may have applied to% H4 h( Y6 H( r/ u, @( Q
the child’s skin. This time the father admitted the3 U5 G) X" g# A/ ]$ k- n( }5 j' G; X
Topical Testosterone Exposure / Bhowmick et al 541
8 i, p; P: D  G  @use of testosterone gel twice daily that he was apply-2 T8 C8 G- r% u% m4 a% S$ C
ing over his own shoulders, chest, and back area for2 W5 T+ Y& ^& K# A4 a
a year. The father also revealed he was embarrassed$ x% S2 c. I. E
to disclose that he was using a testosterone gel pre-7 Z& n) m! A8 W9 }% R, A. N$ `
scribed by his family physician for decreased libido# g  N$ i2 X% d0 r1 R
secondary to depression./ k% @- `% C/ p
The child slept in the same bed with parents.
3 _8 a3 t+ [" B# {The father would hug the baby and hold him on his" j4 ]' L  A1 k  l) W4 Q0 I
chest for a considerable period of time, causing sig-9 I# X  C5 X! G7 a# \
nificant bare skin contact between baby and father./ n2 c' k- E  _! i
The father also admitted that after the phone call,! z) O* g$ x  [- N/ h6 D8 a
when he learned the testosterone level in the baby
9 ~: ?5 W* G% k" D) |was high, he then read the product information
) ?/ X$ x) a; e& |: Ypacket and concluded that it was most likely the rea-4 b! `* @7 ~* p3 y; Q. M
son for the child’s virilization. At that time, they
1 D/ Q* j, p& ~- A& D' {0 Wdecided to put the baby in a separate bed, and the
" j7 A; e4 ]& S7 nfather was not hugging him with bare skin and had  p) r6 I) T( \1 V# w9 G, I
been using protective clothing. A repeat testosterone
$ o2 u- M8 D! S$ s! z& f/ [test was ordered, but the family did not go to the
; E* d0 _5 g1 f$ alaboratory to obtain the test.
+ F; X- V2 S# n3 W, {Discussion
( T" `  I2 p4 p! c, jPrecocious puberty in boys is defined as secondary* Z" F: ]: O0 G8 L) ]( H
sexual development before 9 years of age.1,4
; Y( @+ T% ?$ C7 tPrecocious puberty is termed as central (true) when
% q& U" S6 U  r! X/ J" U7 zit is caused by the premature activation of hypo-
) n# O* l! W( t- uthalamic pituitary gonadal axis. CPP is more com-+ C' s: S. L# X& B' m8 M
mon in girls than in boys.1,3 Most boys with CPP  \; c9 k: }7 x1 q" k' N
may have a central nervous system lesion that is
8 b- j% t6 |* r( w  Lresponsible for the early activation of the hypothal-
  [$ g# H- K3 N; c8 Y! F3 wamic pituitary gonadal axis.1-3 Thus, greater empha-
. j; Z) P) Q& W( o' j! X" O" `, Fsis has been given to neuroradiologic imaging in8 o8 I0 Q' p, ?% P  t
boys with precocious puberty. In addition to viril-
' r% F/ Z; c7 e0 `" v, ?; T* ~ization, the clinical hallmark of CPP is the symmet-3 ^& Z0 ^$ {) R2 c* ^: v: \
rical testicular growth secondary to stimulation by8 C" p" h9 H/ t8 N$ \  {/ ]
gonadotropins.1,34 j0 w& x, d/ ^" |8 o' k  E
Gonadotropin-independent peripheral preco-1 D/ I. H0 r" C* ~# A2 p
cious puberty in boys also results from inappropriate/ \1 V8 {: l+ w3 \
androgenic stimulation from either endogenous or
: ?/ A) }7 a% W2 Mexogenous sources, nonpituitary gonadotropin stim-
! A& T+ l, n( t  L1 Oulation, and rare activating mutations.3 Virilizing1 X/ }( v  s' T# `0 x
congenital adrenal hyperplasia producing excessive* u  ^" L- ^1 m' V. N" G
adrenal androgens is a common cause of precocious; L$ K7 W8 h9 t, t& G) f6 |- R
puberty in boys.3,47 V$ P# d/ k! ?2 w4 w( j
The most common form of congenital adrenal) M( G% H0 c5 R
hyperplasia is the 21-hydroxylase enzyme deficiency.; K  W  @* n/ ]7 Q! b* l
The 11-β hydroxylase deficiency may also result in$ u5 T; s5 T6 e5 |5 N3 b
excessive adrenal androgen production, and rarely,
; t& {' p5 c4 i, t1 J6 Ian adrenal tumor may also cause adrenal androgen
% I" U( o: \6 {3 |excess.1,33 P3 S' W0 ^4 M; o" D0 G; P
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from4 L+ H8 `) r- R+ a! R, _
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
& A* T, ]. g4 l- \) T+ \A unique entity of male-limited gonadotropin-: M: ?- ^  ^% v$ O! |. T' A
independent precocious puberty, which is also known
9 l+ X, G3 I  V3 i' Eas testotoxicosis, may cause precocious puberty at a% f9 a5 W9 Q% ?3 D; [
very young age. The physical findings in these boys
5 Y- |2 L4 i; E2 d3 D( lwith this disorder are full pubertal development,' L  n0 t, F0 w2 A; x+ }+ f+ F; S
including bilateral testicular growth, similar to boys% j+ [+ N; e# d% K) [( V
with CPP. The gonadotropin levels in this disorder. i7 D. q3 p7 O5 ]+ T2 f; B( j
are suppressed to prepubertal levels and do not show% E% J0 c/ T/ a( J: L1 q
pubertal response of gonadotropin after gonadotropin-
( L$ C7 h4 T. }3 ]5 o% [3 U, q1 ereleasing hormone stimulation. This is a sex-linked
' I6 A9 ~* |' E, \autosomal dominant disorder that affects only
: p. l; \& W9 s  kmales; therefore, other male members of the family
+ ]1 R9 _, N# m9 S8 R! u" bmay have similar precocious puberty.3
6 V& m+ v( m) F! ^In our patient, physical examination was incon-
, e9 D1 ?6 z% Isistent with true precocious puberty since his testi-2 M9 b9 J/ }: Q5 c& s; y
cles were prepubertal in size. However, testotoxicosis
7 C- _) E4 X: e9 T' t6 |was in the differential diagnosis because his father
- K! ^4 }6 K6 H; dstarted puberty somewhat early, and occasionally,
- x( x7 M8 ~% B: A0 R! Dtesticular enlargement is not that evident in the$ p! d, `) E6 s# m$ P4 N; \$ o$ d
beginning of this process.1 In the absence of a neg-
4 U( _3 N) e2 Gative initial history of androgen exposure, our
# ^& @9 U, z& D" v- B1 b5 H, Kbiggest concern was virilizing adrenal hyperplasia,8 K6 ?0 H0 J3 J
either 21-hydroxylase deficiency or 11-β hydroxylase
" @4 E+ e) ?1 ^$ v( Z8 |6 f( {* Xdeficiency. Those diagnoses were excluded by find-+ e- _! J1 |' u5 l1 Z' o8 L, G# h& M
ing the normal level of adrenal steroids.
( p" K# T& R$ IThe diagnosis of exogenous androgens was strongly8 Q6 L9 e+ a3 b6 \- K
suspected in a follow-up visit after 4 months because
9 u+ r4 c5 G5 P2 ^/ e) n2 ^- U/ `the physical examination revealed the complete disap-
% w5 X) L& W) q% y9 Opearance of pubic hair, normal growth velocity, and0 j; k' z( I! T4 s8 G0 h
decreased erections. The father admitted using a testos-
/ z' q' I, x3 z5 R) Q2 Hterone gel, which he concealed at first visit. He was0 g9 H6 `9 P' Q# J5 D
using it rather frequently, twice a day. The Physicians’7 w" l) M  q5 s
Desk Reference, or package insert of this product, gel or
, B: E: n6 r( [! J) I$ Mcream, cautions about dermal testosterone transfer to4 [% j* V, h: ^5 m: S+ {
unprotected females through direct skin exposure.: `7 w( w' s$ ?6 q' b
Serum testosterone level was found to be 2 times the
- l+ B! a9 L$ M7 n" r# l0 ~. Pbaseline value in those females who were exposed to' g% b) K, l2 F8 w" D
even 15 minutes of direct skin contact with their male
$ }0 T2 ?- E& y( v$ j) ypartners.6 However, when a shirt covered the applica-
4 O. a0 s8 m# u- Ktion site, this testosterone transfer was prevented.8 p  y1 M+ D8 A& x" f
Our patient’s testosterone level was 60 ng/mL,3 N" u7 R& t4 J/ ]; f
which was clearly high. Some studies suggest that
: ^6 O0 x2 ]/ F' h# rdermal conversion of testosterone to dihydrotestos-, c5 G% `# t5 N, K8 D
terone, which is a more potent metabolite, is more
/ r- w9 W) w+ k! A) mactive in young children exposed to testosterone( l* q- A  Z* K3 V' h
exogenously7; however, we did not measure a dihy-
. o$ v' d' }) q* u3 a- }8 Jdrotestosterone level in our patient. In addition to
* y/ h, L! S. L) t3 Fvirilization, exposure to exogenous testosterone in
' O9 ^, b: h5 L% ~0 Wchildren results in an increase in growth velocity and
# B" ?2 M8 B" I: Madvanced bone age, as seen in our patient.
2 v6 |# T' M! Y8 j- }The long-term effect of androgen exposure during
: d, A! B" E2 {; z3 tearly childhood on pubertal development and final( ]/ W# t& o) w$ t8 n
adult height are not fully known and always remain- S5 F. C# ]: q9 A# r
a concern. Children treated with short-term testos-+ w' l& \, H5 D
terone injection or topical androgen may exhibit some' A; e) \: @  y4 ~1 v
acceleration of the skeletal maturation; however, after  z' `' T: t, [
cessation of treatment, the rate of bone maturation8 i! [, `, _1 v/ D8 t3 i6 N- [
decelerates and gradually returns to normal.8,9
: z4 \) X% E$ X, |: ^# JThere are conflicting reports and controversy9 U8 [9 y! p9 _; _- Z$ ^; D
over the effect of early androgen exposure on adult
) ]/ T2 D3 I+ E/ T; Apenile length.10,11 Some reports suggest subnormal5 m, \9 f* I) i8 `- T
adult penile length, apparently because of downreg-1 X1 m! o1 R7 S" k* I7 g; y
ulation of androgen receptor number.10,12 However,
5 ^( R4 w% k9 m* f4 q- KSutherland et al13 did not find a correlation between
0 Z# z1 y/ x4 }4 i6 ichildhood testosterone exposure and reduced adult
) ?  Z0 R  `# M# i+ G5 Dpenile length in clinical studies.
" t; c- s- j- gNonetheless, we do not believe our patient is( Y! P0 j5 S4 E  I4 Y
going to experience any of the untoward effects from, p1 S9 u6 Z' N3 @8 u4 G
testosterone exposure as mentioned earlier because, x. y5 G* h" [7 x2 B
the exposure was not for a prolonged period of time.0 v" J+ e1 v6 V
Although the bone age was advanced at the time of
$ C( v! \' O3 c. Q3 _diagnosis, the child had a normal growth velocity at( F! T- F) w- Z* U4 \
the follow-up visit. It is hoped that his final adult! s/ l" f1 ^) {
height will not be affected.3 m) l; d1 A* N
Although rarely reported, the widespread avail-! M4 e+ p: [: k5 N/ F' `
ability of androgen products in our society may
1 V" j: E( \; I$ vindeed cause more virilization in male or female
8 ]0 j. p# r# A% g+ d* |children than one would realize. Exposure to andro-
( ?3 }( ?/ H# Y$ Bgen products must be considered and specific ques-
; i. E6 G, |5 ~( u. M" p$ Utioning about the use of a testosterone product or) l7 z, [3 z# w( Q, B  U
gel should be asked of the family members during, {; L8 Q9 W' _- R9 h) \' H" g
the evaluation of any children who present with vir-. A& H( k, I4 u" ]( ?
ilization or peripheral precocious puberty. The diag-
7 i2 k- @* P# R: n6 K: b! H  Enosis can be established by just a few tests and by
7 h  m; g8 @3 B9 c+ `! A9 C3 p. ]appropriate history. The inability to obtain such a. {3 o3 F+ l( X- Y3 J
history, or failure to ask the specific questions, may; e# g6 Y: R$ \; D2 B
result in extensive, unnecessary, and expensive; F, [7 K& D6 Q- E" Q' x
investigation. The primary care physician should be% F+ P& C( H. e' c4 Y" l
aware of this fact, because most of these children6 L4 |5 d2 b; M! e
may initially present in their practice. The Physicians’
9 j1 h' S* {, d" _Desk Reference and package insert should also put a
' w* e0 ^# H+ p5 H2 dwarning about the virilizing effect on a male or
9 l9 x- w. ^2 Ffemale child who might come in contact with some-
7 x! I- t6 V/ Q( Y8 P! ]4 i; u1 Jone using any of these products.. y% @. H* R! P% M9 _4 q  C
References! _- R2 S, }" @( L& ?7 l2 w" f/ p
1. Styne DM. The testes: disorder of sexual differentiation
4 y9 m6 ?* M) J3 i3 D4 K2 H5 |and puberty in the male. In: Sperling MA, ed. Pediatric* v. Y& j9 B. e  r, N/ \: [
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;/ C6 z1 I- O3 i9 @5 ]  t
2002: 565-628.4 N8 _( |% m' g& P6 X) ]9 A6 U5 k
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
; R+ H+ ^2 x% X- N# F# ?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
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
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
5 K" {1 f1 U2 C3 v6 U9 ?
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!
您需要登錄後才可以回帖 登錄 | 立即注册

本版積分規則


快速回復 返回頂部 返回列表