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
0 n0 R/ p( E5 D0 qBoy Induced by Indirect Topical
" S1 o6 B2 K' G" K, K$ ~0 IExposure to Testosterone# @; E( i4 [' W. `; Y3 c5 @  n$ I
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
% S* P# Y1 o3 T% n# Sand Kenneth R. Rettig, MD1' T4 g# p* \7 A, P4 q" t
Clinical Pediatrics+ B* {* F/ I9 j# U; ~
Volume 46 Number 6
, N& X0 o3 s8 l$ G. RJuly 2007 540-543
+ K9 G6 E+ G# |; I0 R) @© 2007 Sage Publications; T4 e* u& r) f8 }% b
10.1177/0009922806296651) G3 m( H5 b; w1 H$ i4 T; x' h  `* F3 p
http://clp.sagepub.com" [5 p3 o: ~) b9 V+ U, i) R
hosted at
0 q2 U: Q  Z* _8 G0 x) Vhttp://online.sagepub.com
9 g1 U, T3 L4 i" F, aPrecocious puberty in boys, central or peripheral,
' o! d9 s3 H8 l0 ~* P5 Z8 jis a significant concern for physicians. Central
: g- j- M5 c0 d# Y9 C8 hprecocious puberty (CPP), which is mediated9 b3 v$ n7 f/ E  z+ n4 b7 @8 {
through the hypothalamic pituitary gonadal axis, has
4 o' G4 Q" n9 O# \  H+ |/ Ha higher incidence of organic central nervous system
; a! r. n6 W/ g6 h0 Y; u$ Mlesions in boys.1,2 Virilization in boys, as manifested0 U7 M  e0 h) {3 F8 c8 _3 ]
by enlargement of the penis, development of pubic- t, [) B0 o1 Z6 z9 ]
hair, and facial acne without enlargement of testi-
2 w; X) M7 ~1 m8 Ecles, suggests peripheral or pseudopuberty.1-3 We
' i8 K( F( C6 ^8 K: F. Freport a 16-month-old boy who presented with the' u/ W1 R7 z' F7 z$ @. [/ n* e
enlargement of the phallus and pubic hair develop-! ~" w' @; V5 e
ment without testicular enlargement, which was due1 u3 q6 D) m9 i. S1 k; l
to the unintentional exposure to androgen gel used by
  J# s2 o: u  J% H5 ]the father. The family initially concealed this infor-3 A9 v2 F; V. ]3 r4 V1 L
mation, resulting in an extensive work-up for this
! Q: C3 S1 l: o2 R) h" g: fchild. Given the widespread and easy availability of
) o7 N- d/ U4 K3 u, M/ x+ p+ Btestosterone gel and cream, we believe this is proba-
2 Z2 T6 m4 C' _8 P! cbly more common than the rare case report in the
* _4 f0 c2 r( f. i" Tliterature.4
# v4 R1 F2 F+ t; yPatient Report6 I, D/ Q, l) q# k
A 16-month-old white child was referred to the1 y8 {  y* W+ K& e  w& ?4 |
endocrine clinic by his pediatrician with the concern, E0 N8 F; K  D; b, ?% u6 V. M- W7 W
of early sexual development. His mother noticed
4 r  l+ a- C" @$ N$ B4 x! {- zlight colored pubic hair development when he was
( y1 A) p3 D2 C9 j  K$ QFrom the 1Division of Pediatric Endocrinology, 2University of. a! v! x2 @4 ?8 ^* S4 f
South Alabama Medical Center, Mobile, Alabama.
3 H, L2 T1 R& E7 i4 k: a+ E7 i+ Y1 KAddress correspondence to: Samar K. Bhowmick, MD, FACE,
' P# A; S( m$ A8 pProfessor of Pediatrics, University of South Alabama, College of; m7 Z6 k& H5 L0 h# U4 s
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;- j6 V' s5 M0 D0 A. _, n1 s
e-mail: [email protected].
2 J' ]# W+ D, n) Z3 nabout 6 to 7 months old, which progressively became/ w; q" K' `0 j6 b
darker. She was also concerned about the enlarge-
! M% E  N& O8 O6 g3 J" H+ Y6 ~ment of his penis and frequent erections. The child
7 ^5 b  q* T. E" p5 O* ]+ owas the product of a full-term normal delivery, with
1 W( z, C9 z7 _5 Ja birth weight of 7 lb 14 oz, and birth length of
. |) C  p* e- C) T& t. d4 n20 inches. He was breast-fed throughout the first year
% Q0 X9 s5 q' w8 nof life and was still receiving breast milk along with% o- y: f! @8 A+ h% r
solid food. He had no hospitalizations or surgery,, {5 h; ?7 v4 E0 O6 E7 R' O
and his psychosocial and psychomotor development
/ @& V- q4 r2 d  }+ c: p$ Kwas age appropriate.
) K7 }4 t. A& y2 v/ rThe family history was remarkable for the father,
, S2 h$ {% H6 I% Gwho was diagnosed with hypothyroidism at age 16,9 T' H# b. g8 n2 ^; Y) ~
which was treated with thyroxine. The father’s) I; G$ A; P' T/ a8 ^9 p3 z( O, t
height was 6 feet, and he went through a somewhat
) k4 d" [/ I5 _2 yearly puberty and had stopped growing by age 14.
' z' Z* z( S/ }; k( N9 v/ MThe father denied taking any other medication. The8 n  I; e3 o7 ~7 C! ~
child’s mother was in good health. Her menarche
0 N: t6 X; |# T# T! J0 lwas at 11 years of age, and her height was at 5 feet0 W+ ~6 `' k8 L; t* |" G6 \. r
5 inches. There was no other family history of pre-' i7 z# i! _: G! N+ F5 f" Y/ k! M
cocious sexual development in the first-degree rela-
: j, L% E/ z7 U, |: z- P2 C$ Y) e5 dtives. There were no siblings.5 R& G( Q: _0 W6 d- |1 M1 |9 R, Y
Physical Examination
" H  H" f% q8 E0 C' a. V2 C( x; n* MThe physical examination revealed a very active,
$ P7 b9 S7 q: C: Eplayful, and healthy boy. The vital signs documented
' A3 G, {' x0 H! |a blood pressure of 85/50 mm Hg, his length was
& ?) L# x5 C! `4 n. u90 cm (>97th percentile), and his weight was 14.4 kg, p9 l8 T; \" c
(also >97th percentile). The observed yearly growth) v3 p2 i. y. [; v4 Y+ h
velocity was 30 cm (12 inches). The examination of
% ~8 C+ e( s: y8 w% x: Sthe neck revealed no thyroid enlargement.* A5 S7 P) e" q6 q( F$ s, K
The genitourinary examination was remarkable for
3 T, y4 r% R2 D& Y4 r9 G# O& Denlargement of the penis, with a stretched length of2 `# m/ D% K# o6 ~
8 cm and a width of 2 cm. The glans penis was very well- s2 [$ |3 Q" |* n8 R  h' B
developed. The pubic hair was Tanner II, mostly around2 x& q: m8 F1 N
540
& A) [5 J% b# W7 X% yat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
1 {0 f* j) b' n; mthe base of the phallus and was dark and curled. The
& p  O& _( T; m  {& ftesticular volume was prepubertal at 2 mL each./ w/ k, U* i  F0 m
The skin was moist and smooth and somewhat0 e1 q; E; f$ ]$ S; g
oily. No axillary hair was noted. There were no
4 Q( r7 u* N, I6 {, S3 y7 Zabnormal skin pigmentations or café-au-lait spots.
# \# T( b" u1 v! t: ZNeurologic evaluation showed deep tendon reflex 2+
5 m+ }2 ^$ m# p) X  Bbilateral and symmetrical. There was no suggestion1 j( q9 z) `: S! d2 ]9 g7 n  C  \
of papilledema.0 R9 u0 a6 |# {/ u  S- R+ B
Laboratory Evaluation" L, k, g9 g: W/ h6 a. V
The bone age was consistent with 28 months by& f9 g# y9 _/ g) p- f6 H' x% n
using the standard of Greulich and Pyle at a chrono-
8 f9 j) R& }2 I9 E4 ^) x5 zlogic age of 16 months (advanced).5 Chromosomal, ~8 f' X  E2 f7 V. b" ~
karyotype was 46XY. The thyroid function test& t/ k4 y+ L% y% D( L
showed a free T4 of 1.69 ng/dL, and thyroid stimu-1 u2 _, V! T' F" d) y  _
lating hormone level was 1.3 µIU/mL (both normal).
; y* i7 J2 F( D* Z, e# lThe concentrations of serum electrolytes, blood. A8 s! x, [0 V6 g2 P
urea nitrogen, creatinine, and calcium all were
6 F0 o) k1 ?7 d. Ywithin normal range for his age. The concentration$ G% {+ g, Z- ?( t% K: u" I
of serum 17-hydroxyprogesterone was 16 ng/dL" n3 a& E: N$ Y0 O9 S+ I3 {
(normal, 3 to 90 ng/dL), androstenedione was 20  `. f; G3 U( `
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
! d9 f0 Z9 Q8 L, F7 P; c- v, Z4 ?terone was 38 ng/dL (normal, 50 to 760 ng/dL),* S, H: K- j3 Z, ~7 a0 `2 p
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
$ e! k0 y" i1 K( |49ng/dL), 11-desoxycortisol (specific compound S)
5 P. D+ ~# O2 n! A" ~was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-) ]; _9 C+ ?4 U8 |$ @2 e" W5 r
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total1 m3 V4 V& v2 N0 i/ k2 t
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
, S/ t  i$ o/ w) |' xand β-human chorionic gonadotropin was less than
# g" N% B& n6 I( G5 mIU/mL (normal <5 mIU/mL). Serum follicular7 W/ q% P! S9 y; z+ Y+ {
stimulating hormone and leuteinizing hormone
. N3 n/ q3 @5 a3 fconcentrations were less than 0.05 mIU/mL/ h; T4 m$ P4 _
(prepubertal).
5 J# J- a$ y: C, x' o3 e6 YThe parents were notified about the laboratory2 g6 k8 T. X0 d% t8 C2 i; c7 f+ E& k
results and were informed that all of the tests were+ q$ S, P# ~  P* i2 o* n& A5 H  x
normal except the testosterone level was high. The
' K$ w- z' \0 d4 Pfollow-up visit was arranged within a few weeks to
# k" X. |1 w' \+ Q+ K+ j- d7 ]. Uobtain testicular and abdominal sonograms; how-
, S3 M! ^6 T( ]7 aever, the family did not return for 4 months.1 `& X' N* b  x
Physical examination at this time revealed that the
+ s* e1 [% r0 x  d0 Z; p7 `child had grown 2.5 cm in 4 months and had gained: o8 g" C- W/ e& b
2 kg of weight. Physical examination remained" B/ c6 Y% \/ Y
unchanged. Surprisingly, the pubic hair almost com-
- E; ~# p4 ~9 ]& N, I) ]! @3 Npletely disappeared except for a few vellous hairs at) M! d- P4 }1 [. x. ?. B" v
the base of the phallus. Testicular volume was still 2
- w- i  c7 V* T. [3 M1 v6 ~/ RmL, and the size of the penis remained unchanged.
0 T! @& a% B, I" [The mother also said that the boy was no longer hav-, j/ @" Y' J: L( W* @- {  v- E. _$ P
ing frequent erections.
0 z- J; K5 p9 t0 D4 \" V  B$ [" y9 JBoth parents were again questioned about use of
/ Z6 n$ D3 }, r# @8 D5 Kany ointment/creams that they may have applied to
: ~3 R* }& d3 z- i+ F* P( [' zthe child’s skin. This time the father admitted the  e. t: q- R+ s( a  K9 D- Z' j
Topical Testosterone Exposure / Bhowmick et al 541
7 h0 v* h- p+ x7 p% \5 M4 Huse of testosterone gel twice daily that he was apply-9 {/ C# B7 N* q9 B0 G& c8 v
ing over his own shoulders, chest, and back area for$ t5 H' N* w; y* s1 V( @/ _, P5 j
a year. The father also revealed he was embarrassed
- k4 H0 g& U' Y6 Z3 y% s; gto disclose that he was using a testosterone gel pre-
1 V6 z, _4 u, a4 R- |7 F2 e) |scribed by his family physician for decreased libido5 v2 L1 b) f% v' {
secondary to depression.
# D3 {+ F9 f" I( q* b5 e/ _' R( LThe child slept in the same bed with parents.4 M: m/ s" b1 S5 V8 V: b6 q
The father would hug the baby and hold him on his
6 R* A5 ~$ V' F* d8 O' C) jchest for a considerable period of time, causing sig-' _% h) }) g9 Q( }* ]) B
nificant bare skin contact between baby and father.: {2 R3 m2 s! h& v7 r
The father also admitted that after the phone call,
' e" O9 t3 |! _* Fwhen he learned the testosterone level in the baby
: E$ T/ }& |$ ~) Swas high, he then read the product information0 V% R! p7 R4 K6 b/ w+ g$ e
packet and concluded that it was most likely the rea-
2 `- ?# h+ s$ Q! z& N! xson for the child’s virilization. At that time, they
2 S' E* x+ w  B3 sdecided to put the baby in a separate bed, and the4 U- Y. M7 B) |; K8 l. {
father was not hugging him with bare skin and had- a  f  G( B5 s4 }5 a' m" ~0 O5 X
been using protective clothing. A repeat testosterone
: ~3 N. q$ h" o( o) ^/ r) Dtest was ordered, but the family did not go to the. Y' J. X" x( X" z5 D/ S
laboratory to obtain the test.
2 W$ E$ P+ N7 n/ U6 @2 N& Z* ~Discussion
7 k! b9 W. ]' Z! E) r" E. SPrecocious puberty in boys is defined as secondary
! n% u# x; L2 T) N! gsexual development before 9 years of age.1,46 S/ H7 B" L4 Z
Precocious puberty is termed as central (true) when1 ?) F/ e7 B" Q& a$ X: p
it is caused by the premature activation of hypo-1 v- Q: o( D( I) @) Z6 E
thalamic pituitary gonadal axis. CPP is more com-1 i; |2 F( R  n2 X
mon in girls than in boys.1,3 Most boys with CPP3 q( x$ f; C0 u! G4 s8 U! p4 _
may have a central nervous system lesion that is
% o: K2 |4 C5 v. J( _responsible for the early activation of the hypothal-% p% `# W2 _6 L$ {' Q
amic pituitary gonadal axis.1-3 Thus, greater empha-
$ t0 X1 U# D1 @sis has been given to neuroradiologic imaging in
% T+ u9 i! U+ a* g! U# v+ i, J* m3 hboys with precocious puberty. In addition to viril-
( v5 p# O) @! N6 `2 hization, the clinical hallmark of CPP is the symmet-8 P7 i: v) g- t* [* d5 P+ r# ~
rical testicular growth secondary to stimulation by8 e, L$ o! n: f* N+ w1 y1 p
gonadotropins.1,3  J& B. P9 O: u+ U+ N
Gonadotropin-independent peripheral preco-
( H2 C: |" o0 D- |8 Q6 D5 I# Qcious puberty in boys also results from inappropriate3 u6 o) j2 Q3 o& m
androgenic stimulation from either endogenous or  Q% J( }9 f2 ~/ A  i4 s3 A
exogenous sources, nonpituitary gonadotropin stim-9 g4 D2 O& a" u3 g  i9 k
ulation, and rare activating mutations.3 Virilizing
. X% e; H1 X( Dcongenital adrenal hyperplasia producing excessive
9 I( f7 S/ d4 c; iadrenal androgens is a common cause of precocious' I; \$ f# l2 ?4 _
puberty in boys.3,4
& R5 w1 ^. l5 tThe most common form of congenital adrenal
" f: [0 {. `0 E% uhyperplasia is the 21-hydroxylase enzyme deficiency.
5 E9 \) }! L- n, `) |1 _The 11-β hydroxylase deficiency may also result in/ O+ [5 O7 ?# Y8 z
excessive adrenal androgen production, and rarely,/ {2 }% l  G3 o* V
an adrenal tumor may also cause adrenal androgen0 L& ?7 t) M& L6 K( s9 G, B
excess.1,3  N7 T% f# M* m: V2 i. r& o$ X* d
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from/ S" K) L3 C' f5 {% g- c1 P
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
8 A; m4 x) k) C' g; yA unique entity of male-limited gonadotropin-1 ^  X+ j  H" y* y  |
independent precocious puberty, which is also known
: E" X( M5 F1 |  ~/ K$ qas testotoxicosis, may cause precocious puberty at a4 D( |2 f! d2 ~
very young age. The physical findings in these boys8 p$ [# n' [& x* V' o. C
with this disorder are full pubertal development,
! L: Z7 F5 t2 ]+ C8 ^& {including bilateral testicular growth, similar to boys
! y( }1 l; N8 l% I- `  S+ ~with CPP. The gonadotropin levels in this disorder" ~5 d% q9 a# J0 w! }2 I8 x
are suppressed to prepubertal levels and do not show
* i1 |! T# x8 K  dpubertal response of gonadotropin after gonadotropin-
1 `* D8 v/ G/ g0 v) k* ]' t/ Creleasing hormone stimulation. This is a sex-linked. r! u, S. E4 ~
autosomal dominant disorder that affects only
; N8 F/ P9 d$ R2 g1 Nmales; therefore, other male members of the family6 a. R% i9 S; l. W8 s* d) G# y5 t
may have similar precocious puberty.3+ i% k$ i7 }9 y' X0 l
In our patient, physical examination was incon-, |2 H) G- }5 _7 V" R9 ?* S, {" {# o8 i
sistent with true precocious puberty since his testi-& e1 x5 H( }$ o: a( l4 E, i& d
cles were prepubertal in size. However, testotoxicosis
& M$ @/ k* \5 Fwas in the differential diagnosis because his father' K2 @. e9 L7 T+ K  |
started puberty somewhat early, and occasionally,
$ _& @5 [, X- u( w4 X, O+ Z: @testicular enlargement is not that evident in the& }: K' X0 d. t) p1 A, s% z
beginning of this process.1 In the absence of a neg-4 O. R0 k7 ^% E$ C! P$ y
ative initial history of androgen exposure, our: p) j2 ~! s; C
biggest concern was virilizing adrenal hyperplasia,) w9 [) o& [' C2 k1 }+ M$ c
either 21-hydroxylase deficiency or 11-β hydroxylase
' _' x( l5 x4 q) c5 z) r( ddeficiency. Those diagnoses were excluded by find-
6 u8 l# H2 V* D3 l( c4 ^ing the normal level of adrenal steroids.
; }9 ?3 E4 P& A9 U2 p! Y: |2 CThe diagnosis of exogenous androgens was strongly- [4 |( q/ e! s4 I
suspected in a follow-up visit after 4 months because
/ G# b& X2 [9 f4 ]- Rthe physical examination revealed the complete disap-9 x- ~& q3 f$ P, ]
pearance of pubic hair, normal growth velocity, and
9 f+ o4 X2 p, Qdecreased erections. The father admitted using a testos-* Z4 R. a* F# [: b
terone gel, which he concealed at first visit. He was
3 O# {/ u% c" B5 L) D8 Husing it rather frequently, twice a day. The Physicians’  \5 B# I  {" U- u
Desk Reference, or package insert of this product, gel or
) y  ]  s$ |/ W1 }& Zcream, cautions about dermal testosterone transfer to
+ V5 Q+ Q+ y0 F7 E, \0 Wunprotected females through direct skin exposure.
# A* r: F3 W( U5 d2 e! s$ i' ZSerum testosterone level was found to be 2 times the
& f  `' M( _  Q( T' kbaseline value in those females who were exposed to* n7 |. `* J. D! b) d
even 15 minutes of direct skin contact with their male7 d* c$ K9 j/ Z* q) n
partners.6 However, when a shirt covered the applica-
" l3 ?! C9 f% w7 e( K0 Gtion site, this testosterone transfer was prevented.: X4 z4 F8 F6 x/ I# [; f! G: p
Our patient’s testosterone level was 60 ng/mL,
5 h* q( y" c* o; Jwhich was clearly high. Some studies suggest that& ?$ G* f' S/ m3 P7 m
dermal conversion of testosterone to dihydrotestos-% ~/ n( ^7 ~% a$ O6 b# S! R
terone, which is a more potent metabolite, is more
1 _) M8 N' J' m) C4 s: gactive in young children exposed to testosterone1 M! [( ?$ R4 N
exogenously7; however, we did not measure a dihy-
/ V: |  H+ l6 b4 Edrotestosterone level in our patient. In addition to
5 V5 d* M! |6 i: Zvirilization, exposure to exogenous testosterone in, i3 O* r1 K0 @
children results in an increase in growth velocity and
9 Q, k) ^* q5 A* r3 K$ wadvanced bone age, as seen in our patient.
& H# |9 P/ _" B: sThe long-term effect of androgen exposure during" A: P' b8 V! Z& [% e* U
early childhood on pubertal development and final
3 \6 k  v9 o8 N6 d" b  |8 qadult height are not fully known and always remain% R7 ^! N' _2 B
a concern. Children treated with short-term testos-: @9 W& ]6 G; R" Y
terone injection or topical androgen may exhibit some$ a1 }+ p  C  L1 c: ~% j# Q9 {! [0 y
acceleration of the skeletal maturation; however, after1 t# `$ L% T9 q' |/ N  R$ z
cessation of treatment, the rate of bone maturation
1 k) W0 u* `& ~1 y! j9 w. m$ C4 Ndecelerates and gradually returns to normal.8,99 e) Q( h0 R- s. j8 S. f1 w
There are conflicting reports and controversy1 y. p6 K+ Q' ?4 z; N
over the effect of early androgen exposure on adult* g$ {  e8 O& _
penile length.10,11 Some reports suggest subnormal" U) I# Q2 X& b0 u' k1 z: S
adult penile length, apparently because of downreg-
5 y: S! s# h: q( G  X- B  sulation of androgen receptor number.10,12 However,
9 {- k; G) W/ v4 x; t4 g' ^Sutherland et al13 did not find a correlation between2 m, W0 ]  {# N; s( l
childhood testosterone exposure and reduced adult
0 U+ |5 Z4 m- D2 p% x" I% m& npenile length in clinical studies.1 E( e9 ]  u/ A  S  K
Nonetheless, we do not believe our patient is! g) A: ?( P" v$ u: I! I" q. P
going to experience any of the untoward effects from
  w4 q5 V9 Q7 h# ?: d4 D' x% ltestosterone exposure as mentioned earlier because- T/ q) c- F8 |) @8 O
the exposure was not for a prolonged period of time.
  }3 t7 G1 M9 a1 s; x/ oAlthough the bone age was advanced at the time of, V% C( m/ p' Y, q
diagnosis, the child had a normal growth velocity at
% @6 a4 S, V. ?0 H9 N& M! uthe follow-up visit. It is hoped that his final adult
' m7 ?, t9 g& h6 t# r# Rheight will not be affected.
* d; f! [% x* B; X7 dAlthough rarely reported, the widespread avail-
7 {" @3 {+ Y* V" [ability of androgen products in our society may3 V; L) n- G+ F3 _+ i+ j: g
indeed cause more virilization in male or female
: k6 V$ v1 M4 [/ M& I. S" T3 Achildren than one would realize. Exposure to andro-
5 Q( c8 a9 {. k6 U& Z  z" tgen products must be considered and specific ques-
2 D# t  O' v3 n) Y& V5 Etioning about the use of a testosterone product or
0 p4 k, a* F( m) X4 Mgel should be asked of the family members during
5 Y7 G; `* n3 A' |1 H3 kthe evaluation of any children who present with vir-
7 {& ^+ y) K# H7 B- ^: q* vilization or peripheral precocious puberty. The diag-# K9 h' c+ b+ J& q! Z' k
nosis can be established by just a few tests and by
* \/ {  ~. X" ^' B/ jappropriate history. The inability to obtain such a
* X3 O$ g1 M# b3 j( M5 phistory, or failure to ask the specific questions, may
- p0 d  P1 x+ _; i! p* U! d1 B" K/ p# G4 mresult in extensive, unnecessary, and expensive
8 [% l! Y) W& qinvestigation. The primary care physician should be3 a8 U, B: W1 w" E. y, \/ [
aware of this fact, because most of these children8 W) l+ X- q! ^6 m
may initially present in their practice. The Physicians’
0 N4 h7 h* \* A2 ^6 fDesk Reference and package insert should also put a( |+ v9 t! Q( s* ^
warning about the virilizing effect on a male or4 x0 M1 R% N7 f6 X  s6 D
female child who might come in contact with some-% k3 }+ g2 K/ }6 U7 v+ `: {4 E
one using any of these products.  h3 a9 u" g+ I/ q
References/ D1 O: S6 z+ Y: W; N3 j4 B" x* J! I4 l
1. Styne DM. The testes: disorder of sexual differentiation
6 r' C. d4 v& s9 z4 Oand puberty in the male. In: Sperling MA, ed. Pediatric4 S& Y  F  y$ g: ~, E- t
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
/ ]5 O1 `% B' i. T; ]/ c& \2002: 565-628.( U2 v. e6 W% l
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
- g( Y0 b$ o  h+ V7 ^  j2 ~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
' W: R$ K( l+ u1 g& Q1 m& h6 H, vBoy Induced by Indirect Topical
* h' y) u& D) [' k& {Exposure to Testosterone
) F3 x" m" S$ ?Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2( w8 [3 h" e9 ?  E: I) H3 M
and Kenneth R. Rettig, MD10 Q6 K  a1 ]! h4 b% q5 \
Clinical Pediatrics
( i8 G/ n2 }* v0 ?* pVolume 46 Number 6) O4 W3 O! C0 J" m/ p" }8 `  N
July 2007 540-5439 M* M4 r: j8 W6 W4 y$ F3 P
© 2007 Sage Publications" \* t! K* ]* p; s9 k/ p0 s
10.1177/0009922806296651
- n3 G5 a( e# Z; f$ F9 m7 I, c# thttp://clp.sagepub.com+ N: V+ J1 k5 @0 E! w  Y
hosted at# p# `# w) I8 |
http://online.sagepub.com
4 `  F% i0 k, S) h! @+ t) xPrecocious puberty in boys, central or peripheral,5 m# G9 D* f/ W# N
is a significant concern for physicians. Central
4 Z2 m4 L8 ~& e% x5 Xprecocious puberty (CPP), which is mediated
; S* p( @5 H  j! @% f+ ?through the hypothalamic pituitary gonadal axis, has% {/ G* B& R  y) H2 }5 E
a higher incidence of organic central nervous system
) J& n3 X& s- D  o3 u  g' o5 ]lesions in boys.1,2 Virilization in boys, as manifested
4 C7 i' x, _% b  X! Jby enlargement of the penis, development of pubic
; ~4 ~6 [; P9 }9 d% \8 {- \  M. yhair, and facial acne without enlargement of testi-) K5 U( V0 @5 [- q, \. x
cles, suggests peripheral or pseudopuberty.1-3 We
& ]1 u" f. E' o& [- mreport a 16-month-old boy who presented with the& ^  }' O5 e1 x' n
enlargement of the phallus and pubic hair develop-
# f+ F/ L. s4 }4 q5 d4 V' Kment without testicular enlargement, which was due" _4 B1 j! f' d% o. w
to the unintentional exposure to androgen gel used by+ K3 r' d* r  v
the father. The family initially concealed this infor-3 \+ ]0 y: q1 f* h
mation, resulting in an extensive work-up for this
- L# D6 B7 J6 u( n* t8 e. r. {; uchild. Given the widespread and easy availability of0 J2 j& o9 p; Z3 Q
testosterone gel and cream, we believe this is proba-
- X3 ?. o$ B2 j3 e5 E" ibly more common than the rare case report in the
  `, O4 T/ ?7 A: J: Xliterature.4
/ K' V  [" A& `; c! o0 YPatient Report1 C8 H% J9 s9 z$ T( f+ I4 T
A 16-month-old white child was referred to the- I- \# {/ E8 N  j; u( b) e  D/ j/ F
endocrine clinic by his pediatrician with the concern
5 }( [4 H! U( y3 I. Jof early sexual development. His mother noticed& f3 q2 X. u3 q0 N/ `& @* h* T
light colored pubic hair development when he was
7 c& V3 H% p$ Y6 ~9 UFrom the 1Division of Pediatric Endocrinology, 2University of$ ]4 L0 b1 W* h" o# {0 q
South Alabama Medical Center, Mobile, Alabama.5 w! e; h  n7 A  u! d5 D
Address correspondence to: Samar K. Bhowmick, MD, FACE,
! X# m; ?+ J' W8 O; X& ]& C& i. AProfessor of Pediatrics, University of South Alabama, College of
) m8 ?0 E* r( O* }9 |& E& J+ iMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;4 v( H7 ?" {$ C7 }0 F
e-mail: [email protected]./ n4 \" O" K. w! l1 }3 @. J% B/ e
about 6 to 7 months old, which progressively became; M. Y) r$ F  k( T$ b$ ~; Y% m5 T& Q, p
darker. She was also concerned about the enlarge-: Z- V; F  @& l7 O
ment of his penis and frequent erections. The child, M' j: \2 j% L  ]4 N! @
was the product of a full-term normal delivery, with) j2 O6 L. h3 M1 p% S; c/ E
a birth weight of 7 lb 14 oz, and birth length of/ Q, a8 l$ P! G7 w
20 inches. He was breast-fed throughout the first year6 \6 ], ~. S, U( K9 e
of life and was still receiving breast milk along with
* y5 `( ?8 H! Z( Hsolid food. He had no hospitalizations or surgery,3 k9 E& I  B) M* s& j8 V
and his psychosocial and psychomotor development
0 f9 c% |+ b5 Z( H# y1 P  ]/ pwas age appropriate.
! e8 Q3 r; k& O; YThe family history was remarkable for the father,
, w& D& Z( q3 F7 O) f( uwho was diagnosed with hypothyroidism at age 16,
8 T" g( x5 z& K+ L8 Ewhich was treated with thyroxine. The father’s! C! o; T  L8 m- @/ J3 C, F" c% Z
height was 6 feet, and he went through a somewhat
! r6 y3 c* ]3 ?4 mearly puberty and had stopped growing by age 14.# r! S; S0 M$ o' K- M# T
The father denied taking any other medication. The5 ~- y& X( q; t
child’s mother was in good health. Her menarche
$ k" o$ I& _1 z: I" Y7 ~was at 11 years of age, and her height was at 5 feet
1 C1 b# K2 J4 {/ D5 inches. There was no other family history of pre-1 J6 C" I" Z: ]) B) |# y: n+ i% \
cocious sexual development in the first-degree rela-
1 l7 [4 q- }8 r$ i! Xtives. There were no siblings./ C! E! s; P  C) d2 v
Physical Examination
) ~) v* I8 a% h4 W2 K! ^$ @The physical examination revealed a very active,
4 ]8 u- N4 b( Iplayful, and healthy boy. The vital signs documented
) h+ D9 s* c% g3 ga blood pressure of 85/50 mm Hg, his length was8 e& R) |- I; _: a/ ?& |- o# v2 Z
90 cm (>97th percentile), and his weight was 14.4 kg8 |8 Z& ^/ `9 f$ b& A( v
(also >97th percentile). The observed yearly growth) Y0 i8 F6 O8 @3 Q
velocity was 30 cm (12 inches). The examination of+ A$ l  G) X: M. j. ^( @6 I& F' e
the neck revealed no thyroid enlargement., D" h! d: @) {% s# A3 B" Y+ Z2 B
The genitourinary examination was remarkable for
4 \9 A3 H" N5 S1 V5 a# H* y; ?- eenlargement of the penis, with a stretched length of. p7 ^. r& y+ F
8 cm and a width of 2 cm. The glans penis was very well! G$ p: e5 b9 N! Z( d# z& o
developed. The pubic hair was Tanner II, mostly around
7 x# F% _) h) D9 h540: ]4 H& t3 r- i+ [( Z
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
4 t1 U/ ?; L8 p+ N$ y: L9 cthe base of the phallus and was dark and curled. The; z" h+ u$ I6 g0 `- @
testicular volume was prepubertal at 2 mL each.
8 Y9 Q, o" T$ ?. C* {3 m' j' P" T# \The skin was moist and smooth and somewhat
$ S$ P7 m3 Y; |) a& _( Ioily. No axillary hair was noted. There were no
4 S; F; [9 k, f3 q& Nabnormal skin pigmentations or café-au-lait spots.
% j  I1 z/ k3 R$ g+ nNeurologic evaluation showed deep tendon reflex 2+
% V1 ?9 N1 E8 K6 B# d3 ~bilateral and symmetrical. There was no suggestion
7 ~$ B. ?, [1 q+ G- ?# }, ~of papilledema./ n3 L; F- D- k/ b& C, z
Laboratory Evaluation) v  I' ]. A* V. F
The bone age was consistent with 28 months by6 Z6 h) h* t" t' ]
using the standard of Greulich and Pyle at a chrono-
: `$ k( R# h6 n7 H+ e3 ?$ Flogic age of 16 months (advanced).5 Chromosomal# u0 q  \" U% J( o
karyotype was 46XY. The thyroid function test
) j' Q  k- j% I7 k. d  V  `showed a free T4 of 1.69 ng/dL, and thyroid stimu-
$ x2 {2 `) U' N( Ilating hormone level was 1.3 µIU/mL (both normal).  N( x$ r, L5 R$ x
The concentrations of serum electrolytes, blood
- c! f( D- S; lurea nitrogen, creatinine, and calcium all were
8 J* p. G; w9 Iwithin normal range for his age. The concentration4 o* ?+ |* u4 i& j3 _: M
of serum 17-hydroxyprogesterone was 16 ng/dL  A7 |3 j. W3 N, v7 f4 _9 D+ {' w
(normal, 3 to 90 ng/dL), androstenedione was 20
8 x* r' l. ]/ ~2 f& D7 Y1 rng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
3 Q! ]. p8 n) I4 P# e% Tterone was 38 ng/dL (normal, 50 to 760 ng/dL),
! A. d: u; J+ D0 Odesoxycorticosterone was 4.3 ng/dL (normal, 7 to/ d* B1 N6 d2 M: r& p8 H# U
49ng/dL), 11-desoxycortisol (specific compound S)- ?0 Y& P( B0 [  h# V7 k
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
* j$ C9 a  `3 T+ `tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
1 _0 d4 A/ a$ atestosterone was 60 ng/dL (normal <3 to 10 ng/dL),2 H; |8 H2 X2 }, @, [
and β-human chorionic gonadotropin was less than" V8 |. j; U' O3 m
5 mIU/mL (normal <5 mIU/mL). Serum follicular
( Y/ h  m* K9 Q) x. T1 M9 Zstimulating hormone and leuteinizing hormone
$ H0 M9 |4 K( ?2 {/ m5 @. lconcentrations were less than 0.05 mIU/mL
4 O* t8 m$ K' O7 M0 @% [(prepubertal).4 C9 G5 _4 w4 v" ^
The parents were notified about the laboratory$ F0 M6 f: |7 r3 U* n2 x
results and were informed that all of the tests were
" s% `' `- {0 j8 Onormal except the testosterone level was high. The
1 P/ j- F% s/ i! Efollow-up visit was arranged within a few weeks to
" f! m3 ?3 d; ?9 O$ P4 ^5 ^$ Sobtain testicular and abdominal sonograms; how-
9 E: R; M/ n$ O+ V% x7 Hever, the family did not return for 4 months.
1 q* v* ~" g& BPhysical examination at this time revealed that the& Z: x/ H+ M- m  H
child had grown 2.5 cm in 4 months and had gained, j$ n2 u6 ~  p% x1 X4 u- Y
2 kg of weight. Physical examination remained" y# E: ]- z- ~
unchanged. Surprisingly, the pubic hair almost com-! t2 e6 i0 |( M9 X2 M5 A
pletely disappeared except for a few vellous hairs at
& I. a) S0 y# I8 o$ _8 wthe base of the phallus. Testicular volume was still 2
9 |; \' ~% I" x3 V8 _8 K+ UmL, and the size of the penis remained unchanged.- u# V6 t; k* Q2 T3 e/ A
The mother also said that the boy was no longer hav-) L/ o# U& }4 X* d# B! T& Q
ing frequent erections.
% `4 K4 C; A" z* DBoth parents were again questioned about use of
- p- Z: [. k0 J& ?: h& B& wany ointment/creams that they may have applied to
6 Q- {! q6 j! Bthe child’s skin. This time the father admitted the6 m% V! I. W- y- B: x
Topical Testosterone Exposure / Bhowmick et al 541
- ?6 p4 X$ J$ Q1 S" Y4 H, ~1 Ruse of testosterone gel twice daily that he was apply-: V+ A2 T. w! Y6 S( D4 n+ @+ f
ing over his own shoulders, chest, and back area for4 w1 R. o+ W3 x( {' o
a year. The father also revealed he was embarrassed) `; ~3 @9 `# A- y! G% x
to disclose that he was using a testosterone gel pre-; E0 V  ]4 U, T5 s9 `- x# M
scribed by his family physician for decreased libido: A# ^2 t% I% H  A' R9 H2 e3 A
secondary to depression.
8 @: h9 F9 f8 H7 ^The child slept in the same bed with parents.
9 v' X% L% f- c2 m. ~+ Y; e: z$ uThe father would hug the baby and hold him on his
2 h2 {7 |; i  l9 {7 B. I4 Ychest for a considerable period of time, causing sig-1 Q1 G3 u" `0 O# ]/ e
nificant bare skin contact between baby and father.
) a( A, @7 }/ \* t* h6 N, MThe father also admitted that after the phone call,1 P% Y) D, T5 y; U- `' I: Z
when he learned the testosterone level in the baby+ w* ?: S  U  _# F: s2 D0 H) Z6 O" p
was high, he then read the product information
! `. l6 s3 Q3 ~" z7 Zpacket and concluded that it was most likely the rea-
% K; j! A; I* r; T8 a1 wson for the child’s virilization. At that time, they( ]/ R: l* o$ K+ q1 h* N) H, d/ T
decided to put the baby in a separate bed, and the+ M5 A& q3 g9 d0 C( O
father was not hugging him with bare skin and had7 |- h" T  k& g5 B' ]  ]
been using protective clothing. A repeat testosterone
0 ^, M9 e9 u7 j: _! f  ltest was ordered, but the family did not go to the2 y- n% S8 _3 M: E
laboratory to obtain the test.8 s$ M. b! Z3 M% P5 I) }
Discussion) M% L) r' \% g6 \9 j6 f% z
Precocious puberty in boys is defined as secondary
. D" l. Y( i. {& H9 i- E6 n7 xsexual development before 9 years of age.1,4# H$ B% @. m" |. y
Precocious puberty is termed as central (true) when" @# x* h" Y1 S+ ?8 ]+ p5 j
it is caused by the premature activation of hypo-9 }$ ]9 g- @' Y3 U# F
thalamic pituitary gonadal axis. CPP is more com-
2 Z/ a9 s. B# T  s" Cmon in girls than in boys.1,3 Most boys with CPP
/ n/ W1 x1 ?( Ymay have a central nervous system lesion that is
* l: X- g& H& F9 Q) G7 hresponsible for the early activation of the hypothal-6 ]: ^8 n% [7 H& k7 S
amic pituitary gonadal axis.1-3 Thus, greater empha-
/ C8 S5 s9 O$ _+ }) n- w6 Dsis has been given to neuroradiologic imaging in
) y. K2 b; i' I0 ^boys with precocious puberty. In addition to viril-* b0 o4 t9 G8 x: t2 L; s
ization, the clinical hallmark of CPP is the symmet-
9 I8 @: \4 P; W3 t" M7 Lrical testicular growth secondary to stimulation by
. K" B1 T+ k5 k2 \& U! [gonadotropins.1,3
1 m) z! q3 v* n+ D& t, ^% GGonadotropin-independent peripheral preco-
$ y" H4 I( \" m  gcious puberty in boys also results from inappropriate% _2 M* o% l1 k# N
androgenic stimulation from either endogenous or
9 C4 B4 i, i  Kexogenous sources, nonpituitary gonadotropin stim-0 y2 }' E6 \8 r& Z5 q& G( E, }
ulation, and rare activating mutations.3 Virilizing) J; u6 ?: l' K2 W- k- s0 Q' M
congenital adrenal hyperplasia producing excessive
. T8 e' I- _) J  q, H, f# `& Padrenal androgens is a common cause of precocious, c6 L& `5 F1 w  d( q
puberty in boys.3,4
  N% u5 l3 A' JThe most common form of congenital adrenal7 A* B& _1 N# ~2 o& k" Z. _
hyperplasia is the 21-hydroxylase enzyme deficiency.  W9 H, w1 x7 i' g7 R! m
The 11-β hydroxylase deficiency may also result in3 {7 x' j: s5 B
excessive adrenal androgen production, and rarely,
: G/ s' T" g% ^9 Fan adrenal tumor may also cause adrenal androgen$ R+ b+ L  b" X$ Z6 ~5 b
excess.1,3( l  J# [6 z1 t& n0 ^  `/ e" e
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
0 D2 b% C( {) k4 U+ G/ g  l3 `542 Clinical Pediatrics / Vol. 46, No. 6, July 2007, V2 F$ A7 W) q# t
A unique entity of male-limited gonadotropin-
( [# `' g9 H. V& r7 aindependent precocious puberty, which is also known) M7 {2 ?# L+ f! D$ ^5 F" o" k
as testotoxicosis, may cause precocious puberty at a
0 t# _  {- b. C% Zvery young age. The physical findings in these boys
$ z/ W8 M1 u% O: u5 f" i# p6 {with this disorder are full pubertal development,* Q$ G3 R/ Q: Y6 m- x0 E
including bilateral testicular growth, similar to boys
8 q) l0 t; O. lwith CPP. The gonadotropin levels in this disorder: `. e4 b( e( n4 S  M
are suppressed to prepubertal levels and do not show
8 c. L+ j# S! U$ L4 F$ xpubertal response of gonadotropin after gonadotropin-# e% \+ {! T  R; B  W
releasing hormone stimulation. This is a sex-linked& O" [% i& Z$ R' U, J) r; W; s
autosomal dominant disorder that affects only
8 T3 h2 a3 J- Ymales; therefore, other male members of the family
, u9 r2 P. b' z8 g9 Q3 l0 \1 Z5 }may have similar precocious puberty.3
  Z& a2 R$ y7 e6 O( E& ?) ~1 ^In our patient, physical examination was incon-
# ^# g: ]* a$ Y: h+ ^sistent with true precocious puberty since his testi-7 y+ B  e7 E; l/ ^' t# |
cles were prepubertal in size. However, testotoxicosis& L* K6 N) J6 @3 b7 t7 O1 W
was in the differential diagnosis because his father
8 M% F" L6 u1 l6 S6 I0 \* @started puberty somewhat early, and occasionally,
8 ^0 P  d% N: ptesticular enlargement is not that evident in the2 l+ w+ v2 Z8 b/ v* ^" r" v
beginning of this process.1 In the absence of a neg-
! F! u1 K: b+ U# _; x0 Yative initial history of androgen exposure, our8 y5 ^# e* s$ g& U7 ~2 I
biggest concern was virilizing adrenal hyperplasia,7 n. n1 t- u& k7 B  ^( c
either 21-hydroxylase deficiency or 11-β hydroxylase
. f$ H7 J' h5 o* gdeficiency. Those diagnoses were excluded by find-, s8 R: Z2 B) x
ing the normal level of adrenal steroids.5 B; [* K6 r( P' g/ Y. `
The diagnosis of exogenous androgens was strongly6 r7 o  [+ L' F# O9 _4 \
suspected in a follow-up visit after 4 months because
1 y2 V8 g! T8 }, `the physical examination revealed the complete disap-% j/ W. v9 }2 R6 ~
pearance of pubic hair, normal growth velocity, and! ~6 y, P* X) s, ^/ B$ u, {# G
decreased erections. The father admitted using a testos-
* `; D; k6 y# h( d# \terone gel, which he concealed at first visit. He was
; ~5 z" r$ V" g; S* `# }; _& Y! @& lusing it rather frequently, twice a day. The Physicians’5 Z/ r  V7 P3 Y9 @
Desk Reference, or package insert of this product, gel or5 [% p/ N% C0 w5 P! k
cream, cautions about dermal testosterone transfer to
( ]4 j  l" X; S2 E( Q+ `0 e' |" r5 dunprotected females through direct skin exposure.( x. }  h. q3 m$ a9 X: {* k
Serum testosterone level was found to be 2 times the+ t' V) W  E! Q. ?7 ?
baseline value in those females who were exposed to
2 y0 x( u" p1 Yeven 15 minutes of direct skin contact with their male5 \3 j( N5 j4 u9 J
partners.6 However, when a shirt covered the applica-2 Q' B  E$ t& A7 U% F3 R
tion site, this testosterone transfer was prevented.- H( v/ B3 U  u4 d. S/ }
Our patient’s testosterone level was 60 ng/mL,
" b$ w: K0 N; J) L( Z8 g' ]. `which was clearly high. Some studies suggest that
  c5 Y. u$ }9 h8 Z  `dermal conversion of testosterone to dihydrotestos-
2 y6 z( K9 ^1 P0 Cterone, which is a more potent metabolite, is more
, x: N2 W8 K6 K, s1 @) {0 E  Aactive in young children exposed to testosterone
7 ^6 t9 O) [: m6 ~3 M; Lexogenously7; however, we did not measure a dihy-
* }! W* N  N" n/ m7 p4 D( \drotestosterone level in our patient. In addition to
1 o% e% H- x/ Gvirilization, exposure to exogenous testosterone in
+ U" A# E# }2 a8 `children results in an increase in growth velocity and3 p: w! I: ~: s/ o1 i" S
advanced bone age, as seen in our patient.
; C6 z, p8 Z' z. ~% o9 kThe long-term effect of androgen exposure during9 T7 B0 S- R+ Y$ P5 D
early childhood on pubertal development and final4 c9 K7 G$ @: P4 N
adult height are not fully known and always remain
, v$ n5 ]( g7 m6 O% E' }a concern. Children treated with short-term testos-
/ s$ I- r, r; f+ H  e( Fterone injection or topical androgen may exhibit some# x2 D+ B% g" ~3 u; ^1 o+ m
acceleration of the skeletal maturation; however, after
/ K. e  i: H9 W- x0 D# _7 v; Tcessation of treatment, the rate of bone maturation2 c/ }+ Y! E" Z1 H" U; o
decelerates and gradually returns to normal.8,9& T6 E# w7 H* W
There are conflicting reports and controversy4 e# `5 K. p: L% @
over the effect of early androgen exposure on adult/ o8 R! C* a# p2 K$ x4 i
penile length.10,11 Some reports suggest subnormal# c  `3 E9 I/ K; y
adult penile length, apparently because of downreg-7 [, B# f* I) c
ulation of androgen receptor number.10,12 However,
: V6 u  d- o4 W% ?Sutherland et al13 did not find a correlation between
' `& P. n! G7 l# d, |childhood testosterone exposure and reduced adult7 h  \* A4 w. g( V
penile length in clinical studies.
# ~  \: f- W, _2 U4 lNonetheless, we do not believe our patient is
  B- N" X9 E7 Fgoing to experience any of the untoward effects from
; @7 f  T  q$ I( ]3 ~testosterone exposure as mentioned earlier because
/ F8 b" l; Y& Z$ s4 {the exposure was not for a prolonged period of time.. O, e/ i* J8 Q) o
Although the bone age was advanced at the time of$ |+ h; x+ `( e$ O# i; m
diagnosis, the child had a normal growth velocity at/ t! N( x' d0 d8 _" E
the follow-up visit. It is hoped that his final adult0 A1 c8 S% I* C' E8 _
height will not be affected.
7 A$ [9 \9 Z8 pAlthough rarely reported, the widespread avail-9 A# t( K5 ^! x/ z" ^9 P: r
ability of androgen products in our society may, d* {+ A0 A, e
indeed cause more virilization in male or female7 O5 ?6 `% g8 ~' J/ g0 A) l
children than one would realize. Exposure to andro-( @' q: I4 _8 n# d
gen products must be considered and specific ques-
$ `! q, Z5 U$ W1 I4 ~! qtioning about the use of a testosterone product or3 A. B# ]- f( l4 _
gel should be asked of the family members during( X& {% e( g1 r" k1 A
the evaluation of any children who present with vir-
9 ~4 r" u8 l% d' C% Xilization or peripheral precocious puberty. The diag-( m5 o& m7 d; X6 q+ P& N
nosis can be established by just a few tests and by
. s6 R0 S, i2 C0 S9 I6 gappropriate history. The inability to obtain such a
5 [, R4 j) N+ J$ y; _" dhistory, or failure to ask the specific questions, may
6 l8 o) P; X9 R$ ?% D' p" vresult in extensive, unnecessary, and expensive
! ]0 r4 T! v+ O. [3 finvestigation. The primary care physician should be
& P( |+ _1 u; o' h) x2 Q6 [  kaware of this fact, because most of these children# V) g) f9 a7 b/ J
may initially present in their practice. The Physicians’9 B' s4 _  k- v4 p
Desk Reference and package insert should also put a
7 C) k0 p2 Q9 c1 Swarning about the virilizing effect on a male or- H/ T/ h# c) p6 L
female child who might come in contact with some-
1 q/ u+ B& L. m) aone using any of these products.) m2 I3 f$ X$ ^6 i
References
" Q) {) Q" J5 t) ^2 B1. Styne DM. The testes: disorder of sexual differentiation1 c2 @. c) t6 c6 S
and puberty in the male. In: Sperling MA, ed. Pediatric" X4 d/ K1 W) g; n9 M6 v  D7 R
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;  _% D! z( _3 I  ], q5 b
2002: 565-628.% L5 Z* P# n7 I3 G: R4 O
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
& K* P, H' r2 a, Z/ upuberty 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
  f+ F9 ^; X' t/ [: H3 p! b
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