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
2 @% a8 C) L5 JBoy Induced by Indirect Topical
- t6 f8 T9 D$ M+ q4 j' d1 ?5 LExposure to Testosterone
0 M1 E7 g3 t$ _  Y0 C& wSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2  O1 n. P- L/ i" D# E3 B: w
and Kenneth R. Rettig, MD1
1 A6 Z, w$ ^. c, d. a, F( i& e+ d/ Y/ ^Clinical Pediatrics5 C% t6 Q! M* I: N. c8 S
Volume 46 Number 6
! H2 `0 @1 S$ X  J9 U2 c. j) d, W$ fJuly 2007 540-5439 M; a1 J( w6 j9 z0 h" b
© 2007 Sage Publications; Y6 S# s% a5 F$ q: k
10.1177/0009922806296651
+ M3 c3 l/ w% s4 E' F9 E. s( phttp://clp.sagepub.com( P+ c* O, _4 I4 Y1 x' B% B
hosted at$ Y: }# @. C9 @
http://online.sagepub.com2 Q1 P( o( r, G- R3 \* [: c6 V
Precocious puberty in boys, central or peripheral,( l( J) _- T& B/ q7 M9 J$ L' ^+ {. @
is a significant concern for physicians. Central( X2 [( t& b, h7 k- `! u4 n
precocious puberty (CPP), which is mediated0 _# {5 Y5 }+ P; b, u8 W5 l$ n
through the hypothalamic pituitary gonadal axis, has6 U5 l+ M& P. F( [* N9 x
a higher incidence of organic central nervous system/ h2 Y% _0 x. }; F6 q' Y3 R
lesions in boys.1,2 Virilization in boys, as manifested
! f$ {3 a$ Q4 Y& iby enlargement of the penis, development of pubic9 [5 \# o8 M7 P8 c- i
hair, and facial acne without enlargement of testi-) g! d, Q' |6 }6 j  U0 B- C
cles, suggests peripheral or pseudopuberty.1-3 We
6 a6 `$ V) J# k( A6 nreport a 16-month-old boy who presented with the
) h! t9 J1 a) kenlargement of the phallus and pubic hair develop-1 M% k4 b7 y5 q/ S2 b: V3 e% u; c
ment without testicular enlargement, which was due
/ j4 }: \  p, n9 C( Q8 k. xto the unintentional exposure to androgen gel used by
3 m' h( n$ [- n$ k/ ~! ]the father. The family initially concealed this infor-) K0 o5 d2 @5 G8 f
mation, resulting in an extensive work-up for this
5 x: F' u/ h4 Q' g9 b( X: P1 P1 _child. Given the widespread and easy availability of$ H8 G8 Y$ t; N/ u: v
testosterone gel and cream, we believe this is proba-
6 N+ w2 D( o- ^+ Kbly more common than the rare case report in the& A" j7 q& T# f
literature.41 W9 F( ?. T2 o" a0 v' \0 L
Patient Report; ]6 G1 L6 s' Y( E
A 16-month-old white child was referred to the
3 @( U+ ?2 y: i) E9 T* h9 Tendocrine clinic by his pediatrician with the concern' D4 W- Q$ N: I0 {
of early sexual development. His mother noticed3 \2 ]& G0 U- d
light colored pubic hair development when he was
6 i! E/ n( ^. L& c/ c. n2 X! qFrom the 1Division of Pediatric Endocrinology, 2University of  f  P! V8 H9 r
South Alabama Medical Center, Mobile, Alabama.6 \  I' F! y  a& l
Address correspondence to: Samar K. Bhowmick, MD, FACE,+ K: Y" p# P  d
Professor of Pediatrics, University of South Alabama, College of
% k6 c( t7 y& y4 cMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
: X& ?2 @) E3 ^$ Z  We-mail: [email protected].
& v- y! _! N3 i+ l" }about 6 to 7 months old, which progressively became
. ~2 M: y, \, {8 Udarker. She was also concerned about the enlarge-) S8 |, }: Y6 ~  B; Q0 z
ment of his penis and frequent erections. The child
4 b8 p% _" C0 x1 x% Owas the product of a full-term normal delivery, with  ^; n$ Y# c; C/ q4 l
a birth weight of 7 lb 14 oz, and birth length of
2 l# B: L! m) t5 w) w20 inches. He was breast-fed throughout the first year/ T. ]) o) y- c% ^4 s$ |8 h
of life and was still receiving breast milk along with; w$ ~- q, H5 m
solid food. He had no hospitalizations or surgery,
3 B) F" R9 ^: X6 S/ hand his psychosocial and psychomotor development8 p7 E1 \9 f; t
was age appropriate.+ L2 k; c* \( Z, P& H+ o- T/ z
The family history was remarkable for the father,
! k7 u! O5 ^3 [/ \+ N. awho was diagnosed with hypothyroidism at age 16,
% o% Q6 l  c! P4 Nwhich was treated with thyroxine. The father’s5 v! q9 L! ~4 @  l
height was 6 feet, and he went through a somewhat$ S/ w7 e* P- ~) a; ?% h7 V5 Y
early puberty and had stopped growing by age 14.: J- G( m+ y7 m; b9 R# w! N. l3 r
The father denied taking any other medication. The/ W' X% Y8 r9 K7 I/ \5 e) A
child’s mother was in good health. Her menarche
) e$ d5 a; P( {; w- r! y* jwas at 11 years of age, and her height was at 5 feet5 Q# U: B1 j. Q/ _+ l: a
5 inches. There was no other family history of pre-
6 g& `% q0 a! i  ~" O# }* N/ p7 ~) \cocious sexual development in the first-degree rela-
2 c9 z( P& p+ u9 A3 mtives. There were no siblings.
% y/ |1 N2 G$ a( V  x$ BPhysical Examination
+ D0 P6 z* k! d4 f. tThe physical examination revealed a very active,
" @: |: o1 X# u$ ]6 t- q( J5 E  o  E8 iplayful, and healthy boy. The vital signs documented
9 J0 M# l8 }! M" Qa blood pressure of 85/50 mm Hg, his length was
) X  ]+ J5 P" X) x1 ]' m90 cm (>97th percentile), and his weight was 14.4 kg
. @$ B  L1 H# ?% q% ~5 ]: z" y: \  g(also >97th percentile). The observed yearly growth
7 }) e& p+ G: C: c* k" vvelocity was 30 cm (12 inches). The examination of
8 A% K5 H/ n3 _$ kthe neck revealed no thyroid enlargement.8 ]! X0 N; N% u/ D- ?6 ?
The genitourinary examination was remarkable for
8 t1 P# d9 n# Xenlargement of the penis, with a stretched length of9 R8 o* f1 W) c
8 cm and a width of 2 cm. The glans penis was very well
# l* {+ H$ a! o4 c) Jdeveloped. The pubic hair was Tanner II, mostly around
& I2 w! \* t/ Q540
  D6 M3 h9 a% zat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
4 C* _9 p1 Q$ a  R# vthe base of the phallus and was dark and curled. The0 B" r! S; k  D5 u: @
testicular volume was prepubertal at 2 mL each.  L7 b$ y" j8 Y+ ^; x, q
The skin was moist and smooth and somewhat
" T( q5 c3 H, ioily. No axillary hair was noted. There were no
1 S. M/ N5 i+ C2 c% w8 Tabnormal skin pigmentations or café-au-lait spots.
4 h6 F- D: Q4 W5 A, zNeurologic evaluation showed deep tendon reflex 2+  r  [) Z7 i5 e$ F
bilateral and symmetrical. There was no suggestion$ |, l& Z2 ]" H! F* ?
of papilledema.; a; M% r! K5 `6 ^9 q! k/ l, ^
Laboratory Evaluation
/ N% O/ Q) R# N4 q  UThe bone age was consistent with 28 months by  k/ N% W- ?# U9 \+ d2 o8 s
using the standard of Greulich and Pyle at a chrono-+ f, f- Z1 t& |; E
logic age of 16 months (advanced).5 Chromosomal
3 A1 j  k9 W; J- V* G- w$ x6 ?& dkaryotype was 46XY. The thyroid function test
, P4 p8 r4 d# ]; @5 ]* kshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
0 o; a% ~) l8 v# s: Ilating hormone level was 1.3 µIU/mL (both normal).
  g; G$ @! I2 X& M( b' ^The concentrations of serum electrolytes, blood
" a* W0 b6 R* @3 J+ Lurea nitrogen, creatinine, and calcium all were
( l: N1 t( ^% c! o7 s+ qwithin normal range for his age. The concentration
* K  u6 E. Z9 Z5 B) rof serum 17-hydroxyprogesterone was 16 ng/dL: F6 P) b1 g% Q  c
(normal, 3 to 90 ng/dL), androstenedione was 207 l  o1 e% F8 w& d7 }
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
( O0 x  N5 C! J1 }5 c/ _1 q/ jterone was 38 ng/dL (normal, 50 to 760 ng/dL),! N1 e2 F6 Y0 I$ x2 J0 F& d
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
4 d  U. ]1 E4 M49ng/dL), 11-desoxycortisol (specific compound S); X2 \; f) Y2 y7 _+ Z2 _. {
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
7 ~8 \" `" l: O' B* r, ]tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
3 T/ [8 w  _2 x% p- i" E& N; Q7 etestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
1 X/ b9 [6 `, ~4 I8 D! i% P: oand β-human chorionic gonadotropin was less than% C" K! |4 E+ j# I1 k) Q
5 mIU/mL (normal <5 mIU/mL). Serum follicular1 T& S/ V0 Y1 l! m( L9 I6 P8 V
stimulating hormone and leuteinizing hormone' a! J9 p; `% K( k2 v6 `
concentrations were less than 0.05 mIU/mL
) k% N  @- k* k) @(prepubertal).% F0 _; g  j/ f. [2 `' X7 R9 t
The parents were notified about the laboratory: T( K, d9 A# R# i" r
results and were informed that all of the tests were
; B/ H+ K' j0 G- m0 g! _( unormal except the testosterone level was high. The
" F$ q2 Z& K( x8 ufollow-up visit was arranged within a few weeks to
/ c" D. ~* ^8 i3 Yobtain testicular and abdominal sonograms; how-
' b( }0 r( q1 ]2 Q" Aever, the family did not return for 4 months.
6 Z* E" i7 i9 s* @1 `0 g7 B* JPhysical examination at this time revealed that the
1 \5 N: ^6 x) kchild had grown 2.5 cm in 4 months and had gained
) _2 I  S' W2 t$ U; H2 kg of weight. Physical examination remained; H6 ]0 A  L0 n  B
unchanged. Surprisingly, the pubic hair almost com-
8 }$ q9 s2 _' [* }5 x0 ]9 Z6 jpletely disappeared except for a few vellous hairs at1 R/ W) t8 n6 l' b" c" m
the base of the phallus. Testicular volume was still 23 x7 ?3 p* G$ O+ I" N1 h& S$ z
mL, and the size of the penis remained unchanged.
4 y& |' W; K1 QThe mother also said that the boy was no longer hav-/ M# d, H) ]9 g. j5 l
ing frequent erections.6 f) b  N- A5 U6 q2 l( q  t' p
Both parents were again questioned about use of5 p/ ~2 ?) S7 z% P, m
any ointment/creams that they may have applied to6 G$ H4 Y; g( }  J! p
the child’s skin. This time the father admitted the' B9 K8 Y1 a# @* E
Topical Testosterone Exposure / Bhowmick et al 541
/ K5 a5 ^4 z' w8 E+ d, L' d8 ause of testosterone gel twice daily that he was apply-
, I7 _4 `: [3 t# N  `ing over his own shoulders, chest, and back area for
' d8 |$ s7 L  D. na year. The father also revealed he was embarrassed, ?' ^5 }+ H. w# z4 u4 D
to disclose that he was using a testosterone gel pre-
. t: A8 t; t( ^7 n) }scribed by his family physician for decreased libido3 S  `$ l  b0 }7 P
secondary to depression.+ F* g5 r  I7 C  ?  E7 T* L
The child slept in the same bed with parents.
, d% e( f: h1 a3 @+ {& M: u* C/ ZThe father would hug the baby and hold him on his
  M: q) O, ~, }& f& _% A0 |' schest for a considerable period of time, causing sig-
. Y: k$ X5 V0 A5 o! Nnificant bare skin contact between baby and father.
/ g6 @& D$ S- G: \The father also admitted that after the phone call,
. d! `$ w& h0 c4 I# @3 cwhen he learned the testosterone level in the baby
% P* ^1 f9 j5 e" x: E9 y, Xwas high, he then read the product information
2 G9 x5 B! V  K; B1 Q7 D; |- K9 rpacket and concluded that it was most likely the rea-3 b! p9 G# B% _) \' m: g( I$ G' h
son for the child’s virilization. At that time, they
' O2 i3 i5 m8 Z0 r* Zdecided to put the baby in a separate bed, and the
5 [: m8 x0 `2 p1 \3 R1 |father was not hugging him with bare skin and had( S0 V1 K7 I# ]( G9 c) [, k. ?
been using protective clothing. A repeat testosterone+ f: p( G9 w, P. X9 o
test was ordered, but the family did not go to the* L& P% w, g, b8 D; ~# ?# l6 D
laboratory to obtain the test.9 w% ~: j! B/ ]) d! q: d; u" T
Discussion5 v$ T3 c3 {/ P6 C. q1 {
Precocious puberty in boys is defined as secondary% m- `# a4 y$ W# L. C2 p" H
sexual development before 9 years of age.1,45 S" Z9 s. Q3 d" X" k
Precocious puberty is termed as central (true) when
% h& {1 a% E9 a) _: v" ~- j( Yit is caused by the premature activation of hypo-1 y% a5 s/ _: c; S0 J
thalamic pituitary gonadal axis. CPP is more com-
3 X5 c# q( z: c& Gmon in girls than in boys.1,3 Most boys with CPP4 }$ u* T# g% ^' }$ `
may have a central nervous system lesion that is
4 W$ r9 D# }% J6 |: k- Qresponsible for the early activation of the hypothal-$ o4 _% W" `# F# Q4 m: I" b
amic pituitary gonadal axis.1-3 Thus, greater empha-' Y+ {0 _0 d* C, I
sis has been given to neuroradiologic imaging in
  T" R4 \6 J4 {! D9 a; A* J- eboys with precocious puberty. In addition to viril-
0 f, z* b; X9 K) L7 S9 ]& uization, the clinical hallmark of CPP is the symmet-
: |7 {. a  ?2 H) v) y2 t8 Q" Erical testicular growth secondary to stimulation by+ W- e0 F7 V% n. O; g
gonadotropins.1,3* }  y$ V9 ]2 r% M
Gonadotropin-independent peripheral preco-
% P. ~( I  s/ G# R; C7 Hcious puberty in boys also results from inappropriate
% u3 }1 v6 U; Iandrogenic stimulation from either endogenous or5 E' x* |0 r, R0 u
exogenous sources, nonpituitary gonadotropin stim-
0 F) B6 `) g; l9 B/ Fulation, and rare activating mutations.3 Virilizing
0 d; w: i* {3 d7 I/ D+ _: v- T* econgenital adrenal hyperplasia producing excessive
0 d+ [% w1 p/ madrenal androgens is a common cause of precocious/ }9 s! ~6 V: E; ]$ a' o& L3 l
puberty in boys.3,4
" J: S. t2 }2 U3 b1 R+ uThe most common form of congenital adrenal
; \, a) U. F- P% }! g6 {hyperplasia is the 21-hydroxylase enzyme deficiency.
  }) C. N& y/ d0 q, rThe 11-β hydroxylase deficiency may also result in
0 k9 I5 q8 f5 h, w$ Vexcessive adrenal androgen production, and rarely,
$ L; \+ ~6 ~$ m8 r- H# uan adrenal tumor may also cause adrenal androgen6 w+ U- o  w9 A* f' P: z
excess.1,3. l, x$ M2 G3 a! J# D/ B
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
  Q) z$ D* ?# `+ f% K9 F3 w542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
  S/ S( Z1 S/ T. zA unique entity of male-limited gonadotropin-
. N: d' E. n) @" @$ uindependent precocious puberty, which is also known
2 T/ R. s& }1 {& Fas testotoxicosis, may cause precocious puberty at a. m& u; X2 g, C1 w! K' r
very young age. The physical findings in these boys
  W: N* \% M) B7 J, `& r4 S1 hwith this disorder are full pubertal development,. C& M+ ?: |' L! W6 U1 Q
including bilateral testicular growth, similar to boys4 [! T6 g) l# V( H+ n, b! q' R1 z
with CPP. The gonadotropin levels in this disorder0 b! W& K8 O4 d$ h4 b$ s+ k( H, p
are suppressed to prepubertal levels and do not show
0 q% E6 b/ h- |pubertal response of gonadotropin after gonadotropin-$ R% X) g2 W+ s
releasing hormone stimulation. This is a sex-linked
: X8 U: ], e% s0 [autosomal dominant disorder that affects only
6 a% N( N! O- ]. s- A3 j$ smales; therefore, other male members of the family
# Y% o: l5 W/ U$ `0 X2 p# omay have similar precocious puberty.39 g, c! U; d+ W. x
In our patient, physical examination was incon-
) X4 {0 V. }% T* x( b' Jsistent with true precocious puberty since his testi-
3 n1 s3 }0 B3 Fcles were prepubertal in size. However, testotoxicosis8 \7 F1 p; ^" H+ g( z. q/ ~* a
was in the differential diagnosis because his father
7 ]+ L: t9 F0 ?+ u# pstarted puberty somewhat early, and occasionally,
/ ~" i" ^0 p! l# V: I% I" t% w$ Etesticular enlargement is not that evident in the
6 j& z  o. K$ A$ X* Ebeginning of this process.1 In the absence of a neg-! D, ~, f# T. |: K, `
ative initial history of androgen exposure, our: w7 H. [7 ]3 G+ {
biggest concern was virilizing adrenal hyperplasia,
$ o# ]& z0 S: _2 s& w8 Qeither 21-hydroxylase deficiency or 11-β hydroxylase
7 Z- B# K+ K) U4 H8 o3 ]8 Pdeficiency. Those diagnoses were excluded by find-
' t4 P1 ^8 j, G# b/ R* eing the normal level of adrenal steroids.
: V# @3 _( h/ D- t5 YThe diagnosis of exogenous androgens was strongly
0 I. T3 z! a5 k/ G2 T1 b8 e7 ksuspected in a follow-up visit after 4 months because, g  c& m8 Y4 F/ {
the physical examination revealed the complete disap-
; e  p: R5 u  F7 t7 O% O% Tpearance of pubic hair, normal growth velocity, and
% P8 T2 O$ _2 [decreased erections. The father admitted using a testos-6 e1 g4 q' l9 L! j  m  e0 U& P
terone gel, which he concealed at first visit. He was& a( l# G7 E, d; l" x( R& O3 Y
using it rather frequently, twice a day. The Physicians’
% W5 Z2 m- C- g: f+ V+ `3 e' GDesk Reference, or package insert of this product, gel or9 P7 A4 [' C# O" }$ D' c
cream, cautions about dermal testosterone transfer to
# P5 Q' G" W$ Z  @; yunprotected females through direct skin exposure.7 d; T5 p/ [9 F% Y  c' u1 c3 B
Serum testosterone level was found to be 2 times the
$ o) y/ R3 r2 C9 y# Y! M. Ubaseline value in those females who were exposed to
+ L' \% ]: ]: Ceven 15 minutes of direct skin contact with their male
: Y5 Q/ k" e/ B9 e* spartners.6 However, when a shirt covered the applica-
" D. _# j' r  y9 g) Z6 ption site, this testosterone transfer was prevented.
8 a+ z* c" t! i) g5 ]1 COur patient’s testosterone level was 60 ng/mL,5 g' A- i( K$ c0 b' u% }# I
which was clearly high. Some studies suggest that
/ W' B9 W- Z) a6 ?' z$ X5 cdermal conversion of testosterone to dihydrotestos-' f0 P2 b. F8 D$ U
terone, which is a more potent metabolite, is more; b0 ^+ t# C4 y( B) x
active in young children exposed to testosterone5 @# j; p: D+ @$ J* S
exogenously7; however, we did not measure a dihy-: }9 I, ~+ R" s, \8 F* g% I1 t8 E
drotestosterone level in our patient. In addition to; t2 l; p: j! Z6 {) ~
virilization, exposure to exogenous testosterone in
# t" C% E; q' g& ^  o' V" echildren results in an increase in growth velocity and
/ N; U- Q5 [& ^9 L$ d4 {6 Iadvanced bone age, as seen in our patient.9 @% c7 d" k2 {: Q) ]
The long-term effect of androgen exposure during5 y9 D( Y) D  Q( k/ B) C* n: \
early childhood on pubertal development and final3 V; l8 R8 i/ I4 u8 n- x$ Y: L
adult height are not fully known and always remain
% F$ b3 m( e' b) ia concern. Children treated with short-term testos-
" o; z/ [2 `* |* x% mterone injection or topical androgen may exhibit some
% E/ R: |( q7 n9 kacceleration of the skeletal maturation; however, after
! l/ }3 u) {8 \6 jcessation of treatment, the rate of bone maturation/ ?8 z9 m! z* b) e7 M5 u0 y
decelerates and gradually returns to normal.8,91 Q" V, E6 [0 p# N- \. o! y# p
There are conflicting reports and controversy) r( b$ B" N$ ?6 a
over the effect of early androgen exposure on adult
: G" _# ^" R' R6 s) x* i- o" Cpenile length.10,11 Some reports suggest subnormal
  d- j6 c+ j, Xadult penile length, apparently because of downreg-
* I" A; ?* X% aulation of androgen receptor number.10,12 However,
; d  H- @( _, j% z; J/ f2 h! h$ tSutherland et al13 did not find a correlation between
; y# a1 M8 g/ B+ j- Bchildhood testosterone exposure and reduced adult
- J6 r+ T8 L/ {  z7 Mpenile length in clinical studies.! o: \+ a( g! r  w
Nonetheless, we do not believe our patient is% s, {0 `; o5 m, d. H0 `
going to experience any of the untoward effects from
* b1 E+ h" l# y5 n, \testosterone exposure as mentioned earlier because
" N6 K5 k4 t0 j- {$ _; }* M$ }the exposure was not for a prolonged period of time.
& Q  c% V/ r) O3 ?, S2 X- G, O( _Although the bone age was advanced at the time of
: `' d7 h+ U  n& X  z+ Q) D# qdiagnosis, the child had a normal growth velocity at, x! n4 I$ E6 d
the follow-up visit. It is hoped that his final adult
% w2 A' l4 c0 \& [height will not be affected.7 a) Z0 E' S- D2 X- H# O! y, c
Although rarely reported, the widespread avail-
- ]: S/ v8 E' R& c( w$ F$ Fability of androgen products in our society may0 R+ f( Q' r1 B) L' h
indeed cause more virilization in male or female! T) a. g0 @0 I( w, P/ I6 n
children than one would realize. Exposure to andro-, ?; r2 `3 ~& w+ @- ^4 i
gen products must be considered and specific ques-
# h  M1 o3 z, j. x$ y# ~5 }2 Rtioning about the use of a testosterone product or
3 R& x8 R+ b9 u. j9 Y. C* u. E3 @/ \, ?/ jgel should be asked of the family members during
8 F8 l/ ?  e# q6 kthe evaluation of any children who present with vir-/ R- P/ T6 i: R: Y
ilization or peripheral precocious puberty. The diag-
6 ]/ u( e# o2 B5 q) Tnosis can be established by just a few tests and by; U4 J1 W  X# ]- m( s6 m
appropriate history. The inability to obtain such a8 c* A$ N8 u) D) {' P, d
history, or failure to ask the specific questions, may0 W. W' R+ Z/ v+ M( c* R" ~% i- \
result in extensive, unnecessary, and expensive
$ n8 F. ?" B: Q# Y9 kinvestigation. The primary care physician should be. m- Z& m6 \& A9 l* N' L, U7 `
aware of this fact, because most of these children1 m+ ]& T' s1 h
may initially present in their practice. The Physicians’* w% [7 l6 k% L/ |4 k2 f, v: a6 F8 R
Desk Reference and package insert should also put a& L, f4 E- M. w0 n
warning about the virilizing effect on a male or* G4 A' W0 u  }- c1 H& s7 B
female child who might come in contact with some-2 W5 h. u! ]3 Z' {: l- t
one using any of these products.5 b; g# r( W4 u* f5 h
References
7 E, w5 r* S- g1. Styne DM. The testes: disorder of sexual differentiation! C$ L' i) a3 n$ d
and puberty in the male. In: Sperling MA, ed. Pediatric5 t3 D# j8 x6 T6 |1 \, [  Y
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
3 `# d2 B0 O1 Y3 G4 {6 }! _2002: 565-628.+ x4 E* R( a8 v
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
0 `3 I8 }6 V. Upuberty 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
! `) M* U$ I5 g  |. t3 m, nBoy Induced by Indirect Topical; h2 K, [- x) m* e/ ?
Exposure to Testosterone
, U6 v: [+ E+ r7 _; dSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2& C5 U6 ~, Z# P6 r# W5 K# d
and Kenneth R. Rettig, MD1
/ Z# B1 Z& `& h  sClinical Pediatrics2 w' V& b7 u, E& q/ B- m
Volume 46 Number 6$ T  A2 I0 P& q- M3 |7 n; B# w; S
July 2007 540-5432 f; s. R6 p4 l' |+ G1 Y
© 2007 Sage Publications
+ s2 L0 G; v( E7 t, t/ N& {7 h4 x10.1177/0009922806296651; L4 a2 O+ S& e' M0 M! r) @
http://clp.sagepub.com2 z2 _) Q8 ?: U! w
hosted at) r, ~3 K' {9 j" d6 U4 y
http://online.sagepub.com' f, E1 T) ^4 w0 B( x5 z$ O
Precocious puberty in boys, central or peripheral,
" c4 `! \! a& u# F  uis a significant concern for physicians. Central
" e- f4 E7 s! y  h! Gprecocious puberty (CPP), which is mediated
' r5 r9 X' D. E: L1 _) n, athrough the hypothalamic pituitary gonadal axis, has6 d7 i: }9 X; ?/ b+ Z- G
a higher incidence of organic central nervous system
8 k+ ^6 t+ c: @* U0 t( Mlesions in boys.1,2 Virilization in boys, as manifested
' O! {& X# N9 \4 ^) Hby enlargement of the penis, development of pubic
9 ^+ O6 D! e$ N  ~hair, and facial acne without enlargement of testi-
  I; e; J- _0 ^6 {. O) Gcles, suggests peripheral or pseudopuberty.1-3 We) Y  `4 I; s( @
report a 16-month-old boy who presented with the1 \% A% I# X3 E
enlargement of the phallus and pubic hair develop-; ^% Z& |: t. C6 R( ~: ~
ment without testicular enlargement, which was due( ]+ t* d' z3 Q$ ?  s7 M
to the unintentional exposure to androgen gel used by
: E, B1 C8 U- p  }' N" A1 P- ?8 @the father. The family initially concealed this infor-( J2 W' t$ x7 p- U4 v/ Y0 T
mation, resulting in an extensive work-up for this, [; u1 i. q; |0 [# N! \% ~7 E: S
child. Given the widespread and easy availability of
  k. X0 ^$ F7 G& K1 Ytestosterone gel and cream, we believe this is proba-
7 x8 ~4 G' f7 H$ N: t8 Y' Ibly more common than the rare case report in the
# ^7 s- w$ \  g- }literature.4; v8 \0 X6 S6 z( ~( ]6 g
Patient Report
6 c! ^- C. u( X" t) C" y& kA 16-month-old white child was referred to the
8 `, K5 h' W4 e; Wendocrine clinic by his pediatrician with the concern; T. `" J! Z6 U0 }. P
of early sexual development. His mother noticed
' G+ W# Q9 q8 l, H8 }$ {light colored pubic hair development when he was
  b- k% J0 ]5 [% ~From the 1Division of Pediatric Endocrinology, 2University of; B2 P7 ?, e2 G# K
South Alabama Medical Center, Mobile, Alabama.
0 @$ g2 c' H* U6 w2 H* uAddress correspondence to: Samar K. Bhowmick, MD, FACE,3 C" S/ \" R1 ^0 H! T! b
Professor of Pediatrics, University of South Alabama, College of
+ |8 f/ A9 F9 D. KMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
: Z% }% Z% w2 m# Fe-mail: [email protected].
5 d& e! K" B2 labout 6 to 7 months old, which progressively became
5 j+ Q6 ^: s, Y# udarker. She was also concerned about the enlarge-& q" a* ^. l2 e- c
ment of his penis and frequent erections. The child
% v; p0 h5 t7 A# K; ^2 W; c( Vwas the product of a full-term normal delivery, with
8 O# Z6 D8 S1 Fa birth weight of 7 lb 14 oz, and birth length of( V; `( u/ Z) o" `2 Y
20 inches. He was breast-fed throughout the first year" v; g( R) E# `+ Y% c0 |( w! G& f8 H3 `
of life and was still receiving breast milk along with
9 _* U1 X/ W5 S4 G1 dsolid food. He had no hospitalizations or surgery," u1 C7 b) C4 k; y3 i0 `
and his psychosocial and psychomotor development
5 K' u+ K$ J9 f0 W9 ywas age appropriate.
2 \+ {; w# |; N# v2 nThe family history was remarkable for the father,: `$ Z! x) X; _" Q( C
who was diagnosed with hypothyroidism at age 16,
) @7 V0 ^  C/ k* x/ D9 _  @2 Xwhich was treated with thyroxine. The father’s
# O: B# E$ ?) X8 f, K7 L# {' |height was 6 feet, and he went through a somewhat3 D  z. q: v5 J$ s  P$ E: X
early puberty and had stopped growing by age 14.
6 E2 p+ L3 Q! X, U) ZThe father denied taking any other medication. The
5 ]1 y  k% C- `4 M6 ^# T6 `child’s mother was in good health. Her menarche7 l! }6 L, N" P! E* b" i- E3 @
was at 11 years of age, and her height was at 5 feet
6 V& s3 I. d. k) H7 z5 inches. There was no other family history of pre-9 h- A- Z4 E4 m% r+ o
cocious sexual development in the first-degree rela-$ U9 L1 v, Y; s5 `0 u6 C
tives. There were no siblings.1 ~9 A) H" m( _
Physical Examination, t  t& f+ p, l% h1 x
The physical examination revealed a very active,* @: A& I* T8 n7 F6 N, ]) c* U( U
playful, and healthy boy. The vital signs documented
+ z: O/ ?& [/ K( z2 n& _a blood pressure of 85/50 mm Hg, his length was
$ ^# x) ?! t9 E6 l& N9 I8 `90 cm (>97th percentile), and his weight was 14.4 kg
9 v( E! ?  T$ N3 S$ G5 p(also >97th percentile). The observed yearly growth9 f5 l4 q/ J$ d9 e' c( r
velocity was 30 cm (12 inches). The examination of
9 k6 [# ?+ b7 [, `, M7 Dthe neck revealed no thyroid enlargement.
  K* t9 H7 P! ?The genitourinary examination was remarkable for
8 T( c7 G$ V- }& R9 Lenlargement of the penis, with a stretched length of
' @/ m3 ~0 [$ G% r( r! s5 v8 cm and a width of 2 cm. The glans penis was very well
: Q# {+ v7 N$ c2 L8 N  ?developed. The pubic hair was Tanner II, mostly around
8 i5 A7 |$ b/ x) q, z5401 I2 {  Y* p3 ]1 x4 s
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
* ]8 G: S0 J# v% \* g+ N/ Wthe base of the phallus and was dark and curled. The- U; n' k4 X+ n( R! H
testicular volume was prepubertal at 2 mL each.
1 Z+ x/ Y- Y+ u! ^5 xThe skin was moist and smooth and somewhat6 O0 T1 E1 F1 d4 O1 d& h
oily. No axillary hair was noted. There were no7 B- k$ ^5 `- d5 r
abnormal skin pigmentations or café-au-lait spots.( w; o; T2 Q; Y# f3 i3 D& o0 U
Neurologic evaluation showed deep tendon reflex 2+  _6 d9 q  |8 v9 {2 v
bilateral and symmetrical. There was no suggestion2 [( E6 d5 b7 k6 Z" G. |5 o
of papilledema.. q$ b* t+ S0 w* L: E4 ^7 P* |
Laboratory Evaluation; V. S! M$ S$ j* ]) J
The bone age was consistent with 28 months by  Y; L5 i: Y4 C# p
using the standard of Greulich and Pyle at a chrono-6 v6 `/ v/ ]3 c1 h2 h" d' E
logic age of 16 months (advanced).5 Chromosomal9 a/ {$ N* U1 `5 Z+ B; m/ {
karyotype was 46XY. The thyroid function test
4 O+ x& u# F: @showed a free T4 of 1.69 ng/dL, and thyroid stimu-
. Z3 a: n5 w/ U, f% y9 blating hormone level was 1.3 µIU/mL (both normal).( S8 \  v) c) t- k. u- [4 t* L
The concentrations of serum electrolytes, blood
' S! U/ w2 H1 c. J6 Z2 aurea nitrogen, creatinine, and calcium all were
- ]( l( R7 c7 Bwithin normal range for his age. The concentration
4 r+ P: r7 y9 ?+ o8 w0 Q! Z* j( Dof serum 17-hydroxyprogesterone was 16 ng/dL
) t5 E. K' Z2 n(normal, 3 to 90 ng/dL), androstenedione was 20
2 a% Y/ O9 ]  M0 Dng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-- E& d3 T: E/ h( ~: U& w
terone was 38 ng/dL (normal, 50 to 760 ng/dL),) K, V, }9 B" U2 T. {
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
; L9 N6 M/ d5 o& O" N8 _& c49ng/dL), 11-desoxycortisol (specific compound S)& [; S$ ]& c1 b) V
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-* B; a/ b% s2 E3 i5 t% f8 T7 f
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total9 z, F8 O& ~3 ?! q
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),  d: g, Q( ~5 A
and β-human chorionic gonadotropin was less than' y4 W) m: x4 @" Z! q7 {, v
5 mIU/mL (normal <5 mIU/mL). Serum follicular
7 d, o; S' C- n( }3 G& s# lstimulating hormone and leuteinizing hormone
# [7 G% `# L6 g& h2 t+ }9 n7 Jconcentrations were less than 0.05 mIU/mL, p6 b! \  m9 P" M2 c
(prepubertal).
4 G; q; ^. [+ jThe parents were notified about the laboratory4 q& Y  T( c4 R  S9 T  |3 j
results and were informed that all of the tests were
6 I5 w. e; h+ O7 E" |normal except the testosterone level was high. The+ L/ A; o( D+ }
follow-up visit was arranged within a few weeks to( b0 k' ?& G. ^3 h& j# {
obtain testicular and abdominal sonograms; how-8 l4 _3 E& W: x. Z- s
ever, the family did not return for 4 months.! I1 v4 k. r3 J
Physical examination at this time revealed that the
" z5 }( }' p) z* ]child had grown 2.5 cm in 4 months and had gained+ e+ N4 I2 V. {' f, N4 e+ h8 U
2 kg of weight. Physical examination remained- m9 n( u/ F) Y0 j
unchanged. Surprisingly, the pubic hair almost com-
. v. F9 M+ Z) hpletely disappeared except for a few vellous hairs at
) G, i( i, G. Qthe base of the phallus. Testicular volume was still 2
8 A) ^1 f5 a9 ?0 {* ^& d3 QmL, and the size of the penis remained unchanged.# W5 c; y' K& q0 P
The mother also said that the boy was no longer hav-
" ]4 J9 _0 s* Z, Uing frequent erections.: s4 d8 i: M8 S
Both parents were again questioned about use of1 E  M9 N' |% t
any ointment/creams that they may have applied to8 V" I& a0 H' T
the child’s skin. This time the father admitted the: t: Z; B. ?7 Q; y. Q
Topical Testosterone Exposure / Bhowmick et al 541
5 {; v( R2 `+ `6 {use of testosterone gel twice daily that he was apply-0 J( n: P3 j$ r1 U5 f# B
ing over his own shoulders, chest, and back area for+ p" Z( w) g( ^& `! ~9 \7 u
a year. The father also revealed he was embarrassed
; E: p+ P1 Y) ?% q0 a8 F/ V: Xto disclose that he was using a testosterone gel pre-
( S4 r: }4 {) {, B. pscribed by his family physician for decreased libido1 }6 n* Y0 _" n8 D0 s! j5 w
secondary to depression.
; D& J( i: @  P0 ~6 d! dThe child slept in the same bed with parents.
- r9 s: O7 r8 ]. U, W3 HThe father would hug the baby and hold him on his5 r2 a: X8 y5 ]. S6 {
chest for a considerable period of time, causing sig-, S* V7 @  M$ Z1 V% t5 h
nificant bare skin contact between baby and father.
0 m' [( @6 e. P+ b3 cThe father also admitted that after the phone call,7 G  y$ b2 D. L1 Q, c* ~
when he learned the testosterone level in the baby( ^# U' @: u$ D; f5 B
was high, he then read the product information
* I/ E& r; S$ s* Upacket and concluded that it was most likely the rea-
/ I3 p7 d! L5 A. J8 c3 R1 gson for the child’s virilization. At that time, they7 I. y) p/ N0 ^3 K
decided to put the baby in a separate bed, and the
, w6 @" e. q: g) Hfather was not hugging him with bare skin and had
* A, A- {* _0 T) n0 sbeen using protective clothing. A repeat testosterone7 {% Z: U( i6 D, K3 w) Y2 {
test was ordered, but the family did not go to the4 z; J6 ]6 n! E% r
laboratory to obtain the test.
  K9 h- J- {2 d7 |1 cDiscussion
" l7 h" U' h  c. QPrecocious puberty in boys is defined as secondary, y! l& p: ]* C5 g4 i5 ^
sexual development before 9 years of age.1,4
* ?! b6 m' x# l6 J+ e2 n9 b$ e7 bPrecocious puberty is termed as central (true) when3 u8 `. W$ r& h! T; c1 Y' Y; Y- ~) u
it is caused by the premature activation of hypo-( H& M. L( n; I& C
thalamic pituitary gonadal axis. CPP is more com-
& O7 t7 ]  L% v6 J# B9 Rmon in girls than in boys.1,3 Most boys with CPP
4 D3 ^, G! a( amay have a central nervous system lesion that is
0 Y% O  U4 h8 Z6 V8 ], Kresponsible for the early activation of the hypothal-
0 m, W2 j4 M; a+ P. f3 n- Namic pituitary gonadal axis.1-3 Thus, greater empha-1 a8 p3 T* ~+ T) |% S
sis has been given to neuroradiologic imaging in8 v$ J  x  y6 L% z1 M7 r" c# ?" L
boys with precocious puberty. In addition to viril-/ Q& E$ N! P6 a. p' {2 I# q
ization, the clinical hallmark of CPP is the symmet-  t& m: ~7 r3 B( u
rical testicular growth secondary to stimulation by
/ B/ R! K! D- N/ S" V6 p, [/ W1 tgonadotropins.1,3
; m) i( l8 ^9 x, f" @Gonadotropin-independent peripheral preco-
& Q! u+ I: U* B- O( lcious puberty in boys also results from inappropriate
1 D7 Z3 u& Y+ {androgenic stimulation from either endogenous or4 `6 o5 i/ W5 y
exogenous sources, nonpituitary gonadotropin stim-$ ?4 n7 s* _+ z5 F  Q
ulation, and rare activating mutations.3 Virilizing
' ^" k7 v9 y% ?- P- kcongenital adrenal hyperplasia producing excessive
, t2 y9 y6 L$ _3 Q6 e5 H; T7 Badrenal androgens is a common cause of precocious
5 }: R) n$ E  u5 E% {8 X* T) Lpuberty in boys.3,4* V% t8 X8 b, Q4 Q; V* L5 F# z( `$ n
The most common form of congenital adrenal  p9 e; C. d) x' T  W* ~
hyperplasia is the 21-hydroxylase enzyme deficiency.) {8 |! `$ {4 j0 ~- ]$ R4 z: C) I
The 11-β hydroxylase deficiency may also result in/ c) J4 n4 C5 }) l
excessive adrenal androgen production, and rarely,5 }* q, x+ @9 Z' S( S) }
an adrenal tumor may also cause adrenal androgen
! m8 ~+ I  p  z# |9 xexcess.1,3
* V6 U% s4 q" f' a8 z, tat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
& U, U1 b  N! R9 [3 D4 y' z542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
0 W. W$ c0 Q% L( U4 D9 F, KA unique entity of male-limited gonadotropin-7 O- S9 k$ {5 y  z# P
independent precocious puberty, which is also known
' I& y/ I) \8 y' {/ H" o& |6 q0 @as testotoxicosis, may cause precocious puberty at a- I7 W" ?  S( R' d% ~
very young age. The physical findings in these boys
2 B6 [) U! p* ], p9 x5 Twith this disorder are full pubertal development,
  B- U! U7 T6 Q" H# J( M2 A. t8 q' fincluding bilateral testicular growth, similar to boys
) ^7 x" l3 @5 u( e" Twith CPP. The gonadotropin levels in this disorder
, k1 h8 T3 p; |. D: Y- R% Rare suppressed to prepubertal levels and do not show
9 D$ A5 P: S' l; T9 J5 g! m1 cpubertal response of gonadotropin after gonadotropin-8 U) W1 ?% d" C7 P+ I0 q/ @
releasing hormone stimulation. This is a sex-linked; _6 B8 x$ a5 f3 `# }  Y
autosomal dominant disorder that affects only
% c3 d; I1 p+ g$ d4 c1 t! M6 Mmales; therefore, other male members of the family3 l% S% B: s6 u! S) Y4 t
may have similar precocious puberty.33 ~2 O3 L3 I& q" ]; b; X) e1 j
In our patient, physical examination was incon-, l, u! r& }$ O5 O. a; b4 _
sistent with true precocious puberty since his testi-/ m) M! G* U; w( o
cles were prepubertal in size. However, testotoxicosis
# |5 {* a0 D: R9 n: _3 F7 |was in the differential diagnosis because his father9 T' m2 S8 ^$ y% H8 t
started puberty somewhat early, and occasionally," W% c0 I* q9 z
testicular enlargement is not that evident in the
5 D* u, n6 d' g  r, O+ }beginning of this process.1 In the absence of a neg-0 P* N" ~7 h- {5 j" S( _) Y4 o
ative initial history of androgen exposure, our+ O% ]0 s& h2 B+ x3 P+ H% G  F% U
biggest concern was virilizing adrenal hyperplasia,
5 _- s/ [4 Z9 h6 W5 f0 zeither 21-hydroxylase deficiency or 11-β hydroxylase
. d1 `4 t) P3 qdeficiency. Those diagnoses were excluded by find-
* P. J& [2 K. j: ying the normal level of adrenal steroids.) V' H; X' ~; |2 z, S" w3 t) d9 E7 N
The diagnosis of exogenous androgens was strongly+ S) r( x1 N$ [
suspected in a follow-up visit after 4 months because' m3 W% C- U- T( k. |- R( i
the physical examination revealed the complete disap-* }$ g- g& f6 U
pearance of pubic hair, normal growth velocity, and6 V( T# j4 I# y% B
decreased erections. The father admitted using a testos-
6 C2 _5 R8 [1 z) g. Q! ^terone gel, which he concealed at first visit. He was
  P0 v! g& w+ d& n- j8 Husing it rather frequently, twice a day. The Physicians’8 G: n! m6 Y$ J! _  ?7 U
Desk Reference, or package insert of this product, gel or
. q- L, |+ l$ p3 g$ @7 f+ \1 lcream, cautions about dermal testosterone transfer to7 b( ?3 o4 I, b. W
unprotected females through direct skin exposure.
8 a& e- C1 J8 v) O, ~Serum testosterone level was found to be 2 times the
% N- x- U, K. C+ t. }4 S' M( Lbaseline value in those females who were exposed to+ [$ P9 o  o! {" L7 V
even 15 minutes of direct skin contact with their male
6 v# `& M/ V, `2 N* [partners.6 However, when a shirt covered the applica-& i; G9 ?1 }  q  z' s) n) b
tion site, this testosterone transfer was prevented.
: ~9 z9 ^4 o# @3 YOur patient’s testosterone level was 60 ng/mL,! U! D5 D4 p! z' f  O" j* Q
which was clearly high. Some studies suggest that; O# g% a, }  }- {- i8 W5 ~
dermal conversion of testosterone to dihydrotestos-
- c) M# N3 n  T& rterone, which is a more potent metabolite, is more5 S$ L5 l5 K; Q8 y' W, v
active in young children exposed to testosterone; \' u: Z* f( r5 f. W* _# D; g
exogenously7; however, we did not measure a dihy-
" Y  p$ C$ j4 D" _3 z) Cdrotestosterone level in our patient. In addition to
' Q- m3 X) y5 {4 @* O- i3 Gvirilization, exposure to exogenous testosterone in
3 @- b$ r0 j* B2 c6 b* |( R; bchildren results in an increase in growth velocity and# G5 E4 L8 A+ G" K( D7 G. n( U
advanced bone age, as seen in our patient.2 `7 x( m7 O& b1 a  @/ O% V! |
The long-term effect of androgen exposure during0 h- h# @, i6 N# A) p0 |. B$ X
early childhood on pubertal development and final7 \! v+ y  J2 V4 X+ Y; i6 y; ~
adult height are not fully known and always remain3 `% o; y# h! Q) Y0 e8 h* l, B
a concern. Children treated with short-term testos-9 ^, `3 N6 C/ M  N4 X, u
terone injection or topical androgen may exhibit some
. G9 q% }% J1 H: ~( `' [acceleration of the skeletal maturation; however, after0 K% e, v) r) o% p
cessation of treatment, the rate of bone maturation. c. U0 O& b3 e4 g1 C% I" E  P
decelerates and gradually returns to normal.8,9/ |% c) u: @; G4 u; X
There are conflicting reports and controversy
( b* x/ R) K9 i7 wover the effect of early androgen exposure on adult9 ]* _5 w3 I/ D( k9 E1 o! i
penile length.10,11 Some reports suggest subnormal4 D3 j: ?1 r. O4 w$ U
adult penile length, apparently because of downreg-5 Q; q0 N# P1 ?: K0 t- L
ulation of androgen receptor number.10,12 However,
5 \" w) u9 O2 B* H3 S, X* @Sutherland et al13 did not find a correlation between  L( u3 }7 {* ?4 V
childhood testosterone exposure and reduced adult
5 Y& f, P2 ?3 v) Zpenile length in clinical studies.
  X( c( I4 e" A6 eNonetheless, we do not believe our patient is
/ H0 T' S" H+ x4 s0 J8 }going to experience any of the untoward effects from- k' \: G4 S! Y* f# |7 b/ K. ?
testosterone exposure as mentioned earlier because! H8 }- i; g( B9 ]7 }# @( w
the exposure was not for a prolonged period of time.
( w1 M2 r$ x- s% m/ OAlthough the bone age was advanced at the time of! G% e5 S0 [4 A" x" q
diagnosis, the child had a normal growth velocity at
6 D2 e' q1 j  t" E9 N- S6 ~the follow-up visit. It is hoped that his final adult( _- H5 p9 T4 y4 m0 Y( X! N
height will not be affected.
6 C8 G* Q, E2 g  zAlthough rarely reported, the widespread avail-- _) a- s7 t  [: v- E/ a% N$ t& O, |
ability of androgen products in our society may
) \; G$ x8 Z% T$ x  V* X: nindeed cause more virilization in male or female& ]2 D! h' v4 c
children than one would realize. Exposure to andro-
5 W( E# [+ }3 u' Qgen products must be considered and specific ques-
/ i1 s# t1 O" w. Z& @) A- `tioning about the use of a testosterone product or
# L. ~* |9 r& b1 ?gel should be asked of the family members during7 i3 w7 P+ l- i! }1 e5 {
the evaluation of any children who present with vir-0 E! f4 J6 C- Z& z
ilization or peripheral precocious puberty. The diag-
9 A7 P7 `- P4 l$ V1 P4 Dnosis can be established by just a few tests and by
5 C0 S+ r! y  d6 k* f+ Eappropriate history. The inability to obtain such a  h4 }& y* {5 T6 T5 ~( D" M
history, or failure to ask the specific questions, may0 ~* F" d9 j  R/ W
result in extensive, unnecessary, and expensive
, \, f3 g9 {; G; G4 {$ Sinvestigation. The primary care physician should be8 N  t! C* F; l  D. s' O
aware of this fact, because most of these children
  _; p. A8 R- f, {) x9 b$ ^) l7 nmay initially present in their practice. The Physicians’
. Z8 H, F" C$ N' {Desk Reference and package insert should also put a
5 O1 M. T! C9 g) P/ k; ewarning about the virilizing effect on a male or
) U0 B4 B  R' t) ^& a7 hfemale child who might come in contact with some-: T, U1 [4 X* U3 C/ ]0 [
one using any of these products.
0 y  F) u/ k0 c% n0 @7 R& G8 Z7 NReferences
& ^4 x" a! A- [# I5 [1. Styne DM. The testes: disorder of sexual differentiation
( F" I- D0 L7 U8 d' i% qand puberty in the male. In: Sperling MA, ed. Pediatric
2 U. p, ~/ e$ j+ eEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
% X# b/ n7 d- `  U. k; D2 f2002: 565-628.' G: w" Q5 \* m/ U- ^2 g! E' a: R
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
% v7 c  O$ P  Z; h3 apuberty 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

2 q7 c& `1 _7 l9 ]; f1 d' f6 L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