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
3 q# i- J' ^; o5 lBoy Induced by Indirect Topical, I2 U& E5 ?  Y% ]
Exposure to Testosterone" u, E& a* c/ {$ s+ [$ A8 ~
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
- e( R" @) V! {& e+ h; S0 ~6 g  [and Kenneth R. Rettig, MD1
& \2 b% k  F: `+ u) h3 h1 u7 EClinical Pediatrics
* s& d9 E0 i* W9 BVolume 46 Number 6# m3 T# L0 c  k( k$ t
July 2007 540-5433 d3 U* |6 O9 U  [9 U% X
© 2007 Sage Publications
0 y- z1 k) j" D+ l( U10.1177/00099228062966512 z( i+ E* M4 P9 Q' u
http://clp.sagepub.com
( S& y6 @1 b* ~! a5 U$ [hosted at8 O( O  `8 S, y# T4 f' _; r
http://online.sagepub.com
# X( o: J9 X& W: W; O) ePrecocious puberty in boys, central or peripheral,6 `- L% ]3 ?# S; J; j8 E
is a significant concern for physicians. Central
% h) C4 w- A% K) ?8 q6 Qprecocious puberty (CPP), which is mediated
( I! T  ], m7 q4 G8 y4 y& C; h0 `2 }through the hypothalamic pituitary gonadal axis, has
8 f0 _. n" O7 x. V( d$ ta higher incidence of organic central nervous system- o! [- e! M" D
lesions in boys.1,2 Virilization in boys, as manifested
3 C7 d& L. U* T- j. F# I/ y. hby enlargement of the penis, development of pubic
# P4 @$ {) _0 _5 U. Y' Vhair, and facial acne without enlargement of testi-# |2 N! M. a1 G% S
cles, suggests peripheral or pseudopuberty.1-3 We
3 J. T. X5 {4 r% R7 Q3 A& Treport a 16-month-old boy who presented with the
' @- Y" c7 I* h, k  F( K6 R4 henlargement of the phallus and pubic hair develop-: i- H  F) _+ C6 m( i
ment without testicular enlargement, which was due& n/ N9 {) ^( L% P2 j* z8 g
to the unintentional exposure to androgen gel used by
# o. i0 s- r3 A9 [$ y% D3 Wthe father. The family initially concealed this infor-( D' K0 W5 q* b' ]2 l7 G- a
mation, resulting in an extensive work-up for this
0 f) P( K  l* F' Nchild. Given the widespread and easy availability of0 j% ~" J# i3 p+ Q7 i, h/ L
testosterone gel and cream, we believe this is proba-7 o# X2 A6 H( q6 g* F
bly more common than the rare case report in the
$ o+ \' Z0 j: ?) Z% o7 S1 Pliterature.47 R8 l1 z) x) K. y# V: z
Patient Report* s0 t& }4 J, v4 f1 ~9 W" p
A 16-month-old white child was referred to the
2 s# F* ^' L& e- g- Vendocrine clinic by his pediatrician with the concern
: i7 d1 c9 O8 h1 l# y9 e  G" n. B& cof early sexual development. His mother noticed
7 t, n0 m) a3 q$ T4 vlight colored pubic hair development when he was1 A- ~5 q: M" w; \4 `
From the 1Division of Pediatric Endocrinology, 2University of! f: D0 f& x5 f9 j$ v" \) C
South Alabama Medical Center, Mobile, Alabama.6 |0 S0 L+ y, v& x0 `1 G
Address correspondence to: Samar K. Bhowmick, MD, FACE,3 k2 |8 G" j/ ]( ~- W. A
Professor of Pediatrics, University of South Alabama, College of
' [$ x" m7 c9 w, a  j4 L* x* NMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
0 V6 s0 t7 O3 F5 H  S' he-mail: [email protected].; h7 U2 g" O8 s# C
about 6 to 7 months old, which progressively became8 E& F2 d: J" ~# `* k4 b4 w- h
darker. She was also concerned about the enlarge-) f6 F# |6 B1 ^5 I. P7 e& k' z
ment of his penis and frequent erections. The child
1 ~0 o" t5 p' k9 A/ pwas the product of a full-term normal delivery, with
9 y! W8 G* t  n0 a% v0 \" Va birth weight of 7 lb 14 oz, and birth length of8 ~0 T( \8 Q) H; o2 z" W
20 inches. He was breast-fed throughout the first year
; b% L5 [* _  C9 e* z% |of life and was still receiving breast milk along with. ^6 _5 G! F2 ?9 o
solid food. He had no hospitalizations or surgery,
8 b" z3 }4 ^6 f) i) dand his psychosocial and psychomotor development. O" k4 H7 p4 a
was age appropriate.
, i, P$ U% K9 D3 S* c. @. ]% DThe family history was remarkable for the father,# K1 ?: f1 X- t+ D  C
who was diagnosed with hypothyroidism at age 16,
: t7 ^! }) V2 m  c: S. f* Uwhich was treated with thyroxine. The father’s+ f9 g, {1 z5 e# R
height was 6 feet, and he went through a somewhat7 o0 D+ X) c6 u' C
early puberty and had stopped growing by age 14.: p5 n$ }& K: F
The father denied taking any other medication. The
  v; N. v" H& e4 w+ f$ E8 s/ F2 T5 schild’s mother was in good health. Her menarche3 ~' f) t4 X$ [+ K; [$ j
was at 11 years of age, and her height was at 5 feet$ c- e& E7 r6 ]$ {$ |' F/ q/ k
5 inches. There was no other family history of pre-- K  p0 T, L: p) G/ A
cocious sexual development in the first-degree rela-+ }" N( @; l- c( Y& |$ T3 ~8 K
tives. There were no siblings.# ^7 g3 M5 G+ \0 |) Q" s
Physical Examination+ W7 }0 U- W  h9 U: l2 `
The physical examination revealed a very active,
) ~9 z4 k2 M+ Q8 e. tplayful, and healthy boy. The vital signs documented
0 y* {; D" e  d6 D$ y; M' c1 k2 ja blood pressure of 85/50 mm Hg, his length was- |0 V" G2 V* G+ S5 \; @; j5 V
90 cm (>97th percentile), and his weight was 14.4 kg
- w" [/ I  y: H9 Q3 k, C(also >97th percentile). The observed yearly growth
7 {" l# p, D: dvelocity was 30 cm (12 inches). The examination of
) [" _: G& ~  l) H$ V8 wthe neck revealed no thyroid enlargement.
6 z( k1 ]7 Y6 L+ L& hThe genitourinary examination was remarkable for1 j- P6 @7 e* Z5 I3 d  p0 E
enlargement of the penis, with a stretched length of/ ]: h. Z/ W7 _
8 cm and a width of 2 cm. The glans penis was very well0 ^" F* D. Z2 N& r) q
developed. The pubic hair was Tanner II, mostly around
# ^' s* W0 u; c  o4 D0 M6 l) L, C540# G( g  Q7 y& l) q& @" |4 Z; f
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from! v- h6 I. w, C. }" r* I
the base of the phallus and was dark and curled. The3 s: V! M( i2 I8 Y! q8 |6 w! R
testicular volume was prepubertal at 2 mL each.1 ]8 w+ P# M" b4 g; T
The skin was moist and smooth and somewhat$ f5 r: j+ }; u2 u% z3 {
oily. No axillary hair was noted. There were no% m: q# i( n5 o( w) p2 }
abnormal skin pigmentations or café-au-lait spots.9 w5 S/ _" T. G! x
Neurologic evaluation showed deep tendon reflex 2+& r# {) F/ j8 }7 n
bilateral and symmetrical. There was no suggestion
" N/ ^) P* X4 j4 M8 wof papilledema.2 C6 H# w: y8 _: I# d
Laboratory Evaluation' p' \" T+ p+ o& k3 a- Z; t
The bone age was consistent with 28 months by7 n7 l' p# h# {
using the standard of Greulich and Pyle at a chrono-
1 e% V  c1 K( l0 d% J+ nlogic age of 16 months (advanced).5 Chromosomal' h( m* u" p: ?
karyotype was 46XY. The thyroid function test* A3 s% R- n' G  x/ T8 d6 k* Q
showed a free T4 of 1.69 ng/dL, and thyroid stimu-, k& j6 O' y, Z) h3 [' G5 L; r$ n
lating hormone level was 1.3 µIU/mL (both normal).
. I9 v4 W, t# k$ hThe concentrations of serum electrolytes, blood( @6 U: y! p" o8 `: A, j! G+ H: b
urea nitrogen, creatinine, and calcium all were* O9 @3 ?$ M! m8 L0 s
within normal range for his age. The concentration. }- w0 E& \) b* Z& A: i
of serum 17-hydroxyprogesterone was 16 ng/dL# x( F% }7 m1 M( |
(normal, 3 to 90 ng/dL), androstenedione was 20
4 P& d4 J- G; K# O6 u4 mng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-: v% D2 \1 E3 t6 t9 P
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
4 ^' |2 {' c: Q, adesoxycorticosterone was 4.3 ng/dL (normal, 7 to
8 N8 n" `  k' t# A2 J49ng/dL), 11-desoxycortisol (specific compound S)( P. S) z( M- e' i6 h( \
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
5 }' y3 c0 X, @; N$ m( Ztisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total. v6 V0 ]. r/ |4 ^4 m5 }' `6 ?
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),( J7 U9 f4 ^4 p0 h
and β-human chorionic gonadotropin was less than+ r1 x1 p5 |9 y% K
5 mIU/mL (normal <5 mIU/mL). Serum follicular/ k) @4 S# z% X" c: ]% a+ N
stimulating hormone and leuteinizing hormone
4 f$ ~: F: V/ ?3 Y) yconcentrations were less than 0.05 mIU/mL
3 f- _7 h! L6 i(prepubertal).
& t/ e2 j) L4 U# S; LThe parents were notified about the laboratory; `# p3 x+ c: `; {' {
results and were informed that all of the tests were6 [! U6 x, c: V. b; g' U% T' y$ Q
normal except the testosterone level was high. The/ V. y5 Y: `- `
follow-up visit was arranged within a few weeks to/ v0 G$ a. [3 v$ Z$ f+ a1 v
obtain testicular and abdominal sonograms; how-
$ g8 t+ j" E0 Vever, the family did not return for 4 months.2 k# c- A9 H* a( d6 Q: }1 Z6 \
Physical examination at this time revealed that the( C4 Y( [" C/ c4 w/ W' g
child had grown 2.5 cm in 4 months and had gained
8 ~5 w: C; j; I. `7 q2 kg of weight. Physical examination remained
. P  z1 i& r- J7 O1 L3 i6 P& {unchanged. Surprisingly, the pubic hair almost com-
! w- ^5 ~, e* `4 \pletely disappeared except for a few vellous hairs at& z9 G1 p8 [. R9 c
the base of the phallus. Testicular volume was still 2
6 z8 P. f! Y, }& p1 T, UmL, and the size of the penis remained unchanged.
) p6 {3 F% W# L6 [; x8 IThe mother also said that the boy was no longer hav-
* z6 ]+ k& {+ o2 N& {ing frequent erections.
' y5 b2 p& @. `. RBoth parents were again questioned about use of9 ^6 h! f) }. O& O( [! J5 \, e# r
any ointment/creams that they may have applied to4 K5 J3 `- M" p& B8 c
the child’s skin. This time the father admitted the
  ~! c7 i/ \- P9 L* _4 O  [# G9 ATopical Testosterone Exposure / Bhowmick et al 541
1 {2 s  _1 ~5 S& ^& {3 zuse of testosterone gel twice daily that he was apply-) D: g0 n. p0 R0 Q3 ~9 Y  I: ~9 Z9 X
ing over his own shoulders, chest, and back area for
. i* q$ `: g5 a9 ua year. The father also revealed he was embarrassed) r0 l7 s  M& R
to disclose that he was using a testosterone gel pre-& N" U: s4 Y. D! U; g$ V
scribed by his family physician for decreased libido3 e, q1 Y; ]/ o4 t3 j$ ?7 M. P
secondary to depression.
1 y0 E% ]4 `- @) L, n) YThe child slept in the same bed with parents.
3 A' {* G7 p8 b1 ~% {7 N1 @( V$ FThe father would hug the baby and hold him on his
5 `1 c" q# Z! G/ O( Rchest for a considerable period of time, causing sig-
1 E; A- Z, W  E# n& a* wnificant bare skin contact between baby and father.
% b: X  e8 B7 Y" {  BThe father also admitted that after the phone call,
+ o/ ~! b  l* V4 g! pwhen he learned the testosterone level in the baby
8 ~  g9 r. z) v) Twas high, he then read the product information, n( a* u% C+ L7 p8 @4 v
packet and concluded that it was most likely the rea-2 Z0 H& ]0 V( f% b
son for the child’s virilization. At that time, they
0 ]( D% T2 _/ Q7 _/ Sdecided to put the baby in a separate bed, and the
6 L% V$ w2 O' ?% y- `3 pfather was not hugging him with bare skin and had
& \. f) l) ^: I7 nbeen using protective clothing. A repeat testosterone0 ?- f! m- J$ Z: u/ x
test was ordered, but the family did not go to the9 v; {& M5 g+ p4 ^; S  |0 N
laboratory to obtain the test.
4 A- o8 v9 {2 o5 {4 [4 ^  o3 sDiscussion
5 M8 _5 E1 e6 t( CPrecocious puberty in boys is defined as secondary" ]9 B4 ^4 h; ]9 O1 g4 ^2 A
sexual development before 9 years of age.1,4) t+ _0 K0 D8 x9 C6 W1 S' F
Precocious puberty is termed as central (true) when- x% a- @' Z- s4 N6 l/ S- {5 s! c. F+ ^
it is caused by the premature activation of hypo-) n! I. |9 K) r, z
thalamic pituitary gonadal axis. CPP is more com-
- E6 j3 q7 V  g0 x1 B9 Z; Qmon in girls than in boys.1,3 Most boys with CPP
. V. D% _1 c% R- imay have a central nervous system lesion that is8 B1 ^( \( |' ]$ W! b
responsible for the early activation of the hypothal-
# A4 K. ~# v6 @amic pituitary gonadal axis.1-3 Thus, greater empha-% \' u8 m0 n! ?- J$ `" \; g
sis has been given to neuroradiologic imaging in2 ~9 d, Q1 v/ ^
boys with precocious puberty. In addition to viril-% Y; n5 O4 O9 e- T! A
ization, the clinical hallmark of CPP is the symmet-
: I/ q, x+ V) t- Hrical testicular growth secondary to stimulation by
  b7 R8 T* L# T3 j! C" i, wgonadotropins.1,3
* ^% O! U: U: H& {- WGonadotropin-independent peripheral preco-
$ w* |6 B* \/ [1 Ucious puberty in boys also results from inappropriate9 C2 i! p# Y; L; N5 X5 }! j$ t
androgenic stimulation from either endogenous or$ Z- a! L$ r2 ^9 j6 q2 g) y
exogenous sources, nonpituitary gonadotropin stim-$ [- @& [+ h# K2 ]' r8 G; i) h$ b7 e
ulation, and rare activating mutations.3 Virilizing
( d3 t" b' ]7 F1 a, c2 M; B+ |, econgenital adrenal hyperplasia producing excessive
% _0 U7 f3 [6 ^adrenal androgens is a common cause of precocious
# S1 }  C$ |* K. Kpuberty in boys.3,4& U% s7 }7 o: W
The most common form of congenital adrenal3 f' `) V+ l6 W3 S+ F- X+ I9 X9 G
hyperplasia is the 21-hydroxylase enzyme deficiency.
& E0 ]& r! }! v$ J, z, rThe 11-β hydroxylase deficiency may also result in
0 v' s0 T0 }7 g9 S$ u: b4 Sexcessive adrenal androgen production, and rarely,
! z6 v$ @( S% S  `an adrenal tumor may also cause adrenal androgen
8 a4 `- N, G& \4 x8 |excess.1,3) |( F; H# V$ N# I
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from  e. k9 Q) A% o5 Y) a; `; x5 Y
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
+ p( X: R- D3 Z) RA unique entity of male-limited gonadotropin-
* b6 z, _3 R3 aindependent precocious puberty, which is also known
9 _* f$ E. f; ]2 g! I" Nas testotoxicosis, may cause precocious puberty at a: v+ d$ m0 u% t, R  l" D
very young age. The physical findings in these boys, \9 m! A( l0 n, v$ Z1 r( @
with this disorder are full pubertal development,
! g; ^+ M+ J3 G* d$ B# {1 Iincluding bilateral testicular growth, similar to boys
& X7 d- c' S( Q. c1 r+ e- {with CPP. The gonadotropin levels in this disorder
1 M0 ]' l5 T2 o7 d9 `% r* M* H. iare suppressed to prepubertal levels and do not show
) E2 X# y6 c" D# epubertal response of gonadotropin after gonadotropin-
9 x. [0 y/ D8 W4 [releasing hormone stimulation. This is a sex-linked& i" g7 F' e) s/ r" n
autosomal dominant disorder that affects only
- ]6 ?  W  H) |& [8 U  |' rmales; therefore, other male members of the family0 v+ i" C- l6 c. X
may have similar precocious puberty.3
% Y2 R! Q3 E( u0 o- t! XIn our patient, physical examination was incon-
) H6 h1 O# Y! u6 }" nsistent with true precocious puberty since his testi-" v: {; Y8 u) P9 X
cles were prepubertal in size. However, testotoxicosis
3 F& G' e. K2 jwas in the differential diagnosis because his father
" T# R8 T3 x+ x5 x% Tstarted puberty somewhat early, and occasionally,
7 ^/ l$ y; X. i/ t5 |/ O% w' Etesticular enlargement is not that evident in the9 L- i8 R' c' L4 v& B
beginning of this process.1 In the absence of a neg-* v, |% K# R3 i& T) x; ?9 [' f
ative initial history of androgen exposure, our! n6 x; R2 C% j, b1 P
biggest concern was virilizing adrenal hyperplasia,* N$ V: J5 v/ {6 D" h" B" D
either 21-hydroxylase deficiency or 11-β hydroxylase
% V& v0 U% ~" Cdeficiency. Those diagnoses were excluded by find-+ ?8 w' D* V* ?' _6 U  D2 o
ing the normal level of adrenal steroids.
( e% B/ @( K* q+ I# Y! yThe diagnosis of exogenous androgens was strongly
$ m! G5 z% ~  n: g! Tsuspected in a follow-up visit after 4 months because9 g3 l+ V- ^+ i0 V4 R3 r
the physical examination revealed the complete disap-6 R- o6 A+ J' ]  l- R
pearance of pubic hair, normal growth velocity, and
, G1 L3 ]* i- k5 f% ^- ddecreased erections. The father admitted using a testos-) d& U: [% x9 `) j9 j
terone gel, which he concealed at first visit. He was5 B  F- }( J* M
using it rather frequently, twice a day. The Physicians’
# P% t6 U7 j! R# U2 s# }" RDesk Reference, or package insert of this product, gel or- I; h' ^/ _, t
cream, cautions about dermal testosterone transfer to$ L1 Q7 t7 E  A  b
unprotected females through direct skin exposure.3 v  v. {+ p+ |5 E4 t
Serum testosterone level was found to be 2 times the6 Y8 R7 r. I1 A3 W5 R) P& O
baseline value in those females who were exposed to+ {* F7 k% N) \  k
even 15 minutes of direct skin contact with their male
' w& k9 p( g- }partners.6 However, when a shirt covered the applica-
; M4 F% p: {$ f1 B2 |  n3 G/ }1 Ution site, this testosterone transfer was prevented.
& q6 i/ C7 z  w2 SOur patient’s testosterone level was 60 ng/mL,
) ?" {2 q& Z/ G. K5 y. Nwhich was clearly high. Some studies suggest that
: z( @3 z. @' h) ^0 adermal conversion of testosterone to dihydrotestos-
; X1 F- E! ^; Vterone, which is a more potent metabolite, is more
  H9 k  v7 K( @) r/ \  |active in young children exposed to testosterone
$ N) ?/ ~- n* Aexogenously7; however, we did not measure a dihy-0 h" K, M; W% t& X
drotestosterone level in our patient. In addition to
' M4 N7 w+ c# p6 ^9 n" H7 dvirilization, exposure to exogenous testosterone in. |3 H% s! o6 |: @2 m& U, ^0 c
children results in an increase in growth velocity and
. z3 a1 J0 u6 j* G  F* ]& N% z$ xadvanced bone age, as seen in our patient.
% E3 ^2 Q* f* ~5 V. GThe long-term effect of androgen exposure during! \9 u/ u4 W. {  m
early childhood on pubertal development and final
# O$ H2 ~9 N) `. J# [! Sadult height are not fully known and always remain, P. V. A2 r. u8 F# l
a concern. Children treated with short-term testos-9 g8 T1 Q7 ]5 X; y! c6 r: a
terone injection or topical androgen may exhibit some$ R9 p# ~% n% O9 j/ e! F; l* U; j# O
acceleration of the skeletal maturation; however, after, Q8 l9 R: W# s9 u
cessation of treatment, the rate of bone maturation$ C( @9 |- R! \5 N" n
decelerates and gradually returns to normal.8,93 H+ ?1 G- {6 s( `0 X" O6 x
There are conflicting reports and controversy
" C# @" L' Q2 s# L9 e3 q3 c8 sover the effect of early androgen exposure on adult* \- f: h7 u/ b3 k4 Q3 n# ~  s
penile length.10,11 Some reports suggest subnormal
  L/ }; Q' E% R4 z5 k6 Y+ c+ Jadult penile length, apparently because of downreg-: e2 v+ k$ N$ D" z5 p; x
ulation of androgen receptor number.10,12 However,) [, u% F; X$ }2 F+ i- O! Q* M
Sutherland et al13 did not find a correlation between
6 B6 k$ c2 G" x/ Mchildhood testosterone exposure and reduced adult& B3 b; K! W- y
penile length in clinical studies.
7 c; ]1 D* `1 X$ W8 f% g$ c: LNonetheless, we do not believe our patient is! _9 Y( Z6 S$ J+ Z0 {* R( q
going to experience any of the untoward effects from
$ P6 n) i& O2 Atestosterone exposure as mentioned earlier because0 w) y  @+ x- C: C" U6 m$ t
the exposure was not for a prolonged period of time.' a3 L3 o3 |8 B9 u
Although the bone age was advanced at the time of8 S+ t+ W4 w. J1 \
diagnosis, the child had a normal growth velocity at
, p4 z! ]" F# d1 \& K" q* c7 r: xthe follow-up visit. It is hoped that his final adult, c& X3 E; H6 {; @, {
height will not be affected.: L8 i5 B+ w" G# l* B+ s! D
Although rarely reported, the widespread avail-+ N  _, A+ i6 z: y8 h
ability of androgen products in our society may
2 \/ e- ~% y1 \. Z, i, Xindeed cause more virilization in male or female
0 W% m6 t0 b4 _3 g: u+ Q7 _4 r% y; j0 pchildren than one would realize. Exposure to andro-
- o8 c- T2 {  G1 P, qgen products must be considered and specific ques-; B+ D, W; g- H: H: L8 f
tioning about the use of a testosterone product or! p/ p% N* Q. e( Z% d2 M8 h
gel should be asked of the family members during5 {7 I* l* j2 x9 J& a
the evaluation of any children who present with vir-
5 j" ~  j' W1 Q( j# dilization or peripheral precocious puberty. The diag-; Z: e  V, T& w1 Z4 D( F
nosis can be established by just a few tests and by
( ]6 w. {" V4 Happropriate history. The inability to obtain such a, v/ ?* P) v1 z3 f6 F3 ^+ m' f
history, or failure to ask the specific questions, may; W% J. W4 W6 l" L
result in extensive, unnecessary, and expensive
3 u. `6 e) O6 W$ W3 {investigation. The primary care physician should be8 f' ^7 ^4 o% i3 c! j2 G' i, D
aware of this fact, because most of these children
2 G( C4 u1 e! x; n* I! Z0 g7 N/ Tmay initially present in their practice. The Physicians’  E" l- E& x2 N
Desk Reference and package insert should also put a  Y. Z5 ]# E( E
warning about the virilizing effect on a male or' o7 r1 S+ a; L% c+ b; ^. q5 E
female child who might come in contact with some-* f% H4 U- q& G0 q4 N
one using any of these products.
, K# E5 q2 C0 Y) B& eReferences
7 G2 X9 V4 h+ i9 n1. Styne DM. The testes: disorder of sexual differentiation7 f6 W7 i0 O- a2 N3 C3 [* j
and puberty in the male. In: Sperling MA, ed. Pediatric
: S& s' i/ y8 ?3 D% A9 XEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;! ?/ H/ v. Q: a7 _& L. L" }
2002: 565-628.' w2 E% p' L5 s6 G
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
* b; i; d9 V- O5 Cpuberty 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
- ~! c% r- Z- K8 F; lBoy Induced by Indirect Topical# K/ N+ {) |/ G5 r/ [$ f, d1 m
Exposure to Testosterone
& P4 d6 Y4 T, }+ B' D; o) cSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2+ E, j/ W" J  I( l
and Kenneth R. Rettig, MD1
+ a( ~2 B8 ?8 V4 b# dClinical Pediatrics
9 p6 J$ L$ d0 ^' Z3 d  VVolume 46 Number 69 j! |1 T$ m6 t+ @% ?
July 2007 540-543
8 G2 h# ^% L& |7 Z# c© 2007 Sage Publications0 Z! {+ g7 Y, P* r5 t! |: b# K# {
10.1177/0009922806296651
& j. f# J; T- D5 M3 Ehttp://clp.sagepub.com& P1 e/ A2 \3 Z. t- u( |
hosted at" |( F  n1 e6 j/ `& E2 O% J/ O+ D
http://online.sagepub.com
2 a9 L# e$ Z  `; c5 wPrecocious puberty in boys, central or peripheral,
# O2 |) e' A6 [, j3 w0 Lis a significant concern for physicians. Central
$ S+ s; d/ K9 Jprecocious puberty (CPP), which is mediated
( V! }1 }* N' Q$ Ythrough the hypothalamic pituitary gonadal axis, has1 q' O. S% u1 `! w) L% `' k! p
a higher incidence of organic central nervous system) M/ v0 i, Y- c' W# A* c+ [
lesions in boys.1,2 Virilization in boys, as manifested
2 W/ ^" w3 z# d$ G  `$ e' U' H( Kby enlargement of the penis, development of pubic
  O& z; b+ W# C6 `9 q" lhair, and facial acne without enlargement of testi-' y7 X) _1 V& V+ p+ i) }+ Z7 s
cles, suggests peripheral or pseudopuberty.1-3 We
) f8 n: J- W1 t/ B3 O. u8 vreport a 16-month-old boy who presented with the
9 ^  `3 ]) Y6 c* uenlargement of the phallus and pubic hair develop-
" i$ w8 l* {& F# bment without testicular enlargement, which was due
  J% w. N5 t8 R0 O7 z8 Q; c% Tto the unintentional exposure to androgen gel used by' R' }3 _, K7 J, w8 O( f1 @2 J1 ~: M
the father. The family initially concealed this infor-
* _3 `' r7 s1 `  k) K3 V# ^mation, resulting in an extensive work-up for this
  D. R1 j' r; J9 v! b: b% L. xchild. Given the widespread and easy availability of0 I; r0 a4 O- N' d: v- x% ~: i8 v. k
testosterone gel and cream, we believe this is proba-% ^/ [& I& r$ N+ X8 N/ C
bly more common than the rare case report in the6 q6 a/ O5 [; a9 `8 M0 t* d
literature.4
( V& e0 S' T) BPatient Report
4 N( z* |" n5 ?  H5 {A 16-month-old white child was referred to the
: n/ k% V; j8 v$ xendocrine clinic by his pediatrician with the concern- U1 ^. b; {* x
of early sexual development. His mother noticed6 Q, u6 u0 n) ^4 a! j3 D% a
light colored pubic hair development when he was/ J6 w) L! e' F- m: O& m
From the 1Division of Pediatric Endocrinology, 2University of
# P9 U' {( J) |) B4 d+ ]$ T3 nSouth Alabama Medical Center, Mobile, Alabama.2 \( j: H. C( F6 V+ |$ e
Address correspondence to: Samar K. Bhowmick, MD, FACE,
5 |: S9 q; k0 d. eProfessor of Pediatrics, University of South Alabama, College of
, D4 A) i, B( @, ^3 ?% `8 @- QMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
0 A0 H$ n1 N2 G6 {" J+ U! ze-mail: [email protected].- R" J3 V2 T& Z
about 6 to 7 months old, which progressively became4 [& n) p* Z1 n! G
darker. She was also concerned about the enlarge-
& U7 N1 e+ ~9 x* Z1 {  ument of his penis and frequent erections. The child
; q: G# p! y; ~. b* |was the product of a full-term normal delivery, with/ h  R* \7 a. ?7 g8 G* y; W
a birth weight of 7 lb 14 oz, and birth length of7 U1 B& P" b: h7 U- p, Z
20 inches. He was breast-fed throughout the first year
* l  H: o$ L# `of life and was still receiving breast milk along with
5 u4 [) Y% H' L) ysolid food. He had no hospitalizations or surgery," L4 D3 P( Q' d7 N1 K# D2 n+ L
and his psychosocial and psychomotor development, K$ P8 d; ]" F& _
was age appropriate.
& C  U5 |9 r. v. `: q( m- c6 Y( jThe family history was remarkable for the father,  ?/ `5 [$ ]; h- o+ V
who was diagnosed with hypothyroidism at age 16,  |- N$ ]3 o& w4 w0 K9 @
which was treated with thyroxine. The father’s
7 M' M2 J7 ?* z7 k6 R* Bheight was 6 feet, and he went through a somewhat2 \$ M  g7 _' D, n! Z  n+ \
early puberty and had stopped growing by age 14.
1 Q' E; N( k+ {6 H0 XThe father denied taking any other medication. The8 O, N9 v) `( ^' S( q" @, @& Q
child’s mother was in good health. Her menarche2 N& u& g# S8 {2 G; k! q
was at 11 years of age, and her height was at 5 feet
5 s/ u' }9 L' y& [* Y( |5 [5 P5 inches. There was no other family history of pre-
4 z2 B' e  L6 _! ], m( }cocious sexual development in the first-degree rela-
6 |" k5 T3 I6 e  \tives. There were no siblings.
0 s7 H# Y. [- [, j! @2 UPhysical Examination4 p' P5 X; x' q0 R
The physical examination revealed a very active,* G& n6 }; {/ v" V
playful, and healthy boy. The vital signs documented
9 a- ^9 s- `& _: B/ ua blood pressure of 85/50 mm Hg, his length was
% P, f+ h/ T" r" x90 cm (>97th percentile), and his weight was 14.4 kg
. [. @  U$ e$ }8 V1 J(also >97th percentile). The observed yearly growth# M3 e7 r3 B0 S& r8 {
velocity was 30 cm (12 inches). The examination of  O5 }6 e- Z; Q
the neck revealed no thyroid enlargement.( A, ~2 p. T6 D
The genitourinary examination was remarkable for# B. c* S2 `, l) ]: d; d
enlargement of the penis, with a stretched length of9 t6 E7 G( J6 X2 M$ e; e2 V- p) N
8 cm and a width of 2 cm. The glans penis was very well. K8 l7 h1 N# \: L6 w1 p) w) m0 D
developed. The pubic hair was Tanner II, mostly around' O2 ?4 I/ i0 v/ P
5404 l9 n( K7 G! [/ g/ ]. E4 q! J; [
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from1 b3 t6 {7 M! n6 B* I
the base of the phallus and was dark and curled. The
! T- }/ P: |" i, ~  x; Ftesticular volume was prepubertal at 2 mL each.
2 J& ?  o9 c3 t5 o0 n& v- x0 zThe skin was moist and smooth and somewhat
4 f% |. W# E+ K. r3 _) w8 x; |oily. No axillary hair was noted. There were no# E8 D/ J% A. |& ?( X
abnormal skin pigmentations or café-au-lait spots.4 o2 m+ a+ a; ^" ?, \4 Y, r
Neurologic evaluation showed deep tendon reflex 2+
$ V3 n7 l0 I/ J! V. Z! e' ?, {bilateral and symmetrical. There was no suggestion5 S; z# D+ f: K5 P
of papilledema.
7 ?0 o0 z1 c. R* b- d9 v! ]  QLaboratory Evaluation
1 _; v2 V2 t7 y3 m( i- mThe bone age was consistent with 28 months by; u5 A8 M% l' C/ ^
using the standard of Greulich and Pyle at a chrono-
6 Y0 ]. v6 }" i2 Plogic age of 16 months (advanced).5 Chromosomal
. _' P1 S+ G8 H8 \9 z6 v3 Tkaryotype was 46XY. The thyroid function test8 w+ \: u4 e& Q, Q' I8 u  W  t, j
showed a free T4 of 1.69 ng/dL, and thyroid stimu-# E# B; O% `. @* o2 W
lating hormone level was 1.3 µIU/mL (both normal).
& q! ^/ a* [, q. e" i9 H# i# EThe concentrations of serum electrolytes, blood
2 @' I5 G0 v' `( T0 Rurea nitrogen, creatinine, and calcium all were
9 P1 S( N! o. Cwithin normal range for his age. The concentration
, Z6 O7 O8 v$ M' G1 m( y3 d3 p& k9 jof serum 17-hydroxyprogesterone was 16 ng/dL
; K* A( q* j2 e4 o" l9 _(normal, 3 to 90 ng/dL), androstenedione was 20$ r, O# _7 U! @6 v% T8 x' D- u
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-7 E& G" I7 K! f& ~, R1 J8 L
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
. t+ Q6 Y5 s" i) |/ j' Udesoxycorticosterone was 4.3 ng/dL (normal, 7 to
& ~: i% e! M6 U8 D  T0 q49ng/dL), 11-desoxycortisol (specific compound S)- r% S* W+ D  b. K
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-& @& V0 F% R! ^: a1 b$ N
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
8 ]+ B+ y* g* i& itestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
: {3 e, \! _5 ^7 Band β-human chorionic gonadotropin was less than
3 f" t+ p/ [" N5 mIU/mL (normal <5 mIU/mL). Serum follicular! J  I4 n5 R: W4 @$ h: j$ @
stimulating hormone and leuteinizing hormone
, z1 r( T( x2 \concentrations were less than 0.05 mIU/mL3 p" u. `1 Z$ R
(prepubertal).1 J+ S7 O4 M5 u: u
The parents were notified about the laboratory; j. y  z  @: H: ]
results and were informed that all of the tests were0 m- F: T" h4 e
normal except the testosterone level was high. The
& F+ y3 H; F( ^8 j  H/ efollow-up visit was arranged within a few weeks to1 G1 M# E( E; I% ^9 Q6 Z7 B
obtain testicular and abdominal sonograms; how-) Q: o! b) N/ h& f7 Z" m9 d3 {; Z
ever, the family did not return for 4 months.
0 O& ]% \  O& e2 \3 H, Z4 kPhysical examination at this time revealed that the( v+ E- L6 T' b, t/ \: `' o) W
child had grown 2.5 cm in 4 months and had gained3 h2 ~( h6 _3 Q: ~8 [7 J
2 kg of weight. Physical examination remained+ I9 p3 S6 F' p. {- k  k8 q
unchanged. Surprisingly, the pubic hair almost com-
& r$ l0 ?7 s# a5 |pletely disappeared except for a few vellous hairs at5 A: D* m8 H' Q  j
the base of the phallus. Testicular volume was still 2
. C* {( ]8 X' M0 }2 RmL, and the size of the penis remained unchanged./ K$ ?9 U$ z3 V) }) j, a; i& d3 _
The mother also said that the boy was no longer hav-
$ c' q' z7 k/ S7 @. N! ming frequent erections.' X) \$ L$ c2 V/ G; y5 j
Both parents were again questioned about use of
# J% y! S' e- ^0 Jany ointment/creams that they may have applied to8 F3 D) L  ^3 Q* N2 A/ R
the child’s skin. This time the father admitted the
* ?# w3 y; I& Z% KTopical Testosterone Exposure / Bhowmick et al 541
" U& B5 Y# M5 I% I2 puse of testosterone gel twice daily that he was apply-
  M' {! J8 d! E4 X; g/ d. M% n$ ]# _ing over his own shoulders, chest, and back area for' O% i  [5 _( T* {
a year. The father also revealed he was embarrassed9 U- G# m) M- ?' U- Z" \* B
to disclose that he was using a testosterone gel pre-+ i( ^! r6 h5 c6 ^) I
scribed by his family physician for decreased libido( v; f6 ], u% \+ F+ _' A
secondary to depression.# ~  W" U- S' ~5 Q$ B) F! i, w
The child slept in the same bed with parents.
( h3 k$ F& g6 y$ nThe father would hug the baby and hold him on his
1 f9 [, G! M% Y- K* l% ^9 ^* Bchest for a considerable period of time, causing sig-
1 _0 ]4 V8 c8 v- G4 [& X" |nificant bare skin contact between baby and father.3 l/ ^" E/ g' s
The father also admitted that after the phone call,
/ p/ P! r" W7 V1 p- H4 x- ]when he learned the testosterone level in the baby3 b& r4 @; O* g4 V8 N! J
was high, he then read the product information
( q3 @: i7 {6 Y# \+ w4 |8 Ipacket and concluded that it was most likely the rea-
( D! \! U# U# s7 _son for the child’s virilization. At that time, they
* `$ u2 l4 ^) p5 S. ydecided to put the baby in a separate bed, and the  ?, S" {# V  [6 W* ^+ }/ D
father was not hugging him with bare skin and had. M3 J0 H! W' p4 x
been using protective clothing. A repeat testosterone7 d+ v. w+ Y% O. O2 x! ]7 Y
test was ordered, but the family did not go to the
+ P3 q$ c& g" g2 ilaboratory to obtain the test.
! ?8 I  S) f- K1 r9 z6 ~' NDiscussion' @# X$ w+ f/ \2 s3 w9 ^. @
Precocious puberty in boys is defined as secondary
; i5 A  o/ W6 l3 S% Z6 p0 p. ]+ _6 csexual development before 9 years of age.1,4' s5 n+ E* H# g8 {) f
Precocious puberty is termed as central (true) when
" ~3 X9 L# }+ L# f. b7 Git is caused by the premature activation of hypo-
4 x' B( a  n& a1 j" |; f  Z% Nthalamic pituitary gonadal axis. CPP is more com-
" X/ h7 I- v; k  o4 qmon in girls than in boys.1,3 Most boys with CPP
2 S7 Y' s" z+ pmay have a central nervous system lesion that is
' c! k1 i6 I! iresponsible for the early activation of the hypothal-  [8 w* b* `% m, R: V3 X: Z, d
amic pituitary gonadal axis.1-3 Thus, greater empha-8 X+ E  h) N* @- U, K8 Z" X
sis has been given to neuroradiologic imaging in, ^: I+ }0 h$ i7 i- c! |( y) {" P
boys with precocious puberty. In addition to viril-' d! O7 s& }! X! Y' |0 K% m8 J$ \
ization, the clinical hallmark of CPP is the symmet-
% v# f1 ^3 F5 S) V8 xrical testicular growth secondary to stimulation by
  O; n$ D0 E4 w- K! c4 x4 c9 Pgonadotropins.1,3) W# @' U7 ]: {
Gonadotropin-independent peripheral preco-: M  G9 T+ s( {. W1 q4 f$ w) r
cious puberty in boys also results from inappropriate
) J' i- {5 C7 `% I( E" ~androgenic stimulation from either endogenous or
7 S$ _' @" c- k* ?7 ]exogenous sources, nonpituitary gonadotropin stim-7 D5 y; A( E& n! d6 O  E
ulation, and rare activating mutations.3 Virilizing: |; t  X- L5 j) y4 N2 z6 v3 }, u& Q
congenital adrenal hyperplasia producing excessive# I+ |# {2 R/ l0 v8 t
adrenal androgens is a common cause of precocious
: T  D% ]& Z0 {0 X. Ppuberty in boys.3,4
9 c# H, r' H. PThe most common form of congenital adrenal  H, }: k1 G1 H* ^0 P2 x7 A
hyperplasia is the 21-hydroxylase enzyme deficiency.
9 i' L) ~( D# c4 c! FThe 11-β hydroxylase deficiency may also result in; P! d# d" p' r8 l
excessive adrenal androgen production, and rarely,2 |- N+ n" a: v  l& z
an adrenal tumor may also cause adrenal androgen! Z* R8 y  D! b" j( a' f$ `6 c
excess.1,3
/ U  T/ v, e& Wat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from6 z- v+ c0 o: X0 p- T8 C
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
; V" W& A6 n* V% ~2 qA unique entity of male-limited gonadotropin-8 Y9 n# }! B4 b. i. _6 `
independent precocious puberty, which is also known
( `4 t  V7 W; B# |+ O# Jas testotoxicosis, may cause precocious puberty at a
& {/ S* L; Q/ z5 f0 i$ W7 s2 n0 K5 rvery young age. The physical findings in these boys% B% @  u3 l+ O4 e  i7 e1 ?6 M
with this disorder are full pubertal development,
, D& X( `$ S% o# h& k9 F% Rincluding bilateral testicular growth, similar to boys
# Z3 n6 g  z* F  }, V) i/ Owith CPP. The gonadotropin levels in this disorder
, g) V0 E4 N: U& n' r, care suppressed to prepubertal levels and do not show; A+ s6 V! ^0 J. I, I3 C
pubertal response of gonadotropin after gonadotropin-
8 ^+ K7 f* q# a9 f/ s" Jreleasing hormone stimulation. This is a sex-linked
4 ^4 D  [5 p% Y+ a& Q4 F3 Eautosomal dominant disorder that affects only2 t+ i. k- h* ~' f
males; therefore, other male members of the family
/ z0 W" q: z: G  nmay have similar precocious puberty.3- g- l# `* m( i
In our patient, physical examination was incon-+ K# g' H* S% t& E  Y
sistent with true precocious puberty since his testi-
' D/ m9 _6 z  I2 Q7 b: Gcles were prepubertal in size. However, testotoxicosis
- @2 ?2 b/ J& ~& s1 Lwas in the differential diagnosis because his father
7 s) x, G( H3 e1 l1 L5 zstarted puberty somewhat early, and occasionally,
& `5 o3 I5 b; i% W) ]testicular enlargement is not that evident in the) ?6 a* W0 v  T+ b; o
beginning of this process.1 In the absence of a neg-# P/ B' i7 p7 U4 G. w
ative initial history of androgen exposure, our
8 l4 z& }+ c/ n6 Vbiggest concern was virilizing adrenal hyperplasia,
2 b; ], m) d& x# @. o+ Teither 21-hydroxylase deficiency or 11-β hydroxylase( {$ ?" ?, C7 n+ P5 ^  {
deficiency. Those diagnoses were excluded by find-
" Z4 n: [. s$ M7 x# n0 i' c' ^ing the normal level of adrenal steroids.9 k- |7 z+ S+ H( H6 \7 a! Z( V
The diagnosis of exogenous androgens was strongly
8 g: G6 k* I1 q9 ]) i% F" jsuspected in a follow-up visit after 4 months because
, j) ~& x4 f( G6 Q; {the physical examination revealed the complete disap-% \8 G# @% x1 u. i5 |
pearance of pubic hair, normal growth velocity, and
7 W9 L! g: [  l/ @+ Y4 g# jdecreased erections. The father admitted using a testos-
1 ^0 I4 r7 M  v( Y. R' Oterone gel, which he concealed at first visit. He was. @% z/ l- o3 w+ I. [
using it rather frequently, twice a day. The Physicians’
/ i1 ^! o( Q* a  L; ]2 _* V# O$ }Desk Reference, or package insert of this product, gel or
% O/ i+ o) P3 I0 v7 n6 {cream, cautions about dermal testosterone transfer to; \/ |/ t; H$ E( I/ F2 W
unprotected females through direct skin exposure.2 U: l: u. T8 p4 K8 |3 ]' W' r
Serum testosterone level was found to be 2 times the
8 n0 I4 x" S. N% zbaseline value in those females who were exposed to
6 ]3 g2 s9 C* b( Oeven 15 minutes of direct skin contact with their male
( A0 K9 [- `- X# V, k& j& fpartners.6 However, when a shirt covered the applica-
$ `9 v& r! d! Z7 E* }) i' T* v3 \tion site, this testosterone transfer was prevented.* S, X/ z3 D: i  g1 {5 n0 a& s
Our patient’s testosterone level was 60 ng/mL,$ }! }; F! o: q
which was clearly high. Some studies suggest that8 ~6 A' W0 b% j- I8 J/ v5 Q  ^
dermal conversion of testosterone to dihydrotestos-! z% q( q  t  E2 @9 p3 T/ u
terone, which is a more potent metabolite, is more
( W% }# G5 A: @3 z; l; Z5 _active in young children exposed to testosterone7 ?/ z0 O, B. P: K
exogenously7; however, we did not measure a dihy-0 q! G1 \6 F, D2 c4 F" E+ R: }
drotestosterone level in our patient. In addition to
, Z8 l& O, T9 r. Zvirilization, exposure to exogenous testosterone in9 C1 @& [3 T) _+ R- U  v$ p
children results in an increase in growth velocity and8 X3 Q" }- A; k6 ]( G' I
advanced bone age, as seen in our patient.
6 w/ Y- T2 r* F" w; ZThe long-term effect of androgen exposure during. N0 d0 G5 O; R
early childhood on pubertal development and final. m+ V. W/ Q( D8 J" U
adult height are not fully known and always remain9 X3 Z) P5 J& }$ a8 C+ ]/ l
a concern. Children treated with short-term testos-
! `: H' E% }' d0 q8 X$ ]terone injection or topical androgen may exhibit some& B( y( c6 r6 X( A- j
acceleration of the skeletal maturation; however, after& n; P! t! P/ S) S: u" l4 u; [& e% Y4 ~
cessation of treatment, the rate of bone maturation6 o* Q3 i6 s" W0 R
decelerates and gradually returns to normal.8,9
; {: F5 e0 ?5 u4 u3 Y9 cThere are conflicting reports and controversy2 {8 l! L9 u+ z# g
over the effect of early androgen exposure on adult- F$ g: ]" V4 x- i
penile length.10,11 Some reports suggest subnormal$ F4 _1 D( c/ u7 U5 t0 n2 K3 ^% o
adult penile length, apparently because of downreg-2 Y7 \& r1 F& D
ulation of androgen receptor number.10,12 However,  ?5 q3 T$ [. b, c
Sutherland et al13 did not find a correlation between5 L" @- k4 W& n& A& D7 I
childhood testosterone exposure and reduced adult0 n7 e# m- ]4 w% q5 y
penile length in clinical studies.2 R- M. W/ _0 s' g( P
Nonetheless, we do not believe our patient is  d* u0 v: r: v2 j4 F
going to experience any of the untoward effects from$ F& J* Z; y7 U) d* }1 \
testosterone exposure as mentioned earlier because$ h& e: A# S0 r5 D' u9 d7 A
the exposure was not for a prolonged period of time.: \9 a; K* x2 p1 f$ B, I6 V7 B
Although the bone age was advanced at the time of' [. ~5 M& p% p! n, a
diagnosis, the child had a normal growth velocity at2 C% b5 D+ Q- W. W5 }7 j
the follow-up visit. It is hoped that his final adult- ^6 R8 ?2 B3 [
height will not be affected." }7 ^6 N6 x* R0 ?' S; C  x
Although rarely reported, the widespread avail-; ]" o5 i# r( j4 v, j- R- Y; |$ ~
ability of androgen products in our society may
/ S# H3 A# V( Xindeed cause more virilization in male or female
) g" |0 I8 ], z) M4 gchildren than one would realize. Exposure to andro-
: m2 t' @9 X% }6 T6 |: Ogen products must be considered and specific ques-
) M) a: N( C( q% C; ~+ O$ q7 g' Ztioning about the use of a testosterone product or$ s# k6 S! ?; T+ j6 I
gel should be asked of the family members during( v# h5 {! a' j
the evaluation of any children who present with vir-
8 A% I0 R( {  m0 G8 t3 zilization or peripheral precocious puberty. The diag-& T3 C$ Y- c7 }% r. x) i( f) q; X% O
nosis can be established by just a few tests and by6 x6 G9 Z  u1 v' e
appropriate history. The inability to obtain such a# N  j) [4 @$ I- N
history, or failure to ask the specific questions, may3 k( B6 ]! E2 f* C; T2 ^
result in extensive, unnecessary, and expensive, z* d% P$ }9 y7 N6 f6 A& C
investigation. The primary care physician should be! i5 q" W0 M$ h/ t& U5 L2 T
aware of this fact, because most of these children9 K* H! k8 q& H( S, w$ g
may initially present in their practice. The Physicians’3 I4 W( t7 F& s  c* g
Desk Reference and package insert should also put a
8 `* f" U3 I6 u0 O# A' r5 J- lwarning about the virilizing effect on a male or
- t# O' U- {5 R: V+ s) xfemale child who might come in contact with some-
4 r# y% O, h3 K- D- Vone using any of these products.% B" a& i4 _0 Y# q3 D4 k
References) ?) _) \. `8 T2 z
1. Styne DM. The testes: disorder of sexual differentiation2 N& t2 m+ f3 q* d* a/ G
and puberty in the male. In: Sperling MA, ed. Pediatric8 j0 x2 y& z3 B. O/ H
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;, C& H/ i& H! f1 V
2002: 565-628.0 T! K9 a: S) z# `
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious6 ]! S! \1 B; Z* d
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
3 p; d6 s# S, ?1 V/ J; F% c
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