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
# N. j3 T+ M" n5 |8 e) WBoy Induced by Indirect Topical
& c8 J  P! R+ x) j) b/ cExposure to Testosterone
0 k- x& @* [  L! r8 ]" T( M! ]Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2) j5 B  y" k# _% y$ D8 t
and Kenneth R. Rettig, MD1
. q. C  m& F+ P# n! c/ DClinical Pediatrics3 p: ?8 k3 e. {: |$ |1 G% o
Volume 46 Number 6
: i& S/ c  K' S# j4 ^3 O0 u% b( oJuly 2007 540-543' p0 E5 H; h+ S2 x
© 2007 Sage Publications
8 i/ ^( g" e& N7 _3 e10.1177/0009922806296651! M8 \2 d0 S" F
http://clp.sagepub.com
% V% l2 P, K8 d0 d: @# P1 Z+ i3 |hosted at1 o' g+ A$ [+ P" V
http://online.sagepub.com& h+ H0 i$ Y' B- _; o* i/ }1 m
Precocious puberty in boys, central or peripheral,. T5 l0 y* J/ b+ e8 D* W
is a significant concern for physicians. Central
1 I# g1 n( f) l7 a0 Lprecocious puberty (CPP), which is mediated4 b" h. I$ \0 i6 O; E: R. h3 j
through the hypothalamic pituitary gonadal axis, has
& v- |8 w& g* I2 q" c3 oa higher incidence of organic central nervous system& o2 G5 |4 }' B. u0 q* U
lesions in boys.1,2 Virilization in boys, as manifested
2 O8 N7 Y. r/ G" }5 rby enlargement of the penis, development of pubic3 W0 K8 K; K) _/ B. j. I) i
hair, and facial acne without enlargement of testi-6 l% _3 Y. U$ Z
cles, suggests peripheral or pseudopuberty.1-3 We
5 D, u# x6 B0 freport a 16-month-old boy who presented with the$ v1 \+ \3 |) V
enlargement of the phallus and pubic hair develop-
$ j6 y; ^" A6 x' x6 Q  T6 wment without testicular enlargement, which was due
" [: P  u" }; P: z3 y+ @to the unintentional exposure to androgen gel used by2 K6 x# l3 u! a- w' y7 t* o
the father. The family initially concealed this infor-
. p! c1 a7 e$ X  pmation, resulting in an extensive work-up for this
+ I: ]+ l# {  T4 y! O1 ]9 [% Gchild. Given the widespread and easy availability of
( W- i# N: V) G; atestosterone gel and cream, we believe this is proba-' ~0 R( s3 h; @6 D3 S
bly more common than the rare case report in the
) t3 [  c- o. R  O6 \' B1 jliterature.41 f8 ?/ \2 G8 z3 Q! Y4 X
Patient Report* d' f) F5 s6 H# ^$ }5 G
A 16-month-old white child was referred to the' ~, l' {/ r$ d2 Z, P8 T
endocrine clinic by his pediatrician with the concern
7 y# T. g4 U0 @6 Fof early sexual development. His mother noticed
+ @3 C0 r6 H7 K" C$ I+ ^% y- j0 ]" qlight colored pubic hair development when he was) Y3 t' @& d! C+ r6 B9 _
From the 1Division of Pediatric Endocrinology, 2University of( U# y, _3 s5 Q) M* i; B  p
South Alabama Medical Center, Mobile, Alabama.
& o4 V5 U4 Y. M1 |& f  ?Address correspondence to: Samar K. Bhowmick, MD, FACE,- ?9 e6 g" ]0 ~2 w( H
Professor of Pediatrics, University of South Alabama, College of4 C  }& j2 U' `  f: n  I+ _4 N
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
* x8 X1 `1 A5 x  s" we-mail: [email protected].
3 g. k* F0 G- t2 x  kabout 6 to 7 months old, which progressively became
% D5 O$ w9 q( J8 Q# \darker. She was also concerned about the enlarge-
+ d% @( D% C% A3 F. m1 Wment of his penis and frequent erections. The child
9 w) @+ ~8 y3 x1 F) U. pwas the product of a full-term normal delivery, with
) X# a" X4 K, X$ La birth weight of 7 lb 14 oz, and birth length of
& j8 X3 N6 T& B20 inches. He was breast-fed throughout the first year% A7 E+ B# H  [1 T# d) ]* ], Z
of life and was still receiving breast milk along with
7 a5 X& U* G  \5 ~$ ]; psolid food. He had no hospitalizations or surgery,
; z3 J, `) |0 u# X* U( c/ `* sand his psychosocial and psychomotor development6 o1 y3 j; B% k9 g6 N( l: w
was age appropriate.' @3 i, W. `1 N; |# L0 @- c7 k% x  y
The family history was remarkable for the father,8 c$ U; P( B0 Y3 U7 l. R
who was diagnosed with hypothyroidism at age 16,
" ]4 L4 A2 v- M# l3 {: Mwhich was treated with thyroxine. The father’s  I9 W, u0 J5 r- P, b1 K
height was 6 feet, and he went through a somewhat
7 d2 U. \3 I" U8 C3 [+ i; [early puberty and had stopped growing by age 14.
" d* x( Q% {% \The father denied taking any other medication. The
) _3 g% O  H* }) B( Q/ b1 y7 f# ochild’s mother was in good health. Her menarche0 h! A' l# V: b2 B
was at 11 years of age, and her height was at 5 feet1 Z4 r2 t! M/ A7 p
5 inches. There was no other family history of pre-! t' _# m7 T2 G0 n- b
cocious sexual development in the first-degree rela-+ @2 h2 }* H3 H$ |2 m% |
tives. There were no siblings.
3 Q, l: W; x7 N5 ?! g- ]( i. S  BPhysical Examination
2 |* d$ Q' {/ c* M! uThe physical examination revealed a very active,
2 o' W5 B: H) i( `" L( m1 q: aplayful, and healthy boy. The vital signs documented
8 ^$ R. m1 ~, L' `a blood pressure of 85/50 mm Hg, his length was
: y/ K# M' r; {6 T90 cm (>97th percentile), and his weight was 14.4 kg
! g2 [' i  s/ ~( t/ D+ A- Z4 n" B(also >97th percentile). The observed yearly growth5 b0 r6 `* J: F$ s: s( @3 D% H$ Q
velocity was 30 cm (12 inches). The examination of
: C+ _; B$ \, t/ o% [! Zthe neck revealed no thyroid enlargement.  I& m& B. `; R+ }3 {
The genitourinary examination was remarkable for
$ \( K0 y3 N! {$ B; Penlargement of the penis, with a stretched length of' B* S! C& T+ L7 I4 m
8 cm and a width of 2 cm. The glans penis was very well
; }/ E2 ?% H7 `7 x# L6 hdeveloped. The pubic hair was Tanner II, mostly around- [- e: I, [6 N: n
5401 J# @8 M2 c! |5 ]3 P8 `% p
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from: `3 @/ n) I0 b/ c) u( }
the base of the phallus and was dark and curled. The
+ K& k2 L9 [; M6 P( R" H. L$ ]testicular volume was prepubertal at 2 mL each.6 M. e3 P' F$ @! {; ]7 e4 t# V, d; y
The skin was moist and smooth and somewhat: g  v7 B/ c. a) K! q2 p
oily. No axillary hair was noted. There were no! E, Y6 [0 V- b. |; y) O
abnormal skin pigmentations or café-au-lait spots.% i! x/ |$ B: n' O: g) f" }
Neurologic evaluation showed deep tendon reflex 2+7 Y( W2 W. N( ]; W# O
bilateral and symmetrical. There was no suggestion6 H0 U3 J2 D* ?" S- s
of papilledema.
; g8 x4 g* O, q9 N) Z. ?  aLaboratory Evaluation! e, L6 p7 Z5 D: g& ?5 `7 T
The bone age was consistent with 28 months by
5 {9 ]# ~; ]' Ousing the standard of Greulich and Pyle at a chrono-5 j* n0 Z. ?; Y
logic age of 16 months (advanced).5 Chromosomal  q7 R6 c0 N: v( d
karyotype was 46XY. The thyroid function test
/ E3 y. w1 ~% c' K: kshowed a free T4 of 1.69 ng/dL, and thyroid stimu-) [7 ^2 R0 ~" T5 w4 i5 H% f
lating hormone level was 1.3 µIU/mL (both normal).
3 O! j, S. i' SThe concentrations of serum electrolytes, blood
, ~7 p6 K. I( e, B; ~! Nurea nitrogen, creatinine, and calcium all were  ^0 w2 k/ \+ A( ^2 t% E
within normal range for his age. The concentration" B1 l" l* ?& Y8 \
of serum 17-hydroxyprogesterone was 16 ng/dL5 Q  q7 X* T# H* }0 e* p/ u; {  U% O
(normal, 3 to 90 ng/dL), androstenedione was 20% s* d3 A4 v$ D* R0 t
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
3 M8 v: M) R2 ~: }' fterone was 38 ng/dL (normal, 50 to 760 ng/dL),$ X6 |" k0 I6 d+ ~4 S
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
3 i0 A+ R( P7 N) I! s: r1 I49ng/dL), 11-desoxycortisol (specific compound S)! h9 R/ y  ~) ^, b% J6 E
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
2 [8 X/ u1 ?* D& [8 U  S% O9 |tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total4 M7 F* E8 R  ?% h
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
2 @# t: h- X4 G3 v. v6 T3 _and β-human chorionic gonadotropin was less than8 @) b  n6 f2 o0 n* U$ C
5 mIU/mL (normal <5 mIU/mL). Serum follicular
; @+ c7 A8 p+ J. ~$ nstimulating hormone and leuteinizing hormone
& C' m3 T+ [; m6 U- M1 cconcentrations were less than 0.05 mIU/mL
% ]9 T' g9 ]; H. D(prepubertal).# Y" W* Y) {2 h" C/ {" f1 D
The parents were notified about the laboratory2 j* O4 m0 Y& y9 k! [/ }
results and were informed that all of the tests were
/ m! v; [* A5 vnormal except the testosterone level was high. The
8 ^5 U2 m$ \5 g1 U  Qfollow-up visit was arranged within a few weeks to
+ l2 _: _0 H$ ]* N6 Q( r7 Mobtain testicular and abdominal sonograms; how-
' u" P( X0 `* A& C1 O9 ^ever, the family did not return for 4 months.
* r- C9 ~8 {, r( A. Q! v& LPhysical examination at this time revealed that the0 i' [5 z0 I5 a0 A3 G* T- L8 T
child had grown 2.5 cm in 4 months and had gained6 U4 G2 T- Q  [* s% }, ]% B7 y
2 kg of weight. Physical examination remained) q9 G" k# g0 X* Q5 s
unchanged. Surprisingly, the pubic hair almost com-
! m: P) c: ]9 B) l7 bpletely disappeared except for a few vellous hairs at' E$ p' H! f+ Q
the base of the phallus. Testicular volume was still 2
' K" O! E: N/ ZmL, and the size of the penis remained unchanged.
8 |9 b# b+ i% O6 uThe mother also said that the boy was no longer hav-" c" T% p6 |! C; o3 [/ k1 h' O
ing frequent erections.
) y' O/ r/ E% e) S1 a* @Both parents were again questioned about use of+ n  i$ I" T! P: j" L
any ointment/creams that they may have applied to
* q1 n4 ~% n; p% Nthe child’s skin. This time the father admitted the, x" k& _# M  x8 M. Q6 B
Topical Testosterone Exposure / Bhowmick et al 541
$ m6 @. S5 d, N  y: w$ ?use of testosterone gel twice daily that he was apply-  Q9 t( k4 _. f) b# A( h
ing over his own shoulders, chest, and back area for" |% j% F9 g' @1 D) k+ k, }/ x5 N
a year. The father also revealed he was embarrassed, L# [1 l. `9 p' ]5 z) U
to disclose that he was using a testosterone gel pre-
+ k1 I" z2 B& n: j; R$ vscribed by his family physician for decreased libido
3 ~" t/ `; V& P9 q8 W9 n7 @" ^secondary to depression.: F7 U' D) D/ j; ]
The child slept in the same bed with parents.
! _; ]) r8 I% v1 ]! u, L' w( i/ O, A! Y9 zThe father would hug the baby and hold him on his
: m4 A/ I4 {1 ]% x$ c2 dchest for a considerable period of time, causing sig-! V6 @2 i! d( J: Y/ f
nificant bare skin contact between baby and father.
$ }0 o( m8 m. k8 k* F8 g+ DThe father also admitted that after the phone call,$ b9 ^' X3 w2 F9 F# r2 W% J
when he learned the testosterone level in the baby
1 a1 l' {5 t$ J" u3 B& jwas high, he then read the product information
0 r; U/ ^! g- e* L2 V3 q5 upacket and concluded that it was most likely the rea-
$ ^' s; }  O4 ?son for the child’s virilization. At that time, they, ]  `- G1 x" h+ j1 X4 P% e5 ^
decided to put the baby in a separate bed, and the
9 K3 g) R0 G1 [father was not hugging him with bare skin and had
( q. ]$ ]$ M4 O5 q- |; z; q  S5 sbeen using protective clothing. A repeat testosterone
% F2 Y1 X. X) \# a; mtest was ordered, but the family did not go to the& A  v  M4 I0 l" O# v2 E
laboratory to obtain the test.# t' S- Y8 z& i+ U' c+ i7 b
Discussion% v; C# M* A6 u6 r0 r# ?" l
Precocious puberty in boys is defined as secondary/ v# C/ _: _" Y( Y/ c& y' G
sexual development before 9 years of age.1,46 X  s7 N/ S. ]. v
Precocious puberty is termed as central (true) when
4 d$ u0 ^, B6 e( e- `it is caused by the premature activation of hypo-
& {4 _" H0 X* Jthalamic pituitary gonadal axis. CPP is more com-
; `. L  L1 p' m9 emon in girls than in boys.1,3 Most boys with CPP
9 I. x8 F5 G$ ?" T4 F' emay have a central nervous system lesion that is, F  A& R* F0 V
responsible for the early activation of the hypothal-9 {0 d9 e" R. d' ^$ T7 D
amic pituitary gonadal axis.1-3 Thus, greater empha-$ B$ w+ J  f  v$ }" B! b& I* ]
sis has been given to neuroradiologic imaging in
9 k  Q" z  a# q$ T, U8 mboys with precocious puberty. In addition to viril-
2 _, A1 ?/ X3 b4 G/ s" J9 cization, the clinical hallmark of CPP is the symmet-8 U6 x! S3 g/ m9 o2 g
rical testicular growth secondary to stimulation by
6 L2 n+ P' c' x- {9 _0 lgonadotropins.1,34 y; e+ w! K$ S; i/ U! E: r
Gonadotropin-independent peripheral preco-' P( `5 w, i' n4 `- t9 Y2 Z1 K0 S
cious puberty in boys also results from inappropriate
& i  a5 [# d3 D- Zandrogenic stimulation from either endogenous or
0 j' k! M3 j1 S# q, mexogenous sources, nonpituitary gonadotropin stim-3 R( E( n: U- Q
ulation, and rare activating mutations.3 Virilizing5 w; g( L* E/ I5 v& |$ _8 Q+ i) b  d
congenital adrenal hyperplasia producing excessive% w" {5 m4 _9 s4 o4 ~
adrenal androgens is a common cause of precocious9 g; J2 H! P0 C+ l2 \) B! [5 u
puberty in boys.3,4
7 ?$ _0 o$ P# W/ o9 g1 XThe most common form of congenital adrenal
' z" j, t5 L/ [hyperplasia is the 21-hydroxylase enzyme deficiency.
7 |, U; f9 V% J- z1 KThe 11-β hydroxylase deficiency may also result in& W* K6 ^5 E8 {/ W9 Y
excessive adrenal androgen production, and rarely,3 N& h& P% M3 o7 \
an adrenal tumor may also cause adrenal androgen
/ W3 e$ r; h0 v. ^! Lexcess.1,3
$ j% a/ b5 E7 {0 {: Y: ]3 Xat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
; S  x2 G3 d' a. I! m+ j' l: ?: w542 Clinical Pediatrics / Vol. 46, No. 6, July 20078 {) s+ L$ O5 z' _4 ^& |
A unique entity of male-limited gonadotropin-% ~" ]& r8 s  N# t! A' I
independent precocious puberty, which is also known
$ d0 H/ _6 m3 U# X: M, X6 r" Nas testotoxicosis, may cause precocious puberty at a1 A9 h& Q, x. I  c; M
very young age. The physical findings in these boys
! y) w& A  U$ q9 m; k0 K+ hwith this disorder are full pubertal development,
/ ^- D* O. a+ }0 y2 p, e# R% eincluding bilateral testicular growth, similar to boys
9 G) Q% T0 Q2 R' l5 H7 I& u' iwith CPP. The gonadotropin levels in this disorder( k! e7 g0 b, o- v
are suppressed to prepubertal levels and do not show- P, W0 a( M7 |0 L- N. b0 p
pubertal response of gonadotropin after gonadotropin-
' V8 B* |7 I) v! R( oreleasing hormone stimulation. This is a sex-linked7 l2 C- l( E6 g& w6 ?3 k/ q
autosomal dominant disorder that affects only
# J- T5 o1 r1 L. Q+ v% l% [  Ymales; therefore, other male members of the family
4 x, G) I* f9 s- i3 dmay have similar precocious puberty.3
% m+ t+ v' [  s5 d9 |. d4 @In our patient, physical examination was incon-
  H5 i6 `& u# S% ]% R) j' Y% Bsistent with true precocious puberty since his testi-1 j: l1 s, [4 l0 O0 Y& R
cles were prepubertal in size. However, testotoxicosis
* J3 S- @7 n  Q$ swas in the differential diagnosis because his father2 G+ }7 D( w/ j/ X! G  C! p0 @
started puberty somewhat early, and occasionally,
1 {$ \3 g3 [  c/ ^' q( P6 h& ^testicular enlargement is not that evident in the" u1 @( e: |. Y$ s
beginning of this process.1 In the absence of a neg-! U; b: E' d- Q' X# W- ?
ative initial history of androgen exposure, our
; n5 x7 T! K3 b* V) d+ ^! Cbiggest concern was virilizing adrenal hyperplasia,2 @+ Y  L% q+ q- J; N
either 21-hydroxylase deficiency or 11-β hydroxylase
, b: w/ F/ X8 a' K! A( K' G0 ~, L8 udeficiency. Those diagnoses were excluded by find-
6 x& i5 @7 Q  \4 j" p* q3 P, _ing the normal level of adrenal steroids." h( k* t0 y' @3 j; I6 H1 W/ d
The diagnosis of exogenous androgens was strongly8 d; o1 w9 x* b% p% t* Z2 q, x
suspected in a follow-up visit after 4 months because
" w& y. _1 u2 l! x- [+ wthe physical examination revealed the complete disap-, G, i. v2 B3 {
pearance of pubic hair, normal growth velocity, and
. f9 |* K' j  `& fdecreased erections. The father admitted using a testos-
' o% m! _* Y! F* P+ Xterone gel, which he concealed at first visit. He was# t+ X. [/ k4 V; X
using it rather frequently, twice a day. The Physicians’
( W: \8 U9 `  |4 b; ]. cDesk Reference, or package insert of this product, gel or
( E6 J' J2 f3 {& Xcream, cautions about dermal testosterone transfer to
- B5 z2 L8 G- d; a  \3 k" Yunprotected females through direct skin exposure.
/ V, R5 h" s' d( q* O* t& D& ~0 T' RSerum testosterone level was found to be 2 times the
; X6 g" C8 Q) X3 a6 b2 ?, z/ S4 I7 K$ _baseline value in those females who were exposed to9 c3 M6 m3 G0 {. \+ Y
even 15 minutes of direct skin contact with their male
' M! ?% r# X# Q0 \) q' i8 d' y, z1 Zpartners.6 However, when a shirt covered the applica-
. _/ w6 z7 F7 p. h( @+ h% stion site, this testosterone transfer was prevented.
# m4 T7 _8 |7 p) t; \Our patient’s testosterone level was 60 ng/mL,
  M" Y4 S: S: t  N: swhich was clearly high. Some studies suggest that& B! A0 ^8 k6 Y0 Q) L. g/ C0 u8 R( u
dermal conversion of testosterone to dihydrotestos-
  \' P& W$ _+ [# S" kterone, which is a more potent metabolite, is more
9 R2 L& ^7 Y( {$ |7 d4 _active in young children exposed to testosterone& ]0 J1 ~$ a; s" ?/ m6 s
exogenously7; however, we did not measure a dihy-# j" S1 s# J; F0 ?6 D
drotestosterone level in our patient. In addition to" n8 w8 i  V7 o
virilization, exposure to exogenous testosterone in
  v' g# Y& f1 d$ ~5 R8 U' Ychildren results in an increase in growth velocity and8 h  b5 C9 r% ~
advanced bone age, as seen in our patient.
% m  K6 g) c$ n% R* zThe long-term effect of androgen exposure during* B8 @( S0 U2 S6 F3 a! W0 ^5 L
early childhood on pubertal development and final9 t8 @# D; s" b2 L  N
adult height are not fully known and always remain
* K; v; l! {( oa concern. Children treated with short-term testos-8 ?0 ~3 |0 \! A) Q* ^, q) y
terone injection or topical androgen may exhibit some$ F! C7 }: ]# @
acceleration of the skeletal maturation; however, after; P# @' v( ~9 r3 t0 l
cessation of treatment, the rate of bone maturation5 b2 I6 x* @" `; j6 S: v
decelerates and gradually returns to normal.8,9
  w& V9 Y% j7 I4 N: MThere are conflicting reports and controversy+ j' K' U. @8 a8 _' m- v
over the effect of early androgen exposure on adult
& b: G1 ^& Y0 y4 u2 {& ^" k8 f# `' Openile length.10,11 Some reports suggest subnormal/ a1 V4 z( @( C
adult penile length, apparently because of downreg-% \# e8 h1 k" _. h4 U7 y% O
ulation of androgen receptor number.10,12 However,3 o. g$ z& m7 |: }
Sutherland et al13 did not find a correlation between
& n" q5 @( W  l, ]- Kchildhood testosterone exposure and reduced adult
# w% `% V+ m+ C7 O/ a2 mpenile length in clinical studies.0 D! K% r4 z+ |" o: W; U: ?
Nonetheless, we do not believe our patient is
3 _; ~* Z5 c1 B( h" ]5 l. }going to experience any of the untoward effects from6 A' J/ q$ @+ v! L* P0 B" R, x
testosterone exposure as mentioned earlier because
4 S$ |. O  \$ Jthe exposure was not for a prolonged period of time.
" u/ K3 {/ ]2 NAlthough the bone age was advanced at the time of) ~' M& Y- c( k' q
diagnosis, the child had a normal growth velocity at
+ S- s* ?7 W# p& G) ?7 \5 p- jthe follow-up visit. It is hoped that his final adult( J% z  Q; s4 e$ x5 C2 B
height will not be affected.5 z$ x) S2 O8 |9 _' ?5 t- z9 X3 k) h0 M  L
Although rarely reported, the widespread avail-
. V5 m# p3 U* r& s' Eability of androgen products in our society may
/ |+ D$ x3 F# C. a1 ^+ o0 [! zindeed cause more virilization in male or female, Y7 \/ q% f$ Z0 S; J
children than one would realize. Exposure to andro-6 J1 `9 w, Q) s$ Q1 R0 @1 ?
gen products must be considered and specific ques-
2 ]6 ]5 p$ T9 ?tioning about the use of a testosterone product or
/ m4 g3 c! [# Q! A) P' U$ wgel should be asked of the family members during* D7 m9 w5 d0 @
the evaluation of any children who present with vir-
) z; I8 |% v* ~9 Bilization or peripheral precocious puberty. The diag-
5 M! Y3 Y7 T3 dnosis can be established by just a few tests and by
  t  O/ V/ y' Y, Lappropriate history. The inability to obtain such a6 A3 p# t' s6 t% j4 v+ c+ T
history, or failure to ask the specific questions, may
6 l& U) e- s6 ~result in extensive, unnecessary, and expensive
; A4 e; T- c! K- l( y  ^( O+ [investigation. The primary care physician should be# h( P7 l( C: a. \2 B0 C+ ?
aware of this fact, because most of these children
( J$ Y. G) [" H, X/ b5 C  kmay initially present in their practice. The Physicians’
$ i' t2 g* Y! Y1 QDesk Reference and package insert should also put a
1 T) I8 a6 ~( ]$ Ywarning about the virilizing effect on a male or, F" {8 d8 M" |( |+ H2 T
female child who might come in contact with some-
4 B5 A0 E, D  o8 _3 [( O  n; Aone using any of these products.
+ |+ A- U3 l+ g1 RReferences
1 C; ]  _( Q0 c' W9 h8 ]* K% z5 h7 V1. Styne DM. The testes: disorder of sexual differentiation
  o8 r8 K, [" K0 v, V- E1 a  [and puberty in the male. In: Sperling MA, ed. Pediatric
% M1 W  R( @" `Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
- X$ G6 b6 u* ?- I1 Y2002: 565-628.
2 }: b( @! K6 L/ E2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious# O) z1 Z7 E0 H+ [
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
2 z7 W: W. d' a: S, F6 |Boy Induced by Indirect Topical
" R0 ]$ n& y9 u8 I5 J9 `Exposure to Testosterone
( s7 \! b" }: t2 lSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
, T3 T1 v% u; L0 O# p% G9 M% j2 zand Kenneth R. Rettig, MD11 I5 k: W: ]" k$ ]9 F" r4 q% p
Clinical Pediatrics
5 e2 [' ^5 W3 [% uVolume 46 Number 6
# W4 j8 @. M  |! T3 T' \, JJuly 2007 540-543. t) O0 \1 u6 b: X2 l
© 2007 Sage Publications+ @5 W; s. g# P& M- a2 v$ p
10.1177/0009922806296651
$ I+ C; V/ ]% `  {$ ahttp://clp.sagepub.com
% x# Z+ ~, T/ @7 |* \0 ~# ahosted at
1 F. H5 t$ ?/ }! {0 }! Hhttp://online.sagepub.com" q9 M" v1 e# C' P& z% z0 y
Precocious puberty in boys, central or peripheral,1 ]  P- F" ^  m: ~
is a significant concern for physicians. Central
: u7 o( `7 V! M4 f& Wprecocious puberty (CPP), which is mediated
# |4 L& K. `. r- w! G: Y" T! g, bthrough the hypothalamic pituitary gonadal axis, has6 F/ y9 o% Y& b) g- I' E
a higher incidence of organic central nervous system
( D* p! x8 g, S; {& blesions in boys.1,2 Virilization in boys, as manifested2 K( M' {! k% l8 k8 t
by enlargement of the penis, development of pubic/ F  d# }2 ~- }
hair, and facial acne without enlargement of testi-( k9 N! [. C# b: A" U* q3 F8 U
cles, suggests peripheral or pseudopuberty.1-3 We
; t' m; {# d; |report a 16-month-old boy who presented with the7 C& ^) r& R' [3 q4 N# V
enlargement of the phallus and pubic hair develop-
! x' V% T) t" r+ Iment without testicular enlargement, which was due' `  V* G  `- G' c3 G
to the unintentional exposure to androgen gel used by
2 d- F' x0 V2 o( d7 _) S( ~the father. The family initially concealed this infor-- c' h2 Q6 q5 h: U7 y) I( F
mation, resulting in an extensive work-up for this, \& s" P, m4 N1 i* A
child. Given the widespread and easy availability of
. {: V( ]+ H1 f7 [6 z/ K' a' g1 qtestosterone gel and cream, we believe this is proba-$ z, q3 }  M2 {8 W5 K
bly more common than the rare case report in the, C3 x5 J$ U3 T1 M
literature.44 Z+ S, K- b5 c# Z4 e9 `, D
Patient Report
6 k6 a0 S( [9 ]A 16-month-old white child was referred to the
2 @* w: C+ m& \; Sendocrine clinic by his pediatrician with the concern. ^* q1 o# D4 A/ C
of early sexual development. His mother noticed
$ \8 b# _- p( H9 V2 clight colored pubic hair development when he was4 [3 S* m  z) v) g9 f4 p- [0 Y$ s: ]
From the 1Division of Pediatric Endocrinology, 2University of- e6 C' g3 w2 T" V  _
South Alabama Medical Center, Mobile, Alabama.
/ K* j5 G3 G5 x# @Address correspondence to: Samar K. Bhowmick, MD, FACE,
$ M# l  v) E1 ~5 pProfessor of Pediatrics, University of South Alabama, College of" x2 o4 w7 J' |+ |5 X
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;. O2 Z; M2 ?+ a  X& `, M7 f: Z
e-mail: [email protected].# {+ y& U9 `) }2 g
about 6 to 7 months old, which progressively became
" ?" \: k% I5 X" }darker. She was also concerned about the enlarge-
- I2 ~2 O3 T# r# ]ment of his penis and frequent erections. The child/ s/ `$ V% U% G! A4 {! a8 f
was the product of a full-term normal delivery, with
! u& a; d1 N: B) G2 A3 Ha birth weight of 7 lb 14 oz, and birth length of
7 K6 f& l. z# Z# S. a) F9 P0 B20 inches. He was breast-fed throughout the first year
$ H) p; v" ^1 ^" r" Z) y/ Rof life and was still receiving breast milk along with& d: v: q: T, d8 ?6 O
solid food. He had no hospitalizations or surgery,- Y5 P0 L- y  a. l0 J/ P
and his psychosocial and psychomotor development" X7 h$ f) {' _; N/ \  a  N* Z4 c$ U
was age appropriate.: ~# v* O' Y! ~( _5 ]0 ~  Q; t
The family history was remarkable for the father,1 }6 J* E3 F/ Y! G; v+ ~' N  q
who was diagnosed with hypothyroidism at age 16,
7 W) t8 k4 p1 V& Fwhich was treated with thyroxine. The father’s3 {: v) W$ i9 a
height was 6 feet, and he went through a somewhat+ ?- [, ^; B: s$ M8 O
early puberty and had stopped growing by age 14.
4 I/ p5 h$ p% h! rThe father denied taking any other medication. The
  d( e; h' S  Q% ichild’s mother was in good health. Her menarche. ]/ g$ O+ I# B( {  }5 }
was at 11 years of age, and her height was at 5 feet
3 \2 C* d3 g" x) \6 i5 inches. There was no other family history of pre-
, K! {7 t' i3 [% z9 K0 S9 Kcocious sexual development in the first-degree rela-5 K: X% }3 {& r' N4 r4 N) T5 i
tives. There were no siblings.
% ^+ O! d* ]1 u1 [( w5 a- BPhysical Examination+ ?- P6 w; h7 ^# o; z1 `  o
The physical examination revealed a very active,$ x! a+ }7 P( K' X( O0 n! f
playful, and healthy boy. The vital signs documented
( j! K. Y& T7 h2 f, E& e! da blood pressure of 85/50 mm Hg, his length was' K& K0 |1 F$ m" C5 e
90 cm (>97th percentile), and his weight was 14.4 kg
# e" U) n1 L0 y1 r5 R* j/ ~(also >97th percentile). The observed yearly growth
6 R2 V  w; V& gvelocity was 30 cm (12 inches). The examination of
0 I) m8 g1 b" q: x& |% }8 Ythe neck revealed no thyroid enlargement./ Z# z7 T! S2 E2 \+ B1 h
The genitourinary examination was remarkable for
' D, S0 O5 _/ D3 E! oenlargement of the penis, with a stretched length of
, r2 O) ]# c, H, `2 n8 cm and a width of 2 cm. The glans penis was very well) ^" ^- x5 b* Z
developed. The pubic hair was Tanner II, mostly around1 X8 l! \% ^( r; T" o8 V
5402 ]2 z; m$ h1 ?! K1 g: j- I' q4 i' N
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
- Z7 [/ u: O7 V& D( Hthe base of the phallus and was dark and curled. The( y2 b3 |! t; T, S9 s
testicular volume was prepubertal at 2 mL each.2 O1 s+ D- K# N7 }# d8 N! b, X) n$ a* s
The skin was moist and smooth and somewhat
0 f  M7 K% f( R7 a& X% a3 A3 o- voily. No axillary hair was noted. There were no
% l% f+ q. q4 s& z, Yabnormal skin pigmentations or café-au-lait spots.9 B$ z) P/ c/ S  l( P* `
Neurologic evaluation showed deep tendon reflex 2+6 @' _$ ]7 m2 a: f+ `; W& \# J0 q
bilateral and symmetrical. There was no suggestion
9 r9 f8 Y; @: Yof papilledema.4 z9 R; S  D0 `# f
Laboratory Evaluation
/ F: Z6 h* f; e9 ?" A8 mThe bone age was consistent with 28 months by. l7 ^: A/ R4 u* N' Q2 n
using the standard of Greulich and Pyle at a chrono-
7 R! X& w: g5 n+ V7 R6 z4 o3 {logic age of 16 months (advanced).5 Chromosomal
/ Y% p9 j, d- F) e, I' Bkaryotype was 46XY. The thyroid function test
3 D. c: C9 A5 @! w" q0 a3 ^showed a free T4 of 1.69 ng/dL, and thyroid stimu-4 l$ c6 `) j3 Q2 T2 n2 ~: Z& j& n
lating hormone level was 1.3 µIU/mL (both normal).
2 H1 P6 f  z2 |; BThe concentrations of serum electrolytes, blood
9 p& x% p) f- e5 H4 D$ g" y" Eurea nitrogen, creatinine, and calcium all were
/ u  s) R2 r3 V6 |! |: Rwithin normal range for his age. The concentration; ]. @6 O( X* i* I: T$ u
of serum 17-hydroxyprogesterone was 16 ng/dL
1 C/ c) a8 Z; ^2 Z: I5 g& U4 r2 _( n(normal, 3 to 90 ng/dL), androstenedione was 20
# @! H7 T* u2 ~2 ^+ w( {0 cng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-' n! F( V- R! F7 }! ?
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
2 T8 }7 h" ~; `' P2 ]( Ydesoxycorticosterone was 4.3 ng/dL (normal, 7 to
( T5 \0 ?0 d' d49ng/dL), 11-desoxycortisol (specific compound S)
. f; h4 Y2 N  J8 n( s- _! }2 `4 r1 vwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-4 j( D; C' {" F4 |* g
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
0 T, }5 B8 n; s9 E6 d  d' {testosterone was 60 ng/dL (normal <3 to 10 ng/dL),' u7 v7 q. c+ @+ U& O
and β-human chorionic gonadotropin was less than
/ G& v, `0 r: W4 o" B5 mIU/mL (normal <5 mIU/mL). Serum follicular
6 _# T- }. S6 f! }) rstimulating hormone and leuteinizing hormone
8 e3 q) J3 Q3 `" v3 Xconcentrations were less than 0.05 mIU/mL
1 |6 L: ~0 v. K: K  @% b/ K% R# N(prepubertal).$ \1 b4 L" Q; I
The parents were notified about the laboratory! E4 s! L: {$ O- B( B- B
results and were informed that all of the tests were
  i; v5 ]+ S4 ?- l0 o$ K' ?normal except the testosterone level was high. The
; E" G' `3 w% _* @- E) r9 Gfollow-up visit was arranged within a few weeks to8 F* L7 \: |# O8 @
obtain testicular and abdominal sonograms; how-; i% m' F/ o7 W3 b: S' U
ever, the family did not return for 4 months.
1 W8 @# H) ?: c: u  I2 [1 D$ MPhysical examination at this time revealed that the
% T- L9 d: K1 M( y6 kchild had grown 2.5 cm in 4 months and had gained
" C' Y! s( l. f2 K; @! k2 kg of weight. Physical examination remained; i5 v) v. ?( \1 r* G$ H2 V, B8 g0 p* U
unchanged. Surprisingly, the pubic hair almost com-
$ h% C7 Z7 ?  v( G$ ?" U! I0 r, mpletely disappeared except for a few vellous hairs at3 D/ E% A* p" S9 E% K# h
the base of the phallus. Testicular volume was still 2
' D% j0 W- i& kmL, and the size of the penis remained unchanged.
6 p/ H- x% ^/ i  DThe mother also said that the boy was no longer hav-
  r" e( b5 ~) o" L! h" Ding frequent erections.4 T4 u( K# t' F' ~2 u5 v
Both parents were again questioned about use of* i2 y6 [* _2 k8 _
any ointment/creams that they may have applied to
/ l/ ]4 W; c, uthe child’s skin. This time the father admitted the4 o) ^7 N# a- W3 a# v8 g
Topical Testosterone Exposure / Bhowmick et al 541
( s" a" r- W  [. e& q- i5 w) e3 juse of testosterone gel twice daily that he was apply-
2 {0 U) X' Q1 F1 f9 e" Uing over his own shoulders, chest, and back area for
7 c/ T9 G/ Y: {1 Y8 Z! pa year. The father also revealed he was embarrassed
" h( V3 A* C! a- f6 Q5 Sto disclose that he was using a testosterone gel pre-/ A9 W( o2 E! r% h+ ^' n5 C  P
scribed by his family physician for decreased libido
. j1 ]- l" A) ^- y# y0 F8 }secondary to depression.
, p7 N8 W6 l2 P# y. n: v! m1 cThe child slept in the same bed with parents.
: s# h; i( ?1 F  G+ D; {5 iThe father would hug the baby and hold him on his
4 v* v9 Q2 J6 g% l5 pchest for a considerable period of time, causing sig-+ o  a; W" |; `0 A. c6 ?
nificant bare skin contact between baby and father.* G# i8 C& j# s; @. r) [
The father also admitted that after the phone call,+ s6 s% N* e. B+ R9 k/ C2 X. x
when he learned the testosterone level in the baby
8 M* `& L# D" J" G2 S4 Awas high, he then read the product information/ Y) W. w' B5 _0 f- f4 G
packet and concluded that it was most likely the rea-4 ^: U( B* F/ n, B' |6 u% J
son for the child’s virilization. At that time, they
  c6 l( F; x  B3 i& Wdecided to put the baby in a separate bed, and the" U3 @0 r/ z% F
father was not hugging him with bare skin and had) A" S; t2 U3 Y7 ]
been using protective clothing. A repeat testosterone
4 b- u  E1 I9 K8 o$ ^- Y1 A) atest was ordered, but the family did not go to the" i+ |, _6 g: E7 ?. z
laboratory to obtain the test.
: j$ ?% ?5 P! h% T2 C8 u2 IDiscussion9 s; K: O; X, S
Precocious puberty in boys is defined as secondary
/ Q& }1 ?- N1 S$ F9 N# Dsexual development before 9 years of age.1,4
  A9 C4 N; y' |" C. E" B/ MPrecocious puberty is termed as central (true) when6 e/ G2 ^+ C! N6 i$ E- f
it is caused by the premature activation of hypo-
- z/ o' ?$ C7 Z. G( {thalamic pituitary gonadal axis. CPP is more com-: D3 w0 ~8 z; G" ^, X7 V2 o
mon in girls than in boys.1,3 Most boys with CPP
( f1 z4 n  [$ y3 Bmay have a central nervous system lesion that is. ^4 K2 W3 Y+ ^! l
responsible for the early activation of the hypothal-1 Z  t3 c! t  Z% q/ L+ q1 O- m
amic pituitary gonadal axis.1-3 Thus, greater empha-0 n5 B6 `. v- G, R
sis has been given to neuroradiologic imaging in
/ u+ Q* j/ C. m' q7 mboys with precocious puberty. In addition to viril-4 B* N, b, H8 [3 v3 J% w
ization, the clinical hallmark of CPP is the symmet-; J: T, |! I5 R& p4 z- E
rical testicular growth secondary to stimulation by" x1 Y: U% j; ^- G4 p/ H
gonadotropins.1,3( ]+ T: l" q1 U! F( _0 L: ^2 n
Gonadotropin-independent peripheral preco-+ g' j- T2 D, m  }+ r! {9 l" v
cious puberty in boys also results from inappropriate3 P! P) i* i4 D; U* z" x
androgenic stimulation from either endogenous or
6 j" J+ h2 i6 Zexogenous sources, nonpituitary gonadotropin stim-( X7 i; _) e8 B3 S& B
ulation, and rare activating mutations.3 Virilizing
; X! ]& ]& i6 ocongenital adrenal hyperplasia producing excessive
3 o) R1 i" E8 q0 ^- y' zadrenal androgens is a common cause of precocious
) N/ d. w& X4 K! jpuberty in boys.3,4% F3 U4 S& j) p  m% \
The most common form of congenital adrenal9 l6 v% L: h- \) }8 [9 r
hyperplasia is the 21-hydroxylase enzyme deficiency.
  z9 D0 o1 E! x3 p5 w7 h# RThe 11-β hydroxylase deficiency may also result in# P; `$ v% H# p7 u
excessive adrenal androgen production, and rarely,. Y; E7 X: \, i% g( u
an adrenal tumor may also cause adrenal androgen* T% L5 Q' g6 C
excess.1,3  s- N+ d: I4 w
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from/ p, v& s& L+ ]! f. t0 q( Q8 Y" T- i
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007* v) {( j  `8 A6 Z
A unique entity of male-limited gonadotropin-
7 X9 [5 Z& s' [/ I- aindependent precocious puberty, which is also known! A4 E3 h  w+ L! t
as testotoxicosis, may cause precocious puberty at a
6 b8 Z" a8 ~" F% G! Ivery young age. The physical findings in these boys
+ c* w' g* g# L, ~with this disorder are full pubertal development,  ~: {3 v! H* C1 p) m
including bilateral testicular growth, similar to boys3 k% ]! k8 J4 T  M# q; ?/ ~
with CPP. The gonadotropin levels in this disorder
$ p$ u- n$ G4 B0 }, |are suppressed to prepubertal levels and do not show
$ S. l8 _0 A0 B. R% Qpubertal response of gonadotropin after gonadotropin-3 e% {! Q4 z, ^. H4 A! o
releasing hormone stimulation. This is a sex-linked
8 h; z, a( E. p! g) E7 Jautosomal dominant disorder that affects only  E2 a0 U9 M! |8 u7 W
males; therefore, other male members of the family- Y  I1 D5 [' d5 I
may have similar precocious puberty.32 h  F. k6 P4 _9 y" u5 F
In our patient, physical examination was incon-% _4 S" {7 X: W( f) I% P* j
sistent with true precocious puberty since his testi-
3 _0 _0 X1 V9 K" a* P* Pcles were prepubertal in size. However, testotoxicosis
4 v% q$ j; ]- u( j/ q" ywas in the differential diagnosis because his father
1 F1 i$ z4 t( z6 n2 n. hstarted puberty somewhat early, and occasionally,# y7 G2 W% Y: ~7 z. w
testicular enlargement is not that evident in the# C/ a# K6 K2 }' a) {
beginning of this process.1 In the absence of a neg-
9 @/ G: O2 s4 W0 D0 p6 a' V3 Uative initial history of androgen exposure, our
1 ^" P% m: ~2 v& }biggest concern was virilizing adrenal hyperplasia,3 d1 S% K* I" u; Y$ |$ G5 y
either 21-hydroxylase deficiency or 11-β hydroxylase; I7 `: R! O( H3 K0 Y
deficiency. Those diagnoses were excluded by find-' j7 Q" O1 h  N# {
ing the normal level of adrenal steroids.: [; |6 J$ f, a% M( n+ N1 v  U
The diagnosis of exogenous androgens was strongly7 P# w( K9 J: k- [4 j, w
suspected in a follow-up visit after 4 months because
& M) q' r3 [2 O& W% qthe physical examination revealed the complete disap-% A* y- n9 Q! j, `+ n# c* F6 X
pearance of pubic hair, normal growth velocity, and
# E. j& ]6 v" P5 g9 }+ r, T# idecreased erections. The father admitted using a testos-
2 Y+ e/ o- o4 l0 Cterone gel, which he concealed at first visit. He was* `" d+ [& f  c
using it rather frequently, twice a day. The Physicians’* y$ _' m6 D% w' Q
Desk Reference, or package insert of this product, gel or+ q  a' U0 s$ J0 T3 x# Y, A
cream, cautions about dermal testosterone transfer to
# T$ }! }; a  }! s: Z+ V% Uunprotected females through direct skin exposure.
( X( ~+ ?; ^  n# @3 JSerum testosterone level was found to be 2 times the
1 \; [- J9 Q, d3 ]! fbaseline value in those females who were exposed to" L5 Z0 d# c+ k) j9 M& e- [
even 15 minutes of direct skin contact with their male
0 c) f8 P7 t/ O) ~  @partners.6 However, when a shirt covered the applica-$ B: v/ ]. ^; A; B  S
tion site, this testosterone transfer was prevented.* Y5 `% V4 a  H* I* C$ ^
Our patient’s testosterone level was 60 ng/mL,
6 Y+ x  ~$ f" ]which was clearly high. Some studies suggest that+ G7 m' k9 v) R' q5 `
dermal conversion of testosterone to dihydrotestos-6 u; B# F% `5 M1 }# T/ T
terone, which is a more potent metabolite, is more
7 a- z1 D% o( q' kactive in young children exposed to testosterone5 Q% z4 X  N" i/ v* ^2 n
exogenously7; however, we did not measure a dihy-
8 g( i: T: r4 A7 t% I1 Udrotestosterone level in our patient. In addition to; `# {7 x2 @: J( J
virilization, exposure to exogenous testosterone in
& s& I; n$ x& [& Lchildren results in an increase in growth velocity and
1 h5 y  v9 e4 K! F, Xadvanced bone age, as seen in our patient.3 x7 I3 _% C6 r; c
The long-term effect of androgen exposure during" ~' }# b( Y+ m) d  d$ j* H
early childhood on pubertal development and final
( i& \, T$ d5 H6 A& S; i  Radult height are not fully known and always remain
1 c$ G0 `5 W, `, V. M8 g. J6 Ia concern. Children treated with short-term testos-
7 C# Q: q+ M( w! z/ S9 c+ dterone injection or topical androgen may exhibit some
" o$ l; S3 ?, T0 _acceleration of the skeletal maturation; however, after
, Z  S  J+ H& z) _% ]( [& t& R8 \cessation of treatment, the rate of bone maturation9 y: X) C% r/ y; h9 H
decelerates and gradually returns to normal.8,97 U: s9 F, i4 P
There are conflicting reports and controversy: C  l+ s  p5 w: W; ~# i- f7 R5 L% g6 K( u) d
over the effect of early androgen exposure on adult
" _1 C5 D. I/ V5 h  L+ ~# d2 `penile length.10,11 Some reports suggest subnormal
/ e! N+ W! s: E1 \5 ~& C; wadult penile length, apparently because of downreg-& p8 N1 Q; h8 V
ulation of androgen receptor number.10,12 However,
$ l1 ?( S' A+ y. o6 |$ i1 D8 GSutherland et al13 did not find a correlation between
0 x. [$ P& k0 A1 B: b7 {childhood testosterone exposure and reduced adult) D) E7 a5 D% Z% |9 P4 ?! A
penile length in clinical studies.5 K2 K; \9 h+ w& K$ k% X
Nonetheless, we do not believe our patient is& j9 u3 n3 Z5 M( j
going to experience any of the untoward effects from- V" a  g  w. H3 `" v6 }, C, g3 y
testosterone exposure as mentioned earlier because' k7 Y* m1 a% ?
the exposure was not for a prolonged period of time.
5 y6 y, \& z5 r) HAlthough the bone age was advanced at the time of, ~' g3 U2 R' z5 w2 K$ @5 }
diagnosis, the child had a normal growth velocity at5 r0 g. ^% x3 T
the follow-up visit. It is hoped that his final adult
: i8 p, I5 ~1 zheight will not be affected., H. `8 o% a; f  r" D+ U; e
Although rarely reported, the widespread avail-
9 g  J2 n; A: K5 A: r: Dability of androgen products in our society may) w/ X2 x- I0 O+ ?: C
indeed cause more virilization in male or female$ N1 M/ w) a: w$ ?7 r5 h
children than one would realize. Exposure to andro-4 [7 k* [2 {3 i: s
gen products must be considered and specific ques-- p( ^$ M( R3 a
tioning about the use of a testosterone product or
$ s1 g) `% Y# t, Ngel should be asked of the family members during
2 d/ a! [- C; u4 y( Jthe evaluation of any children who present with vir-
5 S6 b, j* R1 Ailization or peripheral precocious puberty. The diag-
3 G! H$ |9 N1 \, M- Tnosis can be established by just a few tests and by" {/ H  s1 b& ~0 {, b* ?
appropriate history. The inability to obtain such a1 {2 }& X- c9 t  f
history, or failure to ask the specific questions, may
# v# B1 y. [' C. h4 vresult in extensive, unnecessary, and expensive
4 O2 v4 F6 `) l" ~; N- binvestigation. The primary care physician should be
# i- u3 J4 ~8 ]4 A5 {: Q1 p1 kaware of this fact, because most of these children
2 k% O6 J% T% z$ qmay initially present in their practice. The Physicians’
$ Y& r8 j) E" g5 ^+ _Desk Reference and package insert should also put a- T  s% s5 U0 R- w% B+ s, a
warning about the virilizing effect on a male or
6 R, b8 F. V6 rfemale child who might come in contact with some-$ ?7 e- J' _" k+ c) n& @
one using any of these products.
8 j# ?! [* _/ h$ j* Q& ~References
# s. M& b% h: K/ P8 q1. Styne DM. The testes: disorder of sexual differentiation% y# f) U; Y1 S: ~
and puberty in the male. In: Sperling MA, ed. Pediatric
* I0 @5 L) s! M( u6 @, h0 [Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
# N3 x4 c* E, j2002: 565-628." I/ ^  w- o! W% T9 j$ W  V
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious; x- d  ]1 c3 h, E4 f3 u" U
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
9 k& C6 V5 }5 \! E  K4 T9 y5 ]0 }  f
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