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/ ~! `5 {& W9 p3 b; I' ]# ]7 \3 D
Boy Induced by Indirect Topical
  A3 h. B+ {" w4 IExposure to Testosterone
7 s! T0 p6 m; k/ H( E6 O+ ?Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
& |1 @  ?$ A) Y, {and Kenneth R. Rettig, MD1
, r7 r0 c1 h' G$ _Clinical Pediatrics4 z1 y* a0 E6 }& q/ }2 C
Volume 46 Number 6. l" K  f! G7 e" [
July 2007 540-5434 c# l. _9 P, b5 g# C( B5 U/ N
© 2007 Sage Publications
6 z% n( j) X& Y7 N! u( E10.1177/00099228062966515 C7 q" U0 H! b& F
http://clp.sagepub.com$ E- c8 G' @+ a- G9 j1 j4 w% t* y
hosted at: i2 Y3 R8 w, ]3 ]. l' c9 K
http://online.sagepub.com, ~7 @6 @7 f: R! v5 M% l7 W) b, E
Precocious puberty in boys, central or peripheral,
) K% U0 h" o  O4 yis a significant concern for physicians. Central1 u/ A& v2 k- T" E3 N3 f, C
precocious puberty (CPP), which is mediated; s. M' k% M+ [3 {: p' O3 B
through the hypothalamic pituitary gonadal axis, has
2 @2 Q0 o. o9 v% J+ ]a higher incidence of organic central nervous system6 w7 j. C8 ]  z8 s2 l- g
lesions in boys.1,2 Virilization in boys, as manifested9 B3 I. }1 K- {: D
by enlargement of the penis, development of pubic
& x9 t( ?5 z+ j3 h; R/ Ihair, and facial acne without enlargement of testi-
* T1 u( I& `- `2 F5 }& ]) Z; G* ucles, suggests peripheral or pseudopuberty.1-3 We
8 A( T$ W, m3 q1 O" G) hreport a 16-month-old boy who presented with the4 J& l0 f3 e' t& ~- f, K
enlargement of the phallus and pubic hair develop-4 m# t4 H0 B. n- D0 ?  Z9 U
ment without testicular enlargement, which was due. |3 W8 B: ^6 `5 {9 h: P3 X
to the unintentional exposure to androgen gel used by
8 d# a. o% G4 c' [9 g! e, F9 L& ithe father. The family initially concealed this infor-$ X0 o1 U' H0 \- K- }
mation, resulting in an extensive work-up for this. f4 C' a# _  h# Y+ ]; @
child. Given the widespread and easy availability of. M$ ~, G, a2 C. c% d
testosterone gel and cream, we believe this is proba-
( O* Z: p! z* E: t, j5 `2 Nbly more common than the rare case report in the
( j4 _( r  G" O7 Q4 ]literature.42 O" v" s1 C3 K3 H! V" C, k0 d' v
Patient Report- O4 n/ [9 r9 j
A 16-month-old white child was referred to the5 J4 l  R; E  R# v$ u5 R
endocrine clinic by his pediatrician with the concern- B  j  F% L' C
of early sexual development. His mother noticed
* E0 |' x! V9 C" w# y+ o$ Slight colored pubic hair development when he was( |+ h* J/ w- X0 g/ T: t) s  s
From the 1Division of Pediatric Endocrinology, 2University of- G  |* f) k  ?7 Z+ E/ n; P& N
South Alabama Medical Center, Mobile, Alabama.
! _3 k* d7 Z  ~4 J9 V2 q, |Address correspondence to: Samar K. Bhowmick, MD, FACE,6 h; v9 D* c) G. U& B
Professor of Pediatrics, University of South Alabama, College of, C/ C" D6 }% s; J$ M" y
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
- x+ }& @6 J1 W$ k5 Re-mail: [email protected]./ q3 d$ v1 a2 I2 c7 X" X
about 6 to 7 months old, which progressively became
' X5 ]" U& C& M5 e8 h; J1 t3 x0 j+ _& Odarker. She was also concerned about the enlarge-
) H8 i% T4 p2 j- t, {ment of his penis and frequent erections. The child' \1 E% a4 `. `% o5 y* c
was the product of a full-term normal delivery, with
5 V" s3 l) v( \& x1 |# U& Za birth weight of 7 lb 14 oz, and birth length of
& Q1 H# k) D- U+ e  C1 I! s20 inches. He was breast-fed throughout the first year
2 ?2 z& q9 |# ^$ @- C3 v' aof life and was still receiving breast milk along with
) g8 f$ S7 c: r" g5 ~3 w; V4 s5 [solid food. He had no hospitalizations or surgery,& |) N2 s6 E2 ~% |0 @
and his psychosocial and psychomotor development9 J) ~" }7 V7 v$ W
was age appropriate.
$ ^8 S3 h/ L, z; vThe family history was remarkable for the father,4 h/ X8 y* J/ D/ N
who was diagnosed with hypothyroidism at age 16,* E3 z3 Y3 I& v' e0 S; L3 n7 G
which was treated with thyroxine. The father’s
7 U$ D4 y5 q- V( Qheight was 6 feet, and he went through a somewhat
, V+ E& S& F2 [8 fearly puberty and had stopped growing by age 14.
' d+ ?+ _, b/ ^6 G& o. Q- ZThe father denied taking any other medication. The
2 ?' p$ N; s6 \" Kchild’s mother was in good health. Her menarche+ i( O+ E- \7 [4 C: W
was at 11 years of age, and her height was at 5 feet
& r' B. R7 P- h7 P9 o/ U5 inches. There was no other family history of pre-
( t+ U0 b6 f* J+ wcocious sexual development in the first-degree rela-4 ?: R# ^. I' Z" z
tives. There were no siblings.- U* @7 u6 |3 A2 Q" E
Physical Examination+ v' L# U9 {/ U9 X) }/ ~9 ^! L
The physical examination revealed a very active,
$ t" t7 t" U6 H8 ?0 Yplayful, and healthy boy. The vital signs documented
- O  G9 E$ e6 U8 m6 b; la blood pressure of 85/50 mm Hg, his length was7 O' a# b: a5 b5 Q) B0 u
90 cm (>97th percentile), and his weight was 14.4 kg
. A: y4 d: j3 V" M! C(also >97th percentile). The observed yearly growth* V) K( g' z4 l% d7 `* M* R8 B0 [
velocity was 30 cm (12 inches). The examination of% ^1 s( D5 V3 b1 ]. C3 B' _
the neck revealed no thyroid enlargement.
+ r7 }, |6 R% s4 MThe genitourinary examination was remarkable for
& D; l0 F% g! R- q! zenlargement of the penis, with a stretched length of6 C' n' T% m9 ~5 I6 w1 ~9 ]' H  n
8 cm and a width of 2 cm. The glans penis was very well
- s3 ^9 c" k  _developed. The pubic hair was Tanner II, mostly around
: B* V& s, r  D4 \4 D6 U540
* S2 C/ r8 |! b+ c1 l: u+ Fat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from6 i7 K+ x$ h9 ^
the base of the phallus and was dark and curled. The
" z$ i7 x1 N6 M( ~0 ~5 o7 A: p( ptesticular volume was prepubertal at 2 mL each.
0 O( f5 N( ]- O, ^/ S. N. w) ^The skin was moist and smooth and somewhat+ q/ z( x) c" i0 n" r
oily. No axillary hair was noted. There were no' i8 e) F+ [/ C1 T. F9 G
abnormal skin pigmentations or café-au-lait spots.  W6 G2 c0 C7 c7 e1 ^( D9 {
Neurologic evaluation showed deep tendon reflex 2+
0 h: H: C6 M2 i/ V/ `bilateral and symmetrical. There was no suggestion
5 n5 W' B% y5 w( Q0 gof papilledema., \2 V6 b+ [3 o/ m$ c( l- j2 c, ^
Laboratory Evaluation
2 }0 u/ I% s9 f1 }8 t  gThe bone age was consistent with 28 months by
& \- r& i5 ^1 B0 L/ h) O$ F1 jusing the standard of Greulich and Pyle at a chrono-$ @6 _$ W0 Z; d- A5 V
logic age of 16 months (advanced).5 Chromosomal3 ^1 c. h7 z5 k, \+ d( n6 @
karyotype was 46XY. The thyroid function test* M: {* @5 x4 ]
showed a free T4 of 1.69 ng/dL, and thyroid stimu-) \7 C! ^3 v; H) ?' I2 }
lating hormone level was 1.3 µIU/mL (both normal).! B% C( k: c& f- r
The concentrations of serum electrolytes, blood
, X# C' c+ v8 B% v0 e6 Nurea nitrogen, creatinine, and calcium all were
2 H$ N. l4 _+ }: y5 P  pwithin normal range for his age. The concentration
: v' I3 r$ o+ m! Yof serum 17-hydroxyprogesterone was 16 ng/dL) D4 N; b& Y; e  Q0 `+ r
(normal, 3 to 90 ng/dL), androstenedione was 207 q( t( k+ p% N8 f: ]7 C( A
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-2 S8 L8 M( r" ?9 n' A4 X; `) D4 H
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
& s. `3 I! ]6 ]& o' Q7 Udesoxycorticosterone was 4.3 ng/dL (normal, 7 to; D6 a7 m+ U2 O% J  G
49ng/dL), 11-desoxycortisol (specific compound S)
% o1 E% H+ v5 k1 G' Gwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-, D6 r" a$ ^6 @' \1 }8 D& v9 N' {
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total/ }( R" o% H. S! W/ r
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),6 d' R& w& @8 v; ?6 @8 t0 g$ W' R
and β-human chorionic gonadotropin was less than! W2 e2 {7 m6 q$ E
5 mIU/mL (normal <5 mIU/mL). Serum follicular* ?4 w4 B* o! |7 F8 p* I2 V7 b
stimulating hormone and leuteinizing hormone% {$ E! L9 ^$ |9 A+ F% m
concentrations were less than 0.05 mIU/mL. P4 f+ E2 {' C% {
(prepubertal).4 E8 O6 z! ^* b0 R% i$ ?
The parents were notified about the laboratory
* b. Z5 ], `4 k; i! J& B1 c9 G9 ]results and were informed that all of the tests were
3 Y( C; [  i* l/ ~/ ]2 z9 U8 Anormal except the testosterone level was high. The7 e/ K$ ~) F9 A0 |# d- u2 I" u
follow-up visit was arranged within a few weeks to% m3 }: D8 W+ P2 @& M
obtain testicular and abdominal sonograms; how-
' D" j0 L! ?! Sever, the family did not return for 4 months.
. _6 ~6 M1 I' d6 A# @2 HPhysical examination at this time revealed that the
6 |2 s0 |! Q* J- }% A  o( ?) Wchild had grown 2.5 cm in 4 months and had gained+ g1 [# S3 R: _$ P8 M# t) |9 D  B
2 kg of weight. Physical examination remained1 Q5 M8 @' R3 _. q3 {
unchanged. Surprisingly, the pubic hair almost com-* a; [% U9 n5 h
pletely disappeared except for a few vellous hairs at$ u) u3 D+ b8 `- o) @- ]' f7 Z
the base of the phallus. Testicular volume was still 27 }( a" {8 }+ F" h
mL, and the size of the penis remained unchanged.
1 L( b% {0 Y3 hThe mother also said that the boy was no longer hav-1 U) H; c6 Q( u6 ?+ R) U
ing frequent erections.$ \  h. P5 i: p- @
Both parents were again questioned about use of
9 Y+ Y2 c! I9 q, P( tany ointment/creams that they may have applied to
# A. _' ~$ f4 v" N9 N; _the child’s skin. This time the father admitted the* E. z0 M  ?: P4 V
Topical Testosterone Exposure / Bhowmick et al 541
5 n* R: h9 p% z0 g( Nuse of testosterone gel twice daily that he was apply-# ~/ D' w# K1 ^2 r
ing over his own shoulders, chest, and back area for" `2 A# r' q. u% {3 G" `
a year. The father also revealed he was embarrassed
3 a8 q/ ]' N9 _" W  a: K. yto disclose that he was using a testosterone gel pre-
% G/ |" x& G6 Q6 g4 E/ G$ Oscribed by his family physician for decreased libido3 @* S, O( e0 X" e9 Y
secondary to depression.
! g7 d; }, X9 e; J) \" N, t. kThe child slept in the same bed with parents.0 w' S& `5 e$ w" m7 k! c
The father would hug the baby and hold him on his
' ^& A" N$ ]( P4 p1 u0 B9 bchest for a considerable period of time, causing sig-
1 D2 p/ o$ {: v7 r6 @nificant bare skin contact between baby and father.
: f& Y: K% N; c7 Y1 dThe father also admitted that after the phone call,
2 T, Q$ Q; t% R9 T; F9 g! Wwhen he learned the testosterone level in the baby5 _" K, t7 G: g
was high, he then read the product information2 d( u" @: _/ ~) Y
packet and concluded that it was most likely the rea-
* G7 c* I3 x: X( ]0 x) Json for the child’s virilization. At that time, they, S# k" B9 W4 X
decided to put the baby in a separate bed, and the3 `- [- t" ?, ?" }# ^4 ?
father was not hugging him with bare skin and had' G/ ^8 L" C, |9 x) c! p" _" j. _# L
been using protective clothing. A repeat testosterone
/ s6 V1 @4 D; ytest was ordered, but the family did not go to the
1 Q  K( x- g- }% t8 R) B! O4 h/ s- |laboratory to obtain the test.
  P) c$ N2 P" K. ?Discussion
& {; V: w6 s  o8 ~2 YPrecocious puberty in boys is defined as secondary
- f" A$ ?4 a" S6 x1 w7 d+ Isexual development before 9 years of age.1,46 u3 Z( {$ J4 b  a2 P- u8 s
Precocious puberty is termed as central (true) when
) J* a' ?5 f4 A% Zit is caused by the premature activation of hypo-( |/ S* r1 `7 X
thalamic pituitary gonadal axis. CPP is more com-
* Q& w5 o8 [* P7 k/ k* g2 fmon in girls than in boys.1,3 Most boys with CPP
2 J; C0 k) I- E+ \$ l) D* ymay have a central nervous system lesion that is
! m# ]3 r- p3 u& g' C# p: Bresponsible for the early activation of the hypothal-6 K! o6 y' Q; R1 i/ z! i% R3 X: O# n
amic pituitary gonadal axis.1-3 Thus, greater empha-
+ z7 _0 m% |6 w  xsis has been given to neuroradiologic imaging in, `3 i- m, j' p: |
boys with precocious puberty. In addition to viril-1 F3 Y1 V  {2 k" V5 e; F
ization, the clinical hallmark of CPP is the symmet-
, n9 _# I, r6 N8 h; Arical testicular growth secondary to stimulation by
  t( j$ n$ s" d6 d# c: Ogonadotropins.1,3' g: ^% z: F( \7 ?9 I4 I. i) n. a
Gonadotropin-independent peripheral preco-; Y3 P0 Z  h" m" }) g! z2 H
cious puberty in boys also results from inappropriate
6 ?' d  D7 d+ \+ A4 k4 S! pandrogenic stimulation from either endogenous or
% o8 C( I" K5 _$ L- wexogenous sources, nonpituitary gonadotropin stim-/ `+ p0 E0 R& r0 x
ulation, and rare activating mutations.3 Virilizing( \0 q% U) x: d
congenital adrenal hyperplasia producing excessive
8 J. e/ Z1 I6 C+ J, Oadrenal androgens is a common cause of precocious  g/ J7 z  o/ a# D& P  n
puberty in boys.3,4
9 b( r$ I1 o9 L  i" u/ aThe most common form of congenital adrenal
1 T9 i' r+ Q* w, mhyperplasia is the 21-hydroxylase enzyme deficiency.) Z9 K1 E6 l# z' i. ^. K
The 11-β hydroxylase deficiency may also result in
) d8 ^% p: }& E" o" F7 o# B# l4 lexcessive adrenal androgen production, and rarely,
1 p$ a# J/ `$ y8 c& j0 H# a9 \an adrenal tumor may also cause adrenal androgen+ L& J# d2 G' G, x7 c; F* j
excess.1,36 f: Z. e2 L0 Z" Q$ l% I3 B
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from6 Q9 j7 f  Q# a! w6 g& Q2 Y: D9 k
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007; I3 ^2 l- Z/ F6 e# g
A unique entity of male-limited gonadotropin-
: K5 {6 Y4 E0 B0 nindependent precocious puberty, which is also known
5 K8 C. k5 ?! }3 Nas testotoxicosis, may cause precocious puberty at a$ ?3 m' G- E$ H6 ^, q- N
very young age. The physical findings in these boys: y$ R1 O" {( L8 h$ q
with this disorder are full pubertal development,
) m5 y  ]6 y! E; g" T  N" K* f$ x4 dincluding bilateral testicular growth, similar to boys: |7 [! z8 X3 x' ^9 ^. f# Q
with CPP. The gonadotropin levels in this disorder
) s( M% z& @7 U% b( iare suppressed to prepubertal levels and do not show# c, y3 T5 ]! W9 w3 l! Z- \$ o' e
pubertal response of gonadotropin after gonadotropin-- E3 c" A# c4 B: v; R- h
releasing hormone stimulation. This is a sex-linked: P, I( _+ P& H7 ^  u9 ^
autosomal dominant disorder that affects only
9 y$ N# }. Y# m% Z6 B# J5 Ymales; therefore, other male members of the family
* I' X7 e# }* O: `! @may have similar precocious puberty.3
7 v1 _3 A* j; m( {1 _5 _. C/ {, |8 R- QIn our patient, physical examination was incon-
. k  E0 F# p( s' Lsistent with true precocious puberty since his testi-
* o" W) {7 A0 Y" e$ L3 O& Zcles were prepubertal in size. However, testotoxicosis
4 Z1 a* q/ c5 I: l3 n' B7 O" f9 @! Ywas in the differential diagnosis because his father( _5 d) ~& P& D4 i' O  I; o' B. G
started puberty somewhat early, and occasionally,/ U* l7 ?* J1 h( A
testicular enlargement is not that evident in the
1 B0 d$ L. C( S. Sbeginning of this process.1 In the absence of a neg-2 E$ j0 `, T' n1 w! {2 U
ative initial history of androgen exposure, our
2 M9 e5 F' r; ~/ G' }biggest concern was virilizing adrenal hyperplasia,
& \+ y8 m/ e  ^2 ~3 ~6 peither 21-hydroxylase deficiency or 11-β hydroxylase
+ X1 a% G2 O7 K. gdeficiency. Those diagnoses were excluded by find-' o" B' C  b6 f  F: C9 U, L" R
ing the normal level of adrenal steroids.) U$ U3 ~4 i, i, n# k  E9 M
The diagnosis of exogenous androgens was strongly" ]9 A* \. W2 b8 A' j6 t5 j
suspected in a follow-up visit after 4 months because4 v! E9 ^1 S; `7 t0 C$ }
the physical examination revealed the complete disap-0 `- [' ?1 _, q9 W3 \
pearance of pubic hair, normal growth velocity, and
5 F$ h( g; D4 U$ B; rdecreased erections. The father admitted using a testos-/ J6 m  w1 S0 j- f# |2 h
terone gel, which he concealed at first visit. He was* t4 D+ P, W. y! e) u! `
using it rather frequently, twice a day. The Physicians’
5 f  E0 s# D6 }6 @, k, D1 bDesk Reference, or package insert of this product, gel or' z: u( [5 I) N( C6 o$ k* R
cream, cautions about dermal testosterone transfer to6 A8 ^6 `$ Y: m0 }. ~, {
unprotected females through direct skin exposure.
3 V, e# Q! @  _" Z2 QSerum testosterone level was found to be 2 times the
. L, H: H+ f% b" m  zbaseline value in those females who were exposed to
/ f4 v. \$ v5 a3 beven 15 minutes of direct skin contact with their male
9 W0 L& {; c" F; R; E( u" {partners.6 However, when a shirt covered the applica-
$ n( I  P6 j  Qtion site, this testosterone transfer was prevented.
7 N) }9 H' G! y+ POur patient’s testosterone level was 60 ng/mL,
8 P2 t" h4 ^1 K! U' Vwhich was clearly high. Some studies suggest that
6 {3 r! n% `- w- L4 Edermal conversion of testosterone to dihydrotestos-* z6 k$ _, \8 S/ [
terone, which is a more potent metabolite, is more' q0 _! I  e( l. A/ f
active in young children exposed to testosterone3 W' w+ r- a( o, H
exogenously7; however, we did not measure a dihy-( a) R1 s. s, V- {
drotestosterone level in our patient. In addition to
' u- z" C4 z: Svirilization, exposure to exogenous testosterone in
/ K- h9 O  [9 G! v. \children results in an increase in growth velocity and
0 }/ b' e; A/ X+ I2 Hadvanced bone age, as seen in our patient.
4 ?% V5 M) \( B  S  ~2 g4 zThe long-term effect of androgen exposure during( |4 x( P% h: e0 w) D  a* p
early childhood on pubertal development and final
! }' l2 K9 p2 _' z% Radult height are not fully known and always remain& V7 ]! k* Q4 ~4 R& J7 E) R  _
a concern. Children treated with short-term testos-5 Z2 G! z/ F% v5 I5 ^- X; S" v
terone injection or topical androgen may exhibit some. z/ y8 D& t. c: B6 r# w8 @9 o3 F
acceleration of the skeletal maturation; however, after
$ q1 S: s: z1 G% _cessation of treatment, the rate of bone maturation* x7 N7 u& d1 J2 U
decelerates and gradually returns to normal.8,9
. j2 a. {0 A( A2 J2 P# QThere are conflicting reports and controversy$ p, G1 x8 m8 l0 y! O
over the effect of early androgen exposure on adult& M  R( E% J# [9 N5 P; v* u
penile length.10,11 Some reports suggest subnormal
( n- O: {& k4 A; y& b* S9 Fadult penile length, apparently because of downreg-$ |  V1 V( r, j2 x. m! L) ]+ [
ulation of androgen receptor number.10,12 However,& J: s' I; Q6 D3 \0 g6 n: v# w) b. _  s
Sutherland et al13 did not find a correlation between. R9 r( K  W- X5 c  \, F* J
childhood testosterone exposure and reduced adult+ Q$ C7 F6 L4 `) _1 f2 |
penile length in clinical studies.
9 v! ]5 V' V; Y" iNonetheless, we do not believe our patient is, S2 q7 R, x" n% U. n0 _5 n- ?
going to experience any of the untoward effects from
+ h* C" i; [2 m% p( c& ~3 ~9 Atestosterone exposure as mentioned earlier because
! [1 y5 J% T& x! U4 z! F9 P0 Qthe exposure was not for a prolonged period of time.
6 T/ o0 l% M( j5 v9 k5 f1 [Although the bone age was advanced at the time of" m4 i& G9 N' g. R% C+ N
diagnosis, the child had a normal growth velocity at
: x3 h7 g0 r4 ]3 rthe follow-up visit. It is hoped that his final adult" H* g) f, l6 W! y: Q8 G
height will not be affected.
6 ^. y) p( j- zAlthough rarely reported, the widespread avail-! ~' ^$ C1 f& V& Y7 u) m8 d
ability of androgen products in our society may9 k6 {$ }6 T( G8 c6 L2 ^6 c! C$ M
indeed cause more virilization in male or female
  r2 k# _. Q( P4 Q* L& Ychildren than one would realize. Exposure to andro-
& |9 _: E4 q: S, t; \' T" ^gen products must be considered and specific ques-1 x0 R" I( G+ L2 d8 I: n
tioning about the use of a testosterone product or4 M) f) G! A+ p3 F
gel should be asked of the family members during/ t1 B2 D4 d. j, \6 M# ]
the evaluation of any children who present with vir-
9 r9 C# H0 r8 t# Xilization or peripheral precocious puberty. The diag-
, M. D! U: d' \7 k5 H% g( Cnosis can be established by just a few tests and by- \, [0 a. v0 C
appropriate history. The inability to obtain such a
* \- p0 i+ F: P& z: L1 y. a- v) Uhistory, or failure to ask the specific questions, may, C9 i4 S6 _: C) Q* g
result in extensive, unnecessary, and expensive
0 ~! E0 D& {0 E8 }9 ^9 F+ ]  D2 c( Oinvestigation. The primary care physician should be
( E( _* ?1 p0 z! _aware of this fact, because most of these children
/ c+ E9 ]8 `- U- y* Kmay initially present in their practice. The Physicians’6 D. V8 ~4 i% [5 r
Desk Reference and package insert should also put a' b& K; |- W' H: k3 i6 G
warning about the virilizing effect on a male or: P7 [4 U$ x" m9 c3 [
female child who might come in contact with some-
' \9 _5 `5 e4 e  h5 h% u# ~' sone using any of these products.
/ D; A0 w* [$ l% k: YReferences
4 Y  w8 m. y- E' W6 Z1. Styne DM. The testes: disorder of sexual differentiation8 J8 J2 l0 L4 s7 t  d$ ^
and puberty in the male. In: Sperling MA, ed. Pediatric2 l4 K% d  S9 Y1 ~/ J+ f) V
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
( x3 l9 ^5 w$ a( J* X" @- H2002: 565-628.
5 t+ }4 A2 u1 i' G  C  h2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
$ Y6 `7 H2 t- l  tpuberty 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) n9 h2 L+ \& x
Boy Induced by Indirect Topical
+ u7 o1 s  S, b" A2 ^Exposure to Testosterone$ U$ p# R7 y! R! g7 W+ g
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2  ?+ E3 c$ h9 {7 F* }% P
and Kenneth R. Rettig, MD18 A; a: [+ t8 b
Clinical Pediatrics
2 r' t6 j( [3 m/ H; R% NVolume 46 Number 6, I+ v- @+ k8 r5 B2 E
July 2007 540-543
  i* O1 _; j8 [: Z2 @8 Z8 E. F9 o© 2007 Sage Publications
! {5 t  ?  s- E10.1177/0009922806296651/ C, M7 H, Z2 A8 v
http://clp.sagepub.com  l/ B9 e+ m' [( c. \' _
hosted at* r/ b. n. ~' h; p" e+ r. ?- @1 {
http://online.sagepub.com) U  |, _0 G% Q) Z8 E% X# k
Precocious puberty in boys, central or peripheral,
/ T, H  n2 c; y% x5 C5 y3 y7 B2 r, F8 ~is a significant concern for physicians. Central; ^5 n4 W( q1 ~2 ^5 Y
precocious puberty (CPP), which is mediated
: ]- J# O$ Z& F# Pthrough the hypothalamic pituitary gonadal axis, has/ h" t# i: k9 Q' ~' C
a higher incidence of organic central nervous system' q, A* N- K! p0 R
lesions in boys.1,2 Virilization in boys, as manifested" v8 g- e, W# f  Q& `$ b7 T
by enlargement of the penis, development of pubic" v/ R/ v! K2 k" d* }' @; s" f
hair, and facial acne without enlargement of testi-
2 @7 S8 V  c# O! a! g0 W; S3 Wcles, suggests peripheral or pseudopuberty.1-3 We5 S1 V3 b& c* c, A0 x2 N3 t5 l
report a 16-month-old boy who presented with the2 \7 h, z/ \% H, o9 ]- z/ v* A
enlargement of the phallus and pubic hair develop-- ]! j) r# F3 j7 x  s7 R- H' n
ment without testicular enlargement, which was due) t) U. l5 ~1 D0 B4 f0 Z, |
to the unintentional exposure to androgen gel used by
0 \2 J8 j& {6 w! v2 q/ s: p+ }the father. The family initially concealed this infor-0 K2 O0 ^6 n1 g& ^% d& C$ v1 w3 x
mation, resulting in an extensive work-up for this
. ?& j9 F" X! u$ N- j3 Z, n; a( `& `# ]0 kchild. Given the widespread and easy availability of
0 |7 ]4 B/ Z# [7 Wtestosterone gel and cream, we believe this is proba-
' a* W; Q2 G. |0 |9 b# r- {0 hbly more common than the rare case report in the3 T8 m# H+ ]) o: \
literature.4
" q- n! e! S8 x" LPatient Report
) {) h: P/ h9 t0 y7 e5 m+ NA 16-month-old white child was referred to the+ h; [. c: Z; G8 I% B6 `
endocrine clinic by his pediatrician with the concern1 f0 V9 M- \0 ]
of early sexual development. His mother noticed% {- ^/ x3 G8 `& S' ]* p, p
light colored pubic hair development when he was
5 `# e6 q. k+ _1 SFrom the 1Division of Pediatric Endocrinology, 2University of3 T* @! C1 P- K
South Alabama Medical Center, Mobile, Alabama.
. S0 v, y; x! I8 qAddress correspondence to: Samar K. Bhowmick, MD, FACE,7 g! m% I" T" S4 |) L
Professor of Pediatrics, University of South Alabama, College of1 p! O: e: |& P2 T) ^* \
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;/ p5 v( ^! {. z. b& V. o- G
e-mail: [email protected].* Y: _* b; G9 A! X& u& u+ z
about 6 to 7 months old, which progressively became
5 T- U& K9 ]5 K4 Ndarker. She was also concerned about the enlarge-
$ q" L' }1 t! `6 T1 xment of his penis and frequent erections. The child1 u8 J) L% v  w' u. F! I
was the product of a full-term normal delivery, with
/ Z' I6 @/ U1 M* |9 @) l- Ma birth weight of 7 lb 14 oz, and birth length of
. v+ }9 e0 q% V; x8 r) c20 inches. He was breast-fed throughout the first year, p5 m, k* U* S
of life and was still receiving breast milk along with3 R& I; H! \: n. p2 U
solid food. He had no hospitalizations or surgery,. B+ L& R0 E- t
and his psychosocial and psychomotor development# M0 `& [8 P+ C4 x8 |) V
was age appropriate.* G2 g7 [$ e- E* l& {: g( {
The family history was remarkable for the father,
, u+ x0 S/ ]% X! {who was diagnosed with hypothyroidism at age 16,( R% k1 W/ h# P, ~
which was treated with thyroxine. The father’s4 k$ a+ E) H5 E: x7 f: S
height was 6 feet, and he went through a somewhat# d' A+ M9 J' q8 ?6 }
early puberty and had stopped growing by age 14.2 t, f- H/ [4 t! f
The father denied taking any other medication. The- `2 M0 M# S7 M2 ^
child’s mother was in good health. Her menarche
4 s8 [! B$ _4 ^9 Ewas at 11 years of age, and her height was at 5 feet
* F. Y3 a3 e! B# Q! r5 inches. There was no other family history of pre-) D/ d6 f" z9 L1 M5 E
cocious sexual development in the first-degree rela-
+ p* {- s- b, m5 N% f, @tives. There were no siblings.$ u" |+ W2 ^0 P" u4 \
Physical Examination* K: J+ s" {0 H; d" x) w0 X3 M% x" N
The physical examination revealed a very active,( _6 W6 J+ \% C# l4 S8 h+ e
playful, and healthy boy. The vital signs documented2 `, S" X2 \$ A
a blood pressure of 85/50 mm Hg, his length was4 A# [! {& n0 U8 Z' B  F
90 cm (>97th percentile), and his weight was 14.4 kg/ Y8 v6 g9 a. l/ `" f' c
(also >97th percentile). The observed yearly growth
0 x$ \6 g+ s5 Pvelocity was 30 cm (12 inches). The examination of) ^' ~* u) E6 M
the neck revealed no thyroid enlargement.: }2 s/ R+ _+ C. @  B
The genitourinary examination was remarkable for1 f! |9 W! M" O& v! ~5 I  }0 P
enlargement of the penis, with a stretched length of# j$ |3 G5 [, o2 n# `
8 cm and a width of 2 cm. The glans penis was very well
: z9 ^5 [* d$ U/ N) `* edeveloped. The pubic hair was Tanner II, mostly around
& W, l9 @6 u+ f" S9 p7 a. V5401 q9 c! n( y; k
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
0 |0 |) j, V- s+ r) [the base of the phallus and was dark and curled. The
- K5 A* v( V2 F# _4 A. r7 Mtesticular volume was prepubertal at 2 mL each.: K5 n+ ~: ]" v0 F3 `
The skin was moist and smooth and somewhat# u& f  i7 Y4 I; ?8 x* @; S# _
oily. No axillary hair was noted. There were no
6 n0 M, N/ G+ p8 uabnormal skin pigmentations or café-au-lait spots.  a6 M# |; v9 D  |
Neurologic evaluation showed deep tendon reflex 2+5 y% F5 L1 X$ }0 n: h
bilateral and symmetrical. There was no suggestion
: w. ]6 J- r- l, Y: v) Iof papilledema./ w% X. k) R* B; [6 h
Laboratory Evaluation
  Y# h+ Y9 s' h+ p- j9 A# }7 HThe bone age was consistent with 28 months by" h) b. P; \/ J! w" k0 o
using the standard of Greulich and Pyle at a chrono-6 F4 L! x* z' j# k: |9 Z1 E
logic age of 16 months (advanced).5 Chromosomal
& W+ A) S% E# v$ h, |6 m: u& }karyotype was 46XY. The thyroid function test! G$ w7 F9 d. K$ c$ g7 w& L) |
showed a free T4 of 1.69 ng/dL, and thyroid stimu-: l0 R/ I' c0 ^* L4 E
lating hormone level was 1.3 µIU/mL (both normal).; @5 j+ Y5 {7 H( G7 Y
The concentrations of serum electrolytes, blood
( i. p) P; {6 y: A( {$ Furea nitrogen, creatinine, and calcium all were! y6 m+ Y2 k1 E0 G( S* S- e: v
within normal range for his age. The concentration% W& k5 k7 k& _6 f
of serum 17-hydroxyprogesterone was 16 ng/dL$ ]/ f4 F2 ~, S) Z" Q! A- m
(normal, 3 to 90 ng/dL), androstenedione was 20: Y* {: \' j9 x4 J
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-7 t0 n: |! y+ E
terone was 38 ng/dL (normal, 50 to 760 ng/dL),9 ^( p! a2 B' a+ Z
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
, |* k! `  O: T* l5 w1 c- F" h, X' f1 d49ng/dL), 11-desoxycortisol (specific compound S): X2 I' A5 g/ i
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-  P+ ^1 @! c5 z9 o
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total  H. S7 Q3 h$ Q5 E) d' x& n
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
  i# ~+ ]( d- ?$ X' Pand β-human chorionic gonadotropin was less than' @- x, y2 j+ v, x
5 mIU/mL (normal <5 mIU/mL). Serum follicular9 e) j# u+ B8 U5 E! ~; ^
stimulating hormone and leuteinizing hormone
/ A  v% S$ D/ K- Tconcentrations were less than 0.05 mIU/mL
7 r; f6 K! r+ i. B1 u(prepubertal).
( ^/ Y7 H" I6 mThe parents were notified about the laboratory
* K) ], `: M( h9 _" }5 Eresults and were informed that all of the tests were* x! j, k! o  |! P' A
normal except the testosterone level was high. The
9 V) c4 M9 y8 A1 }' Qfollow-up visit was arranged within a few weeks to
# \) x7 B7 h( y% v2 y1 U7 |3 `  uobtain testicular and abdominal sonograms; how-
2 \$ K* N# _: g& C+ }+ h) @ever, the family did not return for 4 months.8 j) a5 _* Y6 t- l# I
Physical examination at this time revealed that the; }0 c; h7 E/ U  \
child had grown 2.5 cm in 4 months and had gained. Q* z4 \3 b$ Z1 F  o/ p" n$ d# P
2 kg of weight. Physical examination remained' ]. q8 g9 I, l
unchanged. Surprisingly, the pubic hair almost com-
- w! |* ~: ^0 u5 d8 Y8 `- _pletely disappeared except for a few vellous hairs at1 h' L- K" [& g4 v$ v7 [6 b9 w
the base of the phallus. Testicular volume was still 2) C$ s- e* i; r" r
mL, and the size of the penis remained unchanged.
9 H3 F+ S3 Z3 W* R1 k- X+ Q8 p  GThe mother also said that the boy was no longer hav-: M) j9 _- U5 G5 s3 T
ing frequent erections.9 Z( H' g* N0 f$ Y( p& J3 S! T
Both parents were again questioned about use of
- |9 T4 P6 P6 s6 B) S4 m. Kany ointment/creams that they may have applied to
& r  @2 i% _: n$ fthe child’s skin. This time the father admitted the
7 E3 a" w2 N/ hTopical Testosterone Exposure / Bhowmick et al 541
! X' y- _! K( e- C" Y) a7 Vuse of testosterone gel twice daily that he was apply-
# V8 A2 y- d8 h' d" Ding over his own shoulders, chest, and back area for
9 ~& m  ~; y# I% M# La year. The father also revealed he was embarrassed
5 i7 r7 w( a2 E$ F$ \to disclose that he was using a testosterone gel pre-# k1 p4 z9 j) x9 U0 @9 o
scribed by his family physician for decreased libido
: U. W& \/ Q9 B/ @' \1 d% fsecondary to depression.; T- @( ~# I5 [. [
The child slept in the same bed with parents.  [" L' ^# A0 z" t
The father would hug the baby and hold him on his) x. h0 f# R4 |6 T7 E  V/ T4 K
chest for a considerable period of time, causing sig-
9 w9 U: O; D9 n- \6 w: E! B" Pnificant bare skin contact between baby and father.  j! {* ^1 [5 ?  a5 c7 P- \7 C
The father also admitted that after the phone call,
4 Y  h  D  C- {# o9 A  T  uwhen he learned the testosterone level in the baby# n' U' N7 I4 I; @1 o& k5 ^1 Z' z
was high, he then read the product information8 I% b% S8 @  ]" @. S
packet and concluded that it was most likely the rea-
8 C3 I2 X/ b1 e% Vson for the child’s virilization. At that time, they3 v1 R2 |3 D4 O4 F" F0 l
decided to put the baby in a separate bed, and the) B$ x. L* ^1 i8 [* M
father was not hugging him with bare skin and had
* k5 }3 F) I: G9 xbeen using protective clothing. A repeat testosterone& b& s! [" y' T' a7 y- |! h
test was ordered, but the family did not go to the
' \/ w4 J( n, W' j7 u: d! }% c7 Plaboratory to obtain the test.& x/ K- @' x2 b- s
Discussion
! v- l( b. r5 i# D" X3 F) s' K* e0 FPrecocious puberty in boys is defined as secondary
. {- {: i$ q- Z% H( X, ~+ O  c- lsexual development before 9 years of age.1,47 \% |- Z3 x# ?
Precocious puberty is termed as central (true) when4 u' i5 C0 X/ I/ ~$ W) l
it is caused by the premature activation of hypo-
$ S0 ~8 H3 L7 q$ v1 sthalamic pituitary gonadal axis. CPP is more com-& T* S* a( F+ h
mon in girls than in boys.1,3 Most boys with CPP( P. ?! z7 S% L% W& O
may have a central nervous system lesion that is; V% s- u( ?6 J+ d! j
responsible for the early activation of the hypothal-
# h0 Z1 J1 o  a5 _  qamic pituitary gonadal axis.1-3 Thus, greater empha-
! \/ a' B" j# @/ u2 p) ^sis has been given to neuroradiologic imaging in3 L3 C0 Z' y! t7 o: u4 S7 R' m
boys with precocious puberty. In addition to viril-6 f3 S% f8 l+ t3 j4 d9 L9 o. r3 ~
ization, the clinical hallmark of CPP is the symmet-" `! A, }& A6 D$ G1 a
rical testicular growth secondary to stimulation by" p0 Y# y: @) X
gonadotropins.1,33 V3 K1 R5 E, P( u+ w& r
Gonadotropin-independent peripheral preco-  j- h5 w9 `+ F8 d4 L: @1 w
cious puberty in boys also results from inappropriate/ K$ ]3 j# Z: s
androgenic stimulation from either endogenous or
1 C- ~& ?9 y$ n* e- I/ fexogenous sources, nonpituitary gonadotropin stim-
* N" D* Z! a7 y, y+ _! @- mulation, and rare activating mutations.3 Virilizing8 [9 M7 v; ]3 d( ]1 k) {+ H
congenital adrenal hyperplasia producing excessive2 b, n1 _1 ]0 z5 h) V6 o" f5 b
adrenal androgens is a common cause of precocious
$ N5 z0 e0 M- T% [puberty in boys.3,4: j' K- Z0 Y$ [2 I
The most common form of congenital adrenal
( U; B* r: L" [0 ?hyperplasia is the 21-hydroxylase enzyme deficiency.
' T/ x8 I/ ?* s) {The 11-β hydroxylase deficiency may also result in
1 A7 I' I0 z5 N9 X5 a! M1 Eexcessive adrenal androgen production, and rarely,% @& q9 x# L9 L! \+ h
an adrenal tumor may also cause adrenal androgen
& P8 |- B; G- \& }7 B( R- |excess.1,3% G) f  Y* l% a& D+ U( E" U8 W
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
3 F+ T4 k: c( X5 I. n8 x3 H542 Clinical Pediatrics / Vol. 46, No. 6, July 2007+ B/ G+ Z) t$ h! A
A unique entity of male-limited gonadotropin-
% N7 F  w& [; Qindependent precocious puberty, which is also known. r: p4 X, m5 Y, B
as testotoxicosis, may cause precocious puberty at a/ B* C) w6 o9 R- M1 A
very young age. The physical findings in these boys
8 J7 U! T/ A) B$ Z$ \with this disorder are full pubertal development,4 U6 e! G% \8 g& L  `$ o( f
including bilateral testicular growth, similar to boys- u6 Y" y8 M. i" r: Y
with CPP. The gonadotropin levels in this disorder9 o5 ?5 |' R- I; w
are suppressed to prepubertal levels and do not show4 g/ q6 u; W$ `
pubertal response of gonadotropin after gonadotropin-
# n. O* i. p3 Breleasing hormone stimulation. This is a sex-linked4 L7 }" T& ?7 @  p0 o7 w; c
autosomal dominant disorder that affects only4 y; o; I1 V7 m2 t6 v4 p
males; therefore, other male members of the family
' h' r7 Y+ D3 Y) G  G- pmay have similar precocious puberty.33 k& H% ^% x+ Q& c
In our patient, physical examination was incon-% V5 v0 Q2 d1 E) |. |. N
sistent with true precocious puberty since his testi-" k& l7 e7 c( y6 _& o3 D. t
cles were prepubertal in size. However, testotoxicosis
' Y/ B  d, n& _1 ewas in the differential diagnosis because his father
9 d- ~8 l3 {$ ~( \started puberty somewhat early, and occasionally,' \, Z! z3 O% I' u
testicular enlargement is not that evident in the6 d) v: @% a. R1 s
beginning of this process.1 In the absence of a neg-
) i! I3 E# H3 C( h7 B1 Gative initial history of androgen exposure, our2 s1 R, g2 s2 F* j/ E: c0 c, l, u) H, x
biggest concern was virilizing adrenal hyperplasia,2 N+ l0 U  u2 i9 ^( t3 l
either 21-hydroxylase deficiency or 11-β hydroxylase
9 `" H) U. ?+ S8 Ideficiency. Those diagnoses were excluded by find-& o+ T( }6 O4 r- w7 m
ing the normal level of adrenal steroids.
( A9 e6 o3 e+ ]4 i- EThe diagnosis of exogenous androgens was strongly
8 Z* l2 E: ]) w8 J+ dsuspected in a follow-up visit after 4 months because
- s+ @* }* S  ?- v0 n7 M0 k7 H: Zthe physical examination revealed the complete disap-
: `- W+ @; h  U+ @9 lpearance of pubic hair, normal growth velocity, and) x' n+ M. S2 ]! i- h' Z
decreased erections. The father admitted using a testos-
  Z8 ]* s& j7 W" |( u) z5 Qterone gel, which he concealed at first visit. He was
2 l0 ?3 r  n. susing it rather frequently, twice a day. The Physicians’
2 R8 \3 [7 S  a- u0 t& zDesk Reference, or package insert of this product, gel or9 j! m! h) P8 K7 R; M1 y3 C  I
cream, cautions about dermal testosterone transfer to
" w5 ~  Y7 L* Y! Hunprotected females through direct skin exposure./ n* ?$ W& F$ j6 C% I0 h* i6 i
Serum testosterone level was found to be 2 times the
" @/ B( t: A+ w9 Y0 |baseline value in those females who were exposed to1 [* @% u$ S0 |
even 15 minutes of direct skin contact with their male! T9 q* I8 u4 Q+ S4 S" r
partners.6 However, when a shirt covered the applica-
+ X8 k7 i% ?# O& x- A; ition site, this testosterone transfer was prevented.' ]3 A$ U8 ]5 O. h9 U* i
Our patient’s testosterone level was 60 ng/mL,
; _5 M7 P# K( Q+ I6 h* Mwhich was clearly high. Some studies suggest that- p8 e/ q: Z% f( ~" n4 C/ k* w
dermal conversion of testosterone to dihydrotestos-$ c. X2 K- L7 N
terone, which is a more potent metabolite, is more& Z  }9 Z# f  V7 H
active in young children exposed to testosterone5 g) C% U8 w* @7 e5 ]2 x
exogenously7; however, we did not measure a dihy-# L, k+ {$ T+ j5 J
drotestosterone level in our patient. In addition to2 e8 Y6 M( W/ K( Y1 B- H7 V
virilization, exposure to exogenous testosterone in
: `. S5 L) u' L; Dchildren results in an increase in growth velocity and
9 h4 x; Z, ~( o4 X7 g" g: ladvanced bone age, as seen in our patient.
2 M1 j* M& G$ d0 GThe long-term effect of androgen exposure during: f* [$ a# ], U! `' }
early childhood on pubertal development and final6 F8 I0 u+ c8 g( }2 i) u1 Q
adult height are not fully known and always remain; f) _7 J% @) S" I( q- J& w
a concern. Children treated with short-term testos-
' m( W2 F. l2 ]* E+ R% Vterone injection or topical androgen may exhibit some
0 x; R. u7 K& ?8 y! @7 i: Vacceleration of the skeletal maturation; however, after2 P/ ~  o/ G% ~9 m+ R. l$ E& A
cessation of treatment, the rate of bone maturation9 ]; f; E$ c% o% Y) {; \, P. I' j
decelerates and gradually returns to normal.8,9' I) P0 o7 v' p# _: |) S: I
There are conflicting reports and controversy
7 ~4 Y; r" ~* c( c6 |over the effect of early androgen exposure on adult+ \9 r; |8 w: H* `; Y$ m# s
penile length.10,11 Some reports suggest subnormal
7 }: w/ h# j* {: y6 D5 ^/ M  }adult penile length, apparently because of downreg-
( t+ ?. Y1 a& v2 {  z8 gulation of androgen receptor number.10,12 However,
. }9 K- a. Z' D: Z7 [. f2 VSutherland et al13 did not find a correlation between: K7 F- s/ a% U. l
childhood testosterone exposure and reduced adult5 S( X, ~3 {- S: T' e
penile length in clinical studies.
2 B  d6 A5 t* ^8 TNonetheless, we do not believe our patient is! E7 d( R  j7 |% ]2 ?$ K. M! O
going to experience any of the untoward effects from
9 C0 R3 c  u& d8 }3 @testosterone exposure as mentioned earlier because$ ?+ I* z5 n8 g
the exposure was not for a prolonged period of time.+ B% _) J- i4 }) P; J: |) w6 r
Although the bone age was advanced at the time of
+ X, R) V$ |3 d: t/ ~  jdiagnosis, the child had a normal growth velocity at
' m* Y7 g$ u1 a6 c. [% Y7 kthe follow-up visit. It is hoped that his final adult. K" w/ h/ J- |8 J0 V( y
height will not be affected.  J) F* G& @! ?- u$ e$ G
Although rarely reported, the widespread avail-: G+ u5 F# c" h. q4 d3 [
ability of androgen products in our society may5 b/ O8 k0 T% X8 |+ {
indeed cause more virilization in male or female
, l$ p- J( H# f3 c3 x( [3 J/ ichildren than one would realize. Exposure to andro-
% w/ u9 Y& f& x, U- ^gen products must be considered and specific ques-
. }! n- @2 D3 `' d8 a7 Ftioning about the use of a testosterone product or
) N% u8 ^3 g# g- W1 jgel should be asked of the family members during5 }5 u5 S, p1 u8 A& ^: F& E% _
the evaluation of any children who present with vir-% E: _- n- |! r8 X* k
ilization or peripheral precocious puberty. The diag-
2 c, m, T$ j$ \- A3 v+ K: ]nosis can be established by just a few tests and by
5 x7 |: S/ z2 Yappropriate history. The inability to obtain such a
" j) J8 j0 S6 Phistory, or failure to ask the specific questions, may5 M0 B5 A. r  t: E3 r6 v# S
result in extensive, unnecessary, and expensive+ a' N0 D0 n" g; l* N3 t
investigation. The primary care physician should be0 N3 _" p, g; @$ f# _: Z! o+ S
aware of this fact, because most of these children8 O7 G) W& o% |- H5 X% F
may initially present in their practice. The Physicians’% A& p/ W% J/ O/ \# r; G3 h9 R
Desk Reference and package insert should also put a
9 n  }1 t; a( }3 n  M2 F. |warning about the virilizing effect on a male or
+ ^6 _% l- {7 K$ cfemale child who might come in contact with some-1 `" c/ q3 |4 u! n! r9 U
one using any of these products.
$ J$ f# }  U1 H6 _9 hReferences, O, N. h" [% K+ T! n, [% d7 M$ H
1. Styne DM. The testes: disorder of sexual differentiation. ]' k% T# q! c8 ^
and puberty in the male. In: Sperling MA, ed. Pediatric3 K5 C& a. v" _- o/ E) z. y
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
- \' n( j% F+ x0 Q2002: 565-628.
- Q. J0 S* I  i( x9 W) t2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious: s: V. u0 n6 x3 Y) _
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 x$ I3 ?/ `+ e/ 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