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Sexual Precocity in a 16-Month-Old7 P. _/ B, g# X% m$ m, P
Boy Induced by Indirect Topical* R1 {5 i2 Q# J4 o4 i6 l
Exposure to Testosterone% W  z1 j( s$ u/ P- @$ U
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2; J8 B) Z* @+ U# b
and Kenneth R. Rettig, MD1
/ K# {+ B# n3 ?5 AClinical Pediatrics5 B: N) K  S9 A3 I2 ?
Volume 46 Number 67 z; q% C) V7 Z9 C, [
July 2007 540-543
: z" `1 S# Z3 n5 P2 N+ Y9 p/ D# _! s© 2007 Sage Publications0 i( v) ]& @/ q$ @0 ^
10.1177/00099228062966512 m+ b& X  O6 [' O0 e7 v" N
http://clp.sagepub.com
/ z+ y" f( C3 `+ W( N8 U8 Whosted at
# A  r, z) S, m5 Vhttp://online.sagepub.com
  a2 Q9 t4 j; u! Q. j4 L& M0 ePrecocious puberty in boys, central or peripheral,
3 ]2 d4 c8 y$ B$ N6 Y) ris a significant concern for physicians. Central
( {! J6 ~4 ?% K! {# `$ }8 T) pprecocious puberty (CPP), which is mediated) _7 ?7 ~9 x/ _: K% G+ K2 n
through the hypothalamic pituitary gonadal axis, has2 A) q2 x8 n. [( ^  U
a higher incidence of organic central nervous system
. d5 f+ F* N4 Q9 k+ L. v- d) s3 n9 f- jlesions in boys.1,2 Virilization in boys, as manifested: o; a9 S, M8 Z" l! e8 A- q
by enlargement of the penis, development of pubic
% X7 V7 D0 w* ~' L! ?. t; fhair, and facial acne without enlargement of testi-7 p" b& {0 r  ]; }  e, ?* E% Z% u: P
cles, suggests peripheral or pseudopuberty.1-3 We
0 Q- |% J; K0 j+ `  vreport a 16-month-old boy who presented with the
6 T2 w- }+ K. D: j0 `# ~7 Aenlargement of the phallus and pubic hair develop-
+ O" w& t: |& ~9 O) C& E7 |ment without testicular enlargement, which was due  B8 q% P1 W8 ?
to the unintentional exposure to androgen gel used by" {& o; q* \8 ]) Y5 M( V5 k
the father. The family initially concealed this infor-
0 B3 h$ L4 s+ t5 I' z& xmation, resulting in an extensive work-up for this, K5 u2 Y% R4 Q( ~
child. Given the widespread and easy availability of
) c9 c2 n$ ], {testosterone gel and cream, we believe this is proba-7 |4 O5 i1 |' W! D4 s5 X
bly more common than the rare case report in the
) |2 W% f* U# w' N; L6 o( W  pliterature.41 C( _0 t2 I# ]$ T' V8 f$ o
Patient Report
: l+ ^, t, q1 ?2 o% {A 16-month-old white child was referred to the
+ A& V* E8 ?! q, [% J8 c0 sendocrine clinic by his pediatrician with the concern! m/ U) z4 e& x. E2 S: n
of early sexual development. His mother noticed
/ G' o" x6 v8 ^9 Mlight colored pubic hair development when he was
3 r3 |4 l+ P' M( NFrom the 1Division of Pediatric Endocrinology, 2University of( T. t# k- B8 a! Z  q
South Alabama Medical Center, Mobile, Alabama.
# ]! m* H, K; ?, Y3 S) EAddress correspondence to: Samar K. Bhowmick, MD, FACE,
9 C+ z# n0 R# `; R3 X2 Z5 a' y- f0 aProfessor of Pediatrics, University of South Alabama, College of
+ \" q& H1 s7 \: nMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;2 P7 V9 i6 h1 b4 h4 V4 a
e-mail: [email protected].
* U" r% K, _" b: `! kabout 6 to 7 months old, which progressively became
7 I  s5 \" t+ p: ]9 B8 kdarker. She was also concerned about the enlarge-; y5 f% G' a& `) O+ [6 N
ment of his penis and frequent erections. The child8 w! b! e$ d$ A8 z% e- s& X
was the product of a full-term normal delivery, with7 k  H! G* P8 E" w  Z0 R
a birth weight of 7 lb 14 oz, and birth length of
  @' ~" r- f# Z5 E( j# W20 inches. He was breast-fed throughout the first year
' E; Z! @8 {5 U: wof life and was still receiving breast milk along with0 h$ p1 e% b: \; i' y
solid food. He had no hospitalizations or surgery,
" |: |$ ]1 i; X4 p, oand his psychosocial and psychomotor development9 @$ ^- b; ?0 l" d" A! O
was age appropriate.7 G( {) z# n) ^
The family history was remarkable for the father,: U7 s; {& r2 s
who was diagnosed with hypothyroidism at age 16,
% Z: W8 C9 e  |, n  o2 f( ~which was treated with thyroxine. The father’s, b8 r+ m; s8 a& t) i
height was 6 feet, and he went through a somewhat# u" c) }6 k9 s/ x
early puberty and had stopped growing by age 14.  `3 I  |7 H. q& W
The father denied taking any other medication. The
0 I8 r. e3 x9 l9 F3 w8 Uchild’s mother was in good health. Her menarche7 `. {0 @9 R+ K+ c: |5 }6 x
was at 11 years of age, and her height was at 5 feet
* B  j: q9 J: M5 inches. There was no other family history of pre-
' W# X, ?; ]8 q: Acocious sexual development in the first-degree rela-
! A  c6 |6 J( B- _, {& Z, k( u; Qtives. There were no siblings.2 D( Z) m5 ~: O% I1 ^7 `+ E
Physical Examination
4 N  r2 C$ Y5 k# W7 s; y$ XThe physical examination revealed a very active,* `; k7 N6 U' w7 u. K! ]1 a* j( C% l
playful, and healthy boy. The vital signs documented. @$ M& h0 M1 P% T
a blood pressure of 85/50 mm Hg, his length was$ V: J5 @2 t6 g* l# B5 Z: ?; N
90 cm (>97th percentile), and his weight was 14.4 kg
' z+ h5 f8 ~. S0 ^+ {(also >97th percentile). The observed yearly growth2 y) r6 Z5 X2 ^  L
velocity was 30 cm (12 inches). The examination of; k& M, K: ^" x, G
the neck revealed no thyroid enlargement.
; d' t. m4 M0 g+ U3 PThe genitourinary examination was remarkable for
( Q+ d1 F7 N3 wenlargement of the penis, with a stretched length of
* _9 k- K8 @/ q. v4 f8 cm and a width of 2 cm. The glans penis was very well
; t7 \! H9 [2 l& Bdeveloped. The pubic hair was Tanner II, mostly around
& d; w. p. S: c5 c/ |' g; Z5400 Q" N% k+ @  p% }4 Y/ B3 W
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
0 J% t( N" U. T8 p( hthe base of the phallus and was dark and curled. The8 m# x0 K" u+ w4 L6 f# u0 G
testicular volume was prepubertal at 2 mL each.
& T7 \/ Z* L6 T! O7 e/ wThe skin was moist and smooth and somewhat. p  p& E, B# C% Y/ Z0 B
oily. No axillary hair was noted. There were no( [4 a0 I6 u; c+ {( \
abnormal skin pigmentations or café-au-lait spots.
/ U0 C7 W3 x+ \& R: NNeurologic evaluation showed deep tendon reflex 2+
5 |  G$ D  `* C# _bilateral and symmetrical. There was no suggestion8 c) u, X. E% m+ f3 _5 h* m. d. h1 j
of papilledema.% s: k$ A2 t, n& N9 a1 t+ b
Laboratory Evaluation
8 H+ h6 M. k* d+ @% HThe bone age was consistent with 28 months by
; X8 Z  R4 ]6 I+ W" o3 c- Z# U; Vusing the standard of Greulich and Pyle at a chrono-5 r2 H6 e/ S+ T) S. v: U
logic age of 16 months (advanced).5 Chromosomal
2 i" z" }1 X$ [9 n6 x% k0 H. Bkaryotype was 46XY. The thyroid function test" L; W' n. e' V2 O! K) g) ?+ t
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
1 j! x) a% f6 q7 i- o3 \lating hormone level was 1.3 µIU/mL (both normal).3 J& [2 b+ k; t! J7 G7 W# z
The concentrations of serum electrolytes, blood
; M6 R2 @9 G$ A! @( q$ i/ Turea nitrogen, creatinine, and calcium all were
' }  T3 X# O  u% Uwithin normal range for his age. The concentration2 J, O; i0 F: D  N' f8 x0 W% v
of serum 17-hydroxyprogesterone was 16 ng/dL* d( c) M* o$ k# r# g1 d
(normal, 3 to 90 ng/dL), androstenedione was 206 b2 g. T0 z) ?8 F, q7 p7 u7 K# o
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
5 k* Q7 k* b) x9 J( o9 r6 Kterone was 38 ng/dL (normal, 50 to 760 ng/dL),
# L) G( Z+ Y( ~: |' x( b: {desoxycorticosterone was 4.3 ng/dL (normal, 7 to
/ `3 l) k! _) X% V; A/ U49ng/dL), 11-desoxycortisol (specific compound S)8 \3 C4 b. R$ z
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
5 B9 J$ p% Y" x* b: z, _" k. }tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
, x! c  b7 k, A- c0 J8 S8 f' U+ ntestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
+ C& \* g5 [6 ?4 k3 L9 Oand β-human chorionic gonadotropin was less than
% s; V* w4 Y( a5 mIU/mL (normal <5 mIU/mL). Serum follicular
* [6 F9 s' ^' c# j' {! j  g+ |, gstimulating hormone and leuteinizing hormone1 j$ d; s( s/ ]2 {+ c% i; F1 T
concentrations were less than 0.05 mIU/mL2 ?) t: C8 x4 k4 J1 I8 p
(prepubertal).
' u) Q- t" W5 @5 k$ xThe parents were notified about the laboratory1 `- z9 ~/ b) Y5 E
results and were informed that all of the tests were
* q6 Z5 Y( S  M$ i5 gnormal except the testosterone level was high. The7 h0 s+ N, J6 p" Y9 W' c$ P
follow-up visit was arranged within a few weeks to6 _$ O6 h( f0 z! Z: e
obtain testicular and abdominal sonograms; how-/ ^. o& k; u) Y( i6 e+ p/ q
ever, the family did not return for 4 months.
9 b7 M7 r, i. L8 ~8 v7 nPhysical examination at this time revealed that the
9 t! M8 I! a+ M) @child had grown 2.5 cm in 4 months and had gained
1 R" p/ J% z9 Q( R7 F2 kg of weight. Physical examination remained3 b; N  `; e% ^: \' m( n/ w
unchanged. Surprisingly, the pubic hair almost com-$ }* Z+ J( a! p0 w/ V3 m" [
pletely disappeared except for a few vellous hairs at
) Y( q9 p2 t* q+ ^( Sthe base of the phallus. Testicular volume was still 2
. f6 g7 S- o7 P( VmL, and the size of the penis remained unchanged.7 @% Q3 y" ]' A: `
The mother also said that the boy was no longer hav-
# `- u" I! k# V" ^" O7 ring frequent erections.
' t$ W' B+ F6 Y& k3 N1 |Both parents were again questioned about use of
  r4 [% v( X) J8 M  {7 `any ointment/creams that they may have applied to. |' y$ @- t+ s7 k8 I" |
the child’s skin. This time the father admitted the
4 G6 I8 Y3 q  @6 T+ fTopical Testosterone Exposure / Bhowmick et al 541
' P% \6 d0 p0 P  K* \5 S/ \use of testosterone gel twice daily that he was apply-
) K. ]- n: }+ G/ ~ing over his own shoulders, chest, and back area for
1 K; p- ]2 d/ Ga year. The father also revealed he was embarrassed
0 D8 Q9 V8 Z) R+ oto disclose that he was using a testosterone gel pre-' M9 t/ j6 ?* B( Z% O- k
scribed by his family physician for decreased libido9 _: r. L. G' w9 G5 ?
secondary to depression.
! c8 Q1 g- ?1 c4 P4 A1 x! M/ y- TThe child slept in the same bed with parents.0 S& }: H3 E3 K' t+ m
The father would hug the baby and hold him on his: J7 @6 X( ?' G9 V! y, y/ l3 G
chest for a considerable period of time, causing sig-" l) N; i0 j/ `# A' d* x" {- Z! A/ M
nificant bare skin contact between baby and father.( C  n# e% ?0 ]& W% e* |
The father also admitted that after the phone call,
( @1 P6 l6 N1 X5 B0 ?& C+ {when he learned the testosterone level in the baby. ^6 h  B+ z7 t+ y2 ^
was high, he then read the product information) T  b2 A1 |" b& A1 g" g
packet and concluded that it was most likely the rea-
& S; m/ r  N, ]/ Wson for the child’s virilization. At that time, they9 b4 m7 l3 x2 {: a2 \. A
decided to put the baby in a separate bed, and the
$ m/ g2 S2 I6 ffather was not hugging him with bare skin and had
3 w1 U! r! R. R# |6 F% O6 u0 t5 `been using protective clothing. A repeat testosterone
  B4 S% C, f* K" Ztest was ordered, but the family did not go to the
8 D/ P: s. M0 N) blaboratory to obtain the test.( H8 W& u# n" U7 s* O2 e
Discussion
9 D3 C7 T& g! D3 Q: XPrecocious puberty in boys is defined as secondary
4 \" v( m* E# ?sexual development before 9 years of age.1,4( r# U  r8 m5 \7 f
Precocious puberty is termed as central (true) when$ I; ?$ O- @" P! v
it is caused by the premature activation of hypo-
2 M9 }! X' [: D' h8 J$ pthalamic pituitary gonadal axis. CPP is more com-
# s" Z% E# @* u3 K9 `mon in girls than in boys.1,3 Most boys with CPP
6 H7 F! Y" ^5 gmay have a central nervous system lesion that is
: K6 K% R# g2 S; }9 E! X5 h9 Qresponsible for the early activation of the hypothal-
( {; N6 ~( [+ C! Z3 t( Z$ Q( Gamic pituitary gonadal axis.1-3 Thus, greater empha-
/ J% G- G" Z: p4 Z; ?5 c! d, `, {sis has been given to neuroradiologic imaging in
" g3 z. f2 h6 T0 y$ U% Qboys with precocious puberty. In addition to viril-
! G; e/ f( x' S$ `. D2 Xization, the clinical hallmark of CPP is the symmet-
  i+ P7 L- p: j! ~2 J) J. G1 Yrical testicular growth secondary to stimulation by
, h5 i: l2 Z/ H# Ugonadotropins.1,3
0 `* h3 Y" y9 G3 m& GGonadotropin-independent peripheral preco-
4 ~% \8 ^) {) \$ j" T' }" q+ B& z4 J+ y9 ?cious puberty in boys also results from inappropriate/ i, E% d! c6 q; a" D1 c% m: W
androgenic stimulation from either endogenous or
" s) x# G5 _( [  d# {  n9 K. Q, Hexogenous sources, nonpituitary gonadotropin stim-, V( p; e* V2 S- y
ulation, and rare activating mutations.3 Virilizing
( Y* Y. h$ f  \2 `$ Jcongenital adrenal hyperplasia producing excessive5 o, A! ^6 E5 o& L6 s
adrenal androgens is a common cause of precocious: p/ B5 M; _$ x. q  k
puberty in boys.3,42 \& J7 ]/ @4 J6 Z
The most common form of congenital adrenal6 ^0 Z3 B+ M2 ?% Y
hyperplasia is the 21-hydroxylase enzyme deficiency.
$ l9 Y- T: A4 f( N- AThe 11-β hydroxylase deficiency may also result in( K: r$ ]# \$ Z" U) O& z& B8 t* q
excessive adrenal androgen production, and rarely,( C8 s' o, B  J& l( @2 ?7 |* p6 o
an adrenal tumor may also cause adrenal androgen
& x2 P! G; O1 T# c, S' }excess.1,3' l* o* S7 W. y! f8 h" x. P( s- z: B
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from( E& B. K" f3 e; W* J3 b
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007& ]- M' E4 `6 T* w; Y! H) E
A unique entity of male-limited gonadotropin-2 J1 L- g6 E& y5 R/ J9 g' }
independent precocious puberty, which is also known
* _# k' O$ N; J+ Uas testotoxicosis, may cause precocious puberty at a+ s- w2 u# q1 a: [
very young age. The physical findings in these boys! b; F+ c7 R' y  S
with this disorder are full pubertal development,
1 H1 T* r* K* ^0 Kincluding bilateral testicular growth, similar to boys/ b5 C5 w% u3 s, M% Y+ y
with CPP. The gonadotropin levels in this disorder
* m7 o: P7 E  K: w. k6 H3 ware suppressed to prepubertal levels and do not show
8 J  |3 f  r0 b+ p8 Y. U3 epubertal response of gonadotropin after gonadotropin-  z# v, }0 P: U2 |/ ~: k0 v$ M
releasing hormone stimulation. This is a sex-linked, T1 k4 ~4 I; P, q2 q4 [
autosomal dominant disorder that affects only8 V3 o( z# Q! w; x* ~
males; therefore, other male members of the family9 R  G4 Q& K( H" z5 C' H0 `  s
may have similar precocious puberty.3
) @3 j# ]) }% n8 _' w% ~In our patient, physical examination was incon-
7 ], Z! G$ \4 {/ asistent with true precocious puberty since his testi-8 g  ~5 ^0 K: P* p; F7 u
cles were prepubertal in size. However, testotoxicosis. E/ S" y# }5 l, V6 ?
was in the differential diagnosis because his father
7 I! b4 L* a9 q4 Y/ R. a6 V/ r; bstarted puberty somewhat early, and occasionally,
$ R4 ^5 U8 M* ]; X1 ?$ Q% wtesticular enlargement is not that evident in the; n# t  _- {; ~& W, H. b" I
beginning of this process.1 In the absence of a neg-  \9 x7 m" c6 c% i' ]
ative initial history of androgen exposure, our
9 h. [, E2 ^* Gbiggest concern was virilizing adrenal hyperplasia,, j# x! h: S; c6 Y6 W. K
either 21-hydroxylase deficiency or 11-β hydroxylase( p) p3 P; G: ~; r# |1 y$ N3 r( G
deficiency. Those diagnoses were excluded by find-
" }6 y) Q8 i$ ]: Ring the normal level of adrenal steroids.
" E9 X: s0 e, X$ DThe diagnosis of exogenous androgens was strongly2 A/ ?; f; T8 t7 `; W
suspected in a follow-up visit after 4 months because
! _) F, A4 {2 V: L2 i+ }the physical examination revealed the complete disap-
& ?: V& z! Y1 K3 U/ ~9 c$ X1 Dpearance of pubic hair, normal growth velocity, and1 `/ Q+ M) b# x
decreased erections. The father admitted using a testos-% `4 r* o- b1 a2 q. Z! H- i
terone gel, which he concealed at first visit. He was( [) |" d0 p: f; d/ l' `3 l0 l
using it rather frequently, twice a day. The Physicians’/ P& i( C) t5 ]2 _" ]
Desk Reference, or package insert of this product, gel or: b9 j8 F. J! R3 d1 s7 l
cream, cautions about dermal testosterone transfer to
3 K8 I$ }# p1 I2 |6 `1 punprotected females through direct skin exposure.. u* R# U% o8 {
Serum testosterone level was found to be 2 times the
7 p3 W, R3 R$ L; M3 g( m$ e5 Tbaseline value in those females who were exposed to
1 h5 i' V4 x6 eeven 15 minutes of direct skin contact with their male1 d2 z! R' k& C: f
partners.6 However, when a shirt covered the applica-
; ?3 {" y* M7 i. }8 \tion site, this testosterone transfer was prevented.
9 r3 f0 q) ^+ L, H  x% F( A* eOur patient’s testosterone level was 60 ng/mL,
8 A8 Q0 J5 H' u' D. U. O. @1 Wwhich was clearly high. Some studies suggest that- C& _  C( {' T3 H1 i& X0 W' c: _
dermal conversion of testosterone to dihydrotestos-2 ]/ J2 n3 h! L$ i3 e
terone, which is a more potent metabolite, is more. s2 E5 u9 [$ \
active in young children exposed to testosterone
5 v0 F, I$ i0 vexogenously7; however, we did not measure a dihy-
. [; g. E+ E/ Odrotestosterone level in our patient. In addition to
' @/ u  q3 K' s( H. M) Bvirilization, exposure to exogenous testosterone in
9 B6 V, A5 r: N- v7 ^children results in an increase in growth velocity and
# H1 w- `3 w& B+ ~. P' P3 F0 Kadvanced bone age, as seen in our patient.$ P; h/ Q9 r. H  G$ E; ^
The long-term effect of androgen exposure during
' r' q  x  g; C1 p1 xearly childhood on pubertal development and final, J; {8 B7 \+ T
adult height are not fully known and always remain
; p" Z1 K0 m5 k  _: va concern. Children treated with short-term testos-. I- T" e$ Z8 N6 l
terone injection or topical androgen may exhibit some
& s& j- v5 s- M' Y7 C& X. pacceleration of the skeletal maturation; however, after
) n2 B" f% m6 l8 G% Y/ l. N. E) t: kcessation of treatment, the rate of bone maturation$ [8 |+ R  h# G
decelerates and gradually returns to normal.8,94 w( i: W& W# \% p* \' K( ?" ^* e' k
There are conflicting reports and controversy. q* Q2 w& F/ E! m- l5 w3 `
over the effect of early androgen exposure on adult& W4 A+ c) Q6 ?7 H
penile length.10,11 Some reports suggest subnormal
1 A) D! r8 P1 B8 uadult penile length, apparently because of downreg-5 k6 q5 y  z: {3 s+ a- e
ulation of androgen receptor number.10,12 However,
* Z, }" K1 x3 ?2 V/ `- {Sutherland et al13 did not find a correlation between
& m! P& w, Q- C& _' w9 _" m& Nchildhood testosterone exposure and reduced adult1 G+ Q; {- R: z) W! s- h! j
penile length in clinical studies.
5 J5 G) w: r2 v6 d2 ~+ q% eNonetheless, we do not believe our patient is
7 i. Y* W) U& ^going to experience any of the untoward effects from
3 h& e7 S6 }$ P' Z. n9 Ntestosterone exposure as mentioned earlier because
+ Z- c' B! U& q- A0 Vthe exposure was not for a prolonged period of time.
3 o# M3 d5 p6 {Although the bone age was advanced at the time of- s' B( T/ a% F& }1 j( }7 ?
diagnosis, the child had a normal growth velocity at) J. H) o# D% ?
the follow-up visit. It is hoped that his final adult
& F5 k8 X6 [* |8 ]height will not be affected.( N! q; X. r7 Y% c
Although rarely reported, the widespread avail-
# p! t. K. K9 f# I( }2 A8 Wability of androgen products in our society may: n9 p; }' @+ Q7 m) b# v$ Z
indeed cause more virilization in male or female
' T( E8 m- }( F6 [" Hchildren than one would realize. Exposure to andro-
) ]* Z" q! o* ]; |gen products must be considered and specific ques-5 g* C, t' W) T- |5 J
tioning about the use of a testosterone product or" {: F# g) f6 e
gel should be asked of the family members during
2 j; v- L, ^" T: T/ \7 n9 E( Hthe evaluation of any children who present with vir-
# _) g. ^3 {% v: \& @" Iilization or peripheral precocious puberty. The diag-+ I$ X5 R  R9 N9 X- Q: G2 l
nosis can be established by just a few tests and by
& O/ Q# s3 n( {& C+ g! Kappropriate history. The inability to obtain such a
& R! \& F0 ]- Y) t, @3 \history, or failure to ask the specific questions, may
0 G5 B' C, S9 w7 \9 n$ W% h; x" presult in extensive, unnecessary, and expensive
  u5 o1 Q  W4 Q! D! U! \investigation. The primary care physician should be
4 l( ]9 h  Q. u- y4 e* N) caware of this fact, because most of these children
4 c4 K. [7 K, [' u& Q; zmay initially present in their practice. The Physicians’5 p" \5 f) G  z) {. K/ T
Desk Reference and package insert should also put a9 G+ k9 `* o+ T; ^: M
warning about the virilizing effect on a male or
2 D7 L6 e: y# r- ^" sfemale child who might come in contact with some-* ~5 Y: d5 @1 t3 y
one using any of these products.
& k5 |6 J5 ]. c8 zReferences+ t" G3 _; V3 G5 S  t
1. Styne DM. The testes: disorder of sexual differentiation, U" J5 q$ n$ e' j* H- ^- o1 o
and puberty in the male. In: Sperling MA, ed. Pediatric
" m1 n) j1 @7 zEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
( |5 Z7 N( t- O1 _: U2 C9 q2002: 565-628.
/ P. G- M# `# j# ~& }8 w9 K1 r6 f2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
. d0 s* a# m( w9 F) lpuberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old; w; z' h3 X) H3 g: X4 s% j
Boy Induced by Indirect Topical
+ Q3 C% G2 d3 T) p: U0 rExposure to Testosterone
; J* S5 j7 Y) [) HSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,25 _# J7 `% L+ F0 D4 \2 x2 o# i
and Kenneth R. Rettig, MD1* A; K! O' v( A) F* Y0 |" ?* j8 _
Clinical Pediatrics+ i  E5 _) C% d, t
Volume 46 Number 6
( b6 V3 I. [/ ?2 |, ~4 B7 g# O' ]July 2007 540-543
6 D, N+ z) a. w: F9 s  l© 2007 Sage Publications" o8 ]  c9 F* G/ ?
10.1177/0009922806296651
8 g: @+ T# E" y6 Dhttp://clp.sagepub.com
7 [& J% A, P% Z8 Khosted at3 g* ?  K& n/ q# Z; p
http://online.sagepub.com
- b: R7 i/ M* m$ p& R, tPrecocious puberty in boys, central or peripheral,( ?' H9 [0 F( V0 ~
is a significant concern for physicians. Central6 U& c. o/ b/ b; x& x2 m/ p
precocious puberty (CPP), which is mediated
' r' X4 Q( L% [" h5 |7 vthrough the hypothalamic pituitary gonadal axis, has( W( O' @0 u: ^
a higher incidence of organic central nervous system
1 |% @: I& Q. _. W, Dlesions in boys.1,2 Virilization in boys, as manifested% o1 t/ T' S" k- {9 E
by enlargement of the penis, development of pubic. b. C, a0 [4 S9 y
hair, and facial acne without enlargement of testi-$ d6 B9 ^" V, _( S- U
cles, suggests peripheral or pseudopuberty.1-3 We
( b3 i' d8 P* L/ T" Y; Vreport a 16-month-old boy who presented with the
% v6 z! g/ W0 `$ }- cenlargement of the phallus and pubic hair develop-8 }/ `& B7 H  U- V/ ?& w8 m
ment without testicular enlargement, which was due. j, u# b% n& l: O
to the unintentional exposure to androgen gel used by
: c" `8 h) E( L3 Y5 Vthe father. The family initially concealed this infor-
8 H* A# i2 _) {" Bmation, resulting in an extensive work-up for this( i* W3 |& t& o' c
child. Given the widespread and easy availability of
( W8 a  E) E; }. O/ Y* o4 d' S# Dtestosterone gel and cream, we believe this is proba-( |8 w7 {; p* D) x/ W- y+ Y  h
bly more common than the rare case report in the3 i7 b4 Q- [% ]0 Z2 _2 g
literature.4
6 j8 u  w7 |: U8 W+ b$ @' cPatient Report
* S0 B/ w: O! TA 16-month-old white child was referred to the
6 P5 k: j8 ]6 D2 wendocrine clinic by his pediatrician with the concern
3 \- I+ _  Q$ G/ ^6 aof early sexual development. His mother noticed
! {) F2 W  C6 U; C" Wlight colored pubic hair development when he was
0 c9 B+ \4 C) u0 E5 pFrom the 1Division of Pediatric Endocrinology, 2University of
: s3 o: l0 a( A" K' ~South Alabama Medical Center, Mobile, Alabama.0 o8 y3 G- C" ~: j9 `2 K5 ~
Address correspondence to: Samar K. Bhowmick, MD, FACE,
' n. j- l7 S) s7 Q2 M0 w# TProfessor of Pediatrics, University of South Alabama, College of( N+ e. @9 e7 ~
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
1 P0 k: i2 Z) w: Q1 `! G2 he-mail: [email protected].6 [* [$ ?  b4 I% H$ t6 y6 l
about 6 to 7 months old, which progressively became6 w% K- r* p' m
darker. She was also concerned about the enlarge-5 P0 Q8 d- O% Q$ X
ment of his penis and frequent erections. The child1 }& X" a5 c( s  H1 k1 n
was the product of a full-term normal delivery, with
! W/ n, Q9 A5 j* _a birth weight of 7 lb 14 oz, and birth length of
' B4 U- I3 ]9 U9 s/ u. a. s20 inches. He was breast-fed throughout the first year
' W3 s# I$ H' q) ]2 h$ ^/ Rof life and was still receiving breast milk along with! [& z* X# r! m& ^1 x
solid food. He had no hospitalizations or surgery,. |! U2 N7 A3 y% `7 [
and his psychosocial and psychomotor development% T2 K5 M3 x# D* C9 Q7 m& s. R
was age appropriate.. Y3 o4 d# O5 R, e/ T1 |( m
The family history was remarkable for the father,
- x9 N, t1 }' B& g9 Awho was diagnosed with hypothyroidism at age 16,
2 C% B# n5 K3 fwhich was treated with thyroxine. The father’s  s# L) _1 V) q+ ], V, o
height was 6 feet, and he went through a somewhat- M! U/ E" A& v& p9 ?
early puberty and had stopped growing by age 14.
& Q. |, V& O  v( d- ~: wThe father denied taking any other medication. The% r* ^+ T. W* u: [
child’s mother was in good health. Her menarche
; K1 S7 [8 u. X# a9 n+ h  l5 Swas at 11 years of age, and her height was at 5 feet2 V2 Q' i: s# s/ u
5 inches. There was no other family history of pre-9 D6 ~. P5 H9 K
cocious sexual development in the first-degree rela-
/ y' S. @, {- W1 b8 ptives. There were no siblings.
4 Z+ f6 b, _! RPhysical Examination6 ^3 j/ ^8 j8 V# G. a
The physical examination revealed a very active,
! `7 U% y& U1 j4 A1 Cplayful, and healthy boy. The vital signs documented
; o+ o; y+ H# V4 ra blood pressure of 85/50 mm Hg, his length was
2 K) l5 h. M7 N- L+ Y! B90 cm (>97th percentile), and his weight was 14.4 kg+ j6 s/ A$ `' a4 k+ w# X+ x
(also >97th percentile). The observed yearly growth5 V% {) d& w) u! q, ^5 J% B$ E9 \
velocity was 30 cm (12 inches). The examination of3 ]: R* i: y8 B7 s
the neck revealed no thyroid enlargement.% R+ z' u# A2 ?5 ^* L8 \$ k. u
The genitourinary examination was remarkable for6 G9 |: E& ~6 o- ?, g3 X5 d
enlargement of the penis, with a stretched length of1 L& S$ H  w' S5 A: Z+ |
8 cm and a width of 2 cm. The glans penis was very well
" o* [0 v6 @1 p+ o3 o9 Xdeveloped. The pubic hair was Tanner II, mostly around
: \$ l% |( V; V. S/ ^( j( o540
* [  @" B/ o& Lat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from4 t% v' s1 \( m' p' m
the base of the phallus and was dark and curled. The) L4 k" G5 F/ C2 t8 Q' d& J
testicular volume was prepubertal at 2 mL each.
) w/ e) n  m- M4 A& C, Q2 ]( ~The skin was moist and smooth and somewhat! A& ~) u9 O4 |4 c
oily. No axillary hair was noted. There were no0 y- e6 M: E+ j$ C8 z
abnormal skin pigmentations or café-au-lait spots.
9 l* j1 M# u1 D5 N/ O5 bNeurologic evaluation showed deep tendon reflex 2+2 r7 x% Y5 o& V+ `( s$ F
bilateral and symmetrical. There was no suggestion' [4 L/ a: F& n% X( {/ Y
of papilledema.
& i8 Q9 m5 l' s! d% u+ mLaboratory Evaluation+ p" K) t4 X) k) w
The bone age was consistent with 28 months by( {0 q8 Y. Z. S$ c% ~; q7 x0 P
using the standard of Greulich and Pyle at a chrono-- \7 ^" P! W* f' x! q! k
logic age of 16 months (advanced).5 Chromosomal3 V6 O! a( ^1 h) M2 ]
karyotype was 46XY. The thyroid function test+ w. l7 L7 G$ ]: U& `9 I& @" q: A! k
showed a free T4 of 1.69 ng/dL, and thyroid stimu-5 O3 S$ d$ C$ p, U
lating hormone level was 1.3 µIU/mL (both normal).% y6 t/ Q$ H3 i9 ]- z. s
The concentrations of serum electrolytes, blood
0 }5 K& J2 h+ D. w$ N8 {9 A, L3 d' Jurea nitrogen, creatinine, and calcium all were; q* m9 q2 n; v- u, W8 t3 G7 g/ y& p
within normal range for his age. The concentration, O; E0 _3 `/ i% V; G+ q
of serum 17-hydroxyprogesterone was 16 ng/dL
! E6 W0 Q6 }9 b8 Y( m(normal, 3 to 90 ng/dL), androstenedione was 20
6 p, ?  x2 ^1 i) m# kng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-! \) _- E% D1 h# N1 B- d
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
$ b, S( r0 U# I. A/ j6 ydesoxycorticosterone was 4.3 ng/dL (normal, 7 to" X1 b6 M" s9 h  V
49ng/dL), 11-desoxycortisol (specific compound S)9 D: L/ u2 N: E7 f. d
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
1 z4 o; G; `+ A  x! Ntisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total; a5 A3 A0 E) B
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
: O! A8 h1 U9 X$ R) R1 Land β-human chorionic gonadotropin was less than
) c, P  Y0 }6 o; b5 mIU/mL (normal <5 mIU/mL). Serum follicular7 {! A& s- ^; g/ Q
stimulating hormone and leuteinizing hormone
$ H9 F- F) R% M- sconcentrations were less than 0.05 mIU/mL
+ u/ Z8 e, k' p# P+ R(prepubertal).; Z" ]& l! ]  H. }6 x
The parents were notified about the laboratory0 k/ `8 g: \; G) H2 Q& c* q0 f7 i& O
results and were informed that all of the tests were
' {0 J( w4 d7 p8 Anormal except the testosterone level was high. The
$ N" {5 Q5 ?" d5 J" x  U- Mfollow-up visit was arranged within a few weeks to% o, o' V! ~4 o5 M0 o: r
obtain testicular and abdominal sonograms; how-2 ?2 ?  i. f2 [; u4 a
ever, the family did not return for 4 months.
' i1 T6 @& d: _Physical examination at this time revealed that the- v3 w" V/ F! o( j4 \( J8 e8 _
child had grown 2.5 cm in 4 months and had gained( _5 N$ b/ Y& w& b& C, S, H
2 kg of weight. Physical examination remained. y8 H5 y" O3 D
unchanged. Surprisingly, the pubic hair almost com-
  G9 E1 k* M: m/ n, T9 ~pletely disappeared except for a few vellous hairs at" h. x2 L' v+ l& O8 Q; h5 N' H3 W
the base of the phallus. Testicular volume was still 2! r" O5 v9 S: j% O) S
mL, and the size of the penis remained unchanged.
8 @, a) ?. T$ Q4 J; ]6 M# r. r2 w+ oThe mother also said that the boy was no longer hav-, M: F( ~* Q5 V7 a% P
ing frequent erections.: J1 ]" S* d/ T% h# R# E2 U3 {3 D
Both parents were again questioned about use of
1 _" `! W' m' T, ]0 `) |- q- a% Wany ointment/creams that they may have applied to; l' h7 H2 \0 x/ z% J" `" J; ~6 {4 [; ^
the child’s skin. This time the father admitted the
0 f, ^7 U4 D6 g& @Topical Testosterone Exposure / Bhowmick et al 541
$ E/ k+ e# N+ H) D) ause of testosterone gel twice daily that he was apply-6 ?! G  K! c& Y: e# M: q0 R
ing over his own shoulders, chest, and back area for
  z/ ]2 T4 G$ n2 r; }a year. The father also revealed he was embarrassed5 M; x  v- L8 y( {
to disclose that he was using a testosterone gel pre-
) v- A7 @# B$ n8 G1 v& s  u* ~scribed by his family physician for decreased libido
: A2 {0 R- c+ m  c; asecondary to depression.
5 J" G+ ^. h5 x* mThe child slept in the same bed with parents." y. V4 r' _) X  ~) @
The father would hug the baby and hold him on his
$ \" F) q, t, z4 v! l$ f) U1 K/ {0 Vchest for a considerable period of time, causing sig-; K5 o' U+ O/ T5 l+ S% |
nificant bare skin contact between baby and father.
: K8 v9 o8 i: k5 W4 ~The father also admitted that after the phone call,; V' a6 A! t; S* c
when he learned the testosterone level in the baby+ l$ B+ F( g# q5 l
was high, he then read the product information
0 M% Z$ e, n$ Z! k. ]/ ]; epacket and concluded that it was most likely the rea-+ C  e" ^, P& v2 ?
son for the child’s virilization. At that time, they8 N! Y5 s. ?, T7 K4 C8 l
decided to put the baby in a separate bed, and the
" X9 K* V5 f# F. Bfather was not hugging him with bare skin and had
. t5 [, P9 d0 r& l, n7 ^1 jbeen using protective clothing. A repeat testosterone
; q  h- w1 K! x% t, @9 O! I/ Stest was ordered, but the family did not go to the
* P8 b! I# ]% H3 B. `' l* k: m# c2 Mlaboratory to obtain the test.
1 g: p9 N  `$ X0 p, G8 c- I0 KDiscussion" u( Y8 r7 j9 \
Precocious puberty in boys is defined as secondary% k# s$ H- @1 A8 u1 T) Y+ f6 ^
sexual development before 9 years of age.1,4
: |  ?9 ?3 d1 ~7 E& w4 HPrecocious puberty is termed as central (true) when6 n& X4 J: B. e5 y7 ]
it is caused by the premature activation of hypo-
; [2 x( M! c1 ]: C& gthalamic pituitary gonadal axis. CPP is more com-7 c2 o" Y# }; Y2 b# Q4 }: H
mon in girls than in boys.1,3 Most boys with CPP
! R9 z! H8 w8 G4 U( |; }; J% ]! M0 Kmay have a central nervous system lesion that is: ]0 p& |2 d( q# q3 J
responsible for the early activation of the hypothal-# ]3 U) F5 g1 k4 \7 R
amic pituitary gonadal axis.1-3 Thus, greater empha-% \2 W) j5 I$ A
sis has been given to neuroradiologic imaging in
9 o2 p, [5 r. f7 A$ @+ aboys with precocious puberty. In addition to viril-- ?  s- j' q' D! g. }* m: m
ization, the clinical hallmark of CPP is the symmet-
% V& e1 O9 A1 f0 Brical testicular growth secondary to stimulation by$ J2 Q9 n6 C- i3 K
gonadotropins.1,33 d( Q7 B5 F6 _# n
Gonadotropin-independent peripheral preco-/ `& u* l2 _) P% y+ B
cious puberty in boys also results from inappropriate7 M# I8 H" h2 Z$ F& k  W
androgenic stimulation from either endogenous or
9 c. Q. i* i* k2 B, e) H5 `) zexogenous sources, nonpituitary gonadotropin stim-. c3 Q) U0 @& ~9 V9 \
ulation, and rare activating mutations.3 Virilizing
0 z% c. K- g7 E# i+ ~3 L  }congenital adrenal hyperplasia producing excessive
! t# `0 P, M) q2 |1 b7 Hadrenal androgens is a common cause of precocious1 H+ X; }4 U8 l' V1 a. G
puberty in boys.3,4: o, G- `9 U& X0 o% {
The most common form of congenital adrenal0 |" ~' k& H0 C/ w' ?1 s, z/ C5 g
hyperplasia is the 21-hydroxylase enzyme deficiency.
: {! U& C, R* z& N5 L7 [The 11-β hydroxylase deficiency may also result in
$ F4 X7 J0 u9 M# f2 p1 D# a3 Fexcessive adrenal androgen production, and rarely,
9 X" m4 j+ R4 \- p* b/ c  }4 i2 zan adrenal tumor may also cause adrenal androgen' h: X2 @& p5 C( D, L- N
excess.1,3- \! t& Q" K0 o1 p7 Z
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
! J$ J3 _. z3 F1 K7 Z% ~1 v542 Clinical Pediatrics / Vol. 46, No. 6, July 20078 P8 _+ A5 b0 r
A unique entity of male-limited gonadotropin-
6 C- _( S$ s( I8 I1 u: c0 e  |4 zindependent precocious puberty, which is also known; I$ H1 v6 [/ }
as testotoxicosis, may cause precocious puberty at a
2 G+ q8 I- M# H& _very young age. The physical findings in these boys
! h6 b. ]9 Q- x% b9 N' Pwith this disorder are full pubertal development,
0 s# P+ n' V' uincluding bilateral testicular growth, similar to boys/ v! Q5 W. j6 \# J6 f
with CPP. The gonadotropin levels in this disorder
8 {- A* @1 s; T  p, Sare suppressed to prepubertal levels and do not show
! a" m; q% n% H, lpubertal response of gonadotropin after gonadotropin-" u2 q/ p, S: e/ m
releasing hormone stimulation. This is a sex-linked
3 U/ n/ o$ E  d" hautosomal dominant disorder that affects only0 `; W5 o1 v: ]0 Y  o8 f; ]- ?8 O
males; therefore, other male members of the family6 ?0 E( X9 C/ A2 s
may have similar precocious puberty.3
' x% Z9 @% \0 @In our patient, physical examination was incon-6 P; ^) G$ i' |- H/ c' ?
sistent with true precocious puberty since his testi-
) I5 q( [5 m+ G9 _, w8 t0 zcles were prepubertal in size. However, testotoxicosis
) ~; A7 v  Z, y) Y# ?$ Ywas in the differential diagnosis because his father" ^2 s' t% f: N9 N/ G
started puberty somewhat early, and occasionally,
2 H3 \: v$ s# `- u  B' j, k! J2 B7 ]testicular enlargement is not that evident in the
0 q4 ^9 C, S& c3 r" Xbeginning of this process.1 In the absence of a neg-+ E% j0 r9 T" a1 R
ative initial history of androgen exposure, our
) v9 O5 X0 z: T, jbiggest concern was virilizing adrenal hyperplasia,/ ^* e8 Q' Y" s: V3 G
either 21-hydroxylase deficiency or 11-β hydroxylase0 {- ?8 {0 \0 F. c4 }$ _+ M
deficiency. Those diagnoses were excluded by find-) R8 k( q; f# \# {9 B! ~6 g* N$ ~& s
ing the normal level of adrenal steroids.
0 R. s- n( v- S: dThe diagnosis of exogenous androgens was strongly
* X" a4 r: K# j$ w3 q) ?, esuspected in a follow-up visit after 4 months because
1 k  c: M. ~' t5 ^& @" ^the physical examination revealed the complete disap-
+ E+ U: v# s' Q) p' g, Z% a! @( Rpearance of pubic hair, normal growth velocity, and
+ e" i. f  ?% Kdecreased erections. The father admitted using a testos-8 z9 ^4 i( |  h
terone gel, which he concealed at first visit. He was4 ?% r( {* N; j
using it rather frequently, twice a day. The Physicians’, \: S  C" M+ \% Y0 ^- j7 f* ?- o
Desk Reference, or package insert of this product, gel or8 c1 f; ^/ L; d* z7 U, j
cream, cautions about dermal testosterone transfer to
7 X  |  S- x# E" ~unprotected females through direct skin exposure.! {0 I1 _5 z/ `0 {4 y% ^
Serum testosterone level was found to be 2 times the- Z5 I8 ^) s  n6 j& r
baseline value in those females who were exposed to* _4 S2 ^- b9 [
even 15 minutes of direct skin contact with their male3 [# s" C9 L2 }0 G
partners.6 However, when a shirt covered the applica-3 H" b1 \6 a$ I( c' f
tion site, this testosterone transfer was prevented.* o# }: g4 x0 j* Z
Our patient’s testosterone level was 60 ng/mL,
- ^5 W* e; n0 Q7 W3 T+ s; w/ Jwhich was clearly high. Some studies suggest that
1 f: ]. Q1 ^' ^; o& _dermal conversion of testosterone to dihydrotestos-
% }1 p2 q; X" y% R  kterone, which is a more potent metabolite, is more5 N9 A2 q$ d. ~4 R' _* F
active in young children exposed to testosterone
2 a$ K# g* l. Z6 x, zexogenously7; however, we did not measure a dihy-8 ]+ Q$ _3 ~" P
drotestosterone level in our patient. In addition to' c, d9 B, e/ f5 A2 z
virilization, exposure to exogenous testosterone in
5 g+ P7 u6 @9 i, J0 M' U$ j. u1 h! gchildren results in an increase in growth velocity and: U6 y+ `4 B, f
advanced bone age, as seen in our patient.
7 ^% n8 p  g$ ?( p* X7 A3 VThe long-term effect of androgen exposure during
8 B+ m" w6 u; m# hearly childhood on pubertal development and final
  _% ~/ K+ d6 s! q7 v7 r+ Jadult height are not fully known and always remain' ?* r+ k7 K- k+ ?
a concern. Children treated with short-term testos-7 j8 _5 q+ t; v+ U: M* C* P
terone injection or topical androgen may exhibit some: z) l8 C; a& L' E3 v9 s" ]  P
acceleration of the skeletal maturation; however, after; b7 q- H2 D& U$ P
cessation of treatment, the rate of bone maturation# B0 k. Y! M  L. H3 @
decelerates and gradually returns to normal.8,94 u7 t9 X8 [% H9 s1 V8 B& o
There are conflicting reports and controversy: _' P9 S7 y0 C
over the effect of early androgen exposure on adult
9 h4 `2 ~. X- k- Hpenile length.10,11 Some reports suggest subnormal
+ P  w$ w) ]' b9 X: b- ^adult penile length, apparently because of downreg-% |2 h4 ]3 u1 k8 |  q  M6 g. Y1 h
ulation of androgen receptor number.10,12 However,9 |. z/ {& [/ @- {& D- I" b7 W
Sutherland et al13 did not find a correlation between  F$ G# X8 X5 i: [
childhood testosterone exposure and reduced adult+ \0 d: c; D! W" u5 v. ^3 u& [
penile length in clinical studies.  ?+ o, X. x/ R2 }1 y) F! ^
Nonetheless, we do not believe our patient is( w" Y! U# d( Q0 W0 a  @
going to experience any of the untoward effects from& \; i+ `4 u3 e. X
testosterone exposure as mentioned earlier because
: m* o& m  O! f4 W' Zthe exposure was not for a prolonged period of time.
. z' H  r$ j1 F! AAlthough the bone age was advanced at the time of: }* {0 g8 _# Z; Q
diagnosis, the child had a normal growth velocity at
% A+ N. ]4 \; B4 j- F- othe follow-up visit. It is hoped that his final adult
& f5 [& _2 y, r$ l& ]/ Xheight will not be affected.
! b& s5 r* x- ^8 D6 u6 ^# lAlthough rarely reported, the widespread avail-) j9 [! L* i% O9 v( Y, \
ability of androgen products in our society may
- |) H5 t3 n/ C/ U7 c! @indeed cause more virilization in male or female
2 W3 @: a$ U3 o7 z' [) ~$ {, W5 Y2 @children than one would realize. Exposure to andro-: i5 I" Y! o* z1 W
gen products must be considered and specific ques-) e1 {/ @8 r0 X; ]( q! L& G  N! T
tioning about the use of a testosterone product or
3 X  |( w5 U' `+ [gel should be asked of the family members during2 n' S0 n+ r+ A% q! g9 d- l0 F) i
the evaluation of any children who present with vir-( F8 [* E" H* z. H+ w/ w4 R/ Z
ilization or peripheral precocious puberty. The diag-
2 e5 n6 F' h; C8 m# {, q+ snosis can be established by just a few tests and by
- ~  U. O2 E) [& ~appropriate history. The inability to obtain such a
+ @- a7 R( Q  |" T5 m# e( phistory, or failure to ask the specific questions, may
' ~) h5 P. D- C* ~# W. y; p0 lresult in extensive, unnecessary, and expensive4 n, I6 o/ Z7 ~! R3 X
investigation. The primary care physician should be
* ]1 S# o$ [4 ^/ m4 Jaware of this fact, because most of these children
$ Q( B5 L/ T8 r: d: D! Zmay initially present in their practice. The Physicians’. _# n( A7 J. H; a6 w
Desk Reference and package insert should also put a9 ~7 @- M% r! g, Y# G" l0 a
warning about the virilizing effect on a male or
3 R/ f. ~: ^; {1 D# o- [* Y6 ?female child who might come in contact with some-: w( {0 U; F. o
one using any of these products.
* I5 B+ u- {; h/ Z$ n7 ^, [+ [" G- FReferences
  a' z" j1 s$ _) o1. Styne DM. The testes: disorder of sexual differentiation
0 m8 z; s3 B6 F+ \& @# oand puberty in the male. In: Sperling MA, ed. Pediatric* b" F4 D7 d# y. ^* \
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
; y0 T- a% L9 o2002: 565-628.% g; b) i+ u, @' ?! y7 y
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
7 G! s$ E) I" `- m/ n( Rpuberty in children with tumours of the suprasellar pineal
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VIP精品區,資源無限好賺金任務區,輕松賺金幣
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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
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4个什么样的?
發表於 2025-1-19 02:41:05 | 顯示全部樓層

" ^* U; G; z' K. V  R1 ~# x' Z( P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!
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