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Sexual Precocity in a 16-Month-Old
4 M1 W+ N2 x$ |# lBoy Induced by Indirect Topical- Z9 t+ D+ b3 z& N
Exposure to Testosterone
- |+ h& |9 E6 X5 j5 L# a8 Q6 _Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2* K4 ]4 m7 @1 \8 ~, ]9 I4 K  \) u
and Kenneth R. Rettig, MD1" C3 k; t8 [- ^
Clinical Pediatrics
# K0 c" ]2 l8 m  W; r0 M9 pVolume 46 Number 62 z8 f" [5 |, x( ?; T7 n. H! c
July 2007 540-543, }  N% Y' @2 G
© 2007 Sage Publications' g6 c& z% [+ R; Z7 e
10.1177/0009922806296651' {. K; k. l+ N# L9 @1 y1 b2 g
http://clp.sagepub.com
$ V( j) v7 o6 i8 fhosted at) A; V/ l2 l9 c/ f& M
http://online.sagepub.com
' D2 G( ~* v" a2 IPrecocious puberty in boys, central or peripheral,
- T7 I% p: ?0 Y/ |/ H9 q( ?& l* E( uis a significant concern for physicians. Central
3 H1 x# h7 K  \3 Q% X7 W# ]' wprecocious puberty (CPP), which is mediated$ ~0 K8 f, ^% N6 T5 v
through the hypothalamic pituitary gonadal axis, has
3 C/ F& i2 g& N* c7 Za higher incidence of organic central nervous system; x5 W( U* ?6 a' y
lesions in boys.1,2 Virilization in boys, as manifested: ]% d, G6 {5 c- m2 V) n3 p
by enlargement of the penis, development of pubic
8 }; d7 h# I: F# _4 I6 _hair, and facial acne without enlargement of testi-
% J2 F4 ~% J) w' h: F+ {; `cles, suggests peripheral or pseudopuberty.1-3 We! H. @: V& a  ~. ~4 _4 \, a
report a 16-month-old boy who presented with the
7 k: d! @* j* fenlargement of the phallus and pubic hair develop-3 o2 |% Y4 l5 @) N
ment without testicular enlargement, which was due7 R' `/ }) W; ~' e
to the unintentional exposure to androgen gel used by
% t" }6 m4 p7 U' I9 ~$ Athe father. The family initially concealed this infor-
, {* Z' ?5 @. f4 ~mation, resulting in an extensive work-up for this
8 V! @, _+ ^/ h( kchild. Given the widespread and easy availability of
; I# u; l) g6 vtestosterone gel and cream, we believe this is proba-
- \4 e7 R& m5 o: cbly more common than the rare case report in the
2 e. Y* f5 |* Q" N. c- R6 zliterature.4
6 M5 G) {* j9 E+ `" _6 R3 tPatient Report! T  m  d/ S, v6 v& a7 x& ]
A 16-month-old white child was referred to the/ Y0 j3 z: v* }" L
endocrine clinic by his pediatrician with the concern
: s% U$ _9 w6 _( r" M% mof early sexual development. His mother noticed
3 G( I' F; h% H. vlight colored pubic hair development when he was2 c% L3 V9 c% n7 `& u3 u7 ~# M3 [% [
From the 1Division of Pediatric Endocrinology, 2University of- x% Q4 u% l) h( O3 g9 u( X
South Alabama Medical Center, Mobile, Alabama.
" c' D3 Q: E7 g* ?& fAddress correspondence to: Samar K. Bhowmick, MD, FACE,
& j- Y, x: A4 i9 v  q% \8 FProfessor of Pediatrics, University of South Alabama, College of
* O6 \" n( G# E% n$ C8 v& _' m7 eMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
7 \8 {; e- \7 i7 v/ Q; E$ @e-mail: [email protected].
2 C8 K; Z2 z( \- ~# W$ l% Oabout 6 to 7 months old, which progressively became+ ]) a+ ~4 [) A( Z
darker. She was also concerned about the enlarge-* V4 H' p4 X, v: n0 a
ment of his penis and frequent erections. The child
( m2 I% U. Q8 I/ Qwas the product of a full-term normal delivery, with/ s3 c( M9 g* H2 d/ D1 t/ M+ W
a birth weight of 7 lb 14 oz, and birth length of0 l6 ]7 c$ J: D$ P
20 inches. He was breast-fed throughout the first year
' p( M9 V8 ~& jof life and was still receiving breast milk along with
  S, ], g/ D8 x+ w* n- Wsolid food. He had no hospitalizations or surgery,1 A; A( ~( H6 {3 e' f
and his psychosocial and psychomotor development! D  P$ r$ f3 F7 @! ~7 a" S
was age appropriate.
" \5 [# \0 G' w* Q) z( r6 Q- \9 oThe family history was remarkable for the father,, l8 H. y" v4 c) w( @$ W  }
who was diagnosed with hypothyroidism at age 16,$ x$ ]" G+ J* N
which was treated with thyroxine. The father’s
0 ?& v( ]( z# r& M' n5 _+ S6 qheight was 6 feet, and he went through a somewhat
' J5 o; ~2 y5 V2 @+ s  h( s. Zearly puberty and had stopped growing by age 14./ S$ J' n2 p: h. }1 U6 h/ ]
The father denied taking any other medication. The
9 K8 S/ M! |1 g( p% U) g5 G. Tchild’s mother was in good health. Her menarche! Q- I1 Q8 [. f( L* w$ S8 X3 Y
was at 11 years of age, and her height was at 5 feet
* M# k: Z. E5 i& N$ I( Z5 inches. There was no other family history of pre-: d5 A* B. P$ [5 z7 b
cocious sexual development in the first-degree rela-
  C: Q3 H( q, E- ]& b9 htives. There were no siblings.$ \. |- a1 \6 @" |1 d" e. P- n5 O
Physical Examination- `% i9 i+ D$ Z$ U2 j
The physical examination revealed a very active,# W% T. \" u5 P( J" `: j. o% v6 M
playful, and healthy boy. The vital signs documented/ S. B. V. n* j. s$ N
a blood pressure of 85/50 mm Hg, his length was  `# ]" h3 s& j- x
90 cm (>97th percentile), and his weight was 14.4 kg
; a, c" V8 c4 {, m, u! W(also >97th percentile). The observed yearly growth
3 X1 ~5 D, i0 \! z& y) pvelocity was 30 cm (12 inches). The examination of2 S: z8 z3 F( {4 C4 K) z
the neck revealed no thyroid enlargement.
& G" B9 M% x# D7 R# [The genitourinary examination was remarkable for
9 c3 C0 `+ V$ ~! E' p% nenlargement of the penis, with a stretched length of' z# T# ?* W" q; T9 ?5 `/ t' n
8 cm and a width of 2 cm. The glans penis was very well
6 L2 t; R4 S4 w! b2 ?1 ideveloped. The pubic hair was Tanner II, mostly around( Z* Z+ l( }  f2 o" N! L
540% ^9 K6 a; a/ \& t- T
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from7 [8 `$ Y8 o9 ]. W8 h  z) `7 |
the base of the phallus and was dark and curled. The
" F3 ]" v1 b7 F' o8 `testicular volume was prepubertal at 2 mL each.  y: N7 v( o$ U9 f3 j& R$ w& F, Q* u
The skin was moist and smooth and somewhat% H% A4 n( V/ }2 M( W8 b0 W
oily. No axillary hair was noted. There were no
0 d/ j% t1 O+ I3 ]( Zabnormal skin pigmentations or café-au-lait spots.  n, Q4 S+ Z2 A3 n9 `6 `* c: K
Neurologic evaluation showed deep tendon reflex 2+/ b" u0 z9 e5 U3 q0 E6 N7 l0 C, x  j
bilateral and symmetrical. There was no suggestion6 l$ O+ |# i$ R- V! @
of papilledema.
9 v. n' u7 `/ @8 ?/ l: d5 A+ Y' hLaboratory Evaluation: F% ~5 o: g7 ]9 T# Z
The bone age was consistent with 28 months by7 f. L4 C9 L" V. `* }
using the standard of Greulich and Pyle at a chrono-2 |% p4 m' k( L
logic age of 16 months (advanced).5 Chromosomal
3 }4 ?" z' \, Q7 p' S) Ckaryotype was 46XY. The thyroid function test2 q  k; G3 J5 [
showed a free T4 of 1.69 ng/dL, and thyroid stimu-# ~2 [. W, G& Y8 Y, g5 l  I
lating hormone level was 1.3 µIU/mL (both normal).& J0 V& t1 {3 Y8 v( g
The concentrations of serum electrolytes, blood9 C7 Q1 V- f, l" _/ o
urea nitrogen, creatinine, and calcium all were
6 y% x8 E3 A/ ?# j+ Fwithin normal range for his age. The concentration
+ r8 W* ~, K. t+ p7 ?7 Y8 ^; Lof serum 17-hydroxyprogesterone was 16 ng/dL
. V1 g# t" Q" q8 L# E# Y9 V1 U(normal, 3 to 90 ng/dL), androstenedione was 202 k4 {) f  }8 Z  L; l$ w
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-$ c! S% T6 g* W* \; D5 I
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
+ G; k% H5 q& j9 J& v) @desoxycorticosterone was 4.3 ng/dL (normal, 7 to' m. [( g  h7 _3 P, W
49ng/dL), 11-desoxycortisol (specific compound S)
5 t+ V) x" s* y1 m9 B5 E7 E; |: awas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
6 s: h; z3 O  ztisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total. t+ ?$ |$ _3 T
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
+ h  r, K3 i: @  Land β-human chorionic gonadotropin was less than
9 v8 b2 }2 M& Y1 g1 b; {# h5 mIU/mL (normal <5 mIU/mL). Serum follicular
1 g4 B- b4 D1 O, d( ^stimulating hormone and leuteinizing hormone8 f' q! }- R2 j
concentrations were less than 0.05 mIU/mL
$ y8 Z0 T% C* Q- g(prepubertal).2 e0 _" n9 T1 ]2 }
The parents were notified about the laboratory
* |  |, M$ w6 f2 tresults and were informed that all of the tests were% s' f6 X2 {1 w0 R% }3 M
normal except the testosterone level was high. The
8 [- m! h2 s# |follow-up visit was arranged within a few weeks to
/ d7 h  r# I. Yobtain testicular and abdominal sonograms; how-+ c' V3 z  I- w  ~6 P8 [
ever, the family did not return for 4 months.
0 l6 P. j3 l0 M  y( MPhysical examination at this time revealed that the
: R+ W& i, N4 f, n2 g& Echild had grown 2.5 cm in 4 months and had gained
6 \! x! o/ u0 D" G8 z/ \3 p* U: X+ |# v2 kg of weight. Physical examination remained' O" p; P( D/ x2 }3 P
unchanged. Surprisingly, the pubic hair almost com-
" D8 f, W& B4 c5 M# q" {pletely disappeared except for a few vellous hairs at
4 B9 s& c7 x0 v+ S; Y  Kthe base of the phallus. Testicular volume was still 2! I0 ^# o1 V/ g% N6 j/ ^
mL, and the size of the penis remained unchanged.6 x% X* B( k$ t
The mother also said that the boy was no longer hav-
6 i/ K; p! P3 I6 D5 v$ [0 ging frequent erections.8 z6 m- R4 G9 V% _% i0 \
Both parents were again questioned about use of
4 |/ X  h6 X6 |# x2 }any ointment/creams that they may have applied to
* K3 O/ [5 K$ z7 n: X$ gthe child’s skin. This time the father admitted the
) p4 h$ s' H4 l: n' h; ]Topical Testosterone Exposure / Bhowmick et al 541
& n  p* ^9 d: m* V5 G1 A. s0 N1 Luse of testosterone gel twice daily that he was apply-. O/ F- d7 `9 |8 J) u5 }& V4 t
ing over his own shoulders, chest, and back area for
0 `: [0 m7 L. m* W+ Za year. The father also revealed he was embarrassed
/ P+ G+ K, r0 d" W9 @( Ito disclose that he was using a testosterone gel pre-3 X  H. d8 o6 P9 r
scribed by his family physician for decreased libido, D" z  P& R8 Y) G' b7 s7 {
secondary to depression.8 z8 ]5 W/ k  k
The child slept in the same bed with parents.5 c* S# @- X, g, d
The father would hug the baby and hold him on his
2 `1 O& j: D: c$ R, S- T* |chest for a considerable period of time, causing sig-
) p# v/ o$ X9 n$ f, Jnificant bare skin contact between baby and father.
8 z+ m. o* F" CThe father also admitted that after the phone call,
+ n0 ~' n( L8 L4 u- F1 Z% ]when he learned the testosterone level in the baby
! K4 S( y7 d* @  h& Q& g' ywas high, he then read the product information
& c9 r3 G/ A7 b) Opacket and concluded that it was most likely the rea-6 W" z' K* e2 N6 b
son for the child’s virilization. At that time, they; a2 v- C0 f  k; ]( h
decided to put the baby in a separate bed, and the+ J1 g  E% B# S1 ]1 R% d; T
father was not hugging him with bare skin and had
! N, E2 z& ?+ @# G9 T- I) ?been using protective clothing. A repeat testosterone: [( x% W8 A5 E: U$ \) t+ X8 i+ M$ q
test was ordered, but the family did not go to the5 ?( e: A: u( R
laboratory to obtain the test.9 f& o3 b1 Q' X: Z! t% k% d
Discussion
9 {* P! t5 m+ @8 `8 |( GPrecocious puberty in boys is defined as secondary, b7 Y; a# z- o' v3 z& Z6 y
sexual development before 9 years of age.1,4
+ P' l% e5 G7 l. @3 e; pPrecocious puberty is termed as central (true) when
% E; r& Z6 O% V  Oit is caused by the premature activation of hypo-& [9 q$ Z; c2 B+ w4 ^5 s6 s
thalamic pituitary gonadal axis. CPP is more com-' L- o0 T8 ^# ^% |
mon in girls than in boys.1,3 Most boys with CPP5 C2 g. J' |1 D+ ]4 f' X8 B- Z+ K* `
may have a central nervous system lesion that is, \3 q& [* I2 `, q2 T% E8 b+ q% X
responsible for the early activation of the hypothal-
4 ]0 K/ W) A5 `0 Hamic pituitary gonadal axis.1-3 Thus, greater empha-, J: G; i5 P# I" [& X! U
sis has been given to neuroradiologic imaging in
# ~' K% i# ]/ Dboys with precocious puberty. In addition to viril-
5 F9 c% {) _2 Tization, the clinical hallmark of CPP is the symmet-0 C1 b: d# K$ ^4 L
rical testicular growth secondary to stimulation by
5 d6 B5 Y* x) Ogonadotropins.1,30 _) k3 |! u1 F8 x: {
Gonadotropin-independent peripheral preco-1 P- d" B2 Q; W
cious puberty in boys also results from inappropriate/ U3 X6 s) p% X, \
androgenic stimulation from either endogenous or
, A+ f2 F0 `: k) W7 Gexogenous sources, nonpituitary gonadotropin stim-) e3 u0 e8 Y* Z+ W. P" K! ~
ulation, and rare activating mutations.3 Virilizing
4 Z9 I# Z* k3 z. ?2 J3 E0 f2 ncongenital adrenal hyperplasia producing excessive
0 ~3 U* O" ~* i" e7 @; _adrenal androgens is a common cause of precocious
! o8 L9 \& |8 `/ C# lpuberty in boys.3,4% {8 I( Q+ i/ p
The most common form of congenital adrenal% {" _" s+ @6 G& H$ G/ O: ^
hyperplasia is the 21-hydroxylase enzyme deficiency.* r! i! m/ b3 c7 A  M2 |
The 11-β hydroxylase deficiency may also result in8 s7 X( x3 W- f7 g+ D+ l
excessive adrenal androgen production, and rarely,
$ E" u3 E/ z7 w8 ?3 n% c& V' ran adrenal tumor may also cause adrenal androgen/ q+ x* q9 t6 i6 _# H* W
excess.1,3  h3 o( U: ^( [& k8 a
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from$ r: A) m# D+ o8 v3 F
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
7 O$ R2 ]  ~- g" E  f1 ^A unique entity of male-limited gonadotropin-
* w# d+ E. ?3 Q/ s* a( e( nindependent precocious puberty, which is also known
1 D! t: t, v! G' t7 F/ \as testotoxicosis, may cause precocious puberty at a
2 J% Q# _: l1 c. ivery young age. The physical findings in these boys) H0 @3 y0 x6 f# Z+ |# ~
with this disorder are full pubertal development,+ D% V4 P4 }% w, r) h9 L1 m6 H5 z
including bilateral testicular growth, similar to boys9 w/ v& ]1 A$ o7 X. G6 ~& X
with CPP. The gonadotropin levels in this disorder1 j( L& b+ ?' N" ~4 U
are suppressed to prepubertal levels and do not show. i. I% n# [0 e
pubertal response of gonadotropin after gonadotropin-
" t5 ^* d9 J: w$ h" z/ mreleasing hormone stimulation. This is a sex-linked
8 X( }# m" d2 A/ s# ?autosomal dominant disorder that affects only
1 o$ \* ?4 t6 q2 Rmales; therefore, other male members of the family
4 h6 i$ ?7 O! b5 b3 V  R3 f8 nmay have similar precocious puberty.3
! u) \5 S2 I) Z; p6 `- N, rIn our patient, physical examination was incon-
7 W( h! Z: \+ D& L) S7 ^1 {sistent with true precocious puberty since his testi-4 p% z$ s4 S1 a" W) ~( G- o) a6 t
cles were prepubertal in size. However, testotoxicosis
6 i" y4 I8 K& m' I' xwas in the differential diagnosis because his father0 u/ r: d0 R3 j" D4 v% a* F+ d
started puberty somewhat early, and occasionally,9 ]5 P* N; ^8 }  V. S% `7 D
testicular enlargement is not that evident in the+ j- D! C2 k$ `9 N1 m: w
beginning of this process.1 In the absence of a neg-
. K* B) D6 T2 Y9 `# lative initial history of androgen exposure, our
# m3 |: ?. v" Q8 x' ~+ u% \biggest concern was virilizing adrenal hyperplasia,/ o7 q; d1 t, \/ Q& @9 q& D
either 21-hydroxylase deficiency or 11-β hydroxylase
  u& F: q6 Y! J* udeficiency. Those diagnoses were excluded by find-  x' k% S+ o! R8 }/ C/ ]9 R
ing the normal level of adrenal steroids./ q9 j4 L' t5 u; \- u2 a6 B/ H
The diagnosis of exogenous androgens was strongly
' N# z# R' ~4 n( S7 v  N3 Isuspected in a follow-up visit after 4 months because! p( v3 [1 s  s9 Y  f" ^: _
the physical examination revealed the complete disap-1 a- {. n% c# J- R  |/ ?) j
pearance of pubic hair, normal growth velocity, and" h' i, Q4 u! _# y  I+ V
decreased erections. The father admitted using a testos-
* N, P& s, x( V, G* zterone gel, which he concealed at first visit. He was7 I* \, Y% _9 {$ p* k
using it rather frequently, twice a day. The Physicians’  ?3 o0 u9 _! Y; [% E- U2 a# \
Desk Reference, or package insert of this product, gel or( R$ p: N5 W2 N% B
cream, cautions about dermal testosterone transfer to
- O; u. l2 t: a* U: \unprotected females through direct skin exposure.
* m6 V# l  H& O6 RSerum testosterone level was found to be 2 times the! a: Y7 {: [& F; \/ h
baseline value in those females who were exposed to' X6 S- ]1 g$ X5 d1 F1 w' k
even 15 minutes of direct skin contact with their male
- i5 }& {; n9 ]0 d4 `' Vpartners.6 However, when a shirt covered the applica-
% q1 i, L8 j9 s# L4 ~tion site, this testosterone transfer was prevented.
% ?0 W% f* A9 J/ }& GOur patient’s testosterone level was 60 ng/mL,3 V9 w* C5 ?6 p0 W+ s  m, y
which was clearly high. Some studies suggest that
1 P  ^6 M+ a; @1 I8 h0 y& adermal conversion of testosterone to dihydrotestos-
- x) D! w" T, p) D! U" p8 \terone, which is a more potent metabolite, is more0 `8 }* @7 j) T! r$ ^
active in young children exposed to testosterone9 |" h1 `! b  F, n, r; p/ i7 `
exogenously7; however, we did not measure a dihy-
/ l( J* {! b# c* e! |drotestosterone level in our patient. In addition to
8 ?3 H6 g. W5 fvirilization, exposure to exogenous testosterone in
. P' H, T# L0 @  W9 p0 xchildren results in an increase in growth velocity and+ Q' r# S; t, k! q6 }9 }
advanced bone age, as seen in our patient.
! b: \2 A# C. {4 z* Q; GThe long-term effect of androgen exposure during
+ ~! ^$ ~$ d1 ]3 \early childhood on pubertal development and final1 T, c- {% W; u+ `$ _6 m
adult height are not fully known and always remain
5 b9 D. b3 e% Q9 ra concern. Children treated with short-term testos-
6 c7 b! {' S+ g$ l/ @3 wterone injection or topical androgen may exhibit some
! Z" K2 m( {9 A' A, Zacceleration of the skeletal maturation; however, after- L! |  e# ~6 V' w
cessation of treatment, the rate of bone maturation
- N4 T* }6 X5 [! }decelerates and gradually returns to normal.8,9
  n: w2 ]3 r. E/ {3 [8 aThere are conflicting reports and controversy* s4 O+ Y( _- F4 d
over the effect of early androgen exposure on adult! \# V5 I, V) @8 Y- R+ s/ N
penile length.10,11 Some reports suggest subnormal' |* B; x/ A5 h* S7 {: W
adult penile length, apparently because of downreg-
, Q8 ]' B% ^* S3 ^+ c: j' Lulation of androgen receptor number.10,12 However,
: e9 Z. B' V& a5 j2 NSutherland et al13 did not find a correlation between1 ]9 u0 f; {6 x! N0 s# o8 O
childhood testosterone exposure and reduced adult
/ F! y& J7 K% fpenile length in clinical studies.6 ^' Q) z, M, L9 h# _
Nonetheless, we do not believe our patient is
  l$ l. N, h- ]* V7 C7 M7 W4 u- ^; Bgoing to experience any of the untoward effects from" w0 d, }* D* e1 e1 d$ k  R# n1 r
testosterone exposure as mentioned earlier because
9 c+ v# A! c. K$ u  J- [; ^+ nthe exposure was not for a prolonged period of time.
& `5 c) o( M3 G$ ?2 @3 lAlthough the bone age was advanced at the time of
, g/ }# r* w5 [! S) _1 |diagnosis, the child had a normal growth velocity at' F2 q, @- n2 E1 @
the follow-up visit. It is hoped that his final adult9 P3 a' V5 p: T9 Q  h8 P# [
height will not be affected.2 K# t& o! i! d3 ]' I: p; P
Although rarely reported, the widespread avail-
( ~5 r9 D8 r' f6 ^) g$ S  N) Pability of androgen products in our society may8 T/ w& T* a. T+ d+ U
indeed cause more virilization in male or female
4 j' ^8 H8 D' c8 L4 E+ |5 ^5 vchildren than one would realize. Exposure to andro-
6 c$ W! ]: Z( K" o9 ugen products must be considered and specific ques-
& v( m4 K+ y6 c; Stioning about the use of a testosterone product or1 b1 d6 }; f5 X. H0 K
gel should be asked of the family members during; f5 ?- ]/ [: G
the evaluation of any children who present with vir-
! e$ @: ^7 V3 Lilization or peripheral precocious puberty. The diag-
+ N( Z( D* z; x( _! tnosis can be established by just a few tests and by
& @  j* u/ M8 ~" s0 |% Xappropriate history. The inability to obtain such a
4 K# y" l7 W1 L" {2 k$ I& yhistory, or failure to ask the specific questions, may( |8 N1 k$ g3 Z6 K7 b
result in extensive, unnecessary, and expensive
* u* ?) C+ O9 c0 ^' Rinvestigation. The primary care physician should be
5 z6 |- N5 G* d; r5 xaware of this fact, because most of these children
6 P1 t" z/ A4 V/ b* V8 Mmay initially present in their practice. The Physicians’
3 F0 I7 A! y6 i' u9 PDesk Reference and package insert should also put a% w- b) X) {8 L: p1 V! @
warning about the virilizing effect on a male or( z+ `$ b3 e1 w1 n& r8 B: l" O
female child who might come in contact with some-! \9 p. G1 f2 e. ~% S; E
one using any of these products.
, z  w9 a/ V1 y5 K% \& ?' F4 O9 `- Y7 PReferences
7 ~% y  p$ O6 l4 |' \$ H1 S. A( \1. Styne DM. The testes: disorder of sexual differentiation
/ w! G9 W6 i5 B9 F+ J5 oand puberty in the male. In: Sperling MA, ed. Pediatric
6 X5 ^  }* N$ u% K% w0 GEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
1 ~0 s4 V/ q9 T( c' I( g, \2002: 565-628." c5 c5 O" r8 i& N! S4 u9 u
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious3 z& C, X, t5 b1 C/ j, b1 s. O
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old! K  L5 c7 E, o! R5 W# C+ K9 L
Boy Induced by Indirect Topical
! F$ G/ h% R3 L2 V. ?6 t1 H; eExposure to Testosterone% S0 ]* M/ p5 l! M7 I  q
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
  X( |7 t( Z$ [9 i! B8 b% Fand Kenneth R. Rettig, MD1- F# _, ?  n0 ~, K9 `8 A. \+ b
Clinical Pediatrics
* Y% m/ ?4 t$ m$ n. A! dVolume 46 Number 6
# p- J$ W  _0 BJuly 2007 540-543% h- u* K2 f6 L3 \6 h& o8 F
© 2007 Sage Publications
% g. m2 O7 m) v5 k( }10.1177/00099228062966515 S2 f2 p# U# a; y( B7 D
http://clp.sagepub.com
2 {8 r/ P# ]- |hosted at
' V" N/ z7 _+ L- yhttp://online.sagepub.com
/ ~8 B( O' z: O+ IPrecocious puberty in boys, central or peripheral,# Z; E8 X4 ?0 T4 ]4 D+ r, j
is a significant concern for physicians. Central6 i' o5 x& I& v+ m# ^
precocious puberty (CPP), which is mediated
9 X  D1 j) g) kthrough the hypothalamic pituitary gonadal axis, has
; c/ ]' @2 L6 _) u: _" w" M7 i8 ^a higher incidence of organic central nervous system; a0 a: ]4 q( x0 a
lesions in boys.1,2 Virilization in boys, as manifested. P* ]$ d7 L5 G6 D0 B
by enlargement of the penis, development of pubic
- p9 u5 V7 y* K2 nhair, and facial acne without enlargement of testi-
$ N" y/ o: \* bcles, suggests peripheral or pseudopuberty.1-3 We% \7 c9 q: E) s* r
report a 16-month-old boy who presented with the
# G) d, M2 I3 R. i8 Uenlargement of the phallus and pubic hair develop-
9 @8 Y8 s5 w% d! ^ment without testicular enlargement, which was due
  _6 G: E& d0 l5 `0 Kto the unintentional exposure to androgen gel used by) Z% ~' ]7 F% c4 q0 \7 `
the father. The family initially concealed this infor-
# d3 I! x. \- e9 dmation, resulting in an extensive work-up for this
8 z5 }+ }9 u% xchild. Given the widespread and easy availability of
+ o1 B5 x5 I4 D. C6 ^2 j# a) _testosterone gel and cream, we believe this is proba-
, [- v, A* S# t9 j' Jbly more common than the rare case report in the
% ?  M8 B7 X- J5 [, ~literature.4
* ^! u& b* O5 k8 l9 i, |8 KPatient Report
6 x. ?6 K7 y& |+ O6 Q; N. F- EA 16-month-old white child was referred to the
: w' L1 W8 u3 j5 z* Mendocrine clinic by his pediatrician with the concern  W4 P1 S8 \* P" W1 i- T
of early sexual development. His mother noticed
4 l. j! Y4 G$ q  Y' a# i: wlight colored pubic hair development when he was9 U/ I! \& b6 T& f, `" l
From the 1Division of Pediatric Endocrinology, 2University of( r  k$ x7 z3 p4 J8 b
South Alabama Medical Center, Mobile, Alabama.- R$ n2 ^+ @, W/ A* a" V
Address correspondence to: Samar K. Bhowmick, MD, FACE,8 T; q% q# v# p: \9 r
Professor of Pediatrics, University of South Alabama, College of
/ s! F  ~" m  _  A9 oMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;" I! r8 C5 l- v1 v
e-mail: [email protected].6 K* c& e! ?( v0 R! c( s" ^
about 6 to 7 months old, which progressively became& K6 [& c5 H: x2 A
darker. She was also concerned about the enlarge-5 F( V+ x# ?" Y
ment of his penis and frequent erections. The child; o1 r% P6 c5 L1 d
was the product of a full-term normal delivery, with
7 C1 u1 S9 O- c4 ?& @+ }a birth weight of 7 lb 14 oz, and birth length of/ x8 s9 y( F" I- O3 i: Q/ c
20 inches. He was breast-fed throughout the first year
8 |: t2 K6 ]' {* h+ }6 z7 eof life and was still receiving breast milk along with
- |" `" }( G. k; |" D% C+ esolid food. He had no hospitalizations or surgery,6 r8 ^7 W: ]/ l, y( {8 s2 ?! [
and his psychosocial and psychomotor development
" _$ o4 R% `8 ^) `% iwas age appropriate.
4 x( B& y; Q# F( q4 m1 jThe family history was remarkable for the father,: n; J1 y7 `4 a" a' C; [
who was diagnosed with hypothyroidism at age 16,  R: ^. a9 ^) G9 ~2 z. r9 P- m  ]
which was treated with thyroxine. The father’s
& [: S0 d1 d& A* u2 s1 yheight was 6 feet, and he went through a somewhat
/ K: c% ~9 H) m# |; O& o, Jearly puberty and had stopped growing by age 14.
7 S# ^- K9 N9 V4 I$ xThe father denied taking any other medication. The
5 o% E2 M# z* ~9 b# n' N% @* Pchild’s mother was in good health. Her menarche' u0 c& q7 V: W# z& u9 T7 t; e# B
was at 11 years of age, and her height was at 5 feet) Q5 r9 `1 ]& K  ^3 Z
5 inches. There was no other family history of pre-
3 |' R; p3 C. W" ~3 y+ z) J( l- fcocious sexual development in the first-degree rela-
4 g. K6 f' x) D4 l  y/ `; _8 F7 wtives. There were no siblings.
; U) Q+ l- A: iPhysical Examination% Y; l" ]( P: \. S6 C3 I+ I( s
The physical examination revealed a very active,
$ d! o& [! ~* F; k" K7 dplayful, and healthy boy. The vital signs documented5 m; G" i' E1 k2 D3 a
a blood pressure of 85/50 mm Hg, his length was
; n  m8 i6 K  h# ^90 cm (>97th percentile), and his weight was 14.4 kg
, h7 S6 |  U% m. q- n8 _1 z(also >97th percentile). The observed yearly growth: q: N3 h/ Z% ]6 ]1 J, o/ [
velocity was 30 cm (12 inches). The examination of  o( [+ }" Z$ p
the neck revealed no thyroid enlargement./ _# V. u6 n( L, K) n3 D/ z0 a- a! j
The genitourinary examination was remarkable for. U$ _- d3 y/ @3 U
enlargement of the penis, with a stretched length of$ T8 t* ]( j0 O6 z
8 cm and a width of 2 cm. The glans penis was very well
  f! A- w/ C7 V, Adeveloped. The pubic hair was Tanner II, mostly around
1 M0 B$ u& ^3 P5 M& ]" {  u540
  B. h1 v: }1 Q# E! x7 ^/ nat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
& l- }% x1 U6 Y  q$ Tthe base of the phallus and was dark and curled. The$ n9 ~) n. K: }
testicular volume was prepubertal at 2 mL each.
& u  s9 i7 k8 P* D, q) N# |6 }* r9 s# l$ I: LThe skin was moist and smooth and somewhat
& l& B4 Q! W- Y3 aoily. No axillary hair was noted. There were no
& H: h/ F0 z. J8 Sabnormal skin pigmentations or café-au-lait spots.% E6 K( B4 k2 j9 Y3 V
Neurologic evaluation showed deep tendon reflex 2+2 G, [0 U' t  G" n5 Y# H! w
bilateral and symmetrical. There was no suggestion
# @! o9 @; \4 Nof papilledema.
  b7 l; a$ w$ h$ a8 j# wLaboratory Evaluation
7 }5 C! ?2 Z7 @The bone age was consistent with 28 months by/ {9 _$ L' P' z
using the standard of Greulich and Pyle at a chrono-! e5 x6 H4 J- V6 {! Y+ ]6 @
logic age of 16 months (advanced).5 Chromosomal5 s% ?4 _. h  C- P7 h9 l9 O
karyotype was 46XY. The thyroid function test
2 |3 E. I% J# ^) F# d# F3 Xshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
# c, x6 L) v5 ]0 h$ `( B! Blating hormone level was 1.3 µIU/mL (both normal).  ^7 ~& a0 g4 f  Q- ~/ e
The concentrations of serum electrolytes, blood' y+ f7 X, @9 Y
urea nitrogen, creatinine, and calcium all were3 q0 Y* N  t, X6 T
within normal range for his age. The concentration
2 ]* I" l+ S9 a9 W! uof serum 17-hydroxyprogesterone was 16 ng/dL2 G" P$ E+ D( L& _
(normal, 3 to 90 ng/dL), androstenedione was 20) F; j! f6 d% R$ C
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
/ c9 l) R9 {( Z+ c9 r. @- ^terone was 38 ng/dL (normal, 50 to 760 ng/dL),# Y8 D: Z# P' n9 H, k) K) R
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
  P/ y7 I3 C) ^49ng/dL), 11-desoxycortisol (specific compound S)
) ^8 O, y) C, x  Ywas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
; a& g) b8 }1 V  M# {tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total4 {! ~5 D8 J* C* @
testosterone was 60 ng/dL (normal <3 to 10 ng/dL)," w% T9 D" R. j  x$ m% O
and β-human chorionic gonadotropin was less than
1 M( ]7 C& Q( P! p2 x1 ~5 mIU/mL (normal <5 mIU/mL). Serum follicular( M+ m* c, S6 D+ X" p
stimulating hormone and leuteinizing hormone7 S& p6 U0 Z8 A. m4 S) c
concentrations were less than 0.05 mIU/mL+ I9 U! G+ e6 f9 F- J5 r
(prepubertal).
3 I5 Y' z  W0 W  |2 ?The parents were notified about the laboratory2 N6 f0 X+ m8 @: d* v. m- U0 F( M0 B) W
results and were informed that all of the tests were
3 F$ `/ _% ?" j8 K2 N$ qnormal except the testosterone level was high. The( @7 b; V" g& n3 o) f& z
follow-up visit was arranged within a few weeks to
3 U6 I) k0 o0 ~+ W  Lobtain testicular and abdominal sonograms; how-7 o; R9 E" \/ [; _4 L; o% r
ever, the family did not return for 4 months.
& y  k2 E* C# ^: Z0 x/ gPhysical examination at this time revealed that the
5 ^3 `. I$ i: U, a4 G* hchild had grown 2.5 cm in 4 months and had gained! j/ X& I5 ?3 e4 F  T8 ]
2 kg of weight. Physical examination remained  |/ G8 V: b6 ~$ ?
unchanged. Surprisingly, the pubic hair almost com-
/ G' ~! G, i  a" t5 }pletely disappeared except for a few vellous hairs at
  x" _4 s0 A  d* U: |0 F6 _the base of the phallus. Testicular volume was still 2
0 W/ @( s7 u6 V! u# s3 smL, and the size of the penis remained unchanged.
6 q6 K/ H4 S" y1 c9 H# ZThe mother also said that the boy was no longer hav-# m! l3 K0 t  S; b
ing frequent erections.
& i3 M) |8 C: u+ EBoth parents were again questioned about use of0 P+ m2 Q: y+ h2 f$ l
any ointment/creams that they may have applied to
) n  ]7 S8 o" }the child’s skin. This time the father admitted the# S0 H: d. d4 j  h# X. `
Topical Testosterone Exposure / Bhowmick et al 541' L- r5 [: }/ `
use of testosterone gel twice daily that he was apply-
/ N2 Q% r& p, P# G9 F( bing over his own shoulders, chest, and back area for
4 H7 r* X0 w& i9 |1 Qa year. The father also revealed he was embarrassed
. v3 z' P3 ~6 L* rto disclose that he was using a testosterone gel pre-
# S+ q8 a0 T2 Yscribed by his family physician for decreased libido/ K. X% r7 U6 V& `) A+ o+ s" F
secondary to depression.: |* [' k# H3 z8 R
The child slept in the same bed with parents.% G- |. n5 ^* l+ z; X  X
The father would hug the baby and hold him on his
" Z3 X, ?+ V/ }. }( Wchest for a considerable period of time, causing sig-. W/ q1 f; p' r. ^
nificant bare skin contact between baby and father.
! y1 K% x* A7 rThe father also admitted that after the phone call,. B. ^$ v0 {6 \+ a
when he learned the testosterone level in the baby: u  o8 B2 q' n4 L/ R5 N0 m
was high, he then read the product information/ f9 u% H/ ~1 ~4 `8 _
packet and concluded that it was most likely the rea-
: |" E- |! H& c: x9 e8 G/ gson for the child’s virilization. At that time, they
" O0 [% j1 y7 Z2 S& u+ ydecided to put the baby in a separate bed, and the9 W* }6 @. f& |1 c( O$ s7 V& i! }
father was not hugging him with bare skin and had7 A1 g: e1 K" Q! ^
been using protective clothing. A repeat testosterone
0 P; M* H! i1 W9 S' q! I( Q4 M6 btest was ordered, but the family did not go to the# u3 f* A' U( B: j7 O
laboratory to obtain the test.6 m9 L* M  O  W: Z+ D( N! o" ?
Discussion: M1 k6 w! Y3 F$ ~6 C/ d2 J
Precocious puberty in boys is defined as secondary: w% [' }; {6 p6 I4 ~/ U
sexual development before 9 years of age.1,45 v4 P( s+ \, H/ |; ^. m
Precocious puberty is termed as central (true) when4 k- c4 k% p( ]# C' j
it is caused by the premature activation of hypo-
1 d. W" M7 y" O1 \0 ]thalamic pituitary gonadal axis. CPP is more com-+ W' D1 N# @7 _6 }$ q0 @# t8 Q
mon in girls than in boys.1,3 Most boys with CPP2 {  @) r. E' I# m
may have a central nervous system lesion that is
! H2 s3 \6 C  }8 o7 @4 ]2 cresponsible for the early activation of the hypothal-  C" L4 f3 F- B1 |
amic pituitary gonadal axis.1-3 Thus, greater empha-
9 x0 n5 z" S0 l+ m  Isis has been given to neuroradiologic imaging in4 T  D" ]' M- A( q' P' s9 @# @
boys with precocious puberty. In addition to viril-
( v. e0 p4 m2 I5 r: ^ization, the clinical hallmark of CPP is the symmet-
' p( c) j. Q6 }$ L7 Yrical testicular growth secondary to stimulation by
# e) s, _4 e* S; o5 F8 ngonadotropins.1,38 n- }& ^3 F' }& h7 B0 I4 H# Y2 j; e
Gonadotropin-independent peripheral preco-
& w" e! G( t$ s! ^3 R1 qcious puberty in boys also results from inappropriate. D8 ^+ \( D3 v) M
androgenic stimulation from either endogenous or2 E4 `  g+ H# u# l$ o
exogenous sources, nonpituitary gonadotropin stim-$ j& d" t4 P( r. F0 }0 [
ulation, and rare activating mutations.3 Virilizing
. G6 s/ J$ o2 `. e% ^. b- v, n1 Gcongenital adrenal hyperplasia producing excessive
/ U5 f. j+ K) d1 v3 T3 fadrenal androgens is a common cause of precocious
  I; ~2 l- |( x: [5 N* D* p8 apuberty in boys.3,4" q- W$ ^( j* W8 w
The most common form of congenital adrenal" I  f* c) G5 |9 [, _, e
hyperplasia is the 21-hydroxylase enzyme deficiency./ u! ~& \! a& {7 Z7 r  k' \7 W0 c) z
The 11-β hydroxylase deficiency may also result in/ h( K& ?$ B& {& |# |: h9 g
excessive adrenal androgen production, and rarely,. u9 ?, y; B& V( F3 f
an adrenal tumor may also cause adrenal androgen
- N/ K2 ?. O  Xexcess.1,3
5 C' A, Q  K2 ~0 vat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from- h; o6 h- A5 a! V$ d2 ]! R
542 Clinical Pediatrics / Vol. 46, No. 6, July 20070 h1 W' L4 x2 b
A unique entity of male-limited gonadotropin-
# |4 o  {( G8 Q8 O7 t  y: m7 A! Sindependent precocious puberty, which is also known
/ Z0 t2 C* ?% f2 P4 Gas testotoxicosis, may cause precocious puberty at a
6 M0 t! h/ ^9 [) H4 w) j9 F* m$ ]" U8 zvery young age. The physical findings in these boys
0 N: x3 q7 p" E6 a; z# G% p! Awith this disorder are full pubertal development,3 J- B7 j3 f: a. F( K: s/ N1 K+ ~
including bilateral testicular growth, similar to boys  A+ q( J1 `0 c) }
with CPP. The gonadotropin levels in this disorder
7 k# Z, @7 Z( ?+ Dare suppressed to prepubertal levels and do not show
; h3 k0 t1 {6 B9 L; g9 I$ Epubertal response of gonadotropin after gonadotropin-
7 @3 d: @3 h2 `) j/ F2 dreleasing hormone stimulation. This is a sex-linked' t8 `( i2 y( H2 \% w& P
autosomal dominant disorder that affects only
/ a' K, z3 R1 b' M5 H& Lmales; therefore, other male members of the family
: x* P1 H+ s4 W8 J! Y' Xmay have similar precocious puberty.3; V8 L6 u/ U' I$ l( U3 [
In our patient, physical examination was incon-3 Y# [" {4 R2 n9 m! [
sistent with true precocious puberty since his testi-
9 j- |- g4 Z5 d. E: l# w. Y. o+ \. I+ Mcles were prepubertal in size. However, testotoxicosis4 Z" E/ Z3 @- D* n* \/ W' G" T- T
was in the differential diagnosis because his father" \' i8 f" y5 K: s- a- E6 P
started puberty somewhat early, and occasionally,* y# k& K* _! G% L& P
testicular enlargement is not that evident in the
, N* A  D5 w4 H( l" ]* V3 xbeginning of this process.1 In the absence of a neg-
0 ~- n8 u, j8 D  S8 G% ~5 Jative initial history of androgen exposure, our3 _4 q+ ~  V' F
biggest concern was virilizing adrenal hyperplasia,: X* d, l) [$ l9 O) D# q
either 21-hydroxylase deficiency or 11-β hydroxylase3 n& B8 a+ p' _2 j
deficiency. Those diagnoses were excluded by find-
/ q+ y- C+ ]; Sing the normal level of adrenal steroids.
* Z/ i% ?6 ^8 }The diagnosis of exogenous androgens was strongly* K, R" X7 c+ C& a
suspected in a follow-up visit after 4 months because, S( O% J! [: W/ R2 B& H
the physical examination revealed the complete disap-
5 h+ G- `+ V  H& c8 ypearance of pubic hair, normal growth velocity, and! J2 P2 V' v' F" S1 J; D, K
decreased erections. The father admitted using a testos-8 ^1 N8 N  g8 b# W8 e% L
terone gel, which he concealed at first visit. He was' S" L: p; q( p0 S
using it rather frequently, twice a day. The Physicians’: S' A0 `8 |+ ?: @5 T+ C; w/ w
Desk Reference, or package insert of this product, gel or
5 W" Z! u/ a. X5 c! [: Dcream, cautions about dermal testosterone transfer to' o8 U% ]& y+ b& q9 M* M* r
unprotected females through direct skin exposure.* G8 A# `9 D3 a6 x  W3 \
Serum testosterone level was found to be 2 times the
& c2 X  d( }1 |; ~baseline value in those females who were exposed to, L! p0 a5 _* ~; U% a9 r+ I7 w
even 15 minutes of direct skin contact with their male
. l" T/ X% J4 wpartners.6 However, when a shirt covered the applica-) m: W( z, X# z' Q% h
tion site, this testosterone transfer was prevented.
/ d# e1 z7 z. _8 c8 g: XOur patient’s testosterone level was 60 ng/mL,! ~  Y/ L, _5 d; n. D. S
which was clearly high. Some studies suggest that$ f$ W* {" j* A- R+ A3 a4 F; I
dermal conversion of testosterone to dihydrotestos-& s% m9 c* v- D" ~( S8 U1 R% ]
terone, which is a more potent metabolite, is more& m! a) o9 e2 n3 o% E
active in young children exposed to testosterone
7 r# o! q1 t7 D! V1 o, r# U: V, U8 Bexogenously7; however, we did not measure a dihy-
2 n* f# B2 Y! v+ z. c7 s. b5 Ndrotestosterone level in our patient. In addition to
  H4 E# R; u9 h  A# o2 C2 Xvirilization, exposure to exogenous testosterone in
* @+ C. o) d" a8 ^  a% Zchildren results in an increase in growth velocity and
6 |) q* ~8 c7 [7 K; F% b0 Dadvanced bone age, as seen in our patient." J3 k2 M/ p: J
The long-term effect of androgen exposure during
. W. m, i# f, n. L$ f5 h9 h5 z- tearly childhood on pubertal development and final
8 H$ R6 t% ], o! S) \- ~adult height are not fully known and always remain( {# a# T) H8 I% N6 L* X
a concern. Children treated with short-term testos-$ ^! \9 ]: L, A3 \. `
terone injection or topical androgen may exhibit some" f+ d1 t8 u# O# p0 m( z
acceleration of the skeletal maturation; however, after
$ h7 |+ y2 f7 A! z8 b- J6 Ycessation of treatment, the rate of bone maturation% u6 ^3 X1 L1 m& B
decelerates and gradually returns to normal.8,92 Q9 b4 l6 k- V; I* R  G8 R8 s' B
There are conflicting reports and controversy* f1 B6 k# z9 y. G# h/ H
over the effect of early androgen exposure on adult# v6 H. `; S! G. M+ v, G0 C
penile length.10,11 Some reports suggest subnormal
% E8 j( O7 f% Q. Y; Radult penile length, apparently because of downreg-
% n; w& }5 M: k1 i/ b7 |ulation of androgen receptor number.10,12 However,4 S2 i4 [& T1 P: n7 f
Sutherland et al13 did not find a correlation between
) A& h& v$ ^1 S" d, T# echildhood testosterone exposure and reduced adult
' n9 P: u% W: y/ u) ]2 mpenile length in clinical studies.
; B1 d- c+ r" x  ^# `5 YNonetheless, we do not believe our patient is7 n9 ]5 S, z9 z$ q9 Z0 B
going to experience any of the untoward effects from% y8 ]# z- k* T8 |
testosterone exposure as mentioned earlier because
6 [; v9 ~) S* k3 M  C4 Athe exposure was not for a prolonged period of time.
9 G8 `+ S# n# y5 |1 cAlthough the bone age was advanced at the time of& E8 C1 D  b: ~; [8 B
diagnosis, the child had a normal growth velocity at
) a$ J2 w/ b' }0 k: Uthe follow-up visit. It is hoped that his final adult
6 y4 H. C0 C& ?% e3 V  rheight will not be affected.
* Z) |: l" V+ n) Q$ yAlthough rarely reported, the widespread avail-
" L: \8 g& q( S1 H1 W( d' Gability of androgen products in our society may
. T/ N% ^7 `3 X, F% W( C% r6 r. cindeed cause more virilization in male or female$ S' r1 Q+ s: A2 S0 s' ?2 ~) N4 @* }
children than one would realize. Exposure to andro-+ W; i" r4 ~* Z) R' u  z
gen products must be considered and specific ques-  O  f7 `2 [" K5 [6 T. `! D
tioning about the use of a testosterone product or, d0 T0 _2 i! }
gel should be asked of the family members during& ?1 K3 R/ I2 P$ q
the evaluation of any children who present with vir-0 p. r) [/ t' {, Y+ x0 _
ilization or peripheral precocious puberty. The diag-
" g( E# B# l. Knosis can be established by just a few tests and by
) ]/ [5 w! _5 I5 Z/ I$ K: U1 A- ?appropriate history. The inability to obtain such a
4 b* S% h  D  \+ Uhistory, or failure to ask the specific questions, may/ M3 I* q/ k+ w7 G  D6 b3 L+ c' w% _
result in extensive, unnecessary, and expensive
+ Q: F6 C& X5 v9 Q! @, W4 |" iinvestigation. The primary care physician should be: g, s8 R1 m# `3 s- r6 l
aware of this fact, because most of these children/ @) b' h" C! a9 b0 ^. G5 k. E; |
may initially present in their practice. The Physicians’% x5 V" q8 K3 E8 i  _
Desk Reference and package insert should also put a
( a& @7 n, `+ e4 Lwarning about the virilizing effect on a male or' Q  H+ v* g) {9 B
female child who might come in contact with some-
! r9 x7 ~1 ]0 t/ J: J, J" u$ [one using any of these products.6 q) O/ _1 U$ N
References
; y; t5 P. w  Y& A6 b1. Styne DM. The testes: disorder of sexual differentiation! V. `! Z. E$ U( v" {$ Q+ ^
and puberty in the male. In: Sperling MA, ed. Pediatric* ?7 [. o# b( C
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;. Y$ \( \" Y- O, u8 Z5 a
2002: 565-628.0 O8 Q- p5 h3 R7 ?& U+ x: M
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious( C3 }1 g, w  W1 P( h: Z
puberty in children with tumours of the suprasellar pineal
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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

& ^! G. R. l! D  M  e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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