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Sexual Precocity in a 16-Month-Old
- P6 V5 Y: i4 r, O1 J% D9 }Boy Induced by Indirect Topical
) F  ?7 X" K& R( p3 _% PExposure to Testosterone
! a" O" F* K% m% h, r* TSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2# X) t  M9 _) F; M! U
and Kenneth R. Rettig, MD1
! C- \7 T5 z% f& J  @8 {5 x2 mClinical Pediatrics6 Q. c7 t; I! d  |( ?
Volume 46 Number 65 d& V$ x0 r( |5 e% \& e1 y5 @* O- t
July 2007 540-543
, q- _" P, Y- M& Z2 o  P$ e5 ]© 2007 Sage Publications
3 K! F2 \. N: T9 A5 O. ^10.1177/0009922806296651
# q2 Q: b+ H! T! bhttp://clp.sagepub.com8 B2 h4 l" Z) `& z
hosted at
5 \& m( }, J! m1 ghttp://online.sagepub.com
6 }& G3 K" w8 ^# c6 j# d$ pPrecocious puberty in boys, central or peripheral,/ F+ ?. V% C" B( H
is a significant concern for physicians. Central
- {" v# D* l5 v8 vprecocious puberty (CPP), which is mediated5 {+ w: A& i( k/ W% W' h7 b* n
through the hypothalamic pituitary gonadal axis, has
. J3 ^' X. N5 g1 Ta higher incidence of organic central nervous system
; V! Z: Y3 D  \$ ~8 A* h2 J3 S3 K/ Plesions in boys.1,2 Virilization in boys, as manifested
4 F/ }( C$ Z0 Q8 W. Y; ~! {& nby enlargement of the penis, development of pubic6 l. s9 {3 q( k$ b
hair, and facial acne without enlargement of testi-6 u( m3 j2 ~9 c$ D4 r3 C
cles, suggests peripheral or pseudopuberty.1-3 We
8 `$ e# K) }( E  O0 [( s# kreport a 16-month-old boy who presented with the
3 l/ s5 B1 y$ l9 j, F+ Venlargement of the phallus and pubic hair develop-- x! M8 }& `0 I$ ^8 l+ \3 ?
ment without testicular enlargement, which was due' {" T9 r7 Z2 \" G" @2 a- o4 X& a: \
to the unintentional exposure to androgen gel used by
3 @6 _' C8 i9 ]7 A% I0 W9 Sthe father. The family initially concealed this infor-+ i# B, P5 I/ ^% G4 B  \
mation, resulting in an extensive work-up for this
) P- O' A) M  Pchild. Given the widespread and easy availability of
4 U( C, R8 e) Q# d/ Z  z; W7 \testosterone gel and cream, we believe this is proba-
% u  Z) m- Z/ Q, A: o- _bly more common than the rare case report in the
. O% |1 @5 u5 _+ X+ D0 zliterature.4
: s3 e& c# q0 a+ R$ ^1 RPatient Report6 x  U; P6 n5 W' {' V- ^
A 16-month-old white child was referred to the8 N0 B5 o6 i/ c) U9 J
endocrine clinic by his pediatrician with the concern2 A6 Z' R  q3 L: E2 d6 k, \
of early sexual development. His mother noticed( H2 g" F" ~/ A5 \
light colored pubic hair development when he was' @  P0 \' y0 c( ~$ [. Z- Q
From the 1Division of Pediatric Endocrinology, 2University of3 x  Y3 K7 F2 }; |) u  ]
South Alabama Medical Center, Mobile, Alabama.
( E, ]+ d! c$ ]" k/ ?Address correspondence to: Samar K. Bhowmick, MD, FACE,' r' B: |' C1 i& B( T9 [
Professor of Pediatrics, University of South Alabama, College of
* V$ }3 ?9 V! J$ Q% _Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
+ i, M" h- n. Q% }  l/ Ne-mail: [email protected].# d+ b5 V9 ~% A  {
about 6 to 7 months old, which progressively became
# ]0 r. n0 W; }6 a3 b$ _darker. She was also concerned about the enlarge-. g; C% D! L, w8 ]
ment of his penis and frequent erections. The child
9 L4 Q2 u4 H; n- o, J. rwas the product of a full-term normal delivery, with
3 T5 o6 d7 S( Q4 z& N3 q7 [% {+ ia birth weight of 7 lb 14 oz, and birth length of/ ]5 _: Z( z1 N5 x: Q; u& @
20 inches. He was breast-fed throughout the first year5 I. N" B  c* I% W
of life and was still receiving breast milk along with: E- E! v& W* _) `( h3 J; c
solid food. He had no hospitalizations or surgery,
7 }: P! y# b! q4 |and his psychosocial and psychomotor development
. k7 ?  \6 c8 o  H% a: Q/ lwas age appropriate.
% y, M6 n) p! yThe family history was remarkable for the father,
9 n8 g5 _  P# p' y" Z' P0 ?who was diagnosed with hypothyroidism at age 16,
) W- [, O" S; twhich was treated with thyroxine. The father’s# e9 |/ q: s9 Q& j- q6 m8 Q- {; m
height was 6 feet, and he went through a somewhat
7 \4 u; [  o# e- B& z8 Qearly puberty and had stopped growing by age 14.
$ F* q- M3 Z$ ^- ~3 dThe father denied taking any other medication. The
7 b" P1 Y/ {; ^! h. @. s# kchild’s mother was in good health. Her menarche
: L8 i8 t4 v+ f1 Y' awas at 11 years of age, and her height was at 5 feet
0 C5 r  h; v/ {/ I  ^, M5 inches. There was no other family history of pre-
) x) H4 ?& Q- l% E9 \# `cocious sexual development in the first-degree rela-* _3 x' Y- |, g8 U8 n4 O
tives. There were no siblings.
1 h. ?. j# B4 Z1 [: m) LPhysical Examination* g- K- O$ e: l0 L9 o+ }- k
The physical examination revealed a very active,  I8 F$ b! n# U" p
playful, and healthy boy. The vital signs documented
) @& m) p" q# V+ f5 x1 ha blood pressure of 85/50 mm Hg, his length was( ~2 Q! E  J+ S
90 cm (>97th percentile), and his weight was 14.4 kg
$ x, A4 A' |9 ~6 f+ }* ^(also >97th percentile). The observed yearly growth( {; U+ D% x2 z' g3 Q
velocity was 30 cm (12 inches). The examination of
5 k8 e6 A7 ~) K5 ~1 fthe neck revealed no thyroid enlargement.
: @3 h, ?; i# h( x1 x  X# n! LThe genitourinary examination was remarkable for
/ }' y( |' ?# X, K( i4 oenlargement of the penis, with a stretched length of1 I; D' f, g8 }! R" y# J8 X/ h8 M
8 cm and a width of 2 cm. The glans penis was very well$ \! n( |' U! t
developed. The pubic hair was Tanner II, mostly around
0 ^/ a# `! K5 S540
* m# \" q- A( L( w* h4 jat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from' d, F6 i4 ]8 l' X
the base of the phallus and was dark and curled. The% M/ |" t0 l# w( u
testicular volume was prepubertal at 2 mL each.
# i4 J& C0 O. K7 w/ cThe skin was moist and smooth and somewhat
; l, K! J5 i9 E* zoily. No axillary hair was noted. There were no) N3 Z2 l$ T& ~7 X! u
abnormal skin pigmentations or café-au-lait spots.
0 J) g& U* P7 lNeurologic evaluation showed deep tendon reflex 2+
* Z, C7 P5 J+ o; R% E6 ^3 wbilateral and symmetrical. There was no suggestion0 y% ~0 t' k# Y6 g6 P
of papilledema.; Q6 _/ {3 k+ t1 O; s+ h. ~1 t  C* J
Laboratory Evaluation
$ W+ `5 e% h- n7 a5 pThe bone age was consistent with 28 months by
7 E; u' }+ B) E' i) g$ kusing the standard of Greulich and Pyle at a chrono-$ A: p0 v+ W& J
logic age of 16 months (advanced).5 Chromosomal( W! L$ k0 a) C" l" }, O2 H1 I4 t
karyotype was 46XY. The thyroid function test5 n% ~" |9 |+ A8 m) W# f
showed a free T4 of 1.69 ng/dL, and thyroid stimu-5 M& K0 }$ ]8 a7 R$ t% c
lating hormone level was 1.3 µIU/mL (both normal).
' P7 S  C  U  t# U* ^: ?The concentrations of serum electrolytes, blood* c6 B+ Q+ [. L# }- ^! f! K1 P
urea nitrogen, creatinine, and calcium all were3 a8 Y' k  B! V5 K0 I
within normal range for his age. The concentration
  H% r; e* x3 Dof serum 17-hydroxyprogesterone was 16 ng/dL
9 w) W* _# g, m/ V# Q' `(normal, 3 to 90 ng/dL), androstenedione was 20
: X' Z, _# k1 i# p& Vng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
9 U& H" e/ S8 Z) w+ n* ?terone was 38 ng/dL (normal, 50 to 760 ng/dL),
2 G  t6 o0 r+ G9 vdesoxycorticosterone was 4.3 ng/dL (normal, 7 to
- h* K  t- b+ X8 Y( y" H0 Q49ng/dL), 11-desoxycortisol (specific compound S)% {; ^/ H$ v. ~! n7 Y$ r0 @) u+ C7 ]
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-1 T- e2 ?. q- f8 Q
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
8 p' X1 w; x2 n# t2 I% C' |3 ^$ `5 Ctestosterone was 60 ng/dL (normal <3 to 10 ng/dL)," g) v8 l1 M1 a: e; @* F
and β-human chorionic gonadotropin was less than
" H3 q* {4 R4 x- W$ `7 P1 p5 mIU/mL (normal <5 mIU/mL). Serum follicular
$ M* p0 I3 N7 u! mstimulating hormone and leuteinizing hormone1 B) b5 a4 ~+ N6 ~7 n9 T8 b" J5 v
concentrations were less than 0.05 mIU/mL0 a) L- E" I% T) g3 z
(prepubertal).
8 ^. {5 J+ \/ u* N. GThe parents were notified about the laboratory  O" V# R6 C9 C3 O6 H
results and were informed that all of the tests were
1 g# j" S4 x) Y' q4 Snormal except the testosterone level was high. The/ H- Z5 p* d# a
follow-up visit was arranged within a few weeks to
7 v& P4 N1 k$ D9 ?( Y) Y/ Pobtain testicular and abdominal sonograms; how-
& w! \* ?1 \( c) |% C  zever, the family did not return for 4 months.
9 h( _4 o9 z4 l. F) c7 _% ePhysical examination at this time revealed that the
5 {* i6 D. t2 V9 }+ ~0 _child had grown 2.5 cm in 4 months and had gained
8 T- P$ k6 {6 t4 t) K5 J2 kg of weight. Physical examination remained* R' q* o  z0 j! H( n9 B% b
unchanged. Surprisingly, the pubic hair almost com-) E) x, F& H3 Y) x/ Z
pletely disappeared except for a few vellous hairs at
4 |! \7 m! H/ j0 h( Xthe base of the phallus. Testicular volume was still 28 i. I1 t! I( [$ \
mL, and the size of the penis remained unchanged.
8 r; |5 T& B- M3 T! r) f- g8 [6 LThe mother also said that the boy was no longer hav-
2 i" d  t$ r1 n, bing frequent erections.
# _" V8 ^# n/ ?Both parents were again questioned about use of& V) v& \" ^5 ~# q+ W* i
any ointment/creams that they may have applied to& e/ ]3 f  c% ?, S' Z, {8 q- t
the child’s skin. This time the father admitted the! x9 i7 y! W# t, H6 p; b% G7 `. n0 j# P
Topical Testosterone Exposure / Bhowmick et al 541  T$ i9 B# h" H. G
use of testosterone gel twice daily that he was apply-
; m$ c3 Y, I5 }- n- N% King over his own shoulders, chest, and back area for
- c9 C- F6 ]! {3 g! |+ q7 e) s- Ma year. The father also revealed he was embarrassed
- I1 y- A) \' M6 m! P- v, L) \to disclose that he was using a testosterone gel pre-5 N6 ]- z' k9 W$ b  y
scribed by his family physician for decreased libido
; a* R9 E  \& j/ o* Y5 ^) y) @$ osecondary to depression.
( ^& w2 V  r; }+ y, \The child slept in the same bed with parents.! q1 M( D' S$ I& v4 [7 U, o
The father would hug the baby and hold him on his8 p0 r! B* O6 A3 e# i8 @2 l' ]
chest for a considerable period of time, causing sig-5 ?  R4 ^# }) H
nificant bare skin contact between baby and father.# E% H2 Z6 O- k
The father also admitted that after the phone call,
+ G3 S1 W. u5 F& fwhen he learned the testosterone level in the baby
4 S  ~# C* q6 W/ E9 ]6 mwas high, he then read the product information
1 w5 K! v9 J5 `1 b; hpacket and concluded that it was most likely the rea-
4 F8 @1 F) G7 ]$ o6 i" rson for the child’s virilization. At that time, they
9 f% D% x/ q. k. \decided to put the baby in a separate bed, and the3 Q+ ]# d! x$ h( ^( k
father was not hugging him with bare skin and had0 W+ f8 w2 R$ |
been using protective clothing. A repeat testosterone% I. c, Y2 L+ D+ @, [
test was ordered, but the family did not go to the" v) K7 N3 [3 I! T3 e
laboratory to obtain the test.1 y8 L; i: R4 w8 X. T, s8 r
Discussion
  |1 o& o  @. j* N  V! J- [, wPrecocious puberty in boys is defined as secondary
$ X* c3 h1 C, S+ M- X9 }sexual development before 9 years of age.1,4
( {8 E3 E8 q* n: PPrecocious puberty is termed as central (true) when0 \* k# q% W, Y$ }
it is caused by the premature activation of hypo-2 P3 C5 q4 w9 H, x; z" d1 d( A/ n% @
thalamic pituitary gonadal axis. CPP is more com-
3 o; {, |& L8 I) {5 O# M9 Kmon in girls than in boys.1,3 Most boys with CPP* P7 Z. I3 j9 i/ x, C
may have a central nervous system lesion that is- Y" L0 W* j$ u3 H1 w0 P
responsible for the early activation of the hypothal-1 X- `, }  f4 c7 S2 n. ~( ^$ I
amic pituitary gonadal axis.1-3 Thus, greater empha-
& Q- n. |. @' ?5 D* q% rsis has been given to neuroradiologic imaging in
0 e3 i1 }4 F6 J& s: L) X, jboys with precocious puberty. In addition to viril-
9 d, r- _! G% X$ p2 J! o8 vization, the clinical hallmark of CPP is the symmet-4 b- C% i4 `$ P
rical testicular growth secondary to stimulation by1 S* e# O9 k6 T/ Q5 Y; }2 T  `
gonadotropins.1,3% F+ [) @6 _" p
Gonadotropin-independent peripheral preco-0 k* A: o) x9 A+ U7 ^% h  o% W& n; r
cious puberty in boys also results from inappropriate7 }8 |% C: T  X* J( E4 t
androgenic stimulation from either endogenous or- a5 v# d/ R' m/ U6 \) d, q
exogenous sources, nonpituitary gonadotropin stim-
! o2 P: t% ~$ o% f( K- Fulation, and rare activating mutations.3 Virilizing
" Z3 R) W' S: s" N4 scongenital adrenal hyperplasia producing excessive
( w. c) F2 q3 U- aadrenal androgens is a common cause of precocious8 Z1 ^" [- r( I3 @/ d: q/ C
puberty in boys.3,40 M; L) D8 b7 Y% f9 U! B5 p, F
The most common form of congenital adrenal
$ e8 N" l2 N' A+ O+ u' v7 Z& s; Yhyperplasia is the 21-hydroxylase enzyme deficiency.
' z. U& p# _2 i+ ~; ?5 f2 zThe 11-β hydroxylase deficiency may also result in
9 A# P! w  s6 ^) P0 i* ~+ f( kexcessive adrenal androgen production, and rarely,
# H0 o# D; p  pan adrenal tumor may also cause adrenal androgen$ R; B; L$ c7 g4 q$ ~4 k7 w
excess.1,3$ ]& G" v1 F! H) h
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
2 i2 j' d5 f; K+ q( T542 Clinical Pediatrics / Vol. 46, No. 6, July 2007; O$ Q3 t$ d! ]3 B7 B/ J
A unique entity of male-limited gonadotropin-% c5 @/ d: U6 n/ |' k3 m0 E; H% B
independent precocious puberty, which is also known$ D& w) Z% Z. a5 B
as testotoxicosis, may cause precocious puberty at a( [" n  l1 t- h
very young age. The physical findings in these boys
9 O2 j$ p. _) awith this disorder are full pubertal development,
; A" o0 T3 n2 dincluding bilateral testicular growth, similar to boys
2 A. M  U5 M' C+ Fwith CPP. The gonadotropin levels in this disorder) b7 v! e/ s9 U, h& X" q
are suppressed to prepubertal levels and do not show2 Z5 }* [( V( H0 k
pubertal response of gonadotropin after gonadotropin-' u* d6 O) {3 U; h1 H. {
releasing hormone stimulation. This is a sex-linked. }, b- X4 m9 M" t
autosomal dominant disorder that affects only
: U0 d9 b; m9 A9 I* C) E  Gmales; therefore, other male members of the family* v3 n: ]3 r) @7 i% _
may have similar precocious puberty.3
3 r, Q: O, D& \9 y" EIn our patient, physical examination was incon-2 |& m$ g; X7 D3 {) |( S3 n
sistent with true precocious puberty since his testi-
* p2 L0 G' f- `$ d; fcles were prepubertal in size. However, testotoxicosis8 `2 w3 c' Y2 ^( ~: k
was in the differential diagnosis because his father
$ u6 s. H6 G2 j7 }& I* W# Astarted puberty somewhat early, and occasionally,
9 [& j, |- D" V1 |- Ftesticular enlargement is not that evident in the$ o8 o% w  T9 }) c9 ]! v
beginning of this process.1 In the absence of a neg-
8 J: T2 Q0 R3 ~# Y  g& N( w# Dative initial history of androgen exposure, our
( C; n( q9 g1 |3 ebiggest concern was virilizing adrenal hyperplasia,7 W9 J6 r9 ^$ W- j* q3 c: o9 J
either 21-hydroxylase deficiency or 11-β hydroxylase
4 q4 O& J, Q6 w; |deficiency. Those diagnoses were excluded by find-
; {1 ^6 d  R6 P% O/ n6 B$ E" O/ J6 Qing the normal level of adrenal steroids.% R+ D! m. O3 h& _0 D, R
The diagnosis of exogenous androgens was strongly
3 d4 e, J) D6 B; hsuspected in a follow-up visit after 4 months because- X8 g; y  W+ p( G! r8 ?8 \
the physical examination revealed the complete disap-$ t# y  k! }+ c. G* f( s) B( I
pearance of pubic hair, normal growth velocity, and
" C& s* `. _5 p# B, Ddecreased erections. The father admitted using a testos-
# h/ Z/ K+ ^5 K) d; e- W: s5 S# O% I8 Dterone gel, which he concealed at first visit. He was! K* J* `4 W+ H$ E7 N6 N
using it rather frequently, twice a day. The Physicians’
' C" ^  Y4 p' p( H( Q1 F- [Desk Reference, or package insert of this product, gel or
, ~- P. _+ g$ wcream, cautions about dermal testosterone transfer to7 k* H6 L1 |2 V. a7 n7 ?6 w/ `
unprotected females through direct skin exposure.% B6 ~) o& Y& U) [+ N
Serum testosterone level was found to be 2 times the
) _1 O, m. y2 i) a& Rbaseline value in those females who were exposed to, f; F  {( k0 o$ k8 {9 }0 ?
even 15 minutes of direct skin contact with their male, \- g. ?4 k$ e6 F% S$ |3 d
partners.6 However, when a shirt covered the applica-2 p. l( ]3 V. [" j9 Q2 l6 |3 |, I
tion site, this testosterone transfer was prevented.; o# z  V; m) \$ [# y
Our patient’s testosterone level was 60 ng/mL,3 @3 u6 z2 v: _8 u* B3 A. H! A. d
which was clearly high. Some studies suggest that
$ ^/ r0 n3 r. K0 _dermal conversion of testosterone to dihydrotestos-
8 b, `4 |) ^1 c2 A: T( fterone, which is a more potent metabolite, is more
  }0 |6 R& u8 k4 \% nactive in young children exposed to testosterone6 L8 m# Q9 h- t$ \
exogenously7; however, we did not measure a dihy-
- B. s) g" |/ _; m+ H4 t2 Xdrotestosterone level in our patient. In addition to
0 L+ F. g: X: g! b3 q7 ?5 [$ Y* ~1 T# Jvirilization, exposure to exogenous testosterone in6 x  {! j# C; T
children results in an increase in growth velocity and: y  @; |4 m8 w" l0 O3 m
advanced bone age, as seen in our patient.1 F4 L+ M% H! N' ]3 m) E1 l
The long-term effect of androgen exposure during
2 f4 q: O/ \  rearly childhood on pubertal development and final- K: w, D: A8 M5 S/ H
adult height are not fully known and always remain9 i- U$ c8 D% r4 G8 ~) c0 P
a concern. Children treated with short-term testos-
  Y) }/ g8 D0 B4 l! Fterone injection or topical androgen may exhibit some
; T* c" X8 k; u( Y4 macceleration of the skeletal maturation; however, after
" h( W" I4 g$ V7 ucessation of treatment, the rate of bone maturation9 R$ d3 S( l# j
decelerates and gradually returns to normal.8,98 B7 I, `2 @1 F$ E
There are conflicting reports and controversy4 y7 ~' S) m5 S. J( M2 ]8 `
over the effect of early androgen exposure on adult; h+ M% R4 f. N4 l
penile length.10,11 Some reports suggest subnormal
3 h  M- j" P0 q$ M  Fadult penile length, apparently because of downreg-, g0 f; O" P; ]: ]% m% ]
ulation of androgen receptor number.10,12 However,
# E  G; D  Z) U9 D  c. ~2 K# MSutherland et al13 did not find a correlation between
: t* \" a/ I! R) A0 z7 [childhood testosterone exposure and reduced adult+ V5 W  ^1 M8 o
penile length in clinical studies.3 p$ y& i/ C/ {% R+ [, [( s
Nonetheless, we do not believe our patient is. l5 V2 P+ \) M5 W
going to experience any of the untoward effects from: d, y6 o# z  e$ _: ?! B) v
testosterone exposure as mentioned earlier because
% G: g1 v( O: m4 K! Dthe exposure was not for a prolonged period of time.5 N! A4 C8 I% [  X. C
Although the bone age was advanced at the time of" l4 Y: O: f5 ~9 J( g5 L
diagnosis, the child had a normal growth velocity at
  n# ]! E6 U# T2 W& a0 Wthe follow-up visit. It is hoped that his final adult4 S8 a- p7 `# m2 \; b* Y
height will not be affected.: L5 J% N- j) ]0 v( o
Although rarely reported, the widespread avail-8 H- |1 `. z5 T
ability of androgen products in our society may2 }% R- G' @: ^4 P: |3 y/ ~
indeed cause more virilization in male or female
% o3 m+ U: \7 R8 H5 ~children than one would realize. Exposure to andro-
" c& s) C- q. ~7 N% rgen products must be considered and specific ques-7 B9 D( n( h  P' Y( ~- s0 D7 k
tioning about the use of a testosterone product or
2 C% l* h3 u5 L+ a  @, N. ogel should be asked of the family members during% N' }$ U2 F5 \! M3 {/ o
the evaluation of any children who present with vir-. e( h! ]! }! Z, H" x+ m# k7 W% l* C% B
ilization or peripheral precocious puberty. The diag-
* _- {( l9 V9 j: @nosis can be established by just a few tests and by5 n" Y  V$ i# R% o. D
appropriate history. The inability to obtain such a" u+ L; l' @6 Y+ p7 q
history, or failure to ask the specific questions, may9 [+ q. [3 I3 i: p9 D
result in extensive, unnecessary, and expensive* \: Q) x4 A) ?$ c& A
investigation. The primary care physician should be; Z$ {( b/ k7 g! g
aware of this fact, because most of these children
- m) U8 z& |+ ?9 H5 bmay initially present in their practice. The Physicians’
8 v# X$ S+ f- N$ Y2 xDesk Reference and package insert should also put a
  ~, ?! S9 X; P# [warning about the virilizing effect on a male or
, ?3 I" T+ I/ w5 Wfemale child who might come in contact with some-2 B& d4 I  @" X& o
one using any of these products.
+ p$ M, ^& _& k4 z/ v! ]. aReferences) D; J0 z& ?  z; d* w8 X6 J# |
1. Styne DM. The testes: disorder of sexual differentiation5 u. `' B- g( }
and puberty in the male. In: Sperling MA, ed. Pediatric- _' c+ u+ x* E$ z/ c
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;! ]& s; w3 W$ T& E
2002: 565-628.
: @, q# Q; S+ K8 U- H2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
. s* ^7 R3 X) S  ~' Vpuberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old3 w. |, l9 L+ H! _8 f
Boy Induced by Indirect Topical2 i% _7 G7 j* U! V; v8 B8 H
Exposure to Testosterone4 g, y/ b$ A. w# R* w3 O
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
! W# ^+ _, A# _and Kenneth R. Rettig, MD1& T. ~) D! i+ r& n' C
Clinical Pediatrics
) l% t& Q9 N% R4 l8 \2 eVolume 46 Number 68 U) D" _; T; I7 R: M# G, z1 h
July 2007 540-543
$ r2 Z4 }; i$ W5 O7 g, L$ p© 2007 Sage Publications
% t% d3 E% v# M3 b) }10.1177/0009922806296651. A3 o% q3 d4 A9 i- I; y  [
http://clp.sagepub.com, Y" D+ ]) h5 O& V' n  f
hosted at' W- M" n" k9 o8 _0 V
http://online.sagepub.com
8 v' w6 y! k4 o0 z/ tPrecocious puberty in boys, central or peripheral,. m# _% ?" V. o8 n# i  i9 O
is a significant concern for physicians. Central
0 l8 N! I) }9 F" fprecocious puberty (CPP), which is mediated0 w$ D( T: o* y$ W
through the hypothalamic pituitary gonadal axis, has
7 I' H6 j# p3 P6 J! q) Aa higher incidence of organic central nervous system0 D' ]0 m/ v0 V& q
lesions in boys.1,2 Virilization in boys, as manifested/ P: s- [0 B  Q: L( L# i
by enlargement of the penis, development of pubic# e2 H6 C7 [) _% F; o: v
hair, and facial acne without enlargement of testi-
4 r# n: h! p( p, b7 u$ _cles, suggests peripheral or pseudopuberty.1-3 We
2 ~* [8 Y" k  Q7 ~3 dreport a 16-month-old boy who presented with the
/ V& n7 S' A0 L+ l4 aenlargement of the phallus and pubic hair develop-
7 o+ ^' U. l( c. B: dment without testicular enlargement, which was due
% R6 T$ p4 i: q( Xto the unintentional exposure to androgen gel used by
* v  W+ Z8 E2 w. nthe father. The family initially concealed this infor-+ C) {% }- y; u9 p+ u: O
mation, resulting in an extensive work-up for this
/ q7 A! i5 W0 c' S  z/ S3 ]/ ]child. Given the widespread and easy availability of
7 E  H+ [# G# i1 w3 Dtestosterone gel and cream, we believe this is proba-
. Z0 }5 h+ H  |: c7 mbly more common than the rare case report in the
2 m+ a* Y9 f3 o& _literature.4
2 y: g7 Q+ j) w6 l  Z9 t6 R7 FPatient Report
6 }7 Z5 Q- i9 R9 TA 16-month-old white child was referred to the
6 ^$ I; B/ G* J7 c5 ^. _, pendocrine clinic by his pediatrician with the concern& j$ S3 u2 O& _
of early sexual development. His mother noticed
: ]( l* ~' {4 j8 r4 zlight colored pubic hair development when he was
% v" `0 k+ L1 K9 PFrom the 1Division of Pediatric Endocrinology, 2University of$ w" Q7 @5 v4 L  c" {
South Alabama Medical Center, Mobile, Alabama.
4 }0 A- R6 w4 A/ VAddress correspondence to: Samar K. Bhowmick, MD, FACE,
/ I# W7 Q2 f0 v- j. _8 _) d- |Professor of Pediatrics, University of South Alabama, College of
, N! u4 c$ z. u9 Y3 _6 LMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
$ c9 T! P& a% l9 P: q  ?e-mail: [email protected].
; W) }) e- M4 w& m2 j+ X  {about 6 to 7 months old, which progressively became' m; G* v% G% p; |7 F. \. B/ e" x' D
darker. She was also concerned about the enlarge-3 y) {+ y! i$ u0 \! i) N! s
ment of his penis and frequent erections. The child
4 ]" z0 M7 |& `was the product of a full-term normal delivery, with
, D* y, A  V: X6 y- Q7 oa birth weight of 7 lb 14 oz, and birth length of
" T; M' O' X1 {. `( e1 ?7 ]20 inches. He was breast-fed throughout the first year) j  w& D6 t: K/ u
of life and was still receiving breast milk along with* T& e5 m: u" r" j. k
solid food. He had no hospitalizations or surgery,
- t' v: Y0 I# J$ ~+ {and his psychosocial and psychomotor development
( N, r6 J! Z' ]8 j1 g% A/ @was age appropriate.. d* M% P$ _4 {; F4 q" C
The family history was remarkable for the father,
, H4 A2 l! V! Q& H+ `+ o4 Lwho was diagnosed with hypothyroidism at age 16,
' c  H  F) F6 g# S7 r/ nwhich was treated with thyroxine. The father’s
$ G8 D: i2 `+ R# wheight was 6 feet, and he went through a somewhat
! q  j  t/ c6 Uearly puberty and had stopped growing by age 14.
9 z/ d" Q& }( N' ]0 h' j! kThe father denied taking any other medication. The
6 V6 B) k( K* B+ l" Z+ Z- Y+ l: y7 ~child’s mother was in good health. Her menarche
- q! L6 k) Q( J: O3 Owas at 11 years of age, and her height was at 5 feet
1 b' ^2 u, F) b7 _5 inches. There was no other family history of pre-( {2 Y/ C( ^% K; a5 {
cocious sexual development in the first-degree rela-
/ W' b' N' U$ R' utives. There were no siblings.) G8 ^4 `+ q8 I
Physical Examination7 x- v% ?% W7 v. b- \! p4 [
The physical examination revealed a very active,- B4 i/ Q9 ~% t0 D$ \+ Y0 F* j' y0 D8 Q
playful, and healthy boy. The vital signs documented* h- |) @2 ?4 x
a blood pressure of 85/50 mm Hg, his length was
" s1 o; Z5 F- G1 a' w90 cm (>97th percentile), and his weight was 14.4 kg3 V! {4 S- N' n7 u
(also >97th percentile). The observed yearly growth  @4 _& Z; b2 Z# t% K/ `: P
velocity was 30 cm (12 inches). The examination of* i3 p( K: Y) W5 Y0 B
the neck revealed no thyroid enlargement.) C9 S5 A( h# S+ E
The genitourinary examination was remarkable for  s% \, B" V! R; ?
enlargement of the penis, with a stretched length of
' @) ~$ @# g1 Y/ P1 W" E' f5 U: y8 cm and a width of 2 cm. The glans penis was very well+ u% ?+ ~6 v' p. D  [0 {! c
developed. The pubic hair was Tanner II, mostly around
2 e& a" p# ^. r2 o: ~. J540/ Z0 Y) [0 c2 T/ V* u. w3 U. i9 Z
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from3 h) b' w' b$ ^- G
the base of the phallus and was dark and curled. The. T$ H4 w. H/ [
testicular volume was prepubertal at 2 mL each.9 e" w: [% \1 R; I( _! q
The skin was moist and smooth and somewhat
3 E4 v1 d/ ?3 t& zoily. No axillary hair was noted. There were no9 {# c2 w9 h! M5 c
abnormal skin pigmentations or café-au-lait spots.
6 K& U& |- F2 WNeurologic evaluation showed deep tendon reflex 2++ g6 i) T  e4 M$ n% ^3 k
bilateral and symmetrical. There was no suggestion3 n7 c, J/ N  f) L6 |
of papilledema.3 q$ K" ~/ ?* T3 x& G# ^+ t2 ]
Laboratory Evaluation$ T/ g  t0 ?9 X1 W  a( o
The bone age was consistent with 28 months by, X0 U+ @. v! G1 O
using the standard of Greulich and Pyle at a chrono-
% S1 K) K  x" Hlogic age of 16 months (advanced).5 Chromosomal2 `% @  _$ O4 N
karyotype was 46XY. The thyroid function test1 x& R* W% s2 {( p# T8 k, x" J
showed a free T4 of 1.69 ng/dL, and thyroid stimu-7 Q4 b4 I! f5 X- `3 p+ E8 g; m" a# S
lating hormone level was 1.3 µIU/mL (both normal).& d) \- R3 b# ]. q
The concentrations of serum electrolytes, blood
% Q4 U. M$ h4 L9 ~  p/ yurea nitrogen, creatinine, and calcium all were" q1 B- @. ~: K" v4 j- @3 f% G
within normal range for his age. The concentration
  h- Y8 n: O3 {$ ~% ^  x- j( S) qof serum 17-hydroxyprogesterone was 16 ng/dL# }3 m8 Y% @4 n! S
(normal, 3 to 90 ng/dL), androstenedione was 20
+ b4 z3 t, D; C% fng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-1 H. R" k! e. R7 [' I  Y
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
6 D% d& k. z. j0 e1 Odesoxycorticosterone was 4.3 ng/dL (normal, 7 to
, \: K2 Q# T. g1 @49ng/dL), 11-desoxycortisol (specific compound S)
! `" ^" v7 h5 p" \# J! fwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
  j( t1 F; U2 H9 Stisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
6 R, N2 G* ]& @/ q# @* k8 jtestosterone was 60 ng/dL (normal <3 to 10 ng/dL),) ]0 u5 P2 v# m1 r1 K9 ^3 R
and β-human chorionic gonadotropin was less than
; O& [- g- ^/ C! M. p3 G5 mIU/mL (normal <5 mIU/mL). Serum follicular
. Y6 M" o! p, ~) Estimulating hormone and leuteinizing hormone) a/ ^9 M# B' Y0 v% D5 t) h
concentrations were less than 0.05 mIU/mL
1 \" t8 N8 B6 t) y$ s(prepubertal).
. p2 S3 y- E0 F, c. t& x0 AThe parents were notified about the laboratory
3 v, r) s: W: ^( }1 m+ nresults and were informed that all of the tests were$ ?$ s2 ]  f- H4 L6 q, H
normal except the testosterone level was high. The
4 W; a* K5 d+ w4 U6 w* s4 i4 z$ \+ \4 ofollow-up visit was arranged within a few weeks to
. Y7 D! y8 L. k& ?, `obtain testicular and abdominal sonograms; how-8 s$ a8 e3 S0 I& F; \
ever, the family did not return for 4 months.9 o7 r5 m- l; i7 k% A
Physical examination at this time revealed that the
3 Q; [# R" ^1 C& Nchild had grown 2.5 cm in 4 months and had gained
- r. a' B4 N( }# M$ {, ?) H2 kg of weight. Physical examination remained
0 }2 V% b" V/ a" b5 [, c6 o" Eunchanged. Surprisingly, the pubic hair almost com-
1 R$ B7 F  P1 l0 p; F# x5 T: }1 X. zpletely disappeared except for a few vellous hairs at7 _9 ?5 O0 W1 A2 x: V9 [8 l
the base of the phallus. Testicular volume was still 2
3 j# V" ~9 g7 z$ c) RmL, and the size of the penis remained unchanged.
' L4 A7 E' j- `( uThe mother also said that the boy was no longer hav-
; V: K+ g' S: \/ Zing frequent erections.  r$ c( W" }* q  ?
Both parents were again questioned about use of
8 |2 j, \0 K  a% W: i5 G7 f* qany ointment/creams that they may have applied to
& z0 t0 E/ D1 i  dthe child’s skin. This time the father admitted the
; X; u: Z; B) H1 o- B4 P% NTopical Testosterone Exposure / Bhowmick et al 541/ S1 |7 R% q$ P1 b6 g- Z/ k
use of testosterone gel twice daily that he was apply-0 T7 K& U+ u( X
ing over his own shoulders, chest, and back area for
6 t* u: R8 j+ [; M4 X$ La year. The father also revealed he was embarrassed
* |8 @9 ~( `$ bto disclose that he was using a testosterone gel pre-1 m& S3 R- Z4 S7 e8 P
scribed by his family physician for decreased libido) a9 {) Z: O& k+ i, Q9 t4 {
secondary to depression.  M; `1 }" a' Q+ d5 i" p) [9 U' D6 V
The child slept in the same bed with parents.6 K. j$ q1 O6 ]" Q0 L# g
The father would hug the baby and hold him on his
* j$ f3 z, }+ [0 |0 o+ Zchest for a considerable period of time, causing sig-/ u/ W, P+ e* v1 f
nificant bare skin contact between baby and father.
) [* H5 h; h; E9 e) W/ i8 GThe father also admitted that after the phone call,
, k! g  i4 o& C. ?% b. m1 h, S) bwhen he learned the testosterone level in the baby
: T, g5 y9 G; zwas high, he then read the product information& v$ A2 w& x3 k- K- h0 {
packet and concluded that it was most likely the rea-
) Y& M* H5 L  m4 A% oson for the child’s virilization. At that time, they: G  c; Y& \2 r& S' R2 n% y/ H7 {, f
decided to put the baby in a separate bed, and the7 ^9 W1 k& I6 f$ W. s9 I7 R
father was not hugging him with bare skin and had. w5 ?2 K$ C4 ~* W/ Z! G( p
been using protective clothing. A repeat testosterone
# [4 L/ x- m" A" Wtest was ordered, but the family did not go to the: g% D5 M$ D% i
laboratory to obtain the test.1 s. `2 {4 M, x% B
Discussion
0 C" t" T+ V% R; H  d% a4 q* d! MPrecocious puberty in boys is defined as secondary
* O$ z/ T% ?! l- |" Bsexual development before 9 years of age.1,4
( t" c1 [6 j4 I: sPrecocious puberty is termed as central (true) when
3 S1 g" J6 e7 x. Cit is caused by the premature activation of hypo-8 o" k( @. X3 {8 b7 p6 }+ k+ J. z
thalamic pituitary gonadal axis. CPP is more com-. S) x* ?) g/ S- A5 ~
mon in girls than in boys.1,3 Most boys with CPP
' p3 c2 E9 L9 X( c% i2 `( _may have a central nervous system lesion that is3 w' p7 l8 x) B
responsible for the early activation of the hypothal-
! w. n' s9 z3 }* {+ ]amic pituitary gonadal axis.1-3 Thus, greater empha-' d3 z: X' ?3 v4 q
sis has been given to neuroradiologic imaging in, G& [# p1 }3 T
boys with precocious puberty. In addition to viril-. d% J4 H3 O+ X
ization, the clinical hallmark of CPP is the symmet-
* w" ]. I3 ^- y2 _( Lrical testicular growth secondary to stimulation by9 `! T7 a- g, ?' ?9 u7 A
gonadotropins.1,3
# N1 `# @. s6 E9 z# ?; ?9 }Gonadotropin-independent peripheral preco-
3 P) V, m9 m: m: vcious puberty in boys also results from inappropriate
3 X) X6 R: J8 o! h: y2 [0 r1 Wandrogenic stimulation from either endogenous or* w5 \, l4 Z' L. Y' {
exogenous sources, nonpituitary gonadotropin stim-& m$ t# ]% X) B. d- X& E
ulation, and rare activating mutations.3 Virilizing
' N* H2 Y2 f; `9 @; Lcongenital adrenal hyperplasia producing excessive
! u0 H6 j: ]3 C& dadrenal androgens is a common cause of precocious8 s5 c$ ^& b& n7 A3 f
puberty in boys.3,4
' [  T# ^! G/ {The most common form of congenital adrenal
9 b/ H' E+ @/ ^9 {1 Z) W0 yhyperplasia is the 21-hydroxylase enzyme deficiency.* K. M2 c3 Q) c4 b; Y
The 11-β hydroxylase deficiency may also result in! ]! p; D' f. p2 v3 K
excessive adrenal androgen production, and rarely,. x( s. }; I  R. ~* {  b
an adrenal tumor may also cause adrenal androgen
8 O0 u: k- P! d# S' M5 pexcess.1,3! M6 ?$ p/ d( Z% D7 U
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
& l) I5 P& b5 V$ J/ r, g542 Clinical Pediatrics / Vol. 46, No. 6, July 20076 N) H/ U" u2 i4 X8 d* y
A unique entity of male-limited gonadotropin-( U1 c' a! |" l  p( H8 W+ o. n
independent precocious puberty, which is also known0 D7 }; A, E4 Y5 J9 e$ S* d) n
as testotoxicosis, may cause precocious puberty at a8 _. B, W  \5 D4 Y* H; }
very young age. The physical findings in these boys. O8 U1 s2 [# P* s* }7 n4 W
with this disorder are full pubertal development,
& w1 P& I( H* N4 P# gincluding bilateral testicular growth, similar to boys
7 @; Y2 F. j! W7 |! n. s, Dwith CPP. The gonadotropin levels in this disorder4 A5 k2 [( s% O6 W% L  m
are suppressed to prepubertal levels and do not show5 Q# ~' e  s5 P
pubertal response of gonadotropin after gonadotropin-& O) u4 X: ]( r& Q: L( `
releasing hormone stimulation. This is a sex-linked
% Y) D: ?2 k9 ~, v& xautosomal dominant disorder that affects only
! V( ]* _$ y& Z$ y) ?$ y0 A( omales; therefore, other male members of the family
9 t; i7 |. Q, F0 D- h' T+ ]4 |may have similar precocious puberty.3
" U/ P; Y( }: hIn our patient, physical examination was incon-
; v& f( v0 y- `$ q) |- usistent with true precocious puberty since his testi-+ ?/ a5 U: c* B& [  e5 a1 G
cles were prepubertal in size. However, testotoxicosis5 y2 `0 m3 m: q
was in the differential diagnosis because his father5 D; q. S. R  A
started puberty somewhat early, and occasionally,
( h' s/ m: C- ^8 n1 d' Jtesticular enlargement is not that evident in the" i& L9 N/ h& R$ c1 W4 Y; Q8 c
beginning of this process.1 In the absence of a neg-3 E1 M) n7 Q. f9 E
ative initial history of androgen exposure, our3 U& I& g6 S- B, p/ ]
biggest concern was virilizing adrenal hyperplasia,
; R$ F! b- ~# t  R: leither 21-hydroxylase deficiency or 11-β hydroxylase
: e) S6 k% O( |1 L* D. \2 y; |* ndeficiency. Those diagnoses were excluded by find-
4 R2 V& b3 u  U* j$ U" Ving the normal level of adrenal steroids.( l& m& u4 M- X" r& m1 [
The diagnosis of exogenous androgens was strongly
! M- T6 ]1 `- z% J$ |9 [; P& b6 T5 bsuspected in a follow-up visit after 4 months because" K; v! [  V) T% _: B5 z# u' e( Y4 Q
the physical examination revealed the complete disap-6 Q9 L1 z1 B& Z' z3 q
pearance of pubic hair, normal growth velocity, and
: |5 k7 Z( v3 bdecreased erections. The father admitted using a testos-: P3 u' z5 p- [$ B  `4 ?
terone gel, which he concealed at first visit. He was2 B; |& ?% c, e" Q, Q- ]' u
using it rather frequently, twice a day. The Physicians’
. c5 ^/ K. Q6 l+ i) _, _Desk Reference, or package insert of this product, gel or3 J6 ?! k( R, r! _
cream, cautions about dermal testosterone transfer to2 c  O" q, S" v7 J) }$ H- y! L- V
unprotected females through direct skin exposure.& Y6 {) t; m* Q' b  y2 j
Serum testosterone level was found to be 2 times the- e" i0 w/ I& X3 y1 H
baseline value in those females who were exposed to
2 n" W+ v; \, ~$ }even 15 minutes of direct skin contact with their male7 {+ r- E. W! J: v  Z5 [( |+ ]& Y
partners.6 However, when a shirt covered the applica-# ^# d$ J- K0 O; f
tion site, this testosterone transfer was prevented.) _9 K: D; ^4 C5 ]4 w0 j$ e/ W" `. p
Our patient’s testosterone level was 60 ng/mL,3 e+ f1 }+ T/ t/ M: h" b: p
which was clearly high. Some studies suggest that8 u7 L2 n& @1 H' }) @6 f3 T
dermal conversion of testosterone to dihydrotestos-, |% \7 I6 A- ^' Y/ y
terone, which is a more potent metabolite, is more8 Q/ [% B4 ~) V4 d/ M& ^# R$ i
active in young children exposed to testosterone6 |$ p; W. Z( V% H; f
exogenously7; however, we did not measure a dihy-
" P4 t/ N6 q  T+ Ddrotestosterone level in our patient. In addition to% k) O! I- t/ Z7 i# t7 M, T
virilization, exposure to exogenous testosterone in5 U5 }0 m' N9 l2 k6 s" j
children results in an increase in growth velocity and
. l5 X, R, G- N* [+ b: D6 _advanced bone age, as seen in our patient.7 w. _# h" A& r; |  w2 T9 y: {
The long-term effect of androgen exposure during
. E* Z6 H/ r& Y2 T  [early childhood on pubertal development and final
- H9 q! @% N  a; o. fadult height are not fully known and always remain; x! _9 ~4 b8 s. [$ M' f& ?2 ?
a concern. Children treated with short-term testos-
+ T& h2 L8 t1 S" z0 f: @terone injection or topical androgen may exhibit some4 ~8 t, V4 U6 L) D9 n  ]! |6 t
acceleration of the skeletal maturation; however, after
6 [3 X- D3 h; p+ q% |- X+ ]cessation of treatment, the rate of bone maturation* }# h0 _( u  j) N* _% z
decelerates and gradually returns to normal.8,9/ K+ c, h2 b  _# W$ g% K
There are conflicting reports and controversy, |# i6 \+ q2 S8 Q
over the effect of early androgen exposure on adult
$ ]! \, W3 H. M& S% q9 Vpenile length.10,11 Some reports suggest subnormal
* G6 q/ c- t2 Eadult penile length, apparently because of downreg-3 i% V9 Q; R  I( ~( M7 ]0 h3 O0 R
ulation of androgen receptor number.10,12 However,0 L4 m' C/ L) h5 v3 r
Sutherland et al13 did not find a correlation between
& [; q/ D5 ~4 r; `4 Ychildhood testosterone exposure and reduced adult( F# Q: y7 f$ a# j& _- K5 Q! T
penile length in clinical studies./ K- `8 \9 `; _
Nonetheless, we do not believe our patient is
) o$ C! [! z: t! Cgoing to experience any of the untoward effects from! F! ?+ ^9 E+ `( x, K
testosterone exposure as mentioned earlier because5 f3 I& J  ]+ k: H. \8 M& p
the exposure was not for a prolonged period of time.
8 |/ P" G" r1 T6 J- C8 tAlthough the bone age was advanced at the time of7 P1 l9 ?& f  M: n6 A# d
diagnosis, the child had a normal growth velocity at5 Q! b" M7 f! x& M* T5 [
the follow-up visit. It is hoped that his final adult. R' B( x  g9 O
height will not be affected.' k4 D7 W7 [  A8 E
Although rarely reported, the widespread avail-$ G' h* d1 c) P& K: A
ability of androgen products in our society may  Z, U% K" R( R3 N7 o" V
indeed cause more virilization in male or female- v$ k* K7 Y, q- C# T$ I, r8 F  {
children than one would realize. Exposure to andro-7 P8 r$ I, h: l$ `6 o- e+ W2 T
gen products must be considered and specific ques-
! _) p% _7 V1 Q+ Z) p- ntioning about the use of a testosterone product or  T, ~7 h; X* M. _" X4 M
gel should be asked of the family members during
% H, h) N& Y2 O' E" Hthe evaluation of any children who present with vir-
4 q* ]2 c, J$ U# F4 i$ nilization or peripheral precocious puberty. The diag-
0 W/ P7 X  U4 t5 lnosis can be established by just a few tests and by
4 k% i6 g- }  R& oappropriate history. The inability to obtain such a# l) e* w: b# v
history, or failure to ask the specific questions, may; G$ z! d$ N8 I1 C3 i& r4 u
result in extensive, unnecessary, and expensive6 c0 H7 [% l$ M8 z* q
investigation. The primary care physician should be
0 a. D/ Z) t0 F: \3 Eaware of this fact, because most of these children% z. p" m9 Q* B. s( l
may initially present in their practice. The Physicians’
' b9 W& D! j, ?% y/ D. u7 MDesk Reference and package insert should also put a6 E* U- n, x$ U$ S/ p
warning about the virilizing effect on a male or
# E2 o/ P* G3 w0 U+ z9 i. Pfemale child who might come in contact with some-- L  D% r0 ?: ?$ x5 |& w6 r
one using any of these products.
1 j, K- t" B/ c* w9 f9 _9 Y- ?) |References# H3 j* V- X8 v4 P
1. Styne DM. The testes: disorder of sexual differentiation# Z3 z; Y) R$ m! k) {4 z4 s
and puberty in the male. In: Sperling MA, ed. Pediatric* P5 I8 l& P8 d2 W6 y+ X# \% o) O
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;4 L: G; L2 t; y" M/ x7 A
2002: 565-628.
4 r# f4 O1 [: K2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious& ~/ |* J+ z' j' [1 C( i# S( M1 K
puberty in children with tumours of the suprasellar pineal
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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

% X' s3 G. |! t0 c精妙絕倫的精品,感謝啊!期待你更多更好的創作哦!
發表於 2025-3-8 22:04:50 | 顯示全部樓層
絕對的好貼!謝謝啊!逐字逐圖地看完這個帖子以後,我的心久久不能平靜,感恩啊!
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