WK綜合論壇, WK综合论坛

 找回密碼
 立即注册
樓主: wk007

鄉下的妹子太便宜,一次四個都要了[12P]

[複製鏈接]
發表於 2025-1-4 03:25:35 | 顯示全部樓層
VIP精品區,資源無限好賺金任務區,輕松賺金幣
加入VIP,享受高級特權宣傳賺金又升級,超級棒
Sexual Precocity in a 16-Month-Old4 m: S* l  U( C- ~$ g! y  {
Boy Induced by Indirect Topical
! ?- J8 B$ V2 }' _, {4 ?1 e% x# `Exposure to Testosterone
2 c( o0 G7 p1 I9 Q5 y5 I+ {Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
9 U# n& P( }; A: u0 o0 [! h7 S% g6 Nand Kenneth R. Rettig, MD1
" s5 ^- c$ G1 n- G9 MClinical Pediatrics0 ~" t! @+ e  P( y2 d$ c
Volume 46 Number 69 K0 A1 X8 @: Y+ P4 E- A. w6 l8 |/ C4 O
July 2007 540-5439 X7 `) R. q" `) B1 y
© 2007 Sage Publications1 ^+ i* [6 x: G% a% u% \
10.1177/00099228062966517 ^2 S$ L4 l( O" A
http://clp.sagepub.com0 l3 M5 Z, O, }' x" U& g
hosted at: `. E6 W" C2 @
http://online.sagepub.com0 y* Y4 ]( l# N; F
Precocious puberty in boys, central or peripheral,
; `* g+ b7 X! iis a significant concern for physicians. Central' r; E( ?) D; i! P6 S# a" b8 ?
precocious puberty (CPP), which is mediated! U3 E2 [1 R0 v/ i
through the hypothalamic pituitary gonadal axis, has4 i$ d) d: t' c# k
a higher incidence of organic central nervous system
1 E4 ?5 \. Y! p3 u. `. Ylesions in boys.1,2 Virilization in boys, as manifested) ^9 n2 j) d: N
by enlargement of the penis, development of pubic& ^8 z' \! f1 k' s
hair, and facial acne without enlargement of testi-9 J  u! N1 G8 s0 D5 r8 H
cles, suggests peripheral or pseudopuberty.1-3 We( t. ^' x3 F3 `& A
report a 16-month-old boy who presented with the; a" x9 L1 |& b6 x: H( }4 V
enlargement of the phallus and pubic hair develop-
) \: G7 I* b, K- I3 Rment without testicular enlargement, which was due
& ?0 Q3 n. t4 t6 x; Y  m* X! C! P+ g) Eto the unintentional exposure to androgen gel used by
* p/ e8 A, k7 i. n$ H0 ~the father. The family initially concealed this infor-4 l7 }2 T+ X" H
mation, resulting in an extensive work-up for this; y, X5 ?, G8 o+ p, s( u7 [) \
child. Given the widespread and easy availability of/ p3 t( |9 s) w- L$ m
testosterone gel and cream, we believe this is proba-8 f! A; I4 `- p
bly more common than the rare case report in the
- i. q* l4 ?* P" aliterature.4; S* c1 A7 G; T" [3 v' F
Patient Report( \; ?. h( P5 |5 g8 p
A 16-month-old white child was referred to the( G6 C5 M; ~- P9 Z
endocrine clinic by his pediatrician with the concern
/ t4 G' N4 [1 y! G; f4 g9 iof early sexual development. His mother noticed
- n, z/ [* ^) e% |) D( zlight colored pubic hair development when he was/ Y; L2 f  j% Q8 J$ A
From the 1Division of Pediatric Endocrinology, 2University of* U9 e, P/ [  Q, }
South Alabama Medical Center, Mobile, Alabama.
. f- D, I! Q( o1 g5 i; o6 @Address correspondence to: Samar K. Bhowmick, MD, FACE,. e4 J& g9 y, S/ K7 T% q* z
Professor of Pediatrics, University of South Alabama, College of. b9 e; e0 a7 m" ?# n' t& G4 o
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
$ [$ S; L$ `0 e( F9 je-mail: [email protected].1 x. R$ m: D9 y. x: N
about 6 to 7 months old, which progressively became% f0 ]$ L: h' `8 }" k
darker. She was also concerned about the enlarge-4 g) W* V4 E  c, m
ment of his penis and frequent erections. The child$ n/ a/ M: }) g
was the product of a full-term normal delivery, with1 x- |, Z5 J' Z) w6 u  m
a birth weight of 7 lb 14 oz, and birth length of, A6 R& c, N# n- t' G: X
20 inches. He was breast-fed throughout the first year2 P# {/ e# a/ y1 b# h
of life and was still receiving breast milk along with
, |/ p# ~- v9 Vsolid food. He had no hospitalizations or surgery,
+ T- c6 r# J$ v6 B5 uand his psychosocial and psychomotor development
! h4 ?. a* i  T; Z( b+ Vwas age appropriate.4 `5 r0 p3 j" }9 T$ W. o' k
The family history was remarkable for the father,3 l1 W; W  m; U; W0 P1 P
who was diagnosed with hypothyroidism at age 16,
( ?! f* H/ @+ r& o( o$ @* x. Uwhich was treated with thyroxine. The father’s8 M( h& T& k* Q9 W0 Q) u
height was 6 feet, and he went through a somewhat: ~. }4 s$ J" I9 ]! o, }* C
early puberty and had stopped growing by age 14.. k5 l  `7 x. ]3 a
The father denied taking any other medication. The9 ?+ B% [& i- R5 m; Z1 q9 t
child’s mother was in good health. Her menarche
1 T: [$ \2 @% G8 w5 dwas at 11 years of age, and her height was at 5 feet
7 W7 ~8 r- p$ |4 [' {* u, X5 inches. There was no other family history of pre-9 H6 d; W7 k, C* M, \2 t+ F: C+ D  S
cocious sexual development in the first-degree rela-
* d2 s' o; c, K3 x# ttives. There were no siblings.
$ y# {; F+ |9 a2 _' F6 d+ W/ WPhysical Examination
5 y7 ]" g! v$ Q  S4 PThe physical examination revealed a very active,
- H1 a3 }8 p& c/ Yplayful, and healthy boy. The vital signs documented2 D: {1 k) X* u8 U: I  @0 d
a blood pressure of 85/50 mm Hg, his length was
. ~8 {: \+ ?  u* ]. [/ x% N90 cm (>97th percentile), and his weight was 14.4 kg) Q, T, B/ o" r  K( ^
(also >97th percentile). The observed yearly growth
7 A0 R3 q/ [' d$ w# Ovelocity was 30 cm (12 inches). The examination of
, G; m9 B3 ^3 T. o; N5 Hthe neck revealed no thyroid enlargement.
, |4 m; I, y, ^- U4 |( gThe genitourinary examination was remarkable for
1 D. j# ~' V% R$ q+ h" J5 q8 w7 ienlargement of the penis, with a stretched length of% ~' j: b) R: H0 W0 \: {
8 cm and a width of 2 cm. The glans penis was very well
- y8 _0 S* s6 v8 xdeveloped. The pubic hair was Tanner II, mostly around
5 l3 W4 l' q5 Y6 v7 Q9 o5 U540
: c' h' C+ W" Gat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from- V3 z6 }4 B1 a4 p3 `  Z) z. }
the base of the phallus and was dark and curled. The
5 O/ G  d. `* \8 M. Ltesticular volume was prepubertal at 2 mL each.( L3 I) o; i1 E' e1 O" [6 W  T8 u
The skin was moist and smooth and somewhat: I" B) E; S8 o! Q8 X0 u
oily. No axillary hair was noted. There were no
6 H. {3 `0 @: A1 B: k5 b' `abnormal skin pigmentations or café-au-lait spots.
# Y2 `2 P& E* R+ W" dNeurologic evaluation showed deep tendon reflex 2+5 P2 ~+ v4 L' {5 E
bilateral and symmetrical. There was no suggestion* x$ W% Q; d& \6 M- _0 A( M: V5 \
of papilledema.
- I: f$ q( z% l& Y2 FLaboratory Evaluation
; G$ j5 ?. Q6 ^  b+ }, y# ]& GThe bone age was consistent with 28 months by
; ~0 t# |/ ~9 K, ]/ Z# n  r1 nusing the standard of Greulich and Pyle at a chrono-
( V+ U0 h0 \+ t8 ologic age of 16 months (advanced).5 Chromosomal
  t4 f1 c/ s5 ?, G% Jkaryotype was 46XY. The thyroid function test
& f" l# ?* N, P& }9 n2 oshowed a free T4 of 1.69 ng/dL, and thyroid stimu-) Y7 j1 P# X$ }8 y0 u9 H# G$ a
lating hormone level was 1.3 µIU/mL (both normal).
; R6 s- Y  M8 t7 U# Q1 t" l$ }The concentrations of serum electrolytes, blood
3 U7 v2 j2 ?+ j0 @) qurea nitrogen, creatinine, and calcium all were
) e3 z& G6 \& ~5 Owithin normal range for his age. The concentration' w* e% R1 q- j6 U  k
of serum 17-hydroxyprogesterone was 16 ng/dL
, Y' X9 q: L1 M8 H(normal, 3 to 90 ng/dL), androstenedione was 20# o8 [& J5 F5 `7 R
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-. U6 y( g2 I  P8 [( S1 N, n
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
4 ^8 D, S; U  p- Z5 U# ^) ydesoxycorticosterone was 4.3 ng/dL (normal, 7 to
& I7 {0 ]' M6 Q! ~49ng/dL), 11-desoxycortisol (specific compound S)0 l* Y1 w; b, q& E. I( e# V& E
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
8 j& c3 A9 w9 a- @) _8 ^" mtisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total" f& L/ f$ q; |  @2 X! E8 }- Z2 |
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
- P5 k" i7 m3 ]; Cand β-human chorionic gonadotropin was less than
+ U. |; \7 D8 u. h8 i* I8 K5 mIU/mL (normal <5 mIU/mL). Serum follicular. Q5 R  C! L$ x; _
stimulating hormone and leuteinizing hormone8 X; A' g$ G! \3 y1 q8 V% ]$ w9 ^
concentrations were less than 0.05 mIU/mL4 g5 ]- X0 P& Y; _/ `  d8 g. U
(prepubertal).
5 k/ n2 P/ V1 uThe parents were notified about the laboratory
) q9 m/ U, `% f4 `; h8 N4 e' ~results and were informed that all of the tests were4 L4 v# r8 s  l" M" q7 o2 t
normal except the testosterone level was high. The/ K" o/ p* X$ a/ t2 E$ @
follow-up visit was arranged within a few weeks to
2 F" G. Z8 K3 S! Xobtain testicular and abdominal sonograms; how-7 `* p: v) O! D! {
ever, the family did not return for 4 months., H' M1 ^* g6 F" o
Physical examination at this time revealed that the% q& |8 h/ j9 R
child had grown 2.5 cm in 4 months and had gained' V( j  y0 c, d% R$ E
2 kg of weight. Physical examination remained
! W2 R" q8 T( F1 W8 }3 ]1 W3 ]unchanged. Surprisingly, the pubic hair almost com-
) c: F% V( e+ E4 X# Upletely disappeared except for a few vellous hairs at6 P4 s8 ~" Z6 ~2 S7 P1 D
the base of the phallus. Testicular volume was still 2' g  C- }& N, V2 f
mL, and the size of the penis remained unchanged.. \3 J& V7 ^+ m5 ?
The mother also said that the boy was no longer hav-
+ m: v/ |5 D0 y0 g4 ]0 h1 Eing frequent erections.
2 P! D( s0 A" Z/ N1 J- r( CBoth parents were again questioned about use of* |3 n4 Z6 t- Z
any ointment/creams that they may have applied to
+ f. P  H0 U5 V1 zthe child’s skin. This time the father admitted the
6 V6 T. {8 y7 y  X$ `6 ~' |Topical Testosterone Exposure / Bhowmick et al 541
) N5 E. f5 f0 b; }% duse of testosterone gel twice daily that he was apply-
* {6 t" E  _: s  ning over his own shoulders, chest, and back area for
5 A- Z( A$ T- |+ `" ka year. The father also revealed he was embarrassed# B) X0 C* A" Q# |9 y
to disclose that he was using a testosterone gel pre-
+ R3 E- r, \# T% \( d4 b8 y; _scribed by his family physician for decreased libido$ A, G5 V/ q5 {# y
secondary to depression.
4 q, |: B: ]) J8 @6 pThe child slept in the same bed with parents.: g: v3 |3 j) D% ]+ }" {6 d
The father would hug the baby and hold him on his7 |. ?& F2 N, F! r7 F% Y  e: P: L
chest for a considerable period of time, causing sig-* [5 t$ V' `$ p/ t& }$ M* N
nificant bare skin contact between baby and father., S0 Q6 t6 \/ |& U# S5 o4 I
The father also admitted that after the phone call,6 t9 n8 A, }' c2 c  L/ o2 T
when he learned the testosterone level in the baby
5 Y8 Z4 X6 _7 Y' J; i+ Hwas high, he then read the product information* @2 X9 a: V) @# U/ a7 A/ r4 T
packet and concluded that it was most likely the rea-2 Y( }# M6 [+ E. `* q: v! p2 x
son for the child’s virilization. At that time, they! v* ~0 p% v6 y$ m( G3 E
decided to put the baby in a separate bed, and the
% a8 ^8 m0 g; ]% Cfather was not hugging him with bare skin and had
" }1 k# Y6 Y4 Z9 y. gbeen using protective clothing. A repeat testosterone
# s" s4 z4 j8 S, Z& u# Gtest was ordered, but the family did not go to the: ^4 T' `: w6 Q
laboratory to obtain the test.
+ Y* G1 b( v; W! U1 j, ^Discussion
: [" t. w3 M+ p9 c. k/ q& nPrecocious puberty in boys is defined as secondary4 Q% q. v5 e( H, e
sexual development before 9 years of age.1,4
3 j) I% f5 a6 Z; \) v3 {Precocious puberty is termed as central (true) when
1 J& ^3 D6 i2 d# i# ]5 wit is caused by the premature activation of hypo-4 h8 f" c( {, V! K. y! \: h) I
thalamic pituitary gonadal axis. CPP is more com-
  c% K2 Y& K/ tmon in girls than in boys.1,3 Most boys with CPP- X, C# ]) J: Q7 O7 Q' k1 r9 u
may have a central nervous system lesion that is! {+ s  ]! I' c
responsible for the early activation of the hypothal-
( @0 F6 ^- d# Y7 yamic pituitary gonadal axis.1-3 Thus, greater empha-
& Z. c2 Z$ j& ~/ o. m* u( Fsis has been given to neuroradiologic imaging in! [* G  H2 a, Y# `0 S* s
boys with precocious puberty. In addition to viril-; B5 E6 {; m* Z. E) o$ Y
ization, the clinical hallmark of CPP is the symmet-
# I6 j9 E$ r- b) c: N7 Srical testicular growth secondary to stimulation by' {* K$ E8 Y' v$ {3 T
gonadotropins.1,3
4 U$ P" N6 x% h) a0 l: bGonadotropin-independent peripheral preco-
& Q; s" j$ X8 J: y  K' p% I$ Xcious puberty in boys also results from inappropriate0 m5 L/ q3 j( j" m" P3 I$ l
androgenic stimulation from either endogenous or
$ R& G7 B7 l( h- Z1 O. Nexogenous sources, nonpituitary gonadotropin stim-! P5 \/ T6 ]4 `3 Y9 W% @
ulation, and rare activating mutations.3 Virilizing
0 X& M; d+ d; u. {+ W8 k- G) U/ Dcongenital adrenal hyperplasia producing excessive
3 A! h7 f  c- E0 X# Wadrenal androgens is a common cause of precocious
  _+ {. s5 D2 g5 v0 M! `' ?: q7 xpuberty in boys.3,4
' k: n6 x, p, ~, C1 H' cThe most common form of congenital adrenal8 t6 g9 {; q( J" Q, g
hyperplasia is the 21-hydroxylase enzyme deficiency.
' I" T" [% w& m/ m+ P" ^; P% KThe 11-β hydroxylase deficiency may also result in
1 u8 W8 Y$ Z1 wexcessive adrenal androgen production, and rarely,7 p" V& h: g% ~( W+ c' [8 w
an adrenal tumor may also cause adrenal androgen3 `4 y# c1 [; E' j6 g4 F
excess.1,33 t1 d5 M# ~! u$ b
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
% J8 }+ r9 B6 o% m542 Clinical Pediatrics / Vol. 46, No. 6, July 2007( v+ Z4 Z$ n) f, ]) d) X1 z" ]! ]
A unique entity of male-limited gonadotropin-4 h$ R6 s- R8 l+ f
independent precocious puberty, which is also known6 C2 C+ ]/ y. e3 ~, D
as testotoxicosis, may cause precocious puberty at a
& ^# |* L! ^: t. p( U8 l" V, \very young age. The physical findings in these boys( b5 B4 j+ J' e3 q! A6 w' b0 f. z. A
with this disorder are full pubertal development,; g, V# M% |' ~+ o( P
including bilateral testicular growth, similar to boys9 P6 ?' n; K5 q* s2 C6 _8 |. m
with CPP. The gonadotropin levels in this disorder% H! @2 g% \( s1 f5 L) p$ h
are suppressed to prepubertal levels and do not show
9 H8 o9 c# |  n8 n* m6 E* r5 Zpubertal response of gonadotropin after gonadotropin-
3 k- S8 X1 g: u" d) z6 Ureleasing hormone stimulation. This is a sex-linked+ c' ?9 U3 d+ o$ z& {0 p. `
autosomal dominant disorder that affects only* K0 D$ M% E. M- l6 V' [2 n
males; therefore, other male members of the family: u# C& _" I2 s3 O1 B( a1 w
may have similar precocious puberty.3
( \. \: R; E0 _8 \% RIn our patient, physical examination was incon-; \# Q' o2 a2 A: B4 g! h/ C; Q
sistent with true precocious puberty since his testi-
3 K0 G( I/ Y; t6 g) ecles were prepubertal in size. However, testotoxicosis$ I$ d( U. f/ N
was in the differential diagnosis because his father
2 \% w+ i# d7 q1 Dstarted puberty somewhat early, and occasionally,  C  ]! X' w4 r
testicular enlargement is not that evident in the
. y( ?& g9 `5 H' d6 C! o& W: pbeginning of this process.1 In the absence of a neg-* m. w$ ^1 Y1 Q4 s; k: G' J: j
ative initial history of androgen exposure, our
2 e- X  w  G7 P6 F9 O0 L; fbiggest concern was virilizing adrenal hyperplasia,! Z; R: t7 f% z2 R: \
either 21-hydroxylase deficiency or 11-β hydroxylase! O' l9 A% |, @; L) w3 |0 j
deficiency. Those diagnoses were excluded by find-
% t' I3 _+ Q2 M, K- ]ing the normal level of adrenal steroids.4 N4 d! i& o& L- z2 I. c7 ~
The diagnosis of exogenous androgens was strongly
6 g, I5 R, `  F- G5 @suspected in a follow-up visit after 4 months because
4 t% m5 h; j* _" x: [7 x+ ethe physical examination revealed the complete disap-6 ], ?( ~3 V) g
pearance of pubic hair, normal growth velocity, and- B  Q9 r, D/ v4 G, R4 m
decreased erections. The father admitted using a testos-
' |* V8 S! e- sterone gel, which he concealed at first visit. He was
% F7 z% e0 h2 @+ h% tusing it rather frequently, twice a day. The Physicians’
, h* @8 Q1 a, S; B) D! ]/ V: {Desk Reference, or package insert of this product, gel or5 j2 I( D2 F, ]+ J1 ~2 k0 S8 X
cream, cautions about dermal testosterone transfer to) z( W; [6 K' M0 `, g
unprotected females through direct skin exposure.
! p/ \/ q+ B# NSerum testosterone level was found to be 2 times the
2 G! s5 h$ |6 x" Ubaseline value in those females who were exposed to. Q. N" U$ ]( U, l7 M1 s4 w1 v
even 15 minutes of direct skin contact with their male
8 @- P" X+ O5 _# vpartners.6 However, when a shirt covered the applica-. \4 R% o$ t, X, u1 ?, `
tion site, this testosterone transfer was prevented.
- u  n5 H& j7 {- fOur patient’s testosterone level was 60 ng/mL,) b3 n( N+ r" r" k! m1 e/ L
which was clearly high. Some studies suggest that
) k* H% w' o7 h: @6 Ydermal conversion of testosterone to dihydrotestos-2 }8 `  ^* Z# I8 U
terone, which is a more potent metabolite, is more% I6 z- o: f% L3 }5 c' p
active in young children exposed to testosterone
4 Q( d# R- ^, }+ B8 l8 Rexogenously7; however, we did not measure a dihy-  R; W& e& m( e0 O! H+ ~" W
drotestosterone level in our patient. In addition to
9 ~9 w; _8 Y- ]* ^: f; B; Evirilization, exposure to exogenous testosterone in4 b& M* o6 e  g# C6 G; @
children results in an increase in growth velocity and5 i, q" H9 C7 `3 \8 y
advanced bone age, as seen in our patient.
. e/ G, t5 u5 V$ W  _The long-term effect of androgen exposure during
3 W. W: x' N" L2 A! x4 _early childhood on pubertal development and final
" d9 J8 r" W2 ~: I% @adult height are not fully known and always remain
3 U3 F) O7 m& g  ka concern. Children treated with short-term testos-
  w. [: P4 o( L, ?, bterone injection or topical androgen may exhibit some4 ?" c  i' Z) R3 Y
acceleration of the skeletal maturation; however, after
6 Q' t  M& `* y$ \/ {cessation of treatment, the rate of bone maturation9 L& F' u$ v  P, j' P  }! y; Q* F7 D
decelerates and gradually returns to normal.8,9
/ M+ `3 {- A& A# u) Y9 q0 YThere are conflicting reports and controversy4 ^& ^' _0 j: A1 r0 q# z
over the effect of early androgen exposure on adult
2 B7 P6 L1 c$ Mpenile length.10,11 Some reports suggest subnormal
! O9 Z9 M' F  j- |" }) oadult penile length, apparently because of downreg-6 u8 ^& \* a7 _5 s4 C/ C- q! ^
ulation of androgen receptor number.10,12 However,
8 i; f$ N- F: ]. i8 T5 ?Sutherland et al13 did not find a correlation between9 ^$ e9 B; w6 ~$ Q, Z) W2 W9 n6 d
childhood testosterone exposure and reduced adult
( @7 p) X3 y- h- D* f5 d3 p9 jpenile length in clinical studies.
. B& z: h) J+ PNonetheless, we do not believe our patient is
, g- M9 V% B1 O. [9 W2 s  ^going to experience any of the untoward effects from6 n- O! q& w+ h' Z
testosterone exposure as mentioned earlier because- H" q& L( P% V% m/ C0 T
the exposure was not for a prolonged period of time.
5 o- z9 C- O5 A$ \* I5 [: }Although the bone age was advanced at the time of; \5 R3 }: N- _. [: k
diagnosis, the child had a normal growth velocity at0 f' f1 ?# q2 ~( I) E* W
the follow-up visit. It is hoped that his final adult
) `3 ~2 l, a) X" kheight will not be affected." z8 k8 i* Q: _+ I6 q: O4 O2 K/ O
Although rarely reported, the widespread avail-$ B3 s- C! e- n# l2 j7 _* M' [
ability of androgen products in our society may
8 g! ^" F4 c/ findeed cause more virilization in male or female5 d/ C: ^+ @% r* }; q
children than one would realize. Exposure to andro-1 L- M! c' _- [/ n9 y) C/ R& n% q
gen products must be considered and specific ques-
* E+ f3 E& O" Stioning about the use of a testosterone product or
  b7 i1 j! I8 @: Igel should be asked of the family members during! X# s) u$ k. q# L
the evaluation of any children who present with vir-# w6 u4 m# q+ x4 p) @# N- \
ilization or peripheral precocious puberty. The diag-6 F: m( C% W7 Q5 d( b
nosis can be established by just a few tests and by
( J2 x& T! y' e9 f8 m* @appropriate history. The inability to obtain such a- c9 S+ S! [! ~, l: u5 l. [- L
history, or failure to ask the specific questions, may
* g/ G! A: _+ G. }+ O. }* Y2 ~result in extensive, unnecessary, and expensive9 \" k6 k( X6 U
investigation. The primary care physician should be
3 n6 |8 Q3 ]9 q# Haware of this fact, because most of these children- q& x' A; F7 E  V0 J- K% i% L
may initially present in their practice. The Physicians’
; a8 }. `$ \, s3 \6 sDesk Reference and package insert should also put a# k& `: I2 F  b
warning about the virilizing effect on a male or
/ P& n  @- [- F4 I9 M) e( L* gfemale child who might come in contact with some-9 n5 g% \9 m8 p5 z
one using any of these products.3 ]7 c3 O% c. h9 E: U" K0 G  ]
References
$ [% G0 J* V8 ]" R4 ]1. Styne DM. The testes: disorder of sexual differentiation" P+ W5 V$ u/ ?4 T' H& ?
and puberty in the male. In: Sperling MA, ed. Pediatric3 w) O& M, v$ f, s
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
7 ^* V8 I% c( J( V. ~) |2002: 565-628.
8 u- l! F& }( q5 h7 l2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious, K* G( c  R7 v: R3 Q8 ~0 U
puberty in children with tumours of the suprasellar pineal
發表於 2025-1-4 03:27:02 | 顯示全部樓層
VIP精品區,資源無限好賺金任務區,輕松賺金幣
加入VIP,享受高級特權宣傳賺金又升級,超級棒
Sexual Precocity in a 16-Month-Old
0 v3 z# p& ]0 D7 t7 x4 cBoy Induced by Indirect Topical) L% z2 {/ i! z- c( R/ e
Exposure to Testosterone7 o1 V: H" o# u$ ]8 M
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
( Y2 {+ Z* d. w  Rand Kenneth R. Rettig, MD12 r+ m) V, m; t, s+ }% p" Y: M
Clinical Pediatrics; D8 y. _7 S- q' e: T  ^
Volume 46 Number 6
; f! w: [5 J; m$ A) UJuly 2007 540-543
/ N# s7 T; ^- x: k% b© 2007 Sage Publications
7 M9 h4 H: f; e. Z: Y) _( `10.1177/0009922806296651
9 }9 j; s$ K. @http://clp.sagepub.com
8 E: j6 q  K' G# t+ a; ]hosted at! ]0 S5 g* C% K* ]
http://online.sagepub.com
+ ?$ ?) z# X* h7 xPrecocious puberty in boys, central or peripheral,
, m" T) W; y5 z& Xis a significant concern for physicians. Central; ?  w, Q# x- f, H  A' G) s& a
precocious puberty (CPP), which is mediated' H, F8 O) E2 a, Z0 Q, c
through the hypothalamic pituitary gonadal axis, has
, m/ R, s! R+ ]! p9 \2 [5 Wa higher incidence of organic central nervous system
7 c( X$ x9 W/ H1 Ylesions in boys.1,2 Virilization in boys, as manifested
* l7 S! r# k5 C; ]  p) `by enlargement of the penis, development of pubic$ u- c# g7 u! W7 O7 ?$ n
hair, and facial acne without enlargement of testi-
' V3 Y7 E' \: p+ acles, suggests peripheral or pseudopuberty.1-3 We
& l8 G1 [8 E; [report a 16-month-old boy who presented with the, E+ A# O/ Z9 L  V+ h1 x% P
enlargement of the phallus and pubic hair develop-
8 ^) Q0 C) u0 }% Ement without testicular enlargement, which was due
" {& C& h/ c) Q  g$ q6 yto the unintentional exposure to androgen gel used by
, \' ?1 g# L' m) Q6 P) P4 uthe father. The family initially concealed this infor-# }% j8 b+ O: b& Y5 q3 H
mation, resulting in an extensive work-up for this; w% r1 ^4 |, d$ p' e
child. Given the widespread and easy availability of( A* E  E* h9 h
testosterone gel and cream, we believe this is proba-
9 t4 M3 i$ w( N9 c& kbly more common than the rare case report in the
0 u; C% t) e; [+ D" {+ _) M; F: I! kliterature.4) |0 P0 K9 z# u! l; x9 P/ ]" R
Patient Report: I5 O( J& [! b/ R5 \
A 16-month-old white child was referred to the3 ?+ Q1 H1 W7 f& p
endocrine clinic by his pediatrician with the concern7 A/ j2 @- {/ A
of early sexual development. His mother noticed. e9 \( x( s4 i9 |
light colored pubic hair development when he was
- K. w) u2 ~* D7 ]0 v* w- ZFrom the 1Division of Pediatric Endocrinology, 2University of/ z1 k5 X# L5 i! h# A0 v
South Alabama Medical Center, Mobile, Alabama.- g' Z0 z4 l# i8 ]; ]! f" z
Address correspondence to: Samar K. Bhowmick, MD, FACE,
: F% S$ M) q# Y& OProfessor of Pediatrics, University of South Alabama, College of
& x1 r8 ~* n3 q0 K1 T) K& @: B4 ~Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
  ]# g: h) Z9 O( e2 _2 i# }e-mail: [email protected].0 e- \- Z8 c  y/ Z8 o" m9 K% B
about 6 to 7 months old, which progressively became
+ F" J: {7 m" `- Y8 l; X% G) [% Tdarker. She was also concerned about the enlarge-( C) j! j+ Z0 V9 B/ A% j) m7 z4 I
ment of his penis and frequent erections. The child
# X3 D5 N% z) d* v2 n! u( Xwas the product of a full-term normal delivery, with
* b) q/ p- n  i$ U. @4 X/ ra birth weight of 7 lb 14 oz, and birth length of
2 a0 E7 ~( I$ G+ l3 C20 inches. He was breast-fed throughout the first year1 h. z/ F+ Z( d# `. m
of life and was still receiving breast milk along with
( e4 q+ r* ^/ R3 D! lsolid food. He had no hospitalizations or surgery,
1 a! C5 `7 j3 X! S" Z7 Cand his psychosocial and psychomotor development" G6 p( K0 U, J# ]9 d' q; E: G* k
was age appropriate.
/ R+ O1 f. a! M2 Q0 RThe family history was remarkable for the father,+ e! h! k( {' f8 w* y1 c9 Y
who was diagnosed with hypothyroidism at age 16,
) i8 y2 w" m6 Y5 u" p7 t( Twhich was treated with thyroxine. The father’s9 s( Z0 V! A% }2 E' f, x' w
height was 6 feet, and he went through a somewhat. \, G5 m* O1 ]: T. i: ~" F1 k
early puberty and had stopped growing by age 14.3 n! U$ ~: B" Z; g; K! }
The father denied taking any other medication. The
; r) k; b6 P7 ?. ~" \child’s mother was in good health. Her menarche
% T- X' L3 W3 h  y* u& D7 }: Pwas at 11 years of age, and her height was at 5 feet
1 i% b  B6 ~' a8 X% ^2 ^1 Y. r5 inches. There was no other family history of pre-, F" z0 A. `- o
cocious sexual development in the first-degree rela-) Z# b" t7 s* E6 h" i
tives. There were no siblings.
8 H* N, V& C& L# E3 [- ]% s; `Physical Examination
8 b* O7 N+ N( F$ ~( {+ Z1 c, KThe physical examination revealed a very active,
2 b9 O! O& @+ k0 ?5 @playful, and healthy boy. The vital signs documented
, Y! n# A. ^% A+ [' Ia blood pressure of 85/50 mm Hg, his length was
+ \8 u7 Y" u9 }0 Y0 I9 G90 cm (>97th percentile), and his weight was 14.4 kg: ~9 _8 [& u7 y' U. L: G5 J
(also >97th percentile). The observed yearly growth, D2 [: B1 C% C8 R
velocity was 30 cm (12 inches). The examination of. y2 @5 a; E& k
the neck revealed no thyroid enlargement.
5 ?. k% @& a) c( EThe genitourinary examination was remarkable for. K5 }! y% `6 H) ~6 }& l- p
enlargement of the penis, with a stretched length of
, y: v! D. J6 ]! O* S" y6 B' B8 cm and a width of 2 cm. The glans penis was very well8 ]# W0 y! o, ^
developed. The pubic hair was Tanner II, mostly around
/ w% d' O4 n0 M540  k& q# H' d0 @3 L: U6 F3 ^
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from- e5 m0 H: f$ w- E/ }* @. `/ ?
the base of the phallus and was dark and curled. The- I4 N$ x  r6 |" Y
testicular volume was prepubertal at 2 mL each.
4 ?, T/ Q, v' I; M+ NThe skin was moist and smooth and somewhat( \0 Y* H  a8 x4 D6 C7 i) l
oily. No axillary hair was noted. There were no( i5 ?+ T# b# ?: m0 v+ J
abnormal skin pigmentations or café-au-lait spots.# X) K7 e$ c& O; r. C
Neurologic evaluation showed deep tendon reflex 2+
- B: j3 G* z' r/ Nbilateral and symmetrical. There was no suggestion* @% z0 x$ b' y! w: L
of papilledema.
0 s  t1 ^4 Y+ O0 t$ g9 C3 ^1 w% ELaboratory Evaluation( K5 R( J# x$ K5 n
The bone age was consistent with 28 months by
6 W8 L1 N" x9 w: p. Z/ D2 E  nusing the standard of Greulich and Pyle at a chrono-  k' Y. q8 q( i+ b* u1 }2 S9 P
logic age of 16 months (advanced).5 Chromosomal
7 W: u0 `4 g# s5 X5 J1 Y2 X8 j8 ?karyotype was 46XY. The thyroid function test8 s4 W: J5 }1 e  o: R! S
showed a free T4 of 1.69 ng/dL, and thyroid stimu-1 f! J( W# C  c: |( ~( b5 p9 E
lating hormone level was 1.3 µIU/mL (both normal).
4 _7 Z- T$ M) G9 {2 BThe concentrations of serum electrolytes, blood! P. u/ G, u9 C" t! [/ d
urea nitrogen, creatinine, and calcium all were2 `4 ?9 u7 N8 u3 V- m" I
within normal range for his age. The concentration! v7 F# _2 p$ o: g6 m) Q
of serum 17-hydroxyprogesterone was 16 ng/dL
  f! }2 H3 c; M0 v: x6 Y" T(normal, 3 to 90 ng/dL), androstenedione was 20  V" Q4 V9 b  p5 D' u% O) w
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
2 P4 U) W( p! L2 c* rterone was 38 ng/dL (normal, 50 to 760 ng/dL),
3 @7 C- `! A& k& M2 \! d3 \desoxycorticosterone was 4.3 ng/dL (normal, 7 to1 l5 W0 U4 t) b6 Q* E) X$ N
49ng/dL), 11-desoxycortisol (specific compound S)
8 K) v1 ]1 `( jwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
: T2 n3 r; l# q5 Ntisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total5 g( s: P& F) W
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
" o& W& k; _3 Land β-human chorionic gonadotropin was less than
! s% r: \7 h  H: j/ x& B. [- @8 p1 Q5 mIU/mL (normal <5 mIU/mL). Serum follicular4 o. P$ R6 s' l& H8 F/ Y3 P
stimulating hormone and leuteinizing hormone, s; U8 Q- G, B4 w( D& |% s
concentrations were less than 0.05 mIU/mL
, K+ m% K: j. o6 {' }) g(prepubertal).% x* p6 m7 N6 h0 A
The parents were notified about the laboratory2 K, O. m4 r8 X
results and were informed that all of the tests were* @0 W7 f3 \- I. J& v6 A- d
normal except the testosterone level was high. The
) h9 |# _; }6 j. S( n  e! o( afollow-up visit was arranged within a few weeks to
# E' I9 g8 Q2 h# R" D7 Tobtain testicular and abdominal sonograms; how-
# X4 O) F) [# U. \; \7 Z7 }* dever, the family did not return for 4 months.5 M$ E+ c! I1 X2 P, ~9 v+ e
Physical examination at this time revealed that the' ]$ [0 s) i7 b  w
child had grown 2.5 cm in 4 months and had gained
/ ~! v& L7 h$ f2 kg of weight. Physical examination remained
. ]9 ~7 E3 u2 o6 w& Cunchanged. Surprisingly, the pubic hair almost com-, _% i6 i3 P: g8 E
pletely disappeared except for a few vellous hairs at, F- M7 \+ y) ?, F3 `4 ^
the base of the phallus. Testicular volume was still 2
! j5 o- w9 z* ?% B2 t9 h7 bmL, and the size of the penis remained unchanged.
$ i: F( R9 a& G  @; S; R% d& UThe mother also said that the boy was no longer hav-0 h. E0 J& H3 f
ing frequent erections.- U  f; `% U6 T9 T$ Z$ Q) j
Both parents were again questioned about use of
" f  n% {  s% C8 d+ j7 x, `any ointment/creams that they may have applied to
) d6 _- ]' x' ?% B$ \the child’s skin. This time the father admitted the2 U5 h$ V! ?) V& {+ g' J- B3 h
Topical Testosterone Exposure / Bhowmick et al 541) |9 }1 V/ W' o
use of testosterone gel twice daily that he was apply-
# S- |7 c; s# f0 ^2 u* X2 s& `ing over his own shoulders, chest, and back area for
$ t+ @# j, C, F3 Qa year. The father also revealed he was embarrassed
# F# `7 {# w& o% o; \, m; Z  Jto disclose that he was using a testosterone gel pre-
3 c+ v6 b& D$ Y4 J) s# nscribed by his family physician for decreased libido* @, ~7 k0 G, _+ y* n0 b1 b8 E
secondary to depression./ l/ z( e' U' }1 C4 ?
The child slept in the same bed with parents.6 N9 a- ^; h% `5 v5 p: S. t  m
The father would hug the baby and hold him on his
5 S8 z5 r. Q9 z4 {6 kchest for a considerable period of time, causing sig-: m- f  n3 H& l' K
nificant bare skin contact between baby and father.
$ Q2 Q: X8 G! K1 E& V$ P: `! AThe father also admitted that after the phone call,
  {$ p0 S, j$ t5 q* Pwhen he learned the testosterone level in the baby, Y5 X' Z: c! X+ Y# h: K! K. e
was high, he then read the product information
" l! |. w5 n( I2 `5 p: B% xpacket and concluded that it was most likely the rea-  m* P" j. j* f; f& z
son for the child’s virilization. At that time, they
. G/ v: |( h! f3 rdecided to put the baby in a separate bed, and the* f2 z' Q7 |! C. k1 Q6 a
father was not hugging him with bare skin and had
5 ?- Y! V+ Q# E" g, ]been using protective clothing. A repeat testosterone
( n2 B  w( r; S8 Y$ v3 T: A' W8 m, ktest was ordered, but the family did not go to the
, V. w/ w& H1 R& H6 ]. Qlaboratory to obtain the test.
- j5 s4 P6 `2 [  J2 |- GDiscussion8 U$ |' M$ A6 I; J3 L
Precocious puberty in boys is defined as secondary
1 v. f  ~/ |8 y5 r8 }0 Z4 Vsexual development before 9 years of age.1,4
5 p+ K) @( _. s3 CPrecocious puberty is termed as central (true) when
# G; c* P0 E! }7 B- @/ y+ B4 Fit is caused by the premature activation of hypo-
) B: V2 T% B  V8 R2 f8 ethalamic pituitary gonadal axis. CPP is more com-- U' e2 T2 k) N* Z( v
mon in girls than in boys.1,3 Most boys with CPP  f. |8 _, h5 W$ ~$ F5 E, O& i
may have a central nervous system lesion that is9 z4 C& R" l  P! B
responsible for the early activation of the hypothal-
+ p+ C4 o" X/ i  D$ Kamic pituitary gonadal axis.1-3 Thus, greater empha-
+ C4 @4 m/ y& s5 u- V8 g4 v" ]sis has been given to neuroradiologic imaging in
0 @9 s4 J/ |3 |7 W+ u: g; Pboys with precocious puberty. In addition to viril-
" O" V7 g1 T" `( o% _ization, the clinical hallmark of CPP is the symmet-8 U/ {. E3 Q' E. w( g( V8 ]
rical testicular growth secondary to stimulation by, G" S5 ]3 X4 j, a
gonadotropins.1,3/ X% f" o- l" ]+ ]% R) P& N1 ~  S: R
Gonadotropin-independent peripheral preco-. f4 n& |: z5 e0 i: r6 z* ~  M
cious puberty in boys also results from inappropriate
) [% O4 V+ |0 h# ?! i: `3 K& ~- xandrogenic stimulation from either endogenous or
# |( }) {) e, Bexogenous sources, nonpituitary gonadotropin stim-, w% V  Z1 y  Z
ulation, and rare activating mutations.3 Virilizing3 B6 L, u0 ~4 ]0 b
congenital adrenal hyperplasia producing excessive
6 o4 W" `0 d- _2 Q3 ~adrenal androgens is a common cause of precocious
( f  \" H1 O- F7 cpuberty in boys.3,4
! M( M) h8 @. X0 J; M; C5 e4 e/ aThe most common form of congenital adrenal
# i$ T; u" G+ Shyperplasia is the 21-hydroxylase enzyme deficiency.2 A$ _* B& q; r3 p9 q$ N, |
The 11-β hydroxylase deficiency may also result in
9 e" I- S+ d' \6 m& H! j- kexcessive adrenal androgen production, and rarely,; c6 R/ ~. h* ^. S" I( g$ G9 p
an adrenal tumor may also cause adrenal androgen. T( N4 Z) R( s( k
excess.1,3
. F4 I0 u: x, q( r: c$ L$ sat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from1 m% V  w; H$ y3 e2 J( _
542 Clinical Pediatrics / Vol. 46, No. 6, July 20074 L4 g" O: {7 i) U8 Z: u7 ^8 k! E' x+ F) o
A unique entity of male-limited gonadotropin-
5 l$ o; c2 T9 Y" w9 uindependent precocious puberty, which is also known
; O# G. \" T% d6 E5 b7 P1 A  w1 |9 Vas testotoxicosis, may cause precocious puberty at a
3 O! f: e, {5 R6 L4 every young age. The physical findings in these boys
/ W( Q* Z1 a' r% r3 Rwith this disorder are full pubertal development,
6 [0 o* V7 M# u7 M7 z  r- Yincluding bilateral testicular growth, similar to boys
9 p  M4 b3 g6 fwith CPP. The gonadotropin levels in this disorder
8 L/ {- B5 O& ~( e; y) Lare suppressed to prepubertal levels and do not show) V" f0 m! x/ \. i7 O, v, c4 I
pubertal response of gonadotropin after gonadotropin-
3 q+ O: d5 x5 n  P7 L1 s  D: ^releasing hormone stimulation. This is a sex-linked; u5 W0 S& G2 z
autosomal dominant disorder that affects only
/ L& Q6 b# [) ], h8 b* nmales; therefore, other male members of the family
4 c1 C5 m5 m' P, n2 `may have similar precocious puberty.3
9 r- P1 s3 y+ O% @5 PIn our patient, physical examination was incon-
$ b, D& a. v8 D: Bsistent with true precocious puberty since his testi-, D" K2 @) r. N7 m+ s+ S4 X* l) {
cles were prepubertal in size. However, testotoxicosis
/ \% j: P5 k( m' M  bwas in the differential diagnosis because his father
7 h) R; [+ m4 E/ T2 Cstarted puberty somewhat early, and occasionally,) x4 P# W( C5 Z" @( Q" E
testicular enlargement is not that evident in the
; X/ M' B2 o( Y4 @. H0 |beginning of this process.1 In the absence of a neg-
  Q" `& D4 F% z% E' O, X1 c5 Aative initial history of androgen exposure, our
' i' [/ @9 P9 O6 D+ R4 nbiggest concern was virilizing adrenal hyperplasia,5 l/ P+ ]& v/ D, \! W
either 21-hydroxylase deficiency or 11-β hydroxylase2 E( z" y7 q* _0 O- b
deficiency. Those diagnoses were excluded by find-
) f9 J) s+ k+ _4 }- Eing the normal level of adrenal steroids.
/ C* M# j( f9 O5 i: lThe diagnosis of exogenous androgens was strongly
4 V0 D' r" j8 m  a& G$ r. S" Fsuspected in a follow-up visit after 4 months because' j9 D5 z) P0 f6 o6 i) U
the physical examination revealed the complete disap-, U* p9 d; L4 {( _8 x% r
pearance of pubic hair, normal growth velocity, and" {9 j2 U, g' t1 m; n7 H
decreased erections. The father admitted using a testos-
* _8 f+ s1 P+ sterone gel, which he concealed at first visit. He was) K" k2 s5 I% q/ m: ?
using it rather frequently, twice a day. The Physicians’, y8 p8 A0 ~* s5 G$ J
Desk Reference, or package insert of this product, gel or; C. ?5 O, u/ X+ H# V
cream, cautions about dermal testosterone transfer to
+ [- j  t7 W' O# Q0 d% Q1 wunprotected females through direct skin exposure.8 s+ V" `+ N% w- V2 `% k/ `5 y7 \5 k
Serum testosterone level was found to be 2 times the
7 K1 `6 H  }+ j0 H* Zbaseline value in those females who were exposed to. C% R1 B% {3 x8 y
even 15 minutes of direct skin contact with their male
, B3 t& I: o( ~1 z' t4 dpartners.6 However, when a shirt covered the applica-' W: X3 m  V5 {# L# {6 W4 M0 R
tion site, this testosterone transfer was prevented.
9 C6 Z1 v+ k+ s! _/ ^) o1 j/ \) [Our patient’s testosterone level was 60 ng/mL,
8 @  B. c& Z* L2 ~7 f( m4 Swhich was clearly high. Some studies suggest that
! [. g8 P, L/ ?0 `; ydermal conversion of testosterone to dihydrotestos-" g4 v' I: m, l; r7 [
terone, which is a more potent metabolite, is more
* O: J) f9 C& k1 h% {# Aactive in young children exposed to testosterone- H2 ~/ t) P0 ?/ V* y
exogenously7; however, we did not measure a dihy-$ O7 N6 I( H3 b3 |) j3 r# t! r
drotestosterone level in our patient. In addition to6 a' Y* B  n8 R: d+ e  ~
virilization, exposure to exogenous testosterone in; n1 @: Z: U: L* J5 R
children results in an increase in growth velocity and
# T) W4 K7 ]7 O0 [( i- Fadvanced bone age, as seen in our patient.# d' d* F" p7 ?3 `
The long-term effect of androgen exposure during2 d" x# }/ _; Z. s( m6 J% ]  U! l
early childhood on pubertal development and final
. Z3 x4 r  m' w) v% E  Eadult height are not fully known and always remain" s# C& P+ V& Y/ ?. j
a concern. Children treated with short-term testos-4 v! R% p5 V( v1 m! F1 K5 }
terone injection or topical androgen may exhibit some
* x! Z! R5 |: H# H& Cacceleration of the skeletal maturation; however, after
( K. J- A3 W% Z2 A( ?cessation of treatment, the rate of bone maturation- P; I5 n/ P* o6 W: }/ \
decelerates and gradually returns to normal.8,9
6 u; D2 S, R" W; SThere are conflicting reports and controversy
2 ]  S( ^$ j2 R8 Q  p* Q" Y2 aover the effect of early androgen exposure on adult% s" c& m( ]3 t: i4 h
penile length.10,11 Some reports suggest subnormal3 e% B, Q6 T8 W+ Z. U
adult penile length, apparently because of downreg-. F9 T1 A9 B6 U
ulation of androgen receptor number.10,12 However,$ K- N# s9 C/ {% R  _
Sutherland et al13 did not find a correlation between
1 F# P7 V* E) j( Schildhood testosterone exposure and reduced adult# A$ y5 x' [# p$ g5 T
penile length in clinical studies.
# D% L4 L7 m/ |0 b7 n' L/ dNonetheless, we do not believe our patient is
# Q: ?: h2 ^, e/ Ggoing to experience any of the untoward effects from
8 c( [& f4 O! `testosterone exposure as mentioned earlier because
4 g+ f. D+ W) J: x. |" mthe exposure was not for a prolonged period of time.
6 @; E/ L2 h  ~: {8 o% i0 A3 jAlthough the bone age was advanced at the time of1 R+ }1 k# t, D2 Y% @- _  h
diagnosis, the child had a normal growth velocity at  x: \# G* ?* w
the follow-up visit. It is hoped that his final adult
/ h3 E6 M) G- A9 z4 P# d" R6 Z2 ~0 D  Nheight will not be affected., o! _( s2 ~- \3 m/ _, K2 c
Although rarely reported, the widespread avail-& A  o8 m" M6 I& t6 f
ability of androgen products in our society may
: n: w/ _# M, |6 O4 Nindeed cause more virilization in male or female
3 E- \2 p* r. w# s: k! i1 A3 n: Schildren than one would realize. Exposure to andro-
" d/ K  `  |  }9 ?  P9 _: Lgen products must be considered and specific ques-
8 e5 p! t! a# g! z  c2 o+ Z! K9 ^tioning about the use of a testosterone product or
; A" P( L% d4 U+ e3 Hgel should be asked of the family members during' r5 a4 O8 [2 A) ?
the evaluation of any children who present with vir-
! p) X! {( l: |' Filization or peripheral precocious puberty. The diag-
' @; \. o; K/ Q( ?: Wnosis can be established by just a few tests and by
/ {; P* O7 x, L8 T4 }appropriate history. The inability to obtain such a
% K! G# Y6 L$ H7 n; ]4 y2 Thistory, or failure to ask the specific questions, may
* n' M$ n; u  R- j5 R7 ]result in extensive, unnecessary, and expensive2 x, A- E! A  \) b: M: G
investigation. The primary care physician should be
9 U1 D) p# h" waware of this fact, because most of these children
. J4 w* ]7 k2 |may initially present in their practice. The Physicians’$ |( H" }- }# F3 L" J
Desk Reference and package insert should also put a
* @0 O7 p9 l( r8 j: K) Xwarning about the virilizing effect on a male or% X5 U2 \, K8 R: c* x
female child who might come in contact with some-
5 s6 i6 q. t# T7 m, P: f9 s; qone using any of these products.
7 C) _. ]6 I7 [References' v5 r9 \+ L3 F0 W2 c1 o4 I
1. Styne DM. The testes: disorder of sexual differentiation
0 m7 F3 x- ~4 M7 j3 g+ u8 S3 Gand puberty in the male. In: Sperling MA, ed. Pediatric# V& k( S: \7 a$ Q* Y2 L5 ]
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
% U& L5 j, U6 `5 W# R7 T4 [. G+ P. f2002: 565-628.
4 B, U1 U% E: b' m# E/ a* W4 R2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious  N- t' r/ F+ R6 I$ @
puberty in children with tumours of the suprasellar pineal
發表於 2025-1-7 21:59:43 | 顯示全部樓層
這個我收藏了!謝謝分享!WK的資源越來越豐富,這少不了大大的辛勞!
發表於 2025-1-10 10:43:39 | 顯示全部樓層
VIP精品區,資源無限好賺金任務區,輕松賺金幣
加入VIP,享受高級特權宣傳賺金又升級,超級棒
感謝大大的辛勞分享!我會繼續在WK關注大大的文章!
發表於 2025-1-11 22:18:01 | 顯示全部樓層
女厕偷拍辅导班主任尿尿老师的逼很嫩还有一点
發表於 2025-1-17 16:31:39 | 顯示全部樓層
VIP精品區,資源無限好賺金任務區,輕松賺金幣
加入VIP,享受高級特權宣傳賺金又升級,超級棒
4个什么样的?
發表於 2025-1-19 02:41:05 | 顯示全部樓層
2 Z; k8 v% ]9 q8 M
精妙絕倫的精品,感謝啊!期待你更多更好的創作哦!
發表於 2025-3-8 22:04:50 | 顯示全部樓層
絕對的好貼!謝謝啊!逐字逐圖地看完這個帖子以後,我的心久久不能平靜,感恩啊!
您需要登錄後才可以回帖 登錄 | 立即注册

本版積分規則


快速回復 返回頂部 返回列表