WK綜合論壇, WK综合论坛

 找回密碼
 立即注册
樓主: wk007

鄉下的妹子太便宜,一次四個都要了[12P]

[複製鏈接]
發表於 2025-1-4 03:25:35 | 顯示全部樓層
VIP精品區,資源無限好賺金任務區,輕松賺金幣
加入VIP,享受高級特權宣傳賺金又升級,超級棒
Sexual Precocity in a 16-Month-Old
" Y6 w: M5 m$ V( v1 K* `  Y7 N( o4 ^Boy Induced by Indirect Topical( b5 @( u8 t# z: `; d
Exposure to Testosterone5 n1 b( c- w) ]8 l
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2, U8 h4 M' Q: y6 U* s6 _
and Kenneth R. Rettig, MD1: H6 E) D4 j8 s/ _& d* P$ X/ D
Clinical Pediatrics
. b. s3 R* a/ G! e6 EVolume 46 Number 6
2 e4 r2 U1 ~$ WJuly 2007 540-543) J- G* w) d: a+ o( @; T
© 2007 Sage Publications
9 N! ~3 a) a9 C" l3 G# R10.1177/0009922806296651
6 p- L% q6 f7 [# _+ `1 p$ P2 @/ Fhttp://clp.sagepub.com1 T. e3 M& `6 K
hosted at; E; y& w( b4 q3 Q
http://online.sagepub.com
7 K3 F! t- A; g- P) d( ]1 mPrecocious puberty in boys, central or peripheral,6 y2 n5 e6 [' p# r( w
is a significant concern for physicians. Central
% q  M- B! |. F! Q4 vprecocious puberty (CPP), which is mediated  r1 R& c0 l1 x1 N# O
through the hypothalamic pituitary gonadal axis, has6 y6 @+ ^  [; K& w3 \
a higher incidence of organic central nervous system
. b% {" a- k& G- l+ M9 K' _' glesions in boys.1,2 Virilization in boys, as manifested4 ~" r3 W9 f( L" N
by enlargement of the penis, development of pubic1 c8 n4 Z  n: o; Z& O0 P
hair, and facial acne without enlargement of testi-6 E" x9 K7 N2 \, O, Z
cles, suggests peripheral or pseudopuberty.1-3 We
/ f) f& `* r4 w/ }' a8 V: Yreport a 16-month-old boy who presented with the
! p+ o* u' S0 d* I2 S6 J; xenlargement of the phallus and pubic hair develop-2 Z, }9 X+ m9 D8 s
ment without testicular enlargement, which was due9 Z. V' }0 u8 s; R7 _) {9 X1 v; N
to the unintentional exposure to androgen gel used by) |& r& K/ F& l% |
the father. The family initially concealed this infor-: S: K+ I, H9 x8 y. B
mation, resulting in an extensive work-up for this
: \& ?" _  {9 F4 k6 D" Bchild. Given the widespread and easy availability of6 ^0 k% v0 @2 B9 w4 @7 l6 }& ?
testosterone gel and cream, we believe this is proba-* Z8 q, {' q8 w$ _3 K9 h/ X6 {
bly more common than the rare case report in the
2 @4 i& i7 g" c) B" _literature.4
) d, a1 m7 S' E) r, n% d- \6 YPatient Report
4 `3 ^. C1 Q. B& c% s! G3 j  BA 16-month-old white child was referred to the9 H9 y9 h# b! ^3 D2 A. D
endocrine clinic by his pediatrician with the concern
5 T2 P7 M, }+ g+ U' o* T& d) U2 Dof early sexual development. His mother noticed
1 z2 G' e% t; k1 m8 ^" H/ s" h) k. plight colored pubic hair development when he was
8 b. ?3 T3 N% O4 RFrom the 1Division of Pediatric Endocrinology, 2University of
0 Y! k$ B, z0 r$ V7 {! ?) ]  wSouth Alabama Medical Center, Mobile, Alabama.
9 R  C6 F' }* v3 rAddress correspondence to: Samar K. Bhowmick, MD, FACE,
8 k$ E7 o2 W7 @  ^4 u5 `Professor of Pediatrics, University of South Alabama, College of
8 x8 t7 E' J' fMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
( ~5 h) x! C: _+ R. ^% V) C( G- ce-mail: [email protected].
  M& h" R# G- X3 A& D3 N# uabout 6 to 7 months old, which progressively became
- d6 ?6 n0 o! \6 I  P% Z" Hdarker. She was also concerned about the enlarge-0 R6 ^$ S, J# s& k) M
ment of his penis and frequent erections. The child$ d% D- _. J! @6 z+ a
was the product of a full-term normal delivery, with
. c3 j5 O9 S9 _4 m8 @* P3 v6 ta birth weight of 7 lb 14 oz, and birth length of) c& r1 ^/ N4 O1 P
20 inches. He was breast-fed throughout the first year; U% k  p! `, A3 g% s9 E
of life and was still receiving breast milk along with6 u& b. @( S, |" w
solid food. He had no hospitalizations or surgery,
, X. a, D" ?# T+ S& }* F4 Kand his psychosocial and psychomotor development
+ Z; ~  u5 i5 K0 Kwas age appropriate.
; R/ w7 }( x5 k6 H5 I! [The family history was remarkable for the father,
$ o% T& x* ?/ Twho was diagnosed with hypothyroidism at age 16,
' w3 A2 X; @  {- @8 pwhich was treated with thyroxine. The father’s& C9 U0 _3 D9 H) R! Q5 g1 t
height was 6 feet, and he went through a somewhat
$ S& [0 e" n/ J& o5 w9 Cearly puberty and had stopped growing by age 14.6 S$ C2 z3 h% `. o7 o# j- d
The father denied taking any other medication. The- G, m  C% ^  `
child’s mother was in good health. Her menarche$ H+ h' W# W! T5 N+ L
was at 11 years of age, and her height was at 5 feet
. u5 j( }, Q  u# B' u. c: Y3 C" ~5 inches. There was no other family history of pre-( s5 u  w( N8 O# [( j
cocious sexual development in the first-degree rela-7 H) n8 \6 I4 K7 n6 C  P
tives. There were no siblings.
2 \! A7 s$ S9 I8 h( RPhysical Examination& l1 \4 Y% x3 l7 ~
The physical examination revealed a very active,
- e0 s: a( D' n$ l, Gplayful, and healthy boy. The vital signs documented
6 g2 h+ ~$ Z1 wa blood pressure of 85/50 mm Hg, his length was
- U5 p9 n2 O% m90 cm (>97th percentile), and his weight was 14.4 kg
$ s4 d1 @5 r' }, x9 s2 c(also >97th percentile). The observed yearly growth
/ P+ C% i% H& f( ^9 @: A8 Y* |velocity was 30 cm (12 inches). The examination of
  \4 ^5 z6 h: H% _the neck revealed no thyroid enlargement., g- g0 M7 H( z4 g8 U. K( ^; ]: `
The genitourinary examination was remarkable for
/ H/ B6 g" N9 L  g% d8 K% o& Fenlargement of the penis, with a stretched length of
% f; s4 s- X/ y8 o8 F8 cm and a width of 2 cm. The glans penis was very well
  h# G& t* F0 T3 U: a! Pdeveloped. The pubic hair was Tanner II, mostly around
1 }. `* }4 N: A: X/ b3 ]5404 \; T. h' p% S( y; {  o4 B: g8 {
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from0 w$ `) o) n+ O, Y
the base of the phallus and was dark and curled. The4 P  f& ]$ y8 W/ `9 m: B
testicular volume was prepubertal at 2 mL each., Y  @, z* t! F0 o* \; I$ ~
The skin was moist and smooth and somewhat, a1 E" Z" W" {
oily. No axillary hair was noted. There were no0 ~6 A( C( m2 r+ W
abnormal skin pigmentations or café-au-lait spots.
4 a* l7 j& T* v9 X! R1 r/ fNeurologic evaluation showed deep tendon reflex 2+
: t" J* E7 @- d% o- bbilateral and symmetrical. There was no suggestion' v& p  R8 J* _9 u8 [
of papilledema." c( w1 H( x8 Z3 |. D
Laboratory Evaluation
' m1 Q5 w5 j; W$ wThe bone age was consistent with 28 months by
3 D+ b0 m2 y) h* X& t: M9 [- \using the standard of Greulich and Pyle at a chrono-
5 [6 d2 f# w  @- d, U! J( hlogic age of 16 months (advanced).5 Chromosomal
: G, B: v* v9 i% h: J4 [karyotype was 46XY. The thyroid function test0 R. Y  m; F: f
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
" c1 n' O* c: w" }5 I% L; ]lating hormone level was 1.3 µIU/mL (both normal).
" O. j0 v7 d6 \1 J7 V. w) iThe concentrations of serum electrolytes, blood
  u3 Y! L) W8 S6 ^+ W8 L% purea nitrogen, creatinine, and calcium all were. R' U" }. x4 e- y$ ?2 v
within normal range for his age. The concentration* j4 C* |% g5 `0 ]) I3 C3 y6 ?* r
of serum 17-hydroxyprogesterone was 16 ng/dL8 E/ P% o& A. Z7 t4 Z
(normal, 3 to 90 ng/dL), androstenedione was 208 s+ p2 _; D, x1 E! D) [( H
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-- N# {. F% ~! m
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
" T9 M  K# k3 odesoxycorticosterone was 4.3 ng/dL (normal, 7 to* g+ Z# n0 _) Z5 F4 f
49ng/dL), 11-desoxycortisol (specific compound S)$ P4 i; j9 ~' r8 L( V; s/ D
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
+ r6 ]" I  O6 R5 jtisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total. H" g. D8 M( g4 X8 {
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
) o  M3 w5 q0 x3 M. p, I: \0 Nand β-human chorionic gonadotropin was less than6 \" P* [: B1 Y; `3 F
5 mIU/mL (normal <5 mIU/mL). Serum follicular) z' s) e. ?, e* t
stimulating hormone and leuteinizing hormone0 Q9 r+ N3 @- z7 o! \
concentrations were less than 0.05 mIU/mL2 s. U3 }" b3 f- |: z
(prepubertal).
4 g% M! a' Z: k6 n0 p2 uThe parents were notified about the laboratory  h: o' l8 ]7 t8 S/ d5 |1 X
results and were informed that all of the tests were: @& K+ G: q8 e7 u
normal except the testosterone level was high. The" X' `9 U0 W8 {2 N& [  p
follow-up visit was arranged within a few weeks to
( f2 H( ?& \( u' k! t9 \; vobtain testicular and abdominal sonograms; how-$ C8 V9 b+ H* y4 o7 C: k  [# |
ever, the family did not return for 4 months.' }& o8 }/ L4 i+ A2 U' ]
Physical examination at this time revealed that the
' X: q( z# P7 O' Zchild had grown 2.5 cm in 4 months and had gained
! R- b2 x% K! b; y8 \2 kg of weight. Physical examination remained
7 U! q' C  S; X0 J; o3 tunchanged. Surprisingly, the pubic hair almost com-  M4 t6 q. z1 z' ^2 s
pletely disappeared except for a few vellous hairs at
! {; h1 s/ N. Othe base of the phallus. Testicular volume was still 2/ i# ~( a  U# a& t" ?- l. m
mL, and the size of the penis remained unchanged.
+ P& E- f5 l( N, l* iThe mother also said that the boy was no longer hav-3 C; h+ B! ?2 Z" K1 F" u( R
ing frequent erections.
- K0 \: M  Z. e0 b$ R7 x: zBoth parents were again questioned about use of
- b, b- Z3 n& O3 yany ointment/creams that they may have applied to; @. p5 ^2 C. K: r
the child’s skin. This time the father admitted the
- m' m* w1 K! O, {* _. PTopical Testosterone Exposure / Bhowmick et al 541
0 {4 f- T; s- X- N' Juse of testosterone gel twice daily that he was apply-- f5 ~* _0 h5 a3 C% A% X/ w
ing over his own shoulders, chest, and back area for
" m6 ~0 S# P9 q% E) m" H9 d1 w" pa year. The father also revealed he was embarrassed
/ z" o( N, C4 F' Z& \. A7 w  L* Z) Uto disclose that he was using a testosterone gel pre-4 }) p. R+ B% y% }0 }! Z
scribed by his family physician for decreased libido
9 u, }5 _- X  X  bsecondary to depression.
& D0 s" X0 n  F  E! jThe child slept in the same bed with parents.+ `4 Z8 d& G- c. c
The father would hug the baby and hold him on his  h* O. B+ ]7 c2 m
chest for a considerable period of time, causing sig-
, @8 s' `$ d$ [nificant bare skin contact between baby and father.& U) C5 s9 \, B/ H8 J
The father also admitted that after the phone call,- V4 M( Y! H" u. r3 B
when he learned the testosterone level in the baby
* q% g# F4 l# M' Q- F" e1 X. vwas high, he then read the product information# {' e) t1 H1 f  ~
packet and concluded that it was most likely the rea-
* F5 S9 i0 q8 d7 nson for the child’s virilization. At that time, they1 H3 v. ~# l9 p4 C. L
decided to put the baby in a separate bed, and the
  B4 S; o2 o0 d2 V( c) M$ Ifather was not hugging him with bare skin and had
* [/ r) s9 s& P% w* h! [$ V4 N4 Pbeen using protective clothing. A repeat testosterone
! ]( p8 A+ \# Otest was ordered, but the family did not go to the
; @5 U- T; k' E# Q2 alaboratory to obtain the test.
0 Z- A8 t& g5 {# t  ?# g" lDiscussion
; x, p; |2 M- b  ^4 o: ?/ v% ]Precocious puberty in boys is defined as secondary, _% n% e3 n2 d5 Z1 ?7 M  V
sexual development before 9 years of age.1,4
' K- }; u8 M$ \. u; F+ xPrecocious puberty is termed as central (true) when
) B& @! [) Y' W! ?it is caused by the premature activation of hypo-
+ B- w; a! r2 p) X% J! Athalamic pituitary gonadal axis. CPP is more com-
* p" {, d8 p) {& F. b# v! l- umon in girls than in boys.1,3 Most boys with CPP
$ ?& m# v! V; xmay have a central nervous system lesion that is
- c) N( H, N7 n# V+ k8 E  Lresponsible for the early activation of the hypothal-( [$ F0 r5 T8 `% m! g
amic pituitary gonadal axis.1-3 Thus, greater empha-# J. r9 x" {9 ^$ S
sis has been given to neuroradiologic imaging in* S' O! Q6 D' x0 u
boys with precocious puberty. In addition to viril-, E" e3 n" ~- @! f& s
ization, the clinical hallmark of CPP is the symmet-  b) Q' |/ ~( T
rical testicular growth secondary to stimulation by6 _' k2 m; |% a% M# a
gonadotropins.1,3! Q2 |0 b, r6 q$ P  Q) r: x
Gonadotropin-independent peripheral preco-$ j+ L: f: [/ i6 U- k+ `) I% q
cious puberty in boys also results from inappropriate
6 Y: ?0 X1 x# a$ Kandrogenic stimulation from either endogenous or
. _3 U" a) h8 xexogenous sources, nonpituitary gonadotropin stim-9 ~) W+ |! K0 l5 |+ Q$ T$ P
ulation, and rare activating mutations.3 Virilizing/ ~. P% S/ ~, d1 G& ?5 @( ^
congenital adrenal hyperplasia producing excessive
' e. s- I% |( {! B& Zadrenal androgens is a common cause of precocious
. N4 ]; Z" P; ?7 \$ Ppuberty in boys.3,4$ E8 f( t- P" f3 D
The most common form of congenital adrenal
$ ~+ Y  f; T; n0 n2 P5 {$ a4 [hyperplasia is the 21-hydroxylase enzyme deficiency.7 c9 q( ^6 t9 p# }
The 11-β hydroxylase deficiency may also result in
9 i: A9 r% _7 q! u- [4 ^$ e& [3 zexcessive adrenal androgen production, and rarely,
1 H$ Z) _$ V! ^8 V& can adrenal tumor may also cause adrenal androgen
$ ?+ N4 f# b6 f8 }7 A% iexcess.1,39 h! x: m: q9 p& J% {  q
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
6 E% F; C4 y- U: c3 Z3 C542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
8 ]# v  g: C: k+ W. sA unique entity of male-limited gonadotropin-8 Y2 c2 n1 G9 d
independent precocious puberty, which is also known
5 I! s- r) f: B. u. Tas testotoxicosis, may cause precocious puberty at a
3 A- z4 a. \3 f) p: f. @very young age. The physical findings in these boys
' q$ T6 |; j1 Wwith this disorder are full pubertal development,
- _$ r; o& c# p0 G) T) r8 r) [+ ?) Iincluding bilateral testicular growth, similar to boys
9 |) ]& I0 [# ~! ]- C6 |with CPP. The gonadotropin levels in this disorder
0 y4 |3 V: v! Z- i# q& o( nare suppressed to prepubertal levels and do not show
( Z' `% {# N8 F( A2 Tpubertal response of gonadotropin after gonadotropin-
7 ?9 d& q5 H' Rreleasing hormone stimulation. This is a sex-linked
  ^3 w( A2 ]7 l: Y4 P/ fautosomal dominant disorder that affects only
/ E& `4 {) h/ u2 x! ^males; therefore, other male members of the family
+ o2 ?4 ?& S% u7 u( |0 i. l6 ]may have similar precocious puberty.3
  u) j& C2 K" f7 t' u; c. }9 X' ?In our patient, physical examination was incon-
" H) ~( [8 _" @, X$ msistent with true precocious puberty since his testi-
" E/ G* X% ?$ N+ z$ G) _4 ~cles were prepubertal in size. However, testotoxicosis8 r- k2 b$ }0 v
was in the differential diagnosis because his father! B' R6 h$ k! J4 S
started puberty somewhat early, and occasionally,
# T3 e% v; n* p% ltesticular enlargement is not that evident in the/ w  @- P2 Y2 H; Z
beginning of this process.1 In the absence of a neg-$ T- F; Q8 U7 C& G
ative initial history of androgen exposure, our
- X3 v, Y7 {; `; x- j4 Zbiggest concern was virilizing adrenal hyperplasia,% \! B' j, d7 f+ k$ y
either 21-hydroxylase deficiency or 11-β hydroxylase
  E6 e: N3 O" |+ z; \" odeficiency. Those diagnoses were excluded by find-
+ I5 o+ W9 Q6 ]5 C, Jing the normal level of adrenal steroids.
' k0 N9 a& B5 h& k& |5 @) v1 ]1 pThe diagnosis of exogenous androgens was strongly
% S. u& H; ^1 D+ E/ fsuspected in a follow-up visit after 4 months because
8 k, j! L7 _2 E2 F5 C2 Fthe physical examination revealed the complete disap-9 Z: ~; _. k; m# J
pearance of pubic hair, normal growth velocity, and4 \8 r* H3 g; Z2 a  P/ o
decreased erections. The father admitted using a testos-+ ~; h6 i* X- K% o+ R( {$ i
terone gel, which he concealed at first visit. He was: J8 `( H0 ^' @5 `
using it rather frequently, twice a day. The Physicians’5 ~0 }' c% h8 ]" O
Desk Reference, or package insert of this product, gel or- l  Y! b( k  H) M6 A" @5 @
cream, cautions about dermal testosterone transfer to
! D( g0 |- ?2 [. j' ?: B. m0 yunprotected females through direct skin exposure." B% k5 e- V7 b+ s( F" O& R
Serum testosterone level was found to be 2 times the: w3 P* y7 s% F* t
baseline value in those females who were exposed to- L) P2 j. F4 s
even 15 minutes of direct skin contact with their male  v  P9 P, n- o5 `! D! \+ J
partners.6 However, when a shirt covered the applica-, D4 T/ y" E) o! O  ^( M; H; b
tion site, this testosterone transfer was prevented.
& [% `/ H  q: r! Q% Z: ?% e& ~; TOur patient’s testosterone level was 60 ng/mL,' I! H, x) w; E6 v/ H
which was clearly high. Some studies suggest that% E" A3 E0 w3 X4 I/ N
dermal conversion of testosterone to dihydrotestos-* @& R2 a" E+ @& d
terone, which is a more potent metabolite, is more: {/ Q, ~" c' O; v
active in young children exposed to testosterone/ u2 a5 y9 e5 \2 @
exogenously7; however, we did not measure a dihy-
" R( \6 d( d. g% j* |1 Bdrotestosterone level in our patient. In addition to1 l6 ~8 n- f7 r
virilization, exposure to exogenous testosterone in2 y+ W, _+ A2 E- l% o1 E
children results in an increase in growth velocity and
1 j1 Y8 S) |6 p5 |% I6 D: j3 ?advanced bone age, as seen in our patient.
4 p, m0 ~7 H6 f% f# H! {  u. k0 k6 k1 eThe long-term effect of androgen exposure during
6 u9 k6 D4 z4 Q3 r$ |$ f5 oearly childhood on pubertal development and final
6 q  W$ y) K5 b# p; W$ Vadult height are not fully known and always remain3 p: F3 R; y' N9 ~
a concern. Children treated with short-term testos-4 C" M& ~7 c, e- ^# B
terone injection or topical androgen may exhibit some# g9 s# L+ {; @8 @7 {2 s0 d9 ]
acceleration of the skeletal maturation; however, after
! `! V1 U' Y. a- {; _: x& Ocessation of treatment, the rate of bone maturation
1 v" j+ c" n9 N9 ]1 ?& i/ _decelerates and gradually returns to normal.8,9/ j6 I7 h: c6 B  P, C  w  Z6 w; S
There are conflicting reports and controversy
8 e7 g% y( U. S) bover the effect of early androgen exposure on adult
0 m  |8 A  t' n- rpenile length.10,11 Some reports suggest subnormal' u( C* I) A5 _' S/ A
adult penile length, apparently because of downreg-
$ w8 `" m3 s, r( w" B3 aulation of androgen receptor number.10,12 However,
% }9 Q1 ^- W! r: d+ \0 \Sutherland et al13 did not find a correlation between
: R+ t  o# \" d# [4 J; x' Kchildhood testosterone exposure and reduced adult
5 B) X/ U" J7 g0 M  k* Dpenile length in clinical studies." z: ]# h- b* s( K
Nonetheless, we do not believe our patient is
' m1 T2 a2 Y* Z! e9 F, x$ G8 rgoing to experience any of the untoward effects from
! O3 F* i3 P" |' h* Y! Qtestosterone exposure as mentioned earlier because
4 G% K: B* Z& D/ Z  c  gthe exposure was not for a prolonged period of time., J: z& u$ r, X
Although the bone age was advanced at the time of' w6 ^% S& x) r# s- Z
diagnosis, the child had a normal growth velocity at
1 ?) l# S! Z# u. l, O6 ^the follow-up visit. It is hoped that his final adult; X9 B" ]* e4 ?
height will not be affected.; G' z; ^4 Y# {) e; _% ]5 [- A) c
Although rarely reported, the widespread avail-
' V0 g' i1 n1 X1 ~( Oability of androgen products in our society may
% V/ Q! [3 k% Lindeed cause more virilization in male or female
4 u( \6 J- y$ E1 `* Zchildren than one would realize. Exposure to andro-' A1 H* Y/ L0 p2 h$ A7 W
gen products must be considered and specific ques-& C" \! [0 d4 @) m( G; A+ f
tioning about the use of a testosterone product or  c+ o; g' y2 u1 V
gel should be asked of the family members during5 S5 g$ D2 z3 z& a% [1 {6 J
the evaluation of any children who present with vir-  ?' j9 ^) D- E5 B: f& O
ilization or peripheral precocious puberty. The diag-
( @$ q$ ~# y& |/ }nosis can be established by just a few tests and by
7 o7 C8 d+ F$ H: J) Tappropriate history. The inability to obtain such a
* P9 ?' J5 k/ j8 N9 w; ihistory, or failure to ask the specific questions, may
+ P) [0 c% f2 u, ?& p! r$ ~+ Jresult in extensive, unnecessary, and expensive  J/ O2 q# b7 x% t7 t
investigation. The primary care physician should be
" O) S2 U6 H+ A! P# M7 t5 D) paware of this fact, because most of these children
3 P3 h3 e/ |: W, a+ [- B  R1 Nmay initially present in their practice. The Physicians’' I5 Z  i5 W0 A: A) O) u7 B3 z
Desk Reference and package insert should also put a
* Q" z$ V. ?6 x& D- G5 Hwarning about the virilizing effect on a male or
' u# p" [* C9 n6 Y; vfemale child who might come in contact with some-
2 S/ e  h! J6 Y, n( T& y) lone using any of these products.
4 \( s4 [& j" k+ [* j/ J+ WReferences- P, g# R( B9 f* s' Q, b- [
1. Styne DM. The testes: disorder of sexual differentiation
) c4 I5 h# c: Land puberty in the male. In: Sperling MA, ed. Pediatric
$ X" U0 }5 @; Y7 _Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;: G# A+ ]. J# d4 |# @
2002: 565-628.; _) ?- H+ g7 n0 @
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
% t, }& I9 l0 d1 Ppuberty in children with tumours of the suprasellar pineal
發表於 2025-1-4 03:27:02 | 顯示全部樓層
VIP精品區,資源無限好賺金任務區,輕松賺金幣
加入VIP,享受高級特權宣傳賺金又升級,超級棒
Sexual Precocity in a 16-Month-Old
; z4 M' G& n& R$ |5 `( KBoy Induced by Indirect Topical, Z2 j+ o" o( A$ m" P8 d- P, M" K
Exposure to Testosterone
- R/ G7 }# v6 MSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
6 E8 b* D8 v' W# R  ?; k) M) [and Kenneth R. Rettig, MD1/ b  J* [0 T- i1 ~) w
Clinical Pediatrics
9 Z6 }8 X* P4 {, i, H/ K7 g! N. QVolume 46 Number 69 n: c  {0 i+ V& o% x( L5 W" d
July 2007 540-543& Y4 E/ C( P* a$ S
© 2007 Sage Publications
8 F" L& w* [3 o* _" o10.1177/0009922806296651
8 W, Z! Q8 a5 b  f' q5 C, Y; [- ehttp://clp.sagepub.com
; }! e. o. j' Jhosted at
% L" V* Q& c" U& L* p$ ]' lhttp://online.sagepub.com  l; Q- Y4 ~9 r0 m6 `
Precocious puberty in boys, central or peripheral,
7 J4 x& a% t2 j" ]9 pis a significant concern for physicians. Central( |* e& l  y  _2 X3 V- ]
precocious puberty (CPP), which is mediated$ C$ ~, ^, s* c! F; G$ n4 C/ e
through the hypothalamic pituitary gonadal axis, has0 U. T+ e2 C4 x, Y7 Q( d+ W( |7 @4 \
a higher incidence of organic central nervous system9 }  E$ D; Q* G
lesions in boys.1,2 Virilization in boys, as manifested
+ d6 P" q: d: a, T& a# @& Oby enlargement of the penis, development of pubic
/ j3 a5 }: r1 N, N3 L7 ^6 phair, and facial acne without enlargement of testi-! ]. j% v8 \) s+ ?& N7 o% f2 J
cles, suggests peripheral or pseudopuberty.1-3 We& C0 a* y' F( J2 n
report a 16-month-old boy who presented with the5 a2 a+ _* s/ \& b4 X9 ~
enlargement of the phallus and pubic hair develop-) W+ q3 f4 `, v- q; H8 A
ment without testicular enlargement, which was due
! J7 l% @! {+ V. |: oto the unintentional exposure to androgen gel used by
3 ^+ F" r' z2 a1 w" t- g% wthe father. The family initially concealed this infor-  y: z' q0 N5 W+ T. f5 H/ [3 [
mation, resulting in an extensive work-up for this. \6 ?) z9 k- P, ]6 ^$ r, T7 j
child. Given the widespread and easy availability of7 V. `2 \' [) N3 @8 b
testosterone gel and cream, we believe this is proba-- O& M8 P" ^1 n0 v" z
bly more common than the rare case report in the( J% ~9 P+ |$ O! H+ `5 V
literature.4
% V5 m4 E8 }3 U" _Patient Report
( {8 X6 Y) f5 r0 n3 q6 G4 g) J8 w1 yA 16-month-old white child was referred to the2 y4 I" |+ y! m( H) p
endocrine clinic by his pediatrician with the concern2 _0 d* J3 f0 K1 q( R! j' n
of early sexual development. His mother noticed4 G' ^$ H: i+ P) g' R8 m% U
light colored pubic hair development when he was
) f+ s, g: v3 I' ]From the 1Division of Pediatric Endocrinology, 2University of% x& P0 [/ r5 \4 |
South Alabama Medical Center, Mobile, Alabama.4 b7 G- x3 m7 ~: ~" y' E4 v2 H, c
Address correspondence to: Samar K. Bhowmick, MD, FACE,
& ]2 Z0 `; j- A" D5 `' tProfessor of Pediatrics, University of South Alabama, College of; y7 z% N& D$ A! _# C+ I+ p
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
6 }2 K) Z2 X( Y* [' N% F! K- w) se-mail: [email protected].
+ e, [4 J1 Y! }about 6 to 7 months old, which progressively became
8 _" H& Q1 _# \- f' P) Bdarker. She was also concerned about the enlarge-" a, w4 }3 Z; h, F
ment of his penis and frequent erections. The child
" d& Y/ v- A% J3 c0 D0 v3 Z% Bwas the product of a full-term normal delivery, with& Q, W0 j# Y: T: ^" v% t
a birth weight of 7 lb 14 oz, and birth length of8 \' ?9 r% g1 A/ t
20 inches. He was breast-fed throughout the first year/ [% _* n% X% @! @' H
of life and was still receiving breast milk along with/ F8 S3 A: G) s4 r! S+ `
solid food. He had no hospitalizations or surgery,3 x& W# W% G  N& m& c, T% ^
and his psychosocial and psychomotor development) U% C4 F! ?0 E! J) s
was age appropriate.+ A, u6 H' F# u% d5 w# |
The family history was remarkable for the father,, ]  g! x2 Z! M0 U+ l& \& W
who was diagnosed with hypothyroidism at age 16,
" i/ h& L5 G4 {3 O% O) jwhich was treated with thyroxine. The father’s
/ i% m- h% V* H8 Dheight was 6 feet, and he went through a somewhat. L1 ~, M9 e9 Q# k  L
early puberty and had stopped growing by age 14.$ U! ~; c! S; p5 P% {4 G9 q" ~! ?
The father denied taking any other medication. The' [- C: k3 |6 l! e
child’s mother was in good health. Her menarche7 u, n$ v# @. p- Q: z  v6 I
was at 11 years of age, and her height was at 5 feet
* R. H/ g( j& l5 inches. There was no other family history of pre-
) Q/ v( S# a2 ]- a  ^cocious sexual development in the first-degree rela-
. ?; _! J1 V4 N9 i/ ^% itives. There were no siblings.
( k5 A6 G4 ~9 e! l1 zPhysical Examination
- V5 U5 |3 n% QThe physical examination revealed a very active,
! v$ q' S9 V- f( c/ D' iplayful, and healthy boy. The vital signs documented6 O! o3 q% h: n+ h
a blood pressure of 85/50 mm Hg, his length was, g/ x4 W: _0 X$ T) T: `0 ~# ]
90 cm (>97th percentile), and his weight was 14.4 kg' x3 |9 A; n" b8 ], v
(also >97th percentile). The observed yearly growth  X, D& s/ m& ]8 ]
velocity was 30 cm (12 inches). The examination of1 a$ e& q6 h2 K0 K2 H; s
the neck revealed no thyroid enlargement.
* t- r2 {# E# l& N5 K; PThe genitourinary examination was remarkable for4 a3 i5 @3 E2 r
enlargement of the penis, with a stretched length of5 g/ v$ q& x2 ?
8 cm and a width of 2 cm. The glans penis was very well/ y0 Z, _) u# l# e, S$ T1 y
developed. The pubic hair was Tanner II, mostly around0 r1 N8 O0 P, z* q: Z
540
8 b  z- ^; s' @/ ?at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
$ ~1 \" C& o+ ?0 u5 U' I) x" Kthe base of the phallus and was dark and curled. The* B7 H* A$ f3 g5 R" B
testicular volume was prepubertal at 2 mL each.  e1 f" J% f9 a: e5 J  y' Z2 p" H0 q
The skin was moist and smooth and somewhat# d) Z" n3 ?% B
oily. No axillary hair was noted. There were no8 s. h& o) r: y
abnormal skin pigmentations or café-au-lait spots.
! _! c: V  q; c- G7 K4 {: O+ YNeurologic evaluation showed deep tendon reflex 2+
2 \! l8 n- r! b$ @; P' A3 Rbilateral and symmetrical. There was no suggestion- U6 y7 T' A' O( ]9 Y1 D" ]$ l2 e
of papilledema.4 r+ `9 Z2 Q2 _0 z2 b
Laboratory Evaluation
' t8 I9 J% v+ t) ~/ O/ vThe bone age was consistent with 28 months by- Z6 k) H  Y2 H' o6 o  n& z
using the standard of Greulich and Pyle at a chrono-
+ p* F1 B7 f, S0 Y5 X6 flogic age of 16 months (advanced).5 Chromosomal0 @: }9 E, z* d% `
karyotype was 46XY. The thyroid function test
/ l9 V2 z. O+ T5 I2 E; x: T0 Pshowed a free T4 of 1.69 ng/dL, and thyroid stimu-  l2 j( q0 S* b6 J* U
lating hormone level was 1.3 µIU/mL (both normal).) c2 y% |9 Z& C, W, K% ^4 r
The concentrations of serum electrolytes, blood
5 v* u1 b/ o' j5 {3 Aurea nitrogen, creatinine, and calcium all were- h: |% e! ]" F1 M: r- C  d+ C
within normal range for his age. The concentration/ _, T7 q& }; W; R$ {; B3 D# ^8 g- a
of serum 17-hydroxyprogesterone was 16 ng/dL
& c/ U. ^4 y9 T! l- m( Q(normal, 3 to 90 ng/dL), androstenedione was 20
- H+ I' E! Q% Q* H9 Zng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
! d, Q: v" q! x  gterone was 38 ng/dL (normal, 50 to 760 ng/dL),  y- `4 Z' I; B) q: ?) T" {
desoxycorticosterone was 4.3 ng/dL (normal, 7 to1 X3 |$ r2 o! f4 W2 H4 v' P! h$ M. U
49ng/dL), 11-desoxycortisol (specific compound S)  V! @1 ]/ ^3 i5 |6 F
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-; X6 v4 B% k8 X' c* s
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total' p. I  B" ?  D8 J8 a3 T
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
) l7 }  T: W* q1 }( ~6 V* Qand β-human chorionic gonadotropin was less than. o1 a4 N3 A  |, t0 y+ }
5 mIU/mL (normal <5 mIU/mL). Serum follicular+ p, J8 i0 U  }$ S1 ~
stimulating hormone and leuteinizing hormone& p* S& f: _3 a9 R3 T" @7 m6 S
concentrations were less than 0.05 mIU/mL3 L( h' J# O4 q
(prepubertal).
3 U$ t) I( l1 P2 v- \" ]/ F; dThe parents were notified about the laboratory1 Y) f  d* R! ]4 k2 b  D  m! W
results and were informed that all of the tests were0 `: f5 P* ]# C
normal except the testosterone level was high. The9 c* _) S2 ?/ _* ^7 A* m9 x# T
follow-up visit was arranged within a few weeks to6 j! y$ m8 J# Y) g
obtain testicular and abdominal sonograms; how-8 V1 Q5 a" L" A# s, M
ever, the family did not return for 4 months.
1 a8 }  R2 r; d3 c+ _! YPhysical examination at this time revealed that the# d7 {: R1 k8 H) d. K& }$ {4 h
child had grown 2.5 cm in 4 months and had gained
* ]' U8 N. h" i" V2 kg of weight. Physical examination remained
8 n" m2 g7 o; v; s9 Vunchanged. Surprisingly, the pubic hair almost com-: X& Q7 E$ e# J" J8 S* Y7 [7 I
pletely disappeared except for a few vellous hairs at2 l, F6 l$ L, ?) L. f
the base of the phallus. Testicular volume was still 20 ^+ ]9 G# U, _& \- z
mL, and the size of the penis remained unchanged.$ I, B* X1 I7 e6 i7 M! h
The mother also said that the boy was no longer hav-1 z1 T( Z( K+ Y- b
ing frequent erections.  D, x7 p! T* u1 |5 H
Both parents were again questioned about use of
8 I% o/ m* v% fany ointment/creams that they may have applied to, ^+ c+ H) b* X9 w9 i
the child’s skin. This time the father admitted the
3 d  v8 j* Y7 y+ hTopical Testosterone Exposure / Bhowmick et al 5410 i# T" f& u" y
use of testosterone gel twice daily that he was apply-
6 R' }$ Q" b8 F" x$ Uing over his own shoulders, chest, and back area for; D: q4 s+ Y. E4 V
a year. The father also revealed he was embarrassed) M! u2 H6 V5 G: g7 P
to disclose that he was using a testosterone gel pre-8 W: Y- U+ S( b2 w+ q2 G
scribed by his family physician for decreased libido
7 |: @# d' T4 `9 y2 Ssecondary to depression.; d. F8 L; Q$ [$ d. V7 p* t- V
The child slept in the same bed with parents.
. `4 w2 _' f% t1 kThe father would hug the baby and hold him on his; B" j: h# @5 H5 G" e) F: R
chest for a considerable period of time, causing sig-
- \/ V" w+ L% }/ B4 znificant bare skin contact between baby and father.( q2 @& \* Y7 s
The father also admitted that after the phone call,
. M  r7 ?& n& N1 l8 |when he learned the testosterone level in the baby
1 }" Y. J- x6 Q. q- k4 Mwas high, he then read the product information5 ]) R. S5 `/ x9 j
packet and concluded that it was most likely the rea-5 f# o. Q* v1 L
son for the child’s virilization. At that time, they
2 X# k9 i3 [! I. f/ h# {  adecided to put the baby in a separate bed, and the
- i% O& Y6 U% ~2 rfather was not hugging him with bare skin and had
: D: R* I+ z" F' u8 O/ ibeen using protective clothing. A repeat testosterone& _" M& I) r) S$ W
test was ordered, but the family did not go to the7 S' y+ ~4 E5 F2 n! O
laboratory to obtain the test.9 I& c6 `" g. _6 s+ W: N$ F
Discussion' j% X) r1 z4 s3 B. J9 X4 i/ S* P
Precocious puberty in boys is defined as secondary( O8 ]$ U! w* b, K2 c' I
sexual development before 9 years of age.1,4
2 I& z( \2 D" x1 J  ?; yPrecocious puberty is termed as central (true) when
8 l, F3 T- p4 O: `& eit is caused by the premature activation of hypo-
" t. @" v6 {2 ^2 l3 ethalamic pituitary gonadal axis. CPP is more com-3 r3 H! E- Q9 s0 D5 d5 }5 ~
mon in girls than in boys.1,3 Most boys with CPP5 y. q; K& p$ r) L1 @
may have a central nervous system lesion that is
, U2 m: w( G1 S( O# E2 w. Tresponsible for the early activation of the hypothal-
. M0 `3 I. F/ L. c. Z+ Xamic pituitary gonadal axis.1-3 Thus, greater empha-
1 _: J% I/ {5 R8 g- ~5 @3 {. zsis has been given to neuroradiologic imaging in/ h2 R2 _$ o/ O& w
boys with precocious puberty. In addition to viril-; Q1 P8 W; N% L) b, q7 e
ization, the clinical hallmark of CPP is the symmet-
6 g! X4 p  ^3 f0 @, Mrical testicular growth secondary to stimulation by
4 r' \2 _, y5 j$ kgonadotropins.1,3
! n- u" S4 l: J# l3 Z- r$ CGonadotropin-independent peripheral preco-2 ]0 P1 x! Y: Y# I
cious puberty in boys also results from inappropriate
) b9 h8 P4 o; V3 Z' ^% Wandrogenic stimulation from either endogenous or5 S1 i! }9 ^8 d2 Q* N* Y
exogenous sources, nonpituitary gonadotropin stim-' z% r; R# z5 V2 {3 P* {1 T: Z8 T
ulation, and rare activating mutations.3 Virilizing. y# B' N4 o3 X
congenital adrenal hyperplasia producing excessive
; _. o& O6 ?; vadrenal androgens is a common cause of precocious; u. ]* U$ s+ v
puberty in boys.3,4
( K1 Z5 e) c: r& lThe most common form of congenital adrenal/ }# L- `5 ]( o5 F
hyperplasia is the 21-hydroxylase enzyme deficiency.
9 C4 Q9 q2 a. X7 Z3 w6 A. PThe 11-β hydroxylase deficiency may also result in8 }7 Q7 e- n+ N& D8 S" y
excessive adrenal androgen production, and rarely,
3 a) @, L' u8 K& f3 ?: O6 Xan adrenal tumor may also cause adrenal androgen
9 i4 B& B; L/ ^* C% e1 m  {excess.1,3
$ p2 t6 X( y% E: j( J- Rat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from, f/ v' z% M6 B- K* c4 u  n+ p) O
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
& O# G0 ]1 o& a7 k, c  {; [A unique entity of male-limited gonadotropin-
+ K+ a( M* s4 A+ ?independent precocious puberty, which is also known
7 d8 w) R+ J9 ~9 z8 ]: C- p9 yas testotoxicosis, may cause precocious puberty at a4 F6 a  B3 A4 l; _
very young age. The physical findings in these boys
1 c. P8 l( q( @* r9 U2 e  wwith this disorder are full pubertal development,
. v& m# ^  M* E) Z! Mincluding bilateral testicular growth, similar to boys
* g9 G" N. u" f: V: pwith CPP. The gonadotropin levels in this disorder5 X5 f7 s- [# V7 {% J, @
are suppressed to prepubertal levels and do not show
; A9 W- W9 g% d( t- |pubertal response of gonadotropin after gonadotropin-
& c" i$ i7 E; V" ?8 Ereleasing hormone stimulation. This is a sex-linked
; l( T( m7 H6 X6 T* iautosomal dominant disorder that affects only
# i  ?2 ~4 E/ h6 K( I0 R7 Hmales; therefore, other male members of the family
* H2 ^8 m% C; q( V5 |: lmay have similar precocious puberty.36 {! j- K# z9 l, ?: G1 L$ H
In our patient, physical examination was incon-
; Z/ ~. E5 T3 i* [3 Q; D4 Tsistent with true precocious puberty since his testi-8 T; R1 S2 s6 ~
cles were prepubertal in size. However, testotoxicosis- ^0 q* [$ z0 i% Z9 @9 A
was in the differential diagnosis because his father% @0 H* ?. `& Y; X6 M- @
started puberty somewhat early, and occasionally,
& D0 G% l0 v2 f: R9 ptesticular enlargement is not that evident in the+ p. {$ d! i+ d# z
beginning of this process.1 In the absence of a neg-
( q9 X8 b# ]: m$ dative initial history of androgen exposure, our- O( S+ R) r8 ?1 |
biggest concern was virilizing adrenal hyperplasia,
) u, u/ F, O' aeither 21-hydroxylase deficiency or 11-β hydroxylase! T9 \) m! Q9 [1 B# ?
deficiency. Those diagnoses were excluded by find-
+ p8 `8 w/ ^2 p$ |. `3 y' ling the normal level of adrenal steroids.
6 L" L5 Z2 I; XThe diagnosis of exogenous androgens was strongly
0 y3 }7 N! c. M5 Tsuspected in a follow-up visit after 4 months because- t5 K* X8 J4 h- l2 L
the physical examination revealed the complete disap-
" j9 v- J$ L+ @1 \: wpearance of pubic hair, normal growth velocity, and2 H9 c7 F- q4 g6 w% x
decreased erections. The father admitted using a testos-
2 B1 O$ \, B& \3 Zterone gel, which he concealed at first visit. He was
1 d5 C# M: ]5 Q- G8 Zusing it rather frequently, twice a day. The Physicians’! F; J2 n! }# ^( t) d+ D+ V
Desk Reference, or package insert of this product, gel or
1 t7 D: @2 U* ]# Icream, cautions about dermal testosterone transfer to
# f# S$ j8 t# F% c1 dunprotected females through direct skin exposure.
: m4 Q2 e9 v* _Serum testosterone level was found to be 2 times the( a( A' g1 P& l2 \3 Y6 b2 v* ~  l
baseline value in those females who were exposed to
% u7 Q  p' X' K& Y, o& Geven 15 minutes of direct skin contact with their male
# `; }' q, P7 \9 y8 C- ?6 x& Hpartners.6 However, when a shirt covered the applica-8 O3 \# ~! O# i! |! B
tion site, this testosterone transfer was prevented.
- K. q) f2 P' k: x2 d  _$ XOur patient’s testosterone level was 60 ng/mL,- ?- \. a6 {2 d5 _4 ~4 f  k  w; i: C9 ?2 y
which was clearly high. Some studies suggest that1 Y/ w$ W; Z' R+ b& F; r
dermal conversion of testosterone to dihydrotestos-
, Z9 V: o; D" {. f& _; j( Kterone, which is a more potent metabolite, is more
! E4 n$ d% d6 q& @. Hactive in young children exposed to testosterone
# Y& J) G' Y1 Y% J8 p, t4 B* texogenously7; however, we did not measure a dihy-
( \9 k. W# w; g: u9 L( fdrotestosterone level in our patient. In addition to$ X) b' ~( G- K/ F
virilization, exposure to exogenous testosterone in- ]$ @2 y+ h2 f  m, c0 E( ]: V
children results in an increase in growth velocity and9 B. r3 \* S+ L- D" C9 h
advanced bone age, as seen in our patient.
% B- q2 ^; o' @5 [$ q8 Q8 P' Z& ^5 fThe long-term effect of androgen exposure during
* Y  L4 L) z( e+ r% ]  d8 S0 ^1 fearly childhood on pubertal development and final
- a* n' |# j5 N% x; v7 @/ oadult height are not fully known and always remain  W" o4 {  g& u4 ~: m
a concern. Children treated with short-term testos-3 e; {. s- T+ d9 w' u: }9 j  m3 J
terone injection or topical androgen may exhibit some
& B) W9 B9 m2 @; X! t, W: aacceleration of the skeletal maturation; however, after
* `$ n( J, X3 K6 C& _  m! lcessation of treatment, the rate of bone maturation
  ?4 j) B) x8 r5 \9 f3 cdecelerates and gradually returns to normal.8,9% Y2 q" B, P  ^/ ]0 N2 R
There are conflicting reports and controversy
$ n$ p1 Z+ ?" V& Jover the effect of early androgen exposure on adult, A0 f$ y& u* f. O
penile length.10,11 Some reports suggest subnormal
( A, D, @3 [# N' V+ M5 U7 Gadult penile length, apparently because of downreg-' S+ O/ I# W6 C+ X  m1 o
ulation of androgen receptor number.10,12 However,
" @7 G+ o. _9 b7 H) cSutherland et al13 did not find a correlation between3 b- n: H  Q& @
childhood testosterone exposure and reduced adult; {- P, }" g2 I5 R) |9 ]% |
penile length in clinical studies.
8 w& E$ Y; y3 {# ^Nonetheless, we do not believe our patient is
+ l( m* @' ?# O* l1 U- X- @/ h5 Ugoing to experience any of the untoward effects from
8 b' ]0 _1 ]( a. i9 L9 i2 U1 ltestosterone exposure as mentioned earlier because" V8 W1 e# Z" l
the exposure was not for a prolonged period of time.9 b0 T6 D& q- w$ q( v
Although the bone age was advanced at the time of- S- I( H5 p! \" f# g: h
diagnosis, the child had a normal growth velocity at
9 t1 j6 r/ o  a) e1 k6 o) Hthe follow-up visit. It is hoped that his final adult) [" K3 y- a3 X' J: I. V
height will not be affected.
4 G& n! ]/ E9 N; A$ mAlthough rarely reported, the widespread avail-
. |( D: \7 D9 F' v7 Zability of androgen products in our society may
2 Z9 Z" I2 ?4 I6 N' r' v+ T& Dindeed cause more virilization in male or female
9 _& L, K  y( Z, fchildren than one would realize. Exposure to andro-
: T4 K/ ~) u6 c! a- jgen products must be considered and specific ques-
, P" w" g- d& x# Y4 \3 c. x% \$ M. E& Xtioning about the use of a testosterone product or
0 b2 `9 q6 ?; N' ygel should be asked of the family members during
+ k% w  @, x( M: V/ tthe evaluation of any children who present with vir-
, A0 P& J( ^" J/ `) I1 hilization or peripheral precocious puberty. The diag-
, x$ i6 g( S& ^2 H9 `- i( Lnosis can be established by just a few tests and by! C8 X/ N# i: b+ E  P
appropriate history. The inability to obtain such a
1 k9 B$ e0 M" Z6 h" l' Y/ Uhistory, or failure to ask the specific questions, may. Y, Y9 t) k* @  J
result in extensive, unnecessary, and expensive; L. H. P/ [; z9 S
investigation. The primary care physician should be
7 }9 S- u" D4 Naware of this fact, because most of these children. Z9 _: H/ C$ _4 s; @  T
may initially present in their practice. The Physicians’
4 T$ b# g' R# h* n7 dDesk Reference and package insert should also put a
0 h& a6 g! z5 [# a) R* H4 Awarning about the virilizing effect on a male or
! T$ N5 p; V+ \1 v( Jfemale child who might come in contact with some-0 n: ^$ {8 ], k: `1 F7 r% U. j
one using any of these products.( E8 S0 d# G9 g2 H$ D& U
References! e" W) x1 Q' l+ T7 p: M& m
1. Styne DM. The testes: disorder of sexual differentiation
8 \" W# t" }+ J$ v7 L' a8 D- t) L' Cand puberty in the male. In: Sperling MA, ed. Pediatric6 V, E1 ?' v. M( D  f
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
5 C& r- F: ?/ P8 j2002: 565-628.
1 n. K  \9 B( [  b( L8 i2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious0 n6 K+ S# `' }: D5 [* Y, p
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

6 r) i! M: Z2 w! P3 @: o  V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