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
6 h; G, T* e  w8 x: kBoy Induced by Indirect Topical+ a, O, I8 i; H/ J& J8 |/ c( a
Exposure to Testosterone! a* ^3 I: C3 b6 z& {
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
2 t: W8 o; V6 `9 T4 C, L3 iand Kenneth R. Rettig, MD1" Q' P2 [* t/ h  C
Clinical Pediatrics" U7 a# h9 a) x+ q0 c5 T
Volume 46 Number 6" I8 m7 m6 e4 q5 C' I1 N. A- ?
July 2007 540-543
3 [5 F! L: f2 I© 2007 Sage Publications
& A! J9 y, i* S2 N. i2 g10.1177/0009922806296651
  q6 L, \; ^+ ^) x2 fhttp://clp.sagepub.com
& N/ r) o5 y, Y3 c7 \7 K% |# Phosted at
8 B  H4 }8 K3 Jhttp://online.sagepub.com* @6 ^. |7 B# e4 L, b
Precocious puberty in boys, central or peripheral,
2 I; E" J, l" Yis a significant concern for physicians. Central
) W5 y& T$ {( K$ eprecocious puberty (CPP), which is mediated
. D# n( j% v1 X* `through the hypothalamic pituitary gonadal axis, has. Q3 f+ c! o0 F' R( `8 k3 @8 _
a higher incidence of organic central nervous system# \# V- m4 P1 g  S* D
lesions in boys.1,2 Virilization in boys, as manifested
. j. o( @1 H- ?" p; g8 P; m7 cby enlargement of the penis, development of pubic
, q" P- n* [" i' L: s! _; Qhair, and facial acne without enlargement of testi-
0 \; w- E" |& L4 W5 q6 S( P+ mcles, suggests peripheral or pseudopuberty.1-3 We( e/ q9 N5 c- V( c
report a 16-month-old boy who presented with the
+ T8 W9 _4 q8 Wenlargement of the phallus and pubic hair develop-2 N- L) C" a. ~( h% r7 ?8 Y
ment without testicular enlargement, which was due
* i; ]3 ~' H2 x& Lto the unintentional exposure to androgen gel used by( t  M) \5 l& v) k8 V6 w5 L: r
the father. The family initially concealed this infor-  b! z# l9 q/ n  b
mation, resulting in an extensive work-up for this
; `! Z$ I( H, h' i/ ]! echild. Given the widespread and easy availability of  k5 g1 Z# I- q$ z4 j
testosterone gel and cream, we believe this is proba-+ M3 ~( F+ M. M
bly more common than the rare case report in the, [: t0 ?6 P/ I% [
literature.4
% ]) |, G" o) y  YPatient Report
( z7 v, B. N. j" s* xA 16-month-old white child was referred to the
3 s# u/ r& M+ h! l8 E/ o$ I4 I$ Dendocrine clinic by his pediatrician with the concern
: r" ?  _' \9 r1 nof early sexual development. His mother noticed8 f; M& [# _! H1 m. f* N" F
light colored pubic hair development when he was/ y9 i3 G) I" V2 X5 Z2 L
From the 1Division of Pediatric Endocrinology, 2University of
2 z) q3 l: T( o" [4 T* bSouth Alabama Medical Center, Mobile, Alabama., }1 ]; D( Q& V
Address correspondence to: Samar K. Bhowmick, MD, FACE,
3 }+ S2 ^2 \6 }7 M, uProfessor of Pediatrics, University of South Alabama, College of
& @! ?+ o9 i! u0 o. D0 f& hMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;$ Y! {6 T% U" H2 q
e-mail: [email protected].9 o5 R' ^8 [7 O3 y) K$ ?
about 6 to 7 months old, which progressively became4 Q; c: `6 v# \% m" ]
darker. She was also concerned about the enlarge-! q0 V, }6 F. E" q
ment of his penis and frequent erections. The child
4 P6 o* T: b; {% w2 _was the product of a full-term normal delivery, with
4 e- l. F: w" A! u: v9 k0 t3 Sa birth weight of 7 lb 14 oz, and birth length of
2 H3 l7 I1 k9 s  Q0 y& P* V4 U20 inches. He was breast-fed throughout the first year; x0 w8 a4 R7 J4 S0 S% y" |
of life and was still receiving breast milk along with/ S2 O! k0 J* I2 L  }
solid food. He had no hospitalizations or surgery,
) y% l. V" W6 f( R1 f  g6 M1 ?; @and his psychosocial and psychomotor development
+ E! U, ^4 K- X6 \/ e6 j9 uwas age appropriate.2 }0 o9 w- H; o) P' J
The family history was remarkable for the father,
0 P& b* x) E) l7 awho was diagnosed with hypothyroidism at age 16,4 Y: b% Y# `# i2 N4 [$ l) h
which was treated with thyroxine. The father’s
( R- f5 b2 M1 M3 }, ]4 E% Uheight was 6 feet, and he went through a somewhat
: N3 Y" c. |: i( N9 ?9 \( c  E* Mearly puberty and had stopped growing by age 14.
! _" |! P& f  h% H$ v$ TThe father denied taking any other medication. The% d8 Y1 x! b3 S# {
child’s mother was in good health. Her menarche
' v$ R& E( S8 L3 h) Mwas at 11 years of age, and her height was at 5 feet# ^* C. c8 P! ^& f5 }$ O
5 inches. There was no other family history of pre-
+ _! t, h% s2 r! f* C* acocious sexual development in the first-degree rela-5 ?4 J+ R8 L! y+ r
tives. There were no siblings.
* I0 J; p. r! r+ L" p3 MPhysical Examination
8 I. @* g7 P6 y; Z( M8 k5 lThe physical examination revealed a very active,* ~# P. S$ w9 A8 l6 C' P
playful, and healthy boy. The vital signs documented/ q+ U% M9 T& Y$ N9 Z9 E! l
a blood pressure of 85/50 mm Hg, his length was  \' n. k7 z) r% U
90 cm (>97th percentile), and his weight was 14.4 kg! {, X$ ~' a4 ~- w# x5 O) |+ C
(also >97th percentile). The observed yearly growth- c# U' {: I* z% X) \
velocity was 30 cm (12 inches). The examination of
5 ?! D3 v! K! @) {& m9 Qthe neck revealed no thyroid enlargement.) R5 @' m; c  G
The genitourinary examination was remarkable for+ X, {9 w; c! h+ d/ o( }+ S
enlargement of the penis, with a stretched length of
3 X% Q8 H8 h$ S& i  Y. h% ]8 cm and a width of 2 cm. The glans penis was very well
$ P  `, g% Y" N# [5 Mdeveloped. The pubic hair was Tanner II, mostly around+ d: ^2 v/ U$ c* V* r. D& N
540
2 H' u  }9 U: o7 _; cat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from- b# J8 k" c1 v, L8 U, w
the base of the phallus and was dark and curled. The
3 k3 R. q6 W! wtesticular volume was prepubertal at 2 mL each.- p& y$ z% I$ q4 a0 @' C
The skin was moist and smooth and somewhat
7 T* A3 k6 ?, m6 uoily. No axillary hair was noted. There were no
3 ^) I$ z5 e3 w+ B+ Cabnormal skin pigmentations or café-au-lait spots.
. u& E! W, c( L: ^' [& ENeurologic evaluation showed deep tendon reflex 2+! a) c0 P# m" \& t. U
bilateral and symmetrical. There was no suggestion9 P- G% }* q- K. m1 m- C' r
of papilledema.8 s. p( S; Y# u5 G/ e. L/ o
Laboratory Evaluation
9 N$ ^) y0 u; `: oThe bone age was consistent with 28 months by
+ f: l/ I3 y8 X- w2 Gusing the standard of Greulich and Pyle at a chrono-
7 O$ \# C$ u  M+ p6 t9 I9 }6 Nlogic age of 16 months (advanced).5 Chromosomal
& c5 U/ R4 ?4 K" w! u6 B$ Akaryotype was 46XY. The thyroid function test, V+ ^, i  d" D8 E8 _/ _4 k
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
6 `$ {0 l8 F$ }& blating hormone level was 1.3 µIU/mL (both normal).
! }8 v8 G- J4 O% ]. y& s+ n. N: E7 PThe concentrations of serum electrolytes, blood
2 H# ^1 q# c/ k* n, A( ?2 Ourea nitrogen, creatinine, and calcium all were9 \. F, i7 F5 X% K
within normal range for his age. The concentration
, m& ], X: i2 k( A+ ^of serum 17-hydroxyprogesterone was 16 ng/dL; Q* Z& A0 U! s" [6 n" @7 b
(normal, 3 to 90 ng/dL), androstenedione was 205 P7 I/ R+ w' F9 |" `5 ]; I
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-: U+ C: e0 d. S& H4 y- [" \, }& [
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
  T( p5 i! j$ m' A; `0 Adesoxycorticosterone was 4.3 ng/dL (normal, 7 to8 X% h- x5 ?0 F8 e' k% u0 L3 Y
49ng/dL), 11-desoxycortisol (specific compound S)
/ a4 Q% v+ g  J* E" Awas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-/ u% w- H+ m- ~( v, o/ G
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
" s) I/ B$ P* H+ M3 i! F( n, W0 rtestosterone was 60 ng/dL (normal <3 to 10 ng/dL),( g! c3 \* Z2 d" N+ g) C4 p
and β-human chorionic gonadotropin was less than2 Q3 ]5 w0 q2 P8 p9 s
5 mIU/mL (normal <5 mIU/mL). Serum follicular- a0 e6 b, W- Z% `  n0 s1 W6 p
stimulating hormone and leuteinizing hormone
% u0 h3 I  R: L2 E5 P- \& E+ c4 Qconcentrations were less than 0.05 mIU/mL$ \: p1 R3 i* Z. q4 ]
(prepubertal).
; \/ a( j9 A0 f  P& _8 g/ l! ^2 Y1 gThe parents were notified about the laboratory
2 p1 u& [. H5 f( ?" M' G" lresults and were informed that all of the tests were
; d/ \( {/ c  f4 Y1 H0 k, pnormal except the testosterone level was high. The
; a" k* _; S; K( C- y& M, _  c8 Ufollow-up visit was arranged within a few weeks to& i4 Z, P5 [) n# [6 r* I* p3 t
obtain testicular and abdominal sonograms; how-# ^6 }5 u$ N9 d; A
ever, the family did not return for 4 months.
& K! ?8 _3 ]: k5 G- ~, F' e( r) YPhysical examination at this time revealed that the
5 L9 u8 q* D! i  [( Q* T4 q; K  dchild had grown 2.5 cm in 4 months and had gained
# y' o, V; k) [6 [0 P! Y2 kg of weight. Physical examination remained
& g) J0 c, f* Y, s& e' j: xunchanged. Surprisingly, the pubic hair almost com-6 m8 g( x. L9 w9 S5 S% h' s
pletely disappeared except for a few vellous hairs at
8 [+ m* `  g8 ?+ @# Pthe base of the phallus. Testicular volume was still 2( y/ c. y0 x; |8 `
mL, and the size of the penis remained unchanged.0 T7 [. U' o" v) t3 K6 t
The mother also said that the boy was no longer hav-) y0 v7 V% Y! A/ L. v' b+ {: g
ing frequent erections.
6 ?1 F( n8 d1 F7 H  T$ P8 a* mBoth parents were again questioned about use of
: N* U0 j+ @7 f) s+ S7 fany ointment/creams that they may have applied to1 t7 d- I! a( v+ D6 q
the child’s skin. This time the father admitted the
/ P/ X3 X+ c( k: `% FTopical Testosterone Exposure / Bhowmick et al 5418 x$ O* `# F% g7 @
use of testosterone gel twice daily that he was apply-, [4 g7 O# `5 K5 k
ing over his own shoulders, chest, and back area for
/ X) g3 t7 L8 A1 Za year. The father also revealed he was embarrassed
% I4 E8 v0 L: A/ N; T% yto disclose that he was using a testosterone gel pre-
5 H, s6 |) e) {' p5 C' qscribed by his family physician for decreased libido. o. d% s, P% F! t9 _2 E! E' j' n" d  \
secondary to depression.
9 O# ?% w) D( X: m7 d5 r9 ~0 vThe child slept in the same bed with parents.( n3 O0 ^7 O5 F9 H, n3 |
The father would hug the baby and hold him on his/ t) u( A& K: `" V
chest for a considerable period of time, causing sig-, k( K$ `6 C) s  ^+ `
nificant bare skin contact between baby and father.- _0 ~% Y" D, {& D0 b) B
The father also admitted that after the phone call,! X" S: c+ A* n  }1 A' _7 e
when he learned the testosterone level in the baby4 a4 W9 m. C- w9 m; Y
was high, he then read the product information
0 Z, P, z' _% b" V* y5 fpacket and concluded that it was most likely the rea-, x+ d: F, }2 @5 O+ c. T5 t
son for the child’s virilization. At that time, they
7 R# f1 \9 E" d3 W: ~4 ]decided to put the baby in a separate bed, and the) s8 U$ h: k$ j! ], y
father was not hugging him with bare skin and had
5 [( h! U2 J* g( |been using protective clothing. A repeat testosterone9 x. J+ k* b: R
test was ordered, but the family did not go to the! G. z! F8 z1 X0 `. r
laboratory to obtain the test.
; T3 i8 M/ p! ?) S, t! T9 \Discussion; O2 K) A# z3 i
Precocious puberty in boys is defined as secondary: b: u- Z) t2 w3 X' x
sexual development before 9 years of age.1,4& @4 _' Y+ w% u/ P: C9 ~
Precocious puberty is termed as central (true) when/ x5 A, `- U1 S4 V- ]
it is caused by the premature activation of hypo-( I# @$ Y5 j- }' k0 u/ }
thalamic pituitary gonadal axis. CPP is more com-, ?( `7 j9 P1 m/ b
mon in girls than in boys.1,3 Most boys with CPP  n- I) j$ b, `$ v8 [
may have a central nervous system lesion that is. a8 K) _  Y8 I5 \! |
responsible for the early activation of the hypothal-
4 R. k3 r# V6 J( Y0 Iamic pituitary gonadal axis.1-3 Thus, greater empha-( u8 i9 p+ s8 s( `2 ?$ ^
sis has been given to neuroradiologic imaging in
8 ^5 o2 ?) Z. T0 M: D2 Kboys with precocious puberty. In addition to viril-
$ w; O( A7 ~! Q# A" }- a% kization, the clinical hallmark of CPP is the symmet-
& X8 T7 ]6 M9 _) Y6 U5 K* ]rical testicular growth secondary to stimulation by* y; |5 W( Q, m7 f1 P
gonadotropins.1,3
5 ^  x2 z3 G- _0 \* G& B8 \Gonadotropin-independent peripheral preco-
" C; ~! S2 r" Acious puberty in boys also results from inappropriate  o$ h* O! p; ^6 Z' j8 a
androgenic stimulation from either endogenous or
- o* k5 L3 }% ?* U: b9 ^$ }* {6 R' [( qexogenous sources, nonpituitary gonadotropin stim-
/ e+ i) d/ \, F& Xulation, and rare activating mutations.3 Virilizing
/ A& J# _* f: ]+ T+ Gcongenital adrenal hyperplasia producing excessive! U0 O( U7 i! V$ P0 k
adrenal androgens is a common cause of precocious
- u" O; E% y9 v, B( zpuberty in boys.3,4  t+ T, ~! H0 [1 N
The most common form of congenital adrenal, w: H! |* L! @
hyperplasia is the 21-hydroxylase enzyme deficiency.3 m4 i* Q) I3 a% n" e
The 11-β hydroxylase deficiency may also result in
" x7 m/ v( Y, Y8 {4 X0 a3 xexcessive adrenal androgen production, and rarely,
: P, V& r! c+ M- ?" l- Han adrenal tumor may also cause adrenal androgen2 t' K  N& [/ P1 ]
excess.1,3; v* a$ c% o; s; X6 b/ q
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
9 _3 [) w+ l# @$ W542 Clinical Pediatrics / Vol. 46, No. 6, July 2007( l0 R4 e5 ?9 v
A unique entity of male-limited gonadotropin-
3 K% ]" M; h# @5 K# Q) lindependent precocious puberty, which is also known2 }& i' S# e5 w; L5 h" l1 B2 W4 w+ ?
as testotoxicosis, may cause precocious puberty at a  K, w5 U, n( f
very young age. The physical findings in these boys! u' @# h' z) `% h( n: H# S
with this disorder are full pubertal development,
5 l/ t% A# m0 o5 s3 l0 Mincluding bilateral testicular growth, similar to boys; }  W! E7 p# Q0 u7 `6 l& C
with CPP. The gonadotropin levels in this disorder
, r! L) L" N' f1 nare suppressed to prepubertal levels and do not show: v1 |  d) M1 X( Z
pubertal response of gonadotropin after gonadotropin-
6 l% o/ x, R" f% f8 jreleasing hormone stimulation. This is a sex-linked" A4 D# @& n$ V% X
autosomal dominant disorder that affects only& Q' X1 p/ B, r( U2 ^- y. Z
males; therefore, other male members of the family
' O5 S, X  |' t3 jmay have similar precocious puberty.3! q4 J2 W, n1 m4 A" U
In our patient, physical examination was incon-
8 _% q) D1 ^5 X* }* w8 @3 J& esistent with true precocious puberty since his testi-
# g9 G( y6 \7 zcles were prepubertal in size. However, testotoxicosis; h9 l' Z. d: }8 t) q
was in the differential diagnosis because his father
% ?  @: G% i$ w$ ystarted puberty somewhat early, and occasionally,
# o1 h  u: d/ d$ Btesticular enlargement is not that evident in the
  c4 k1 p: G" V, `$ Cbeginning of this process.1 In the absence of a neg-3 |7 V+ v' X6 s" z7 D
ative initial history of androgen exposure, our7 h. ^! d% P9 E
biggest concern was virilizing adrenal hyperplasia,7 R: y  I* W, {, f
either 21-hydroxylase deficiency or 11-β hydroxylase1 u5 E3 j6 C) Z" B  D
deficiency. Those diagnoses were excluded by find-7 x, W9 k, x- e9 x' q+ P, L- O
ing the normal level of adrenal steroids.9 x% [& _: m( `+ x# c
The diagnosis of exogenous androgens was strongly, Y9 \4 q7 {; [6 Y
suspected in a follow-up visit after 4 months because: P4 V) N: I  |, d" X1 [( E
the physical examination revealed the complete disap-3 Y$ R7 y. T6 V' f, I
pearance of pubic hair, normal growth velocity, and
* g% G0 ~# ^% [" j0 [7 Vdecreased erections. The father admitted using a testos-/ ?7 a3 W9 a( m! q: v( `5 A) y1 P
terone gel, which he concealed at first visit. He was
3 _% Y- h+ o8 h1 C$ w; ]6 u9 fusing it rather frequently, twice a day. The Physicians’; J9 F$ B2 v3 u& }  S* ]+ ^
Desk Reference, or package insert of this product, gel or# a: V6 K! m8 u& ~# E- g
cream, cautions about dermal testosterone transfer to
4 _0 D: k# ~  o- J- c/ F) y7 ^3 `( junprotected females through direct skin exposure.
: }) U/ Y: W8 z/ B. x3 |Serum testosterone level was found to be 2 times the
. B: x) G  x" @, P9 E' u  Q# F* o2 \. mbaseline value in those females who were exposed to
& ~9 @: y0 J& Q$ ceven 15 minutes of direct skin contact with their male
6 i8 h- q, V7 zpartners.6 However, when a shirt covered the applica-
; o( P) @8 X2 d* ~& t/ r! g! ]tion site, this testosterone transfer was prevented.4 S8 l7 i1 c# F; z
Our patient’s testosterone level was 60 ng/mL,3 h) M, i1 T; w% K+ T' r: }
which was clearly high. Some studies suggest that. u2 r4 g8 h" K$ G- k. N
dermal conversion of testosterone to dihydrotestos-
4 g9 N+ D) g" Qterone, which is a more potent metabolite, is more8 U9 }& B8 S% N0 ?) \$ J* D) S
active in young children exposed to testosterone+ R$ G6 c9 _( ]( i/ E* v' a
exogenously7; however, we did not measure a dihy-( T$ c  }+ I  t, i
drotestosterone level in our patient. In addition to, C. J1 u% E, A7 u$ e
virilization, exposure to exogenous testosterone in9 I) r6 ]9 ?  _* o4 _
children results in an increase in growth velocity and6 u& \; ~& m  o9 ~
advanced bone age, as seen in our patient.2 E: O; I9 k% i) s
The long-term effect of androgen exposure during
. a9 t; a  ?" bearly childhood on pubertal development and final$ Q7 {* W+ |# K, y9 T# }1 t6 ~
adult height are not fully known and always remain  O- L# f  `" G% _
a concern. Children treated with short-term testos-0 {. S; K' A  _
terone injection or topical androgen may exhibit some" S: z4 @. Z! ]) c9 X
acceleration of the skeletal maturation; however, after
0 w% ?7 `3 ^" q( J* r5 rcessation of treatment, the rate of bone maturation& u4 `" d1 K/ o0 j; w0 O/ G
decelerates and gradually returns to normal.8,9
) p( d  a2 \6 d1 cThere are conflicting reports and controversy7 X, D+ s; e. z/ G$ Q8 `
over the effect of early androgen exposure on adult
) ~) @; j3 T* z: V. |/ H$ Vpenile length.10,11 Some reports suggest subnormal
$ X6 K! j" X# `7 Eadult penile length, apparently because of downreg-
6 ?' A5 G' g: Aulation of androgen receptor number.10,12 However,
4 n' |6 t, x; `3 R( s# ^1 O8 mSutherland et al13 did not find a correlation between6 C" s+ {1 l) z" g: m- J7 |1 i
childhood testosterone exposure and reduced adult
& j1 W7 H# x9 i/ p: J! qpenile length in clinical studies.
' X  K4 t  x# ~0 x: J& q& rNonetheless, we do not believe our patient is1 X; ]3 l$ y0 J2 c
going to experience any of the untoward effects from+ N3 q* U8 K, o6 U
testosterone exposure as mentioned earlier because8 c% ]: O2 w8 [% o5 S) {! j* {
the exposure was not for a prolonged period of time.
% Y4 X' k) E- v4 K7 z2 VAlthough the bone age was advanced at the time of1 b" i) v0 g$ U, h7 r2 P- M8 b
diagnosis, the child had a normal growth velocity at( N. c9 ^- H' m, p, u; e4 v
the follow-up visit. It is hoped that his final adult# H) @* \+ c; r0 b7 r# S# W
height will not be affected.
( r; `( J: t, z0 fAlthough rarely reported, the widespread avail-
+ D9 B/ `- r4 lability of androgen products in our society may
/ [) k$ ]6 h7 Zindeed cause more virilization in male or female
4 E$ ]$ f" H: Bchildren than one would realize. Exposure to andro-
+ M" n7 O. E% f( ~& p) sgen products must be considered and specific ques-
8 @- ?2 H4 B/ M$ Ntioning about the use of a testosterone product or
+ F  W' m1 Y6 z8 |gel should be asked of the family members during/ H: N1 J+ `1 m& M1 x9 v. i
the evaluation of any children who present with vir-: g: E% R+ b. N7 r, Z/ f
ilization or peripheral precocious puberty. The diag-2 e; `5 Z7 k' L
nosis can be established by just a few tests and by: v4 @$ Y7 e% W. R3 C( M4 }
appropriate history. The inability to obtain such a8 [* h3 U$ Y/ M& r: @2 T
history, or failure to ask the specific questions, may+ ?- L* e) F0 G, \- H
result in extensive, unnecessary, and expensive
; r# e) O1 A  q5 L5 Tinvestigation. The primary care physician should be
" U( ~+ R2 c1 L/ ]& ^2 n/ jaware of this fact, because most of these children
' U; a: f9 S. _- U: Hmay initially present in their practice. The Physicians’
" O+ X" F6 |7 h; [Desk Reference and package insert should also put a  V5 |7 D  F3 a
warning about the virilizing effect on a male or
  s; [. O  ^/ lfemale child who might come in contact with some-
& ~* u0 g# S4 d1 Vone using any of these products.
) k/ e: u. m5 i( M2 d) ?1 SReferences: h4 R6 O3 j  C0 i
1. Styne DM. The testes: disorder of sexual differentiation! r1 t% p) H# b) {
and puberty in the male. In: Sperling MA, ed. Pediatric0 a6 }6 Q+ L( y/ D
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
. k7 P1 `! \& C# b7 r7 P( e4 j# r2002: 565-628.  d* S* t# ?3 U. ]) G0 T( x/ n
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious6 k* ?4 f& a2 b( h
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
5 g8 G1 G. q' ^7 R1 o4 VBoy Induced by Indirect Topical# ^- [% [' D; s! _9 |9 I
Exposure to Testosterone
4 ?2 z* q% E3 r. N, R7 Q# |  wSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
  F2 a6 z  {- I4 j' |and Kenneth R. Rettig, MD1
" s: g* B8 B+ _8 M# w2 _; OClinical Pediatrics
$ F3 A" w' Y3 r0 V/ u& A5 UVolume 46 Number 6
2 s. D% N, d' b+ \, d5 C' yJuly 2007 540-543% Z( `  [0 F* M0 E- U3 j8 c
© 2007 Sage Publications: l# f8 G+ B# h' K; i3 E6 L
10.1177/0009922806296651
% ?+ ^( |7 t- ]5 D, h- `8 m- n/ m7 Hhttp://clp.sagepub.com4 [. z. S+ x$ A$ x7 Y+ n
hosted at
+ b7 @7 R, o2 ~http://online.sagepub.com
, w" ^5 h: o1 Q" f' i2 xPrecocious puberty in boys, central or peripheral,
# U" u0 _3 z7 R0 ?. lis a significant concern for physicians. Central) m& y# Y/ M- T) g
precocious puberty (CPP), which is mediated% V& h) O/ k* @4 r4 l
through the hypothalamic pituitary gonadal axis, has
5 N. F& B$ D5 s7 |! c1 V9 Q+ @2 Q7 ra higher incidence of organic central nervous system- K2 ]4 L' Z1 E/ B* K- f
lesions in boys.1,2 Virilization in boys, as manifested
' J, k- \! ~# ?, Mby enlargement of the penis, development of pubic' Z3 X3 A) u( R2 ~% O
hair, and facial acne without enlargement of testi-
9 P! O( K7 T: X. E- @* |cles, suggests peripheral or pseudopuberty.1-3 We
) e) Y1 q8 ?% T; K7 vreport a 16-month-old boy who presented with the% l7 k) m9 U5 m2 w7 }
enlargement of the phallus and pubic hair develop-' ]" B& J4 R3 i/ t$ B7 t% S
ment without testicular enlargement, which was due
9 k2 ^7 s2 m1 S# sto the unintentional exposure to androgen gel used by
( l: G! z2 M$ ]/ l' F; ^, R# b. kthe father. The family initially concealed this infor-2 ~6 ~  ~  k8 w+ {  {
mation, resulting in an extensive work-up for this
. |- z$ w( ^, ^. |child. Given the widespread and easy availability of
7 y/ Z2 E) s2 T8 htestosterone gel and cream, we believe this is proba-3 }' `$ `: n# G5 P3 g" P
bly more common than the rare case report in the
9 A2 T; D4 |- C. ]- ?literature.4
, \1 p% d1 A( |' G9 i5 zPatient Report2 D2 _$ x% k4 P. \8 }2 o
A 16-month-old white child was referred to the
6 y* P' G/ G& a) Sendocrine clinic by his pediatrician with the concern" [7 N5 q5 {/ T0 Q$ @1 K
of early sexual development. His mother noticed" e" N) j6 g: a0 ]+ s
light colored pubic hair development when he was
2 [$ i7 B9 @9 u- P' {! R1 MFrom the 1Division of Pediatric Endocrinology, 2University of
8 m4 f# p( G# G$ J& mSouth Alabama Medical Center, Mobile, Alabama.5 W; f. R1 Z: n3 K: J
Address correspondence to: Samar K. Bhowmick, MD, FACE,. [7 D  O' a5 |% N9 L
Professor of Pediatrics, University of South Alabama, College of/ E5 [! Q. X# P1 O; O& @
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
; i( P, K+ t& b% A$ q* o5 we-mail: [email protected].
. f9 T" s. h8 ^- @8 y9 V- Sabout 6 to 7 months old, which progressively became% E2 @! }  l# g' K! I! U' ]
darker. She was also concerned about the enlarge-
9 ?% x% y, @* S! A/ l9 H" G, N" @ment of his penis and frequent erections. The child0 \' t4 u, M7 Y, e" L- _, E
was the product of a full-term normal delivery, with
& L* X0 _: j! ~) q* |; R/ ba birth weight of 7 lb 14 oz, and birth length of
0 x. C' u# U  u. z; n20 inches. He was breast-fed throughout the first year$ C& X' M/ l* {; K: r
of life and was still receiving breast milk along with
# O9 V8 H- a3 D* v7 U! O5 Gsolid food. He had no hospitalizations or surgery,, K1 ~5 m3 A0 [* z
and his psychosocial and psychomotor development
  A1 |7 R0 V3 ~- y& p" hwas age appropriate.  |3 g8 N) ]3 o: ~8 h
The family history was remarkable for the father,2 \  x  B* B* B$ c0 b
who was diagnosed with hypothyroidism at age 16,& f" ~/ a7 o4 n
which was treated with thyroxine. The father’s
4 e) ]9 f: {4 D% Z2 ]* ^7 _height was 6 feet, and he went through a somewhat
' d2 Y8 y( H! ^' J$ J! e. Dearly puberty and had stopped growing by age 14.
8 h- h7 E! q3 }! [* hThe father denied taking any other medication. The7 r, W$ ]( a+ A* e" ]$ z: ]5 y
child’s mother was in good health. Her menarche
7 B) J* k2 @# B5 Nwas at 11 years of age, and her height was at 5 feet
6 m1 H# f; L% N5 x8 {$ w5 inches. There was no other family history of pre-
* f" `# [3 k: n2 M; }cocious sexual development in the first-degree rela-, |7 _% T3 D6 z# s& i% t# q6 `
tives. There were no siblings.
. o, D8 M8 b- |* wPhysical Examination
3 H0 v+ W" e& \The physical examination revealed a very active,* Y% O& w% a6 l' C! U1 i! S
playful, and healthy boy. The vital signs documented
0 Y* H2 z9 [2 ?+ p6 Z9 u5 L# Ba blood pressure of 85/50 mm Hg, his length was
* F- t. s* F8 C# W( z3 P4 t90 cm (>97th percentile), and his weight was 14.4 kg
9 o/ s  B1 U" O6 W(also >97th percentile). The observed yearly growth
& K7 r; |( I/ D  |* x) @- pvelocity was 30 cm (12 inches). The examination of
7 g  p" c  Q: [8 B% F6 athe neck revealed no thyroid enlargement.
% X, R# M' d4 g" v+ ?# P7 ~The genitourinary examination was remarkable for3 z2 ^0 r2 X, ?
enlargement of the penis, with a stretched length of
! k# j* r) Y- o& K( v: p8 cm and a width of 2 cm. The glans penis was very well
) }2 {5 V3 m% _5 E( x& y6 wdeveloped. The pubic hair was Tanner II, mostly around0 @6 x& d8 {1 M9 z
540
0 Q/ ~, ?% `" r/ D7 i7 dat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
, e- N" X' f; D& Fthe base of the phallus and was dark and curled. The
( O. B' N$ M5 |7 Z( U+ y2 Q  mtesticular volume was prepubertal at 2 mL each.
- _& V. ]* f3 |, r+ O' sThe skin was moist and smooth and somewhat
. b+ a8 }$ K# D( Moily. No axillary hair was noted. There were no
3 x" {: J- c- O; Uabnormal skin pigmentations or café-au-lait spots.$ u" ]. L+ _9 @5 {& D
Neurologic evaluation showed deep tendon reflex 2+
; a( j- f+ q" U- Cbilateral and symmetrical. There was no suggestion
+ I4 k7 L4 r. _/ l! K3 wof papilledema.
# R' X* X  I& jLaboratory Evaluation
& T4 i' u- y: R. }2 hThe bone age was consistent with 28 months by6 `1 ]% u2 s9 d* n
using the standard of Greulich and Pyle at a chrono-8 G5 T4 m8 q! J" ~* ?, M
logic age of 16 months (advanced).5 Chromosomal0 ]& o4 k# C7 I' e3 D% x
karyotype was 46XY. The thyroid function test
! ~6 u: f; p7 E! b+ b: ^1 Nshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
6 D( j1 }# k1 i" ?1 \lating hormone level was 1.3 µIU/mL (both normal).5 G+ F) q7 z& s2 S) d  C: F3 R1 [
The concentrations of serum electrolytes, blood1 [( H0 q1 m4 r  B
urea nitrogen, creatinine, and calcium all were
; Z0 x% O8 B# h1 r+ x9 {; @within normal range for his age. The concentration
% Y( Q7 _. N' q( ]4 i9 g, \of serum 17-hydroxyprogesterone was 16 ng/dL
% T  q; u1 m8 y7 n' d% r(normal, 3 to 90 ng/dL), androstenedione was 20: c& P# Y9 `4 d* j
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
  n' _& l1 |+ ?terone was 38 ng/dL (normal, 50 to 760 ng/dL),9 \7 e. ~- U; p' L8 ?
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
, t: M0 C3 n8 Q4 |- c6 ]. P) t; [49ng/dL), 11-desoxycortisol (specific compound S)/ l& j& F8 m( p
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-  s9 o0 S: }1 W8 ~; \
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
( ?5 [8 r. ?% q! j5 btestosterone was 60 ng/dL (normal <3 to 10 ng/dL),, P! b2 M' L9 T8 A7 g2 [2 W9 F
and β-human chorionic gonadotropin was less than
/ N% Q6 A3 p- }" A8 O5 mIU/mL (normal <5 mIU/mL). Serum follicular2 }3 _7 ^  F2 V* }4 |' A4 M
stimulating hormone and leuteinizing hormone7 c9 f8 T3 e$ v' ]" P
concentrations were less than 0.05 mIU/mL
& |% ?4 W# X3 Z* T5 }(prepubertal).6 K8 l! T7 }. k( M
The parents were notified about the laboratory9 ]& }! x! p& a/ B4 }: U
results and were informed that all of the tests were
) g& i& H7 x" A7 a" e) Pnormal except the testosterone level was high. The! ^1 }5 \* S" S8 ~! s
follow-up visit was arranged within a few weeks to. l0 d: S7 z1 `
obtain testicular and abdominal sonograms; how-( o3 y: B% A6 H: n
ever, the family did not return for 4 months.0 V/ R. _: M2 G- @$ R
Physical examination at this time revealed that the" o+ _. P9 s. S
child had grown 2.5 cm in 4 months and had gained5 x. I* M  h4 l2 v/ w6 ^9 t# F
2 kg of weight. Physical examination remained9 o- O9 H5 p0 s
unchanged. Surprisingly, the pubic hair almost com-, o. ~3 {7 k/ r3 f
pletely disappeared except for a few vellous hairs at* u6 m. e6 D$ K- h% I9 l% c. Q
the base of the phallus. Testicular volume was still 2; t$ I: ?2 s( T, ~. c( B* U
mL, and the size of the penis remained unchanged.
1 n5 Z) k' s' \The mother also said that the boy was no longer hav-  }5 I* a+ ?! V! U  ^: q* M/ F( p
ing frequent erections.
$ m3 H3 d& x6 |3 T* j1 Z  I( dBoth parents were again questioned about use of
, ?* b1 X# q1 [. Nany ointment/creams that they may have applied to
8 U6 G& v1 @6 o1 W% t7 D6 }the child’s skin. This time the father admitted the
! U# m! v. j( i6 ^Topical Testosterone Exposure / Bhowmick et al 541
& B: d" a1 J$ w* C* huse of testosterone gel twice daily that he was apply-
8 V. p: J" N% `( O% R8 @ing over his own shoulders, chest, and back area for/ Y2 R! B0 {: u, T  y0 N) d
a year. The father also revealed he was embarrassed
0 n& w! i5 @- d3 E0 E& }" h, u0 fto disclose that he was using a testosterone gel pre-2 }0 o+ l! O% z; k
scribed by his family physician for decreased libido* q5 V1 e. v7 |, e% M5 ~
secondary to depression.6 M, G: C+ [$ \% `+ e7 w  ~  K& |
The child slept in the same bed with parents.
, Q5 g# V$ ]" @+ \7 k4 i( Q5 ?The father would hug the baby and hold him on his1 f6 W' ^* Q: N( F' u' G
chest for a considerable period of time, causing sig-/ @2 o6 }1 F4 _
nificant bare skin contact between baby and father.
/ H+ j% y) P" C$ T# O; bThe father also admitted that after the phone call,$ x5 C0 r7 B4 o& X) j! A, n* A9 T
when he learned the testosterone level in the baby0 R/ U  g% @7 e0 h5 s
was high, he then read the product information% A$ k5 F2 {) u" V& G
packet and concluded that it was most likely the rea-: d+ ?  z3 g& p2 X. O1 J
son for the child’s virilization. At that time, they
: n9 H2 I( m! _, fdecided to put the baby in a separate bed, and the
: @  B  x9 h1 h0 K& h" B1 Ofather was not hugging him with bare skin and had1 R" g! H3 ~* H- b0 Z! b! u# }
been using protective clothing. A repeat testosterone
7 N% d! v+ o$ Z) C& k& b/ utest was ordered, but the family did not go to the
1 P% e0 _4 s8 nlaboratory to obtain the test.
, u7 }( ?5 J% L( m2 B5 tDiscussion
4 R6 N0 A- y- D  d7 H8 FPrecocious puberty in boys is defined as secondary
) w/ V, {5 S+ j" {( e* x) vsexual development before 9 years of age.1,4
+ @8 ?3 [" }' Y7 p, EPrecocious puberty is termed as central (true) when
+ q8 m7 v3 S2 d3 z8 _# J" N6 r" Eit is caused by the premature activation of hypo-, q/ H2 f( v* E/ l
thalamic pituitary gonadal axis. CPP is more com-. g4 l* Y2 _. e: J$ O/ Q' Q; }8 h
mon in girls than in boys.1,3 Most boys with CPP  _( T. H' p9 Q4 C# D% |6 o+ p
may have a central nervous system lesion that is0 D+ q" E2 B; N0 U  A1 Q3 Q
responsible for the early activation of the hypothal-
& J% o" V  o9 e+ Yamic pituitary gonadal axis.1-3 Thus, greater empha-( j1 t9 u/ x& j' ~  D/ E
sis has been given to neuroradiologic imaging in# b0 Y! F9 ^$ g; m2 }! E
boys with precocious puberty. In addition to viril-8 d* @: i" D* I" L+ ~' _7 w# A
ization, the clinical hallmark of CPP is the symmet-6 g& ?2 B7 B9 _5 h6 x( {9 a# ]
rical testicular growth secondary to stimulation by2 F+ N3 _* ?' n% u# P7 M' x1 X4 Y
gonadotropins.1,3
+ F/ i" s3 ?5 o! k. i; _Gonadotropin-independent peripheral preco-& f* t3 Y  k) Z7 G3 c3 w9 J9 Y
cious puberty in boys also results from inappropriate/ @4 x0 y# m+ {* W. U/ N2 Z
androgenic stimulation from either endogenous or7 u' [! M1 L! f! N
exogenous sources, nonpituitary gonadotropin stim-
- t' M: R$ _$ j: dulation, and rare activating mutations.3 Virilizing& U2 `  s8 {$ S/ q- |4 P( X8 L
congenital adrenal hyperplasia producing excessive; Z  x0 J* o; N  j+ x
adrenal androgens is a common cause of precocious
  H2 Q! n3 s: s- _$ n3 Npuberty in boys.3,42 k/ h1 w% S5 X* q
The most common form of congenital adrenal- p5 ^: |9 U2 {3 R( v3 W
hyperplasia is the 21-hydroxylase enzyme deficiency.& e* f& q: [1 K% ^
The 11-β hydroxylase deficiency may also result in, j& l7 K) K* E) I3 u
excessive adrenal androgen production, and rarely,
% J8 [3 W! d" i! W6 aan adrenal tumor may also cause adrenal androgen0 A3 x6 D$ s# C
excess.1,3
# U9 Y. b8 O: X! `3 E' Yat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from  X5 f, O" v; i  y7 s# l  C
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
/ p3 t2 m0 i7 I6 CA unique entity of male-limited gonadotropin-- a$ D$ f. X( v6 o% @
independent precocious puberty, which is also known3 e5 G8 [! w! y) g& I* f8 J7 i
as testotoxicosis, may cause precocious puberty at a
4 q5 h8 g  {# R* t/ S$ tvery young age. The physical findings in these boys( ~( S) ]2 p2 k# h- o' X% J4 m" V
with this disorder are full pubertal development,7 O9 ]! D3 n+ h' g  @
including bilateral testicular growth, similar to boys
- G, m% \- c* X: @  h) ~. dwith CPP. The gonadotropin levels in this disorder+ O" I" B1 p: R7 A6 u# z$ {
are suppressed to prepubertal levels and do not show; s9 ?- |2 T$ Q! S: R
pubertal response of gonadotropin after gonadotropin-
  e$ k" Z* J& w7 i8 x8 S1 c! sreleasing hormone stimulation. This is a sex-linked
- H& y2 K: c( N7 K, E3 m& M4 Cautosomal dominant disorder that affects only
( z; c( {! j/ h. E6 v' }6 K7 D. bmales; therefore, other male members of the family! o, G% o2 n1 z* f; y! P, ~
may have similar precocious puberty.3& z9 R. t5 H+ G: Q* H1 k
In our patient, physical examination was incon-
/ w; y5 g+ n' a& t: J, A8 J. Jsistent with true precocious puberty since his testi-
+ E, j6 w: p8 n! N2 N. u  P* mcles were prepubertal in size. However, testotoxicosis
, u, U$ I7 r  Q9 n7 [$ i8 b! D( N. Qwas in the differential diagnosis because his father
' {; V' B5 }* T$ [started puberty somewhat early, and occasionally,0 B: v) ]  P  ]; A8 L" Z; F/ c9 `
testicular enlargement is not that evident in the/ d' S, N9 K% {. e. [" N
beginning of this process.1 In the absence of a neg-
) ]# [7 O$ x" e% f6 ?! K- Aative initial history of androgen exposure, our7 \9 Z0 ?9 W% \; }+ s
biggest concern was virilizing adrenal hyperplasia,
6 j0 _3 A: A; w" meither 21-hydroxylase deficiency or 11-β hydroxylase
' ]( q( i/ B# N0 m  j5 h0 }deficiency. Those diagnoses were excluded by find-
# S- L/ |( T( |7 }  Y' _ing the normal level of adrenal steroids.
" m7 ?9 c  z1 F* pThe diagnosis of exogenous androgens was strongly
' c3 l: Q8 B- ~$ k- O9 a& X9 |1 dsuspected in a follow-up visit after 4 months because/ C8 S; C: F6 ?
the physical examination revealed the complete disap-
, @  l, i4 G& }$ r$ p6 lpearance of pubic hair, normal growth velocity, and  b+ V. K+ n' ^) x; o0 q% P- Y
decreased erections. The father admitted using a testos-$ I3 _/ I$ v5 o8 }) x% d  M
terone gel, which he concealed at first visit. He was
! u$ J; j/ Q$ g5 v6 Ausing it rather frequently, twice a day. The Physicians’
7 j: u/ v6 h6 @; {. k% IDesk Reference, or package insert of this product, gel or* O+ t' [# v0 e% M5 R( c4 u: I; [
cream, cautions about dermal testosterone transfer to/ d- t) r5 C$ W, Q6 v1 W  Q
unprotected females through direct skin exposure.& @& X9 q5 p+ Q5 I4 ~
Serum testosterone level was found to be 2 times the' w# ?& }+ ~# w+ e: X, A4 Z
baseline value in those females who were exposed to
) @8 m! p2 e0 Jeven 15 minutes of direct skin contact with their male& T. \" K, i3 J3 y
partners.6 However, when a shirt covered the applica-5 K0 C( B0 F' V  r+ X
tion site, this testosterone transfer was prevented.
5 B- Q, ^  v( ~8 j; `- dOur patient’s testosterone level was 60 ng/mL,4 J6 }: ], k0 e- c' E# T# q7 l
which was clearly high. Some studies suggest that3 p$ {: Q# n- p' [6 B9 A# ~
dermal conversion of testosterone to dihydrotestos-. e' q: [1 v8 {5 I" E) c
terone, which is a more potent metabolite, is more# z) S' J( y" V' j) _
active in young children exposed to testosterone3 t& k! Z( G: L, w* h
exogenously7; however, we did not measure a dihy-
# j# U' Z  P6 b1 r1 V6 G- ~drotestosterone level in our patient. In addition to4 h# s0 G: ^" H; y; ?+ O" o
virilization, exposure to exogenous testosterone in
8 i) S9 D* I2 z) \2 F: Jchildren results in an increase in growth velocity and$ a4 T6 T- q: u% w, f$ N! M! J
advanced bone age, as seen in our patient.
8 _( u$ D7 x* s* @  o" DThe long-term effect of androgen exposure during" n# v2 m3 }2 C
early childhood on pubertal development and final
8 k2 P  F+ @/ W& Oadult height are not fully known and always remain
& ~+ U8 l/ V8 {4 W, ta concern. Children treated with short-term testos-- H' v6 j) s2 |1 T* M
terone injection or topical androgen may exhibit some
9 V/ F2 ^  a0 O2 W6 h4 Sacceleration of the skeletal maturation; however, after
! f/ \! B1 V" G: {) qcessation of treatment, the rate of bone maturation) @: q/ @$ T: D/ p
decelerates and gradually returns to normal.8,9
9 H. j5 P& ?% bThere are conflicting reports and controversy
: Q* {2 H# ?& ^4 xover the effect of early androgen exposure on adult
# G  @/ F* d( r7 d" k2 \penile length.10,11 Some reports suggest subnormal
! \+ U0 z  V; [6 S5 Radult penile length, apparently because of downreg-
3 d! l. O$ ^# L3 g6 t) ^ulation of androgen receptor number.10,12 However,
; G9 O7 s' g8 M4 r$ v& ySutherland et al13 did not find a correlation between
+ ]; S9 X) x8 m6 e7 G/ nchildhood testosterone exposure and reduced adult( g1 Y; n8 z; |) f6 N
penile length in clinical studies.1 V8 F0 E, U2 u2 e: \. X$ K
Nonetheless, we do not believe our patient is! \8 z: t% C4 [9 h$ H
going to experience any of the untoward effects from
; V$ R6 V% M2 Xtestosterone exposure as mentioned earlier because
% J. d! k8 n5 w$ I# U5 S* `& |the exposure was not for a prolonged period of time.6 A' \7 v+ B: q& `
Although the bone age was advanced at the time of7 {$ [: j2 @/ i3 S6 @! N
diagnosis, the child had a normal growth velocity at
) k# g1 X/ ]( v7 \the follow-up visit. It is hoped that his final adult3 m5 z2 ]# Y1 |4 j# U
height will not be affected.5 ~. x, ?: l. q- {
Although rarely reported, the widespread avail-5 H0 y6 y5 Z* \7 i4 I  k
ability of androgen products in our society may( g* G: [; Y4 p- |  e4 X
indeed cause more virilization in male or female8 \2 o3 B* n. o
children than one would realize. Exposure to andro-
7 B8 h; Z% e. q8 }gen products must be considered and specific ques-
) f, W2 Q' T1 n# O% C" W# l9 e# Ltioning about the use of a testosterone product or+ a7 B8 m: d% ~
gel should be asked of the family members during3 F) H/ v) b0 a, s: `
the evaluation of any children who present with vir-* N/ G) t( D: e( Q2 |4 s, g
ilization or peripheral precocious puberty. The diag-
7 Q3 O. J' s+ i! I  U' lnosis can be established by just a few tests and by- T: o4 J* g. D* d$ i/ U% \
appropriate history. The inability to obtain such a0 H$ V! M  E( `/ ]% C7 i
history, or failure to ask the specific questions, may" E) F" _  C  ?( `$ w1 g1 T
result in extensive, unnecessary, and expensive
5 C! f1 ?  H* ]) u! C0 f0 ^  V. |investigation. The primary care physician should be& N0 T$ M9 X8 A' C/ J7 K
aware of this fact, because most of these children
( T6 S% R1 A8 n2 g! y, r+ L( ^5 vmay initially present in their practice. The Physicians’
- C3 H- ^- X* F/ c8 s6 ]9 dDesk Reference and package insert should also put a, d0 L0 Q0 R$ W
warning about the virilizing effect on a male or" g' y9 w6 c& @+ I2 y* {
female child who might come in contact with some-* u1 O) m6 o5 R7 l' w1 D
one using any of these products.
& o% g2 q' \2 u; H3 G' P' wReferences
2 M9 |  j5 k) Q7 x  ^; ?8 o0 y1. Styne DM. The testes: disorder of sexual differentiation: L! g( R( Z2 Q8 r2 i& T
and puberty in the male. In: Sperling MA, ed. Pediatric0 k( b+ O- Y* K% l$ u
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
7 R9 \* d& q& `% m3 n2002: 565-628.8 ]4 l% X3 h' ?$ Y: o3 u7 X
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
' s6 z2 N3 z+ K$ p# N0 A9 npuberty 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

7 a% M- ?5 f1 u6 h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