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: s0 x8 F0 m1 v
Boy Induced by Indirect Topical
$ J9 W' h+ n- j9 [Exposure to Testosterone* V1 A# i1 s2 K8 G
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,29 N, g2 A  b% L; F) t5 `
and Kenneth R. Rettig, MD1
5 L0 }1 k% `  {5 x4 oClinical Pediatrics
7 d! z3 m3 p/ A6 D! ^; D/ }  VVolume 46 Number 6
" ?" a4 x9 c4 A7 D2 d1 DJuly 2007 540-543
% R' F  ^* |, C$ S$ J" j' R+ f- o© 2007 Sage Publications
! R  n* v9 o- n# v6 w/ v* k10.1177/0009922806296651
! T! J2 O- ]9 Q5 dhttp://clp.sagepub.com
; ?2 M4 Q7 i6 xhosted at" B. V% [% l1 ^/ \( d4 E+ n4 K
http://online.sagepub.com1 _/ V& L7 h- ~, F
Precocious puberty in boys, central or peripheral,
  F  W! |2 ^/ ?7 B* n$ P) j# Dis a significant concern for physicians. Central% r5 l- u3 y7 c0 o6 i# |
precocious puberty (CPP), which is mediated
* A* `- A* S5 g2 dthrough the hypothalamic pituitary gonadal axis, has
( n6 e" N* K  B, B' ba higher incidence of organic central nervous system
# b1 `! S' h+ C6 y. M3 F. wlesions in boys.1,2 Virilization in boys, as manifested5 b$ a3 U9 Z0 I9 e% e5 A: X
by enlargement of the penis, development of pubic+ e* {( Y5 ~+ j1 g6 X. Q6 ?
hair, and facial acne without enlargement of testi-
, B  F, [7 a! n- e8 zcles, suggests peripheral or pseudopuberty.1-3 We' ]: e" F' O% q  J
report a 16-month-old boy who presented with the
. Q( I; B  ~2 X& @8 m5 U* }1 penlargement of the phallus and pubic hair develop-+ V+ j3 `* j4 d6 U9 L
ment without testicular enlargement, which was due
8 L% p% `7 E* o; [2 b: Qto the unintentional exposure to androgen gel used by
- ~' A! M) h( K9 T! h+ Z7 Mthe father. The family initially concealed this infor-
8 B/ F4 t+ }( H+ ?5 ?5 b7 {; mmation, resulting in an extensive work-up for this
" d1 y$ ]$ o; i3 zchild. Given the widespread and easy availability of
# O- A. ~5 |: g1 mtestosterone gel and cream, we believe this is proba-
3 T  @6 }3 `: h# w+ w$ \bly more common than the rare case report in the8 p- E; l* N* s2 Q1 ~- V
literature.4
3 N7 l$ K# ?  Y# `, vPatient Report1 `6 F" }& Q, _4 G( ]
A 16-month-old white child was referred to the1 ]$ N; O" v: j. m6 e" ^
endocrine clinic by his pediatrician with the concern. p4 ]4 e, ?7 d9 w8 C
of early sexual development. His mother noticed
3 c! u6 Z( F3 k* V, @6 [3 Alight colored pubic hair development when he was" H9 e$ T4 K. @  E4 w
From the 1Division of Pediatric Endocrinology, 2University of
% @- q" u: f( L+ d* KSouth Alabama Medical Center, Mobile, Alabama.% J# K* ~3 J4 M& H/ j) J: p& K; Z
Address correspondence to: Samar K. Bhowmick, MD, FACE,
+ Z! j" v9 ^3 \" I! J4 ?$ wProfessor of Pediatrics, University of South Alabama, College of. u! g( E$ j3 q+ F
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
2 [$ D0 O1 k: Z9 [2 Ye-mail: [email protected].
% ~! _. j- F8 b. U' cabout 6 to 7 months old, which progressively became" Y" {& Z: h& m7 ]9 c, y
darker. She was also concerned about the enlarge-
# _' k- G- V0 e( ]; ament of his penis and frequent erections. The child
6 P# }% j2 G% i1 H9 l# jwas the product of a full-term normal delivery, with/ @+ D. ?5 K/ d2 z1 g+ `. X
a birth weight of 7 lb 14 oz, and birth length of* D! m9 W# }, N( E7 P  k% o
20 inches. He was breast-fed throughout the first year, Y. q$ i+ c, b0 y" t5 A2 O2 l
of life and was still receiving breast milk along with1 x  ]+ n- w9 h  Q" j% w1 A
solid food. He had no hospitalizations or surgery,
1 p, T/ z* s' ~, w: Uand his psychosocial and psychomotor development. C6 ~6 y; f" J5 U6 g) c4 e9 ~4 G
was age appropriate.
+ c- A  @5 X' E+ |* \. @The family history was remarkable for the father,2 ]& O6 g& u  P: N8 m1 h
who was diagnosed with hypothyroidism at age 16,4 o" k4 D" `# A$ l' i
which was treated with thyroxine. The father’s
9 R* n& ~, ?+ X' I: Oheight was 6 feet, and he went through a somewhat( v+ Y+ y& b6 M7 x$ j# E6 H8 W
early puberty and had stopped growing by age 14.' ]% W' y, b6 `" Z, U5 D3 O
The father denied taking any other medication. The
5 @2 t: r: V' i- i. _+ b- nchild’s mother was in good health. Her menarche8 ~4 d0 U  R% l6 C- s7 b- ~. ^
was at 11 years of age, and her height was at 5 feet
' A: ~' q% O  \) D- V% i& j3 A, u5 inches. There was no other family history of pre-6 k( x1 c7 M; Z5 s
cocious sexual development in the first-degree rela-7 m9 D  _, N: k, H! b9 F
tives. There were no siblings.* F. }9 z" F1 o, P; I
Physical Examination, k) H) ~( @# p% D9 r4 k  v6 s1 Q
The physical examination revealed a very active,
$ S" F* o+ c7 C/ \3 H; [* Oplayful, and healthy boy. The vital signs documented
" u( I" u8 e" K9 ua blood pressure of 85/50 mm Hg, his length was
) B9 H: w1 n6 V% [5 f6 p90 cm (>97th percentile), and his weight was 14.4 kg% S9 A, M2 c$ `8 C% w
(also >97th percentile). The observed yearly growth
" q) B) ]8 K7 T0 p2 nvelocity was 30 cm (12 inches). The examination of
3 ?7 X% P9 z, ]3 u- `. Z* H; n9 Hthe neck revealed no thyroid enlargement.. ]0 }6 l$ M4 J& o2 S+ Q5 z- q/ v/ ?
The genitourinary examination was remarkable for; u, i1 @- j# E: o' O8 J9 U  K
enlargement of the penis, with a stretched length of
  r6 ]3 c5 w- P$ k8 cm and a width of 2 cm. The glans penis was very well! z* Y8 @& P7 |4 Y
developed. The pubic hair was Tanner II, mostly around: S' ]5 n9 ?5 F- C
540- _4 e' h; J3 u* M
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from% x! Z9 ~: y. Y- i( f% |- c% z; f
the base of the phallus and was dark and curled. The! `* @0 j' W* _
testicular volume was prepubertal at 2 mL each.
4 X$ w- f4 [  a* S3 q( b, }5 O0 T2 EThe skin was moist and smooth and somewhat
( Z# N( L3 p6 c, ^. Moily. No axillary hair was noted. There were no. a# e  a% J% f, f3 ?+ u
abnormal skin pigmentations or café-au-lait spots.4 L2 g9 ~8 a5 B- |( U8 o
Neurologic evaluation showed deep tendon reflex 2+
2 r' i5 P$ ^/ F6 }2 L! h# E+ zbilateral and symmetrical. There was no suggestion
! j; A' G6 P/ d/ ]* \8 xof papilledema.3 s- j( o. y# }
Laboratory Evaluation
) b8 B1 n! c  MThe bone age was consistent with 28 months by
  X" H8 z0 @, ~0 a! X# |6 zusing the standard of Greulich and Pyle at a chrono-  _) Q# z' C8 a% q  {0 }
logic age of 16 months (advanced).5 Chromosomal
$ O7 c2 X( E) c  q6 C/ ukaryotype was 46XY. The thyroid function test
- s; w, T3 n7 K5 ashowed a free T4 of 1.69 ng/dL, and thyroid stimu-4 d; j. a: S8 l. x
lating hormone level was 1.3 µIU/mL (both normal).3 i. Y1 H# w7 x2 a; s  v; O$ A
The concentrations of serum electrolytes, blood
- K9 ^7 ?0 T. _6 n. @! X* F4 aurea nitrogen, creatinine, and calcium all were6 O2 |* _3 @+ m  S; N
within normal range for his age. The concentration
- T2 Y- i( [; @4 A1 p: a  L7 c4 v7 B  Iof serum 17-hydroxyprogesterone was 16 ng/dL. B3 i8 L0 P+ r
(normal, 3 to 90 ng/dL), androstenedione was 20, ~  O, N& }+ |. k0 I
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
6 u) i9 n3 F* y8 t5 Sterone was 38 ng/dL (normal, 50 to 760 ng/dL),
8 i% T+ k8 k- Q5 A8 G6 qdesoxycorticosterone was 4.3 ng/dL (normal, 7 to
6 y; p" Z8 b3 f9 }$ G49ng/dL), 11-desoxycortisol (specific compound S)
% }/ b5 f2 C5 m" n, n0 E: W: fwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
" T6 h+ E8 {) u. g- \! Mtisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total) X0 @4 M) ?& `) t1 k6 J
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),- h* \. D8 S* h, u  R4 O! c% c
and β-human chorionic gonadotropin was less than
" {/ v' ^4 a5 W' p) f+ T5 mIU/mL (normal <5 mIU/mL). Serum follicular
& v" N7 X% N" a  {stimulating hormone and leuteinizing hormone* S* ?) H  V! u9 Y
concentrations were less than 0.05 mIU/mL6 Q6 E# X2 M& W; O
(prepubertal).4 }$ O$ `2 ^6 G" ]7 T1 `0 ]
The parents were notified about the laboratory) ]4 ?# t( y; ]9 K! P/ D
results and were informed that all of the tests were: Y  Q! `3 O# ?9 L( J% O, x! P
normal except the testosterone level was high. The, ^% k% y4 F  `4 J5 G* F
follow-up visit was arranged within a few weeks to
. ]" @* x+ |9 G! W1 u8 U" B- Wobtain testicular and abdominal sonograms; how-
. }( {  {5 _) l' }6 Bever, the family did not return for 4 months.
* f$ G, a- E! R8 K: H$ @  @Physical examination at this time revealed that the
5 m" i1 V" ?& B( dchild had grown 2.5 cm in 4 months and had gained
- i9 k% k5 F6 o; b" @+ e. Q2 kg of weight. Physical examination remained
4 O2 H1 p1 O; E- U: r" s, H9 y; o; G2 tunchanged. Surprisingly, the pubic hair almost com-
& Y  P0 T8 l( p# M( ~pletely disappeared except for a few vellous hairs at
6 G" [/ o1 p& a$ R& ithe base of the phallus. Testicular volume was still 25 A3 h. ~- |$ u2 ]
mL, and the size of the penis remained unchanged.3 z. z! G; ^, l' d
The mother also said that the boy was no longer hav-
. O2 j2 M7 {; K1 f  Aing frequent erections.: F1 k- r6 F7 X0 Q( X) y; H
Both parents were again questioned about use of
2 E% }( ?/ {& F& o0 x( |3 r! n  Iany ointment/creams that they may have applied to
# g8 Q2 e4 G2 |; y8 A) e2 L# mthe child’s skin. This time the father admitted the
" l& m. I: }* w( c5 eTopical Testosterone Exposure / Bhowmick et al 541
2 H" q; x( G; b- T3 s# juse of testosterone gel twice daily that he was apply-
4 O+ o7 s( T: e. A+ L7 }* Z$ cing over his own shoulders, chest, and back area for
0 u( f- p) g3 W+ W% B+ }! `' }a year. The father also revealed he was embarrassed
4 s( x$ [, q. b+ Q! |; w. sto disclose that he was using a testosterone gel pre-4 @" i8 j: N: w) @! j) [+ ]
scribed by his family physician for decreased libido) g) R  ]) n/ V: j
secondary to depression.
  L! R' c) u; eThe child slept in the same bed with parents., f& e! x4 o" K
The father would hug the baby and hold him on his
/ q2 s" I# u/ I) G8 `* j# e) x. ]3 dchest for a considerable period of time, causing sig-" l1 O6 j7 x: V" u8 \8 g
nificant bare skin contact between baby and father.
% h. `7 Y3 V$ c2 U6 O! X& R- yThe father also admitted that after the phone call,% L5 l8 m# P! z  ?- M$ p
when he learned the testosterone level in the baby: L, D* t4 |& T# N) v/ d
was high, he then read the product information, S& K+ f* f) }" M$ S
packet and concluded that it was most likely the rea-+ |. I7 X8 H, h
son for the child’s virilization. At that time, they
2 N) |% c$ x( j$ P4 d% }decided to put the baby in a separate bed, and the
* ?! L0 `; q( X$ q7 i+ O( rfather was not hugging him with bare skin and had
4 G+ _0 H0 W! y2 Gbeen using protective clothing. A repeat testosterone6 T" U: d' H; F! a
test was ordered, but the family did not go to the( v$ g8 T& `- \1 L% j' n
laboratory to obtain the test.' o+ A. h# T8 W, d
Discussion/ _* T+ B  O* H7 W# m0 u
Precocious puberty in boys is defined as secondary
+ D' Q0 O0 N2 V! o2 c. z+ J* usexual development before 9 years of age.1,4- p$ ?2 [' N9 l* h- f
Precocious puberty is termed as central (true) when8 g4 p4 c& U) u1 v+ K8 Q3 f4 R
it is caused by the premature activation of hypo-
# ]# }3 `0 x4 V7 J9 O/ Ithalamic pituitary gonadal axis. CPP is more com-
5 u) \2 w8 |' N$ N# @mon in girls than in boys.1,3 Most boys with CPP2 F8 \% W# E# e9 S! s! i  ^4 G
may have a central nervous system lesion that is
* V; G! k' y2 P. \; Mresponsible for the early activation of the hypothal-7 Q6 J, g* l3 @; h
amic pituitary gonadal axis.1-3 Thus, greater empha-- o' @( V- D9 i; R9 y! T
sis has been given to neuroradiologic imaging in/ n" Q: L. p" V! C! g  g6 o
boys with precocious puberty. In addition to viril-
# x2 M: C+ S& U& D1 _- Qization, the clinical hallmark of CPP is the symmet-
2 X1 C- ~$ D7 \7 Erical testicular growth secondary to stimulation by* C% k; u9 M$ ]  m3 V8 b/ P( p0 b
gonadotropins.1,3% K0 w: {" o& q( D+ v
Gonadotropin-independent peripheral preco-1 [$ a* L$ q$ x& Q; l
cious puberty in boys also results from inappropriate
1 E. |  p6 b% u; M+ |9 i9 x4 x% landrogenic stimulation from either endogenous or( {. z6 x6 |- S
exogenous sources, nonpituitary gonadotropin stim-' s; i' Q+ {. v6 r/ S% V* m
ulation, and rare activating mutations.3 Virilizing
  H- U9 m1 i$ \* d1 D7 Acongenital adrenal hyperplasia producing excessive
7 E5 y5 c4 e- A/ D/ Dadrenal androgens is a common cause of precocious
! J5 l3 \( b8 ^2 Y0 ypuberty in boys.3,4
* k* g3 C8 o. @, pThe most common form of congenital adrenal
* Y$ b& Y( S, D1 `hyperplasia is the 21-hydroxylase enzyme deficiency.! `2 {+ Z0 w! d4 V& h0 H) `8 ~
The 11-β hydroxylase deficiency may also result in0 `4 T; R0 ]+ d
excessive adrenal androgen production, and rarely,+ r# O# y* s8 J5 W# k0 S4 G
an adrenal tumor may also cause adrenal androgen
$ z/ Q6 Y# _; pexcess.1,3' w* I# ]6 A6 O
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from  E  ^* S; a5 p5 }
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
  H+ h. }6 {- z* R# N- D# f  qA unique entity of male-limited gonadotropin-
' p+ L9 [7 ?% \: Q8 w% jindependent precocious puberty, which is also known/ M& P( ]0 H+ f% }7 R6 R1 I- ?+ T
as testotoxicosis, may cause precocious puberty at a
1 u+ E' l7 C$ overy young age. The physical findings in these boys& E, C. d1 d3 u& n) b
with this disorder are full pubertal development,5 l. `, j7 K* x1 q/ P1 A
including bilateral testicular growth, similar to boys" I- z( `% Q# }; e$ j  u
with CPP. The gonadotropin levels in this disorder
; {. j) F+ y5 Yare suppressed to prepubertal levels and do not show2 w. _8 L3 b& R! u7 ~
pubertal response of gonadotropin after gonadotropin-% m. K7 m) B  Y
releasing hormone stimulation. This is a sex-linked& ?9 i6 X* \" H! l9 [2 x9 }
autosomal dominant disorder that affects only
! J7 n" h5 x. t$ H$ b" Jmales; therefore, other male members of the family. ^3 a' p' F7 I; ?) w; O
may have similar precocious puberty.3
3 e( |* Y' O* n7 rIn our patient, physical examination was incon-2 D& f  i/ D6 l$ T9 q5 |
sistent with true precocious puberty since his testi-) C  }4 t. C- ?
cles were prepubertal in size. However, testotoxicosis% T7 z( a8 b( |
was in the differential diagnosis because his father. Q# ?# d  k5 Y8 x  m, A
started puberty somewhat early, and occasionally,! e  Z# e. |5 E9 j
testicular enlargement is not that evident in the3 B8 S7 N, \& }9 x- }
beginning of this process.1 In the absence of a neg-, g2 x1 c6 ]% l4 `
ative initial history of androgen exposure, our: g$ k4 {, t5 G! |6 N
biggest concern was virilizing adrenal hyperplasia,  ?. u. ], {7 c1 e! V
either 21-hydroxylase deficiency or 11-β hydroxylase
& }7 f- n5 I* Y4 p) }/ Z; ~deficiency. Those diagnoses were excluded by find-
; L9 o5 N% E6 ^# r; |ing the normal level of adrenal steroids.
- s6 `5 v3 a+ U$ w# jThe diagnosis of exogenous androgens was strongly  R8 u% _( G* v9 `6 y$ b4 q2 [! m
suspected in a follow-up visit after 4 months because, M  S0 z, q' d- Q9 c) Z* |: |7 h
the physical examination revealed the complete disap-% B; e. ^0 Q# r+ v/ n
pearance of pubic hair, normal growth velocity, and# n7 x: \9 A* F5 f+ `- l( i
decreased erections. The father admitted using a testos-: `! ?  ^4 I/ t2 Y/ t- d  q& }; w( ^
terone gel, which he concealed at first visit. He was0 h- }$ a5 n8 g% \, @
using it rather frequently, twice a day. The Physicians’, k8 X1 j2 g5 z) l
Desk Reference, or package insert of this product, gel or# }. q4 R* k6 s( U" \  g3 T
cream, cautions about dermal testosterone transfer to, m1 v' B9 k7 R4 g. y
unprotected females through direct skin exposure.* ]2 T* g% m; y7 |
Serum testosterone level was found to be 2 times the
( {7 w  e/ n% _* b+ z; Ebaseline value in those females who were exposed to
( l; e5 g5 C, Aeven 15 minutes of direct skin contact with their male
) S& k) @" R! A6 N) f% kpartners.6 However, when a shirt covered the applica-' k$ `; A8 @# O+ h2 E4 }. w
tion site, this testosterone transfer was prevented.% L( q. D  D3 V7 l! S
Our patient’s testosterone level was 60 ng/mL,
3 u- c. \7 }$ I/ I- ^2 t# S9 `+ nwhich was clearly high. Some studies suggest that/ h' {+ o. D' u
dermal conversion of testosterone to dihydrotestos-
* g- v: `; x' F; Y" [$ tterone, which is a more potent metabolite, is more/ e7 D9 ]0 Y& {. W) g+ d# D
active in young children exposed to testosterone) q4 h5 w: H( B% e! C
exogenously7; however, we did not measure a dihy-2 s& U/ w+ m' z! J6 ~9 ^
drotestosterone level in our patient. In addition to
! U2 t; Q9 v3 v: y" ^9 dvirilization, exposure to exogenous testosterone in7 h$ ?8 e8 Z  Q5 k2 X
children results in an increase in growth velocity and! K1 S+ H; C! b0 M4 ^; k! I
advanced bone age, as seen in our patient.
1 d; q5 R7 W3 I! nThe long-term effect of androgen exposure during9 c& W4 h! ?8 D( h+ W
early childhood on pubertal development and final
: Y4 w$ [& \& I: C% Fadult height are not fully known and always remain
5 y5 q- i" o' f7 La concern. Children treated with short-term testos-
, O# [  O# k/ v- F. j+ H+ {terone injection or topical androgen may exhibit some# a( D; Y( j. N8 B) F: v8 Z9 }$ I
acceleration of the skeletal maturation; however, after
6 O. W2 b4 F6 {7 r8 r9 ~$ t: c/ L3 tcessation of treatment, the rate of bone maturation
2 Y: P* L8 f7 s3 }8 A1 c# ldecelerates and gradually returns to normal.8,98 d/ V  {4 H% U2 {; Z
There are conflicting reports and controversy
+ `+ O* \( S: |  g7 ]: @, H6 L: Hover the effect of early androgen exposure on adult  E7 t% {9 E/ D7 e. Z* r# C- _* K9 L
penile length.10,11 Some reports suggest subnormal
0 a' r. L+ O( [9 n3 F1 U6 Eadult penile length, apparently because of downreg-
7 {8 R: X  s. G4 S1 Y9 t  Vulation of androgen receptor number.10,12 However,# p4 W5 t8 `% c
Sutherland et al13 did not find a correlation between
3 {& k/ {# f5 p, ?7 C' D# M( y. schildhood testosterone exposure and reduced adult
9 [$ [& o& `* ]. `& l$ R+ S2 Vpenile length in clinical studies.4 H0 `9 H  p! ^" W3 G, B
Nonetheless, we do not believe our patient is7 J7 |% j5 q$ h0 b+ A: \( e, }" C! F
going to experience any of the untoward effects from2 m' J9 Q9 [5 Y# s* u0 x
testosterone exposure as mentioned earlier because
# F9 z, F" m, {% C! J( dthe exposure was not for a prolonged period of time.1 g" u8 l$ t5 V' w/ e
Although the bone age was advanced at the time of
- s3 r; p9 J5 u8 Z/ W' _diagnosis, the child had a normal growth velocity at
) m/ o7 \$ V3 ^the follow-up visit. It is hoped that his final adult- y; p+ F/ s+ m1 `" l
height will not be affected.
6 w# A4 {; X: G7 Z2 I" VAlthough rarely reported, the widespread avail-
7 N' n; z4 U$ M$ Q4 M' P' Wability of androgen products in our society may1 p& x0 q" R# F9 u0 y( j3 w
indeed cause more virilization in male or female
4 z3 B/ a, K# xchildren than one would realize. Exposure to andro-
, w/ K$ m5 X  B5 L; w' {7 P% Q1 A) Sgen products must be considered and specific ques-4 C5 g9 l9 u; Z/ h
tioning about the use of a testosterone product or
9 u, F# T* I& c2 Ygel should be asked of the family members during
( t9 x+ M! L9 @% D" c2 Fthe evaluation of any children who present with vir-
9 _, E( d7 X0 K! i: @6 Kilization or peripheral precocious puberty. The diag-
$ f* Y: L3 p' `# W" \nosis can be established by just a few tests and by9 b( D. n7 I/ y- U; F8 P  M
appropriate history. The inability to obtain such a- |' s1 J& N5 L; f8 D, ^
history, or failure to ask the specific questions, may
0 X8 i- k9 H; G. L' _" A. J2 nresult in extensive, unnecessary, and expensive
# x. l0 u- ]# A! r6 Sinvestigation. The primary care physician should be: h7 |' a; v$ J" C% @: |
aware of this fact, because most of these children! p% [  ^% E$ U% T- e! R/ r
may initially present in their practice. The Physicians’
& f& m0 N$ i$ H9 J* K% dDesk Reference and package insert should also put a
% e2 g: Z; P9 q5 b7 x( J& Swarning about the virilizing effect on a male or
) H5 d& Q' b+ A2 Zfemale child who might come in contact with some-
# h$ |0 h) t  k0 y9 u- lone using any of these products.
/ x: b2 q2 C9 a, m$ pReferences3 _( ?* s$ U3 b- o% b8 O% }6 ^  m/ ~
1. Styne DM. The testes: disorder of sexual differentiation
% y8 }1 B) \/ i; {( Vand puberty in the male. In: Sperling MA, ed. Pediatric
% k: u0 I- v0 |1 _- f+ g1 OEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
3 a/ A0 N" A+ f' `$ J2002: 565-628.3 v! O/ I& p1 m% k9 _) U+ }
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
9 q$ z0 s: j, ~; Y3 B2 C6 rpuberty 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/ R, o. ^6 w' \6 Z% o
Boy Induced by Indirect Topical
+ b: b3 r# i4 Q5 j! P5 c7 k" dExposure to Testosterone
) R4 y7 D5 O; B+ ASamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2! a6 Z% V' [- j: ]- G- x6 a, U
and Kenneth R. Rettig, MD1: D2 n9 f; B- C! `# U
Clinical Pediatrics% A$ X4 A5 Y# F3 x
Volume 46 Number 6
7 P- ~& q4 e; K; nJuly 2007 540-5438 |, V- u. Y1 x$ r$ z! Z
© 2007 Sage Publications. \& X' y: ^1 P" H
10.1177/0009922806296651; W; a4 E0 M9 J  j* R
http://clp.sagepub.com
3 m/ c- G4 v0 F5 phosted at
, G: B5 g) C7 ~* l9 e( W, w5 d  }http://online.sagepub.com& I$ o9 @" H* T+ }" ^
Precocious puberty in boys, central or peripheral,
  V2 H7 A; `! `( C$ X# G0 P3 [! ^- Bis a significant concern for physicians. Central
) I& J( n* z9 |, P6 {precocious puberty (CPP), which is mediated& c# {5 w1 `1 M7 V. d  R; H
through the hypothalamic pituitary gonadal axis, has; W5 N: f8 x+ n) V, k8 F% s
a higher incidence of organic central nervous system. n/ P% c1 \9 d; N; \$ _4 ^
lesions in boys.1,2 Virilization in boys, as manifested
, ^1 j: c; M/ Y' v4 cby enlargement of the penis, development of pubic& a3 `" S8 ]! I/ \: I
hair, and facial acne without enlargement of testi-
  H! \; a# N, Z& y, ?cles, suggests peripheral or pseudopuberty.1-3 We8 D( ]! X  ?" ~  ^6 W
report a 16-month-old boy who presented with the
+ a7 k9 ?7 _7 ?/ c8 genlargement of the phallus and pubic hair develop-
0 m: E# W2 |& S" _# z) Cment without testicular enlargement, which was due& D' p# `4 W# l3 _# K& L
to the unintentional exposure to androgen gel used by
! w5 r/ x! s- bthe father. The family initially concealed this infor-
# v8 \! ]5 E  _2 [  Imation, resulting in an extensive work-up for this
4 {# n  i. n& p$ y0 r9 r( {' Wchild. Given the widespread and easy availability of
! C* g! B) }& T3 W/ H. z! ptestosterone gel and cream, we believe this is proba-. o- _$ O  d( Z9 M8 t" B
bly more common than the rare case report in the
+ P/ c9 ~1 E; ~literature.4
& ^* I8 o3 M( V+ @& YPatient Report! n0 W: m/ z3 b
A 16-month-old white child was referred to the
8 f7 m& h8 r( i9 ~endocrine clinic by his pediatrician with the concern
3 z+ z3 O& i2 j0 w  ~1 E) Kof early sexual development. His mother noticed* x4 X1 O5 m" C* \8 `0 a/ d; y
light colored pubic hair development when he was) W* i$ s9 z2 Z* T$ U' k6 Y
From the 1Division of Pediatric Endocrinology, 2University of; h9 C" e* q  j) L
South Alabama Medical Center, Mobile, Alabama.8 b5 h4 X' x1 a, a& D8 t+ L" j9 o
Address correspondence to: Samar K. Bhowmick, MD, FACE,
) y# ?8 N/ p; d8 x& N' [Professor of Pediatrics, University of South Alabama, College of
$ A( g! l& A/ p7 BMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;! w, w6 k1 W0 I* x& `7 _
e-mail: [email protected].
" l& o; K8 j- `8 u* c& sabout 6 to 7 months old, which progressively became
$ L  `+ r8 |; b, k  x+ n! J. cdarker. She was also concerned about the enlarge-
3 I) ?# L0 v: l7 D/ s8 Z( h. [# _( pment of his penis and frequent erections. The child
4 i# ^  N( i" o; ]: A! ywas the product of a full-term normal delivery, with) o9 n3 a; L% B! P
a birth weight of 7 lb 14 oz, and birth length of
. [" c$ U: E0 ~  m# J20 inches. He was breast-fed throughout the first year
* V. q( }. X6 f% Hof life and was still receiving breast milk along with
' T3 b( k% i8 r8 Isolid food. He had no hospitalizations or surgery,7 r. I2 ]; C% c1 o3 ^6 S
and his psychosocial and psychomotor development
) [7 o9 N! N. i6 h" W# M! m: fwas age appropriate.
9 K9 A) h) A+ Z+ a. }, dThe family history was remarkable for the father,
0 E1 G4 s- x1 J, e4 n' [who was diagnosed with hypothyroidism at age 16,5 G& ~: D" D" j% t) L* ~
which was treated with thyroxine. The father’s! i0 _! {# N0 Z  a# ]  X
height was 6 feet, and he went through a somewhat
# C8 r7 ^' K9 t. w, nearly puberty and had stopped growing by age 14.
+ G1 |: R7 V7 TThe father denied taking any other medication. The6 x: v/ @( Z! E6 M. v. l- r
child’s mother was in good health. Her menarche, k. J9 u3 @. k9 F9 k
was at 11 years of age, and her height was at 5 feet2 i& r7 n% m: v! |2 d
5 inches. There was no other family history of pre-
5 x& \6 ^/ |2 b6 C) H6 C  u5 Zcocious sexual development in the first-degree rela-
* P) M5 ?% c4 j* [6 I, M  A1 Vtives. There were no siblings.
) ]9 x/ x  K9 O0 w: o- I9 t# [Physical Examination  k' G. n! Y2 a% w
The physical examination revealed a very active,/ z  z* d1 {, z4 E1 O( }  u# B
playful, and healthy boy. The vital signs documented- ]9 h# B, u5 V4 @; m$ N6 L  X  x
a blood pressure of 85/50 mm Hg, his length was
0 A6 O* w7 u% x# {, C90 cm (>97th percentile), and his weight was 14.4 kg9 a- W! g, H' N9 U
(also >97th percentile). The observed yearly growth6 y4 @1 E2 x( C% v0 w0 Q( H
velocity was 30 cm (12 inches). The examination of
& k9 A0 R/ P- S/ P/ C* Kthe neck revealed no thyroid enlargement.! x( r5 X9 T$ r! q& G' ^$ O: Y
The genitourinary examination was remarkable for
5 p! Y2 \( q: h/ D  v, Wenlargement of the penis, with a stretched length of) d9 ]% u( y2 l' Z& G
8 cm and a width of 2 cm. The glans penis was very well
" E/ M+ [: z( ~' p' Odeveloped. The pubic hair was Tanner II, mostly around7 j# c2 n) @1 L* s2 u
540
* o  O! u, H! H. K: U- `at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from+ N2 t5 \$ r  y# W8 r0 l1 ]* q
the base of the phallus and was dark and curled. The
4 x- I0 F' p+ o" q+ S, }testicular volume was prepubertal at 2 mL each.
0 F/ c& d7 \# Y2 a* C1 T; W# V) XThe skin was moist and smooth and somewhat4 L# ]8 k- {% x3 B7 z$ z+ w
oily. No axillary hair was noted. There were no* B+ B6 l2 r5 n0 Y* @
abnormal skin pigmentations or café-au-lait spots.7 C* M2 N# {0 S
Neurologic evaluation showed deep tendon reflex 2+
- w- z" l3 j7 k' t# p% p% ]bilateral and symmetrical. There was no suggestion0 H3 i9 W; Y/ m. Q
of papilledema.+ o6 W4 `9 q, x, U* ]- h8 E+ j
Laboratory Evaluation
* P# D4 J$ c; x$ l- |4 \- gThe bone age was consistent with 28 months by) Y( y+ S/ D# b" O$ I; E: S( f* c
using the standard of Greulich and Pyle at a chrono-- ~9 W/ L) [& O  Q  E8 X
logic age of 16 months (advanced).5 Chromosomal) R" d1 A! \$ Y  }$ U
karyotype was 46XY. The thyroid function test$ N$ b4 g; G/ F* P
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
" O" f1 y5 c4 l( glating hormone level was 1.3 µIU/mL (both normal)." k3 w1 @0 G% S+ Q! W+ z
The concentrations of serum electrolytes, blood- `, P( M: ]& s5 l* a. d! w
urea nitrogen, creatinine, and calcium all were/ ~6 J$ h1 G# d; `/ e: S
within normal range for his age. The concentration
3 v$ H2 L( s) s8 u  J" Kof serum 17-hydroxyprogesterone was 16 ng/dL
& b- P- K! `* N0 g9 R% k(normal, 3 to 90 ng/dL), androstenedione was 20
5 C; `7 h' \8 I0 v4 {' x4 dng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
$ t5 A$ |% C7 ]4 I) ~+ j) Z" m2 hterone was 38 ng/dL (normal, 50 to 760 ng/dL),( ]- \" J3 k/ o7 b
desoxycorticosterone was 4.3 ng/dL (normal, 7 to) G( D1 R4 B% w% G
49ng/dL), 11-desoxycortisol (specific compound S)( k( s2 t% }2 Q! w
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-  t8 M; c* ^+ ^
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
7 v6 o' L; _& z2 qtestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
9 W3 q3 J, c, I- |8 G. y( oand β-human chorionic gonadotropin was less than
& h' X3 D( i$ h3 X& @" r5 mIU/mL (normal <5 mIU/mL). Serum follicular
& J/ t# ]- W# k8 P$ ystimulating hormone and leuteinizing hormone5 i) l1 ^* l" P9 a4 U: f
concentrations were less than 0.05 mIU/mL
7 `6 j- j1 V! q" L6 Q(prepubertal).
. b. ?1 j; ]& g) M3 \* nThe parents were notified about the laboratory
; ~. \/ S5 s% c: F- X0 }4 f! }# Fresults and were informed that all of the tests were
9 W3 U+ l. A& t$ Jnormal except the testosterone level was high. The
. ^) v  ?! S' Cfollow-up visit was arranged within a few weeks to
* P8 H! V& E* P) h  Wobtain testicular and abdominal sonograms; how-' I( X/ l* P7 u, E$ ~. i/ M# |
ever, the family did not return for 4 months.' m6 j" J; S2 o! R4 j7 x
Physical examination at this time revealed that the3 l9 a( m  }% X7 a& @7 i
child had grown 2.5 cm in 4 months and had gained, A, W/ j3 _4 V  G% P4 N# m
2 kg of weight. Physical examination remained
; ~, j3 O4 `5 d8 Q' O5 Munchanged. Surprisingly, the pubic hair almost com-
2 e( Y1 W# h1 T( G( n7 Ypletely disappeared except for a few vellous hairs at
# }! ^2 f4 B; u' s9 Uthe base of the phallus. Testicular volume was still 25 \( o" j  ~' x& L
mL, and the size of the penis remained unchanged.
/ b5 s7 y7 A8 Q2 T& `The mother also said that the boy was no longer hav-$ R# D  e, z. E& ^  k  Y
ing frequent erections.) S/ W# y: {4 y# R* c
Both parents were again questioned about use of3 N+ _- S/ s  B$ t( v
any ointment/creams that they may have applied to
; j8 h9 C/ w; V( n7 ]- _the child’s skin. This time the father admitted the7 x) A! y$ j5 b; m+ {' Z4 Z: C
Topical Testosterone Exposure / Bhowmick et al 541
9 r3 Z" ~$ [3 r4 l2 N8 ~# X- [use of testosterone gel twice daily that he was apply-7 I& f9 b' c+ Q8 ]' D0 r' k
ing over his own shoulders, chest, and back area for) _- e2 t9 k$ V( r, m  M( b/ h
a year. The father also revealed he was embarrassed
0 q3 Z! L( U4 h  y" Tto disclose that he was using a testosterone gel pre-
' ~8 D/ O$ Q, a# Z9 e. T9 R" l" a& Nscribed by his family physician for decreased libido0 j. r* ]( W3 m9 y5 F
secondary to depression.
6 @* \9 b( A: ]$ s; S% zThe child slept in the same bed with parents.
! A1 A* A/ V. ^! iThe father would hug the baby and hold him on his
( t! A8 m* B, X  m; |chest for a considerable period of time, causing sig-
/ Z* w+ p- w4 P4 f4 q  [nificant bare skin contact between baby and father.. x* z6 e  ]$ u! H, ?7 `* ^) w
The father also admitted that after the phone call,1 E4 {  o5 ?! ^$ y! r, Y' p) ]6 u
when he learned the testosterone level in the baby; L9 V$ l, K" K5 ^
was high, he then read the product information# L' t; G1 F9 J$ E$ r& [! \
packet and concluded that it was most likely the rea-5 i9 q* Z' e. h
son for the child’s virilization. At that time, they
: n$ A: }0 I% [% idecided to put the baby in a separate bed, and the! L% O( S4 \; F- R& ~7 h# O3 l+ R
father was not hugging him with bare skin and had. `8 v0 p, W9 S* V8 a
been using protective clothing. A repeat testosterone
9 W4 ?! o* {" P% Btest was ordered, but the family did not go to the( k7 L+ m: Z* w, u
laboratory to obtain the test.
. x9 i/ {! a# \7 v3 aDiscussion
1 p8 [  H9 p; s  E) }Precocious puberty in boys is defined as secondary, z3 [) b1 p0 V. i2 _" _% `# s! g
sexual development before 9 years of age.1,4$ n: A9 I0 l. b* }
Precocious puberty is termed as central (true) when1 A) Z- G/ k5 F" K3 x
it is caused by the premature activation of hypo-
% F  z% Z5 \& Ethalamic pituitary gonadal axis. CPP is more com-
2 d8 H  X! I4 P4 @7 tmon in girls than in boys.1,3 Most boys with CPP
7 d' {/ |- B: v( Bmay have a central nervous system lesion that is
) q8 j7 n0 D! e" ]3 ]7 i& ]3 L, \7 i6 jresponsible for the early activation of the hypothal-, k: C, ^! I0 ]& U! [6 {
amic pituitary gonadal axis.1-3 Thus, greater empha-
: G5 O% E! u& C+ q+ g0 v$ S6 ?sis has been given to neuroradiologic imaging in
+ n4 @; b* L# b, A* y$ C: Hboys with precocious puberty. In addition to viril-
: f$ z5 o8 G, ]/ `ization, the clinical hallmark of CPP is the symmet-
9 ^7 ?9 |" J1 T5 z. L1 Srical testicular growth secondary to stimulation by) Q/ O/ ?3 `! J( ~  ^
gonadotropins.1,31 T% B4 T1 F: L, h/ D0 V5 |
Gonadotropin-independent peripheral preco-
; F1 q+ ~5 W: bcious puberty in boys also results from inappropriate
+ U4 x/ Z! H9 ]androgenic stimulation from either endogenous or
( o) P$ X# r. O0 c8 Bexogenous sources, nonpituitary gonadotropin stim-
8 R1 E9 ~* N1 |, c) Z0 yulation, and rare activating mutations.3 Virilizing
. w! K7 u0 k! Icongenital adrenal hyperplasia producing excessive( K" l  _0 `6 o( x$ _- M- M
adrenal androgens is a common cause of precocious( Z# `5 G* Y* F5 O
puberty in boys.3,4
- I; j/ B$ F) l. V0 z' CThe most common form of congenital adrenal& m; ^' f9 V5 E6 V2 c9 |, Y. D
hyperplasia is the 21-hydroxylase enzyme deficiency.
8 ]1 P2 r# @( k- RThe 11-β hydroxylase deficiency may also result in
" p: Q) b7 p8 z  Oexcessive adrenal androgen production, and rarely,
2 Y5 k+ A; v; kan adrenal tumor may also cause adrenal androgen
+ a* F$ O, P6 n( j7 E# v' ^% Cexcess.1,3
4 l1 c1 H/ v; C/ W/ b# t3 zat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from1 S2 q/ {/ K: {+ e
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
+ _! d% v2 ?4 u2 W1 @! ]0 z7 qA unique entity of male-limited gonadotropin-# Q. y% [. h! r* a$ N
independent precocious puberty, which is also known
; ~7 q9 O6 ^% g+ C# [as testotoxicosis, may cause precocious puberty at a
/ G: J3 x4 g3 Z1 K* Kvery young age. The physical findings in these boys4 f# q0 ~- l9 J- P0 H
with this disorder are full pubertal development,% J( s1 P9 e8 r: m1 N5 ~
including bilateral testicular growth, similar to boys
) V  Q. F0 H8 T, q) j6 E- L2 Fwith CPP. The gonadotropin levels in this disorder
' a& O1 M) R% _; Y* l7 D; Mare suppressed to prepubertal levels and do not show; d$ U1 h& l" l6 b! C3 Z" B
pubertal response of gonadotropin after gonadotropin-. X1 }* S; p: @3 ^" g6 V5 j
releasing hormone stimulation. This is a sex-linked
+ Z: n: s) F8 ~6 fautosomal dominant disorder that affects only1 @5 K- S8 L8 D: O
males; therefore, other male members of the family2 U, I. J* a: l6 Y% j; a7 K
may have similar precocious puberty.3
+ ~) ~. K0 G: e; D; SIn our patient, physical examination was incon-2 O! i2 M$ k% i6 x% O6 z- H
sistent with true precocious puberty since his testi-
1 T( `2 \! b$ Scles were prepubertal in size. However, testotoxicosis
/ U7 j, e5 ~5 v9 ^7 U, vwas in the differential diagnosis because his father
6 |' W2 q4 J* R1 l* _started puberty somewhat early, and occasionally,
" R7 S8 Z- l8 a- R( h) T6 atesticular enlargement is not that evident in the6 d6 Y5 m- e2 p4 ~
beginning of this process.1 In the absence of a neg-
- {1 q; v  m$ A4 l4 n7 Native initial history of androgen exposure, our
' h* b2 X, @/ s0 A' \biggest concern was virilizing adrenal hyperplasia,$ e7 ~  ^8 _, m1 v5 e% P: M# p2 J3 U
either 21-hydroxylase deficiency or 11-β hydroxylase
' |$ ^1 x6 b! I# J8 ~( [deficiency. Those diagnoses were excluded by find-
: {$ ]* |+ m  R* f7 u% Jing the normal level of adrenal steroids.1 W# t, s( \" c. K
The diagnosis of exogenous androgens was strongly. W+ ?5 k0 k) }0 C2 \: E
suspected in a follow-up visit after 4 months because
/ H' e6 P" D. c; W7 lthe physical examination revealed the complete disap-
% o& }& E; l4 }/ c, B, Vpearance of pubic hair, normal growth velocity, and4 M+ I  K5 y0 U+ R- V. l$ c5 Q
decreased erections. The father admitted using a testos-+ c# O( Y, L0 h; W7 g+ Z* U
terone gel, which he concealed at first visit. He was# M+ J" h) |1 T  P
using it rather frequently, twice a day. The Physicians’
+ ]/ |: Q/ a& ^% v% L$ l$ UDesk Reference, or package insert of this product, gel or
! Q! [1 ^: t, j* S% Kcream, cautions about dermal testosterone transfer to
- j$ u6 j% @2 |3 o+ C! Aunprotected females through direct skin exposure.0 o+ e- T8 o" u* t3 ]
Serum testosterone level was found to be 2 times the
0 C  K3 S8 Z# \. x7 \- ]1 Z7 wbaseline value in those females who were exposed to- a) Y& [  A5 ^/ h# T. \
even 15 minutes of direct skin contact with their male
% O; Z  V+ x6 R6 V7 l; i, Lpartners.6 However, when a shirt covered the applica-6 H: R- V( b7 z' w$ q
tion site, this testosterone transfer was prevented.
2 o3 ?+ B  Z( b5 J7 tOur patient’s testosterone level was 60 ng/mL," I) x+ `; ~8 }
which was clearly high. Some studies suggest that. X1 Y$ N8 r/ n( k  t5 J: w0 p. T6 Z
dermal conversion of testosterone to dihydrotestos-
8 m- g' w% i: e" k/ S+ o* V6 \terone, which is a more potent metabolite, is more' o& f; Q9 s+ {* d- O! f6 q# Q( s
active in young children exposed to testosterone- u5 p5 R8 S$ Z% k; n5 ]7 [
exogenously7; however, we did not measure a dihy-0 u: P8 d! E+ U0 @3 z. H
drotestosterone level in our patient. In addition to
. a; K1 f1 F& c5 B; Q$ H& _# t  F! B% Qvirilization, exposure to exogenous testosterone in5 s6 z, k2 k- G) Z0 }
children results in an increase in growth velocity and# c3 B$ ]1 i! U. f3 }. h! \# o3 y
advanced bone age, as seen in our patient.7 z6 [7 G& C& }# ]7 f7 v$ G
The long-term effect of androgen exposure during
! Y( k' C5 C4 F& I% G& u- Iearly childhood on pubertal development and final% l1 e9 {" o' u- D
adult height are not fully known and always remain, c- f9 j; D$ e! Q9 K
a concern. Children treated with short-term testos-  Q+ e; q2 x, V2 E' R- i3 L0 X
terone injection or topical androgen may exhibit some
1 q% T6 K6 d) n, Q0 O- Uacceleration of the skeletal maturation; however, after, f' s3 I/ V2 a8 w0 P$ ^
cessation of treatment, the rate of bone maturation  O: a; G" G2 b4 D4 S
decelerates and gradually returns to normal.8,9
$ N# N: p. Z9 c- D3 C( b) S4 IThere are conflicting reports and controversy
- v% @1 |5 ~% Tover the effect of early androgen exposure on adult$ d* s) n& {  b0 c
penile length.10,11 Some reports suggest subnormal" X6 a; B3 K( Z. R' v, I3 ~, m3 ?
adult penile length, apparently because of downreg-# _+ [  V  z9 y
ulation of androgen receptor number.10,12 However,
* j5 v) }% t, `3 FSutherland et al13 did not find a correlation between! A' K4 F) i2 Z. {3 j0 E" d
childhood testosterone exposure and reduced adult
2 c- O0 h' i, \8 f/ z8 p& ?penile length in clinical studies.
5 \1 U- n: w- C1 A6 c1 CNonetheless, we do not believe our patient is' \, N3 A! _) T1 _1 k$ o
going to experience any of the untoward effects from
6 l# o8 Y# _) V6 Q1 o% e4 otestosterone exposure as mentioned earlier because' B/ U1 D; e  Z
the exposure was not for a prolonged period of time.
6 S0 E. r1 g$ y( h& b6 ZAlthough the bone age was advanced at the time of
  v. G# r1 E, e, M+ g7 F' S. [diagnosis, the child had a normal growth velocity at
9 G7 s* Q. y# wthe follow-up visit. It is hoped that his final adult5 B8 g: R1 X" _/ h
height will not be affected.
7 R5 o) k+ h9 }! N- {. f" G) h* vAlthough rarely reported, the widespread avail-
% s  }( f0 B7 `3 }% j! Aability of androgen products in our society may1 k/ F8 r' F8 Y' `$ K: q
indeed cause more virilization in male or female
0 _6 Z, h- X; Y9 vchildren than one would realize. Exposure to andro-
3 `( G/ r* d! Tgen products must be considered and specific ques-* q" }1 L% i, ^
tioning about the use of a testosterone product or
7 ~5 Z9 p- f  D  Lgel should be asked of the family members during
1 p( S3 `% d" e) ], mthe evaluation of any children who present with vir-& }0 u3 O5 [/ q7 q" w/ I
ilization or peripheral precocious puberty. The diag-
) a2 T5 ?8 m8 Y9 X; B) i. ^# \3 l2 Bnosis can be established by just a few tests and by
( ]  f* q: x2 ?5 Iappropriate history. The inability to obtain such a
3 K3 v3 `# U) h) X6 z* P( khistory, or failure to ask the specific questions, may
" K; g8 U7 p8 f, m" j- O8 \result in extensive, unnecessary, and expensive# J' |8 `2 N8 l0 S) A* F8 b: j
investigation. The primary care physician should be
' m2 k. S% W& Y& Z: ^, A5 qaware of this fact, because most of these children9 p+ W# t' I' M
may initially present in their practice. The Physicians’  S( }4 e6 S* |$ p$ |
Desk Reference and package insert should also put a. Y$ @  m( F4 H3 ]  t; z2 L
warning about the virilizing effect on a male or6 K0 n( e+ K4 ]3 o  q$ X5 ~
female child who might come in contact with some-+ A+ q# ~/ a" {, o
one using any of these products.
9 B4 c  D) P# @' s9 W6 ]1 QReferences
9 \6 l1 e* q+ p, c; b$ ?. M  H1. Styne DM. The testes: disorder of sexual differentiation3 t! a9 n, L/ S0 ?2 c/ H- o* t
and puberty in the male. In: Sperling MA, ed. Pediatric
* s$ y+ W( t; q3 @. x8 AEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;5 O% N5 ^4 _; [7 o1 p: F  X! q
2002: 565-628.% Q# [* H2 D9 C
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
3 t" n6 E7 O; q* }. r0 wpuberty 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
) L' S' h1 B: z$ v8 K$ {: O
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