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鄉下的妹子太便宜,一次四個都要了[12P]

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Sexual Precocity in a 16-Month-Old
& [; ]$ t- C4 k8 lBoy Induced by Indirect Topical3 X: `" ?% [' C" T0 b) G
Exposure to Testosterone
( Z2 |( c/ p- I* c1 ASamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,23 e8 h. e) |0 [4 h1 Q/ n
and Kenneth R. Rettig, MD1
& [' x# T" A- a9 ?Clinical Pediatrics/ v2 K& M. @2 w2 [* d$ t# u: m6 V
Volume 46 Number 6! p  Y9 q/ I, K& h1 r2 q
July 2007 540-543/ R9 `, @7 _1 _9 l& H6 L
© 2007 Sage Publications
1 i6 |2 u$ r' k( V! F" M10.1177/0009922806296651* d' Y. p) d& ^. D2 @, ?
http://clp.sagepub.com
$ M8 f  O% x, A; g8 \) u! v4 C7 Xhosted at8 J8 u. z+ w; d/ w) c: G2 l
http://online.sagepub.com
+ x% S$ `7 F/ u. u6 ?+ I6 jPrecocious puberty in boys, central or peripheral,
- D+ ^6 S1 u  N- cis a significant concern for physicians. Central6 M, y8 n  {9 W3 ~2 x+ g- ^7 o
precocious puberty (CPP), which is mediated) Z& Z! u$ x; f4 @/ {) `
through the hypothalamic pituitary gonadal axis, has
8 F" X/ G& c; J9 Z# |a higher incidence of organic central nervous system- ^! A7 {  r* [0 J
lesions in boys.1,2 Virilization in boys, as manifested. j$ a4 y( {/ X, E- u6 O
by enlargement of the penis, development of pubic
- f( @( S- T" f* e+ r- Y9 g2 xhair, and facial acne without enlargement of testi-
. q- H4 C8 c  J. J: q; Mcles, suggests peripheral or pseudopuberty.1-3 We
5 C. g2 ]- D9 W" T( T9 [report a 16-month-old boy who presented with the
! s$ }( S% J. }0 |! benlargement of the phallus and pubic hair develop-" O7 f- r+ u. P9 G: j
ment without testicular enlargement, which was due4 @3 B) u6 k0 L( u
to the unintentional exposure to androgen gel used by
, e( D0 p! B4 Z0 Jthe father. The family initially concealed this infor-
4 o6 P7 ^0 v3 ]' nmation, resulting in an extensive work-up for this4 r, Y" U/ D5 l: f. W6 `" h# J
child. Given the widespread and easy availability of- ]* N) `/ w! @7 V5 ?
testosterone gel and cream, we believe this is proba-
5 S& x. ~- ?/ c5 O. B0 x2 A8 cbly more common than the rare case report in the
3 F* [0 D- T. O  ]- |( l3 K/ j. ^literature.49 ~0 c+ O( [( I0 t. q. x
Patient Report) Y6 s+ F5 j1 ?6 k4 s
A 16-month-old white child was referred to the
9 d5 b% j0 G/ G0 p2 oendocrine clinic by his pediatrician with the concern
: X- g, ^) V& |, O+ Q) Q  n! bof early sexual development. His mother noticed
3 @' O+ x+ J; P4 A" [6 G" w  t4 Elight colored pubic hair development when he was
, ~  ?. D1 c: ^/ ^/ jFrom the 1Division of Pediatric Endocrinology, 2University of! t5 D0 r$ E! v8 {0 m
South Alabama Medical Center, Mobile, Alabama.+ O' i' T. ^' i7 B+ w
Address correspondence to: Samar K. Bhowmick, MD, FACE,8 v2 W: H9 r1 W2 X
Professor of Pediatrics, University of South Alabama, College of
' T# O: M8 W+ C5 H8 \Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
" m/ F2 g' ?8 t) Te-mail: [email protected]." W1 z4 i6 N8 a% q2 X  q5 U
about 6 to 7 months old, which progressively became
% Y% J! q6 x: _  H* f5 s2 ]: `5 zdarker. She was also concerned about the enlarge-0 }2 |" X0 k$ }' n& H
ment of his penis and frequent erections. The child
% {* T, M% B. hwas the product of a full-term normal delivery, with3 c5 c' I3 k. @* h
a birth weight of 7 lb 14 oz, and birth length of. `2 [5 M* c! R; R, M! f: \
20 inches. He was breast-fed throughout the first year
6 ^7 ^3 L5 j8 X+ K; N; cof life and was still receiving breast milk along with
# f# p9 m+ w# x4 ]" p9 Csolid food. He had no hospitalizations or surgery,0 W: ^' ~/ W  A2 t
and his psychosocial and psychomotor development# G- l' O. l* o9 r
was age appropriate.
3 |0 T- ]% S$ u2 hThe family history was remarkable for the father,
3 P8 M, B& h! W- ?7 D, {who was diagnosed with hypothyroidism at age 16,
$ I: P- U$ H2 ?which was treated with thyroxine. The father’s
* @. e0 x& P3 u$ D1 K. M3 lheight was 6 feet, and he went through a somewhat# B# K+ N6 X) ?) P/ ]& J
early puberty and had stopped growing by age 14.( F1 Q' m- k0 i: w' Q
The father denied taking any other medication. The/ `4 s) B9 w: g1 l" |5 `
child’s mother was in good health. Her menarche/ t- P% w7 U% N* V/ B
was at 11 years of age, and her height was at 5 feet
" J. Z4 d7 K* D8 x$ W* {5 inches. There was no other family history of pre-8 p- `; H9 _) O7 o3 s& x
cocious sexual development in the first-degree rela-
; Z% Z$ s+ D4 V8 E+ I8 I) itives. There were no siblings.
. u) S. d7 D5 D0 D5 HPhysical Examination2 I' q( N) t/ g" ^! n; h4 w! s3 p
The physical examination revealed a very active,& q1 b) ^: X( B: ?1 f( G* N" K+ N
playful, and healthy boy. The vital signs documented
& U3 F; I0 Q2 a9 wa blood pressure of 85/50 mm Hg, his length was
& y6 \; [  F+ S( J' b0 u( C90 cm (>97th percentile), and his weight was 14.4 kg
8 F+ e# p0 F2 _4 D$ i% h$ k(also >97th percentile). The observed yearly growth
: j  S: j' |4 Z, S# N* ~4 V5 bvelocity was 30 cm (12 inches). The examination of
( L/ E) R9 _3 h' C0 u: athe neck revealed no thyroid enlargement.4 M& S3 Q* R2 Y, H1 h4 N
The genitourinary examination was remarkable for
) ?6 B3 u; c# o2 benlargement of the penis, with a stretched length of0 h% F% g: e, r8 v4 k% P) h8 r
8 cm and a width of 2 cm. The glans penis was very well
: @* m+ n2 _& W+ G9 Xdeveloped. The pubic hair was Tanner II, mostly around
7 @1 k, ~$ {' F% ^+ }: Y8 y540# F2 ]3 z% H6 o+ M  L4 \: W
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from( S  u8 a- q$ I' ~/ `
the base of the phallus and was dark and curled. The
' h) a* ]9 ^5 L  D( o5 A7 u, wtesticular volume was prepubertal at 2 mL each.5 p+ z3 F4 o. q! `& H2 _+ h
The skin was moist and smooth and somewhat3 [2 }7 U5 ?/ r' W% Q4 J( Y3 U4 t
oily. No axillary hair was noted. There were no
# F* `; ^7 _( Z$ xabnormal skin pigmentations or café-au-lait spots.
) t4 K) [6 R0 b1 O  t  K) b! ANeurologic evaluation showed deep tendon reflex 2+
& |& }  q& r: f9 x: x- E- |# Fbilateral and symmetrical. There was no suggestion
/ ~$ S, |( e# o# Oof papilledema.4 s/ b1 Q! W$ o0 E. C" k0 E
Laboratory Evaluation
* Q- K4 A# {2 J+ p" u0 b, ]: yThe bone age was consistent with 28 months by
5 M( n6 B/ T8 Y6 g3 w% E! g; \using the standard of Greulich and Pyle at a chrono-
3 e% W! U+ M7 J# ?" {% x4 zlogic age of 16 months (advanced).5 Chromosomal# n( V3 u  E4 Q: I6 I
karyotype was 46XY. The thyroid function test
6 r  L; B) }, ]$ n  U+ Sshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
( \* `8 m* v2 W, a0 Y- @! T: Qlating hormone level was 1.3 µIU/mL (both normal).
/ O! b# \  Z" zThe concentrations of serum electrolytes, blood
8 `% |) W7 T2 o7 K8 [1 ^, Aurea nitrogen, creatinine, and calcium all were
3 m% |3 I8 Y; l8 O4 rwithin normal range for his age. The concentration
6 o+ T7 a3 o+ J+ {of serum 17-hydroxyprogesterone was 16 ng/dL
* Y9 r9 M, g# j(normal, 3 to 90 ng/dL), androstenedione was 20, o7 ]  g" ^" W: Z7 R  |
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-5 b- R8 k7 b; Y- Q8 h  k
terone was 38 ng/dL (normal, 50 to 760 ng/dL),1 g" \# ]6 f7 g+ R/ d9 L9 a
desoxycorticosterone was 4.3 ng/dL (normal, 7 to2 t: s4 m  `: I  H
49ng/dL), 11-desoxycortisol (specific compound S)  Y, m& ?4 i) I# }! e0 g( ~
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-+ W& Q7 G# G& k& u: l/ M: I
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
! q/ o5 u4 L0 {3 |testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
0 I7 F8 r, R9 |; Dand β-human chorionic gonadotropin was less than
5 p, m' M3 B3 i& ~  o  t( n5 mIU/mL (normal <5 mIU/mL). Serum follicular
4 {$ p4 i3 P, a( astimulating hormone and leuteinizing hormone$ O( L* ?4 ^& J& H7 K
concentrations were less than 0.05 mIU/mL1 I2 x. ]) p! `9 r% ^. k3 P
(prepubertal).6 J# w! S5 U  N% r
The parents were notified about the laboratory0 [! c$ ]; u: y) U
results and were informed that all of the tests were: T1 q7 \" T% V7 y
normal except the testosterone level was high. The
6 s6 j2 q5 C- C. x6 i$ cfollow-up visit was arranged within a few weeks to
3 W# s2 t" K% E1 a; F0 Mobtain testicular and abdominal sonograms; how-
3 j8 Q9 {- o3 t8 H: S0 Z7 jever, the family did not return for 4 months.3 c) \& R4 K, d  M
Physical examination at this time revealed that the* k; V9 w# v: o7 w: l, h. i7 j
child had grown 2.5 cm in 4 months and had gained
& `3 f! O2 w5 I3 W2 J9 C2 kg of weight. Physical examination remained1 g7 q; j! E  P- q9 _7 F$ B
unchanged. Surprisingly, the pubic hair almost com-" P- x# _0 R- {/ y* O  `! x
pletely disappeared except for a few vellous hairs at
1 Q- H8 I* F1 s. g8 L. Hthe base of the phallus. Testicular volume was still 2
9 L. G) ~- L1 {8 VmL, and the size of the penis remained unchanged.
! J8 r& [3 g' ^% V3 p) H! I6 UThe mother also said that the boy was no longer hav-
5 p- c' \: q; c) C' sing frequent erections.
3 ]9 ?7 K3 Y6 WBoth parents were again questioned about use of- k# ^, w0 U6 }" n1 q
any ointment/creams that they may have applied to2 J1 x. }) V2 `) J
the child’s skin. This time the father admitted the' |' D; H: |, U0 h, k0 A. m. A
Topical Testosterone Exposure / Bhowmick et al 541/ R1 }) r5 e4 Z2 [, A! I1 |: x
use of testosterone gel twice daily that he was apply-
4 D% n. g% E! }5 ^, _" w- Q, {6 cing over his own shoulders, chest, and back area for
, }* q+ C0 y7 o, D( [1 fa year. The father also revealed he was embarrassed
% G9 X* \$ g8 v& @! Dto disclose that he was using a testosterone gel pre-% p& Q. t- [" ^1 ?
scribed by his family physician for decreased libido4 {1 O& b1 M' P, ?( Q
secondary to depression.
6 I- S8 Y7 [  [The child slept in the same bed with parents.2 |. L. n0 _) Y
The father would hug the baby and hold him on his# q. @) S# v: _5 x9 @+ O; x
chest for a considerable period of time, causing sig-
1 n" ~2 `- Q' g" Cnificant bare skin contact between baby and father.( D# E  D6 c8 p. a( J6 O
The father also admitted that after the phone call,  N& A* }) T1 w/ j+ A' N
when he learned the testosterone level in the baby3 \* r; v! N" O/ Q4 n( U2 y4 g
was high, he then read the product information
$ T8 k! c' C' Q4 z4 N$ lpacket and concluded that it was most likely the rea-
* p+ E; Q# @, B% [5 bson for the child’s virilization. At that time, they
  T4 i# T) k! Y, Rdecided to put the baby in a separate bed, and the! S; J* A( b5 K  t0 `" A& o
father was not hugging him with bare skin and had
: k, b9 l$ B+ q2 P" C, lbeen using protective clothing. A repeat testosterone$ w& X, b& S! Q
test was ordered, but the family did not go to the$ D* ?: o; {% `4 a1 |
laboratory to obtain the test.
6 D5 @- W% J8 T, \. L, S% x3 bDiscussion$ Q- K- y3 [, c+ M
Precocious puberty in boys is defined as secondary+ w9 e! c; H! \+ ~
sexual development before 9 years of age.1,4
; d1 l: `: S. q* [$ l7 O0 X- SPrecocious puberty is termed as central (true) when- H2 e1 S7 C) U% l
it is caused by the premature activation of hypo-7 g! x5 _" ~7 G5 E9 i8 B
thalamic pituitary gonadal axis. CPP is more com-
& X6 _& ^4 P# wmon in girls than in boys.1,3 Most boys with CPP- {9 l9 S; Y$ r* X! O, w/ ~' {
may have a central nervous system lesion that is& [$ H/ Q5 A( I$ b. h2 `+ h: W. N1 l# c
responsible for the early activation of the hypothal-
4 a# x! L' P. S" Kamic pituitary gonadal axis.1-3 Thus, greater empha-
% p  U9 P$ O# a1 n; d6 f* ssis has been given to neuroradiologic imaging in
4 V! o) g) C0 D5 j+ E3 {- y) A" |( Lboys with precocious puberty. In addition to viril-
0 }: l4 U2 F4 v% D6 E6 `; }! ^! Fization, the clinical hallmark of CPP is the symmet-
* g4 R2 I7 B3 Q1 P3 drical testicular growth secondary to stimulation by* F% e- B3 c' B3 X, ^: P
gonadotropins.1,3
# ?8 j* |9 O+ k" \' _, WGonadotropin-independent peripheral preco-8 f. j8 ]. j6 c3 A: P! K) G
cious puberty in boys also results from inappropriate
' K4 f& R" T* w3 R( Yandrogenic stimulation from either endogenous or3 s6 ~% W. |- N* K
exogenous sources, nonpituitary gonadotropin stim-
0 Y# G- p2 F  L2 j5 b0 nulation, and rare activating mutations.3 Virilizing
/ h$ \5 U# s/ u6 D4 K  p" [congenital adrenal hyperplasia producing excessive
5 b# a3 T8 T( J' i5 G2 ?adrenal androgens is a common cause of precocious% Y. V7 r8 N5 l. C9 |6 E6 o: {  g: ?
puberty in boys.3,42 K4 a# B: B8 n5 _( m
The most common form of congenital adrenal
4 o7 E$ [1 k5 q9 hhyperplasia is the 21-hydroxylase enzyme deficiency.0 I0 O. U- f7 B3 T
The 11-β hydroxylase deficiency may also result in% }7 D5 f# U8 E( o& M6 D) g
excessive adrenal androgen production, and rarely,
) _' X. k- V% h$ o1 fan adrenal tumor may also cause adrenal androgen' _+ e5 r& {: t3 t/ M( ~/ ?; T
excess.1,3
" c0 M' w  W( e( h" }1 t0 Kat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
  \# j# a. \4 [4 J5 \542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
0 |1 @3 Y; T- `, @8 t- }0 {0 N  iA unique entity of male-limited gonadotropin-
4 _$ v2 U: A; @, q3 d0 N! jindependent precocious puberty, which is also known
4 ]" x8 Z1 _# Ras testotoxicosis, may cause precocious puberty at a
! T/ t6 z9 |% j# v- pvery young age. The physical findings in these boys
& N* d4 l' m/ r& Dwith this disorder are full pubertal development,, V# k$ ~4 Z  _9 @
including bilateral testicular growth, similar to boys1 |: s2 o5 P. ]+ r8 `
with CPP. The gonadotropin levels in this disorder# L4 ^  ^1 _2 l- q
are suppressed to prepubertal levels and do not show* y+ [4 |, u- o0 O' M* k# v
pubertal response of gonadotropin after gonadotropin-) h- \' R+ ]! T" J7 f4 Y
releasing hormone stimulation. This is a sex-linked
. m  n$ o# z- W3 J" |autosomal dominant disorder that affects only, a9 h% E: H' h* y1 G
males; therefore, other male members of the family; P5 [! g, y. U7 N7 ~+ Q, u
may have similar precocious puberty.3
1 w6 }6 d7 G% kIn our patient, physical examination was incon-
! S0 z. }; P1 \# s6 {sistent with true precocious puberty since his testi-
, f$ C4 e7 ^; `cles were prepubertal in size. However, testotoxicosis0 U! U1 L( Y$ X7 l, `1 b; \
was in the differential diagnosis because his father7 Y6 n# U  @* X$ q
started puberty somewhat early, and occasionally,
5 Q0 S' D, E# X9 _- [: j6 ytesticular enlargement is not that evident in the
5 ]6 J. ]% _/ E0 A9 c4 ]0 ^beginning of this process.1 In the absence of a neg-
3 E) k, u. D% R; L% Yative initial history of androgen exposure, our
4 L2 m( {# W3 }0 Jbiggest concern was virilizing adrenal hyperplasia,
2 N0 T6 ^1 _3 S0 peither 21-hydroxylase deficiency or 11-β hydroxylase
; u9 ?# y8 f+ Q: i4 f  ~deficiency. Those diagnoses were excluded by find-& s! j! d4 j# t! ^) v
ing the normal level of adrenal steroids.9 L) _8 U+ i% k% G/ m& A4 @) K$ [
The diagnosis of exogenous androgens was strongly
. _3 A- A* [! [* Qsuspected in a follow-up visit after 4 months because
, U) F" c. E$ L" n+ |the physical examination revealed the complete disap-7 C" B0 s+ l( q: a6 b# e7 m
pearance of pubic hair, normal growth velocity, and+ Y) D& L+ @2 T5 X( ?. W+ E
decreased erections. The father admitted using a testos-& p+ C0 g; \: T* @
terone gel, which he concealed at first visit. He was
) H, D: P6 M* N9 a" w/ G1 J4 u$ Qusing it rather frequently, twice a day. The Physicians’% a# w- h3 n' k5 @
Desk Reference, or package insert of this product, gel or* z) b4 ?& J$ E- @3 K4 p2 z
cream, cautions about dermal testosterone transfer to) q$ O4 Z" w- y, g/ J7 ~8 ^
unprotected females through direct skin exposure.
+ e' x% D& A. x! T" t4 r9 P  SSerum testosterone level was found to be 2 times the
7 q$ C# J6 \9 ybaseline value in those females who were exposed to
0 C6 t3 U2 w5 {4 ?even 15 minutes of direct skin contact with their male
7 S" o' A6 U! W  `* @, d' Tpartners.6 However, when a shirt covered the applica-
/ F, ~& Q9 V+ V6 a7 a9 S7 ltion site, this testosterone transfer was prevented.
7 d$ @/ t0 `" w0 G8 VOur patient’s testosterone level was 60 ng/mL,
8 C& [6 H& v5 `2 F) n/ r7 Zwhich was clearly high. Some studies suggest that' D$ J- R% [% s3 a0 b# w+ {+ n
dermal conversion of testosterone to dihydrotestos-
0 w; N% W9 k* e8 A1 {4 l. Aterone, which is a more potent metabolite, is more
: T# Q( x; ]4 |! b4 ractive in young children exposed to testosterone
6 Y' C1 n3 B/ }  q, g/ aexogenously7; however, we did not measure a dihy-" p. {' ?) j9 a1 q/ ~
drotestosterone level in our patient. In addition to
' i! U0 w3 \7 E! a" \5 nvirilization, exposure to exogenous testosterone in& S; `9 E+ {- `3 }: y" t
children results in an increase in growth velocity and
/ R2 v4 L! Z  S/ L0 K  Z1 Vadvanced bone age, as seen in our patient.9 W  I/ A+ t- I, d" ?: r
The long-term effect of androgen exposure during! X# y) O) W% o. F- e
early childhood on pubertal development and final
/ F1 p& e/ R2 g% ]2 h1 h+ G0 Eadult height are not fully known and always remain/ C) j7 H  o  E! B: ~8 t3 w1 ]
a concern. Children treated with short-term testos-0 N# F3 v# e8 d1 m6 k( f% @
terone injection or topical androgen may exhibit some6 a- ^( V- H2 h. N, n
acceleration of the skeletal maturation; however, after0 ^( Y, R0 e) [+ g$ Q
cessation of treatment, the rate of bone maturation
8 K2 }. j, ~  {. f7 t2 adecelerates and gradually returns to normal.8,9! |1 i: L$ M6 H
There are conflicting reports and controversy
; y. T: ~' [" E8 a# n' |over the effect of early androgen exposure on adult6 o) K0 w8 o5 v# P  g  @
penile length.10,11 Some reports suggest subnormal+ {+ [" c& O7 z' E3 z
adult penile length, apparently because of downreg-! X9 M6 I( i& T! r4 P4 Z* F
ulation of androgen receptor number.10,12 However,
6 S; r+ e8 `$ l& D/ rSutherland et al13 did not find a correlation between
1 z  O6 o( k- s6 R3 Uchildhood testosterone exposure and reduced adult( N$ A3 j7 q  t
penile length in clinical studies.
  _" R6 M7 t3 h2 Z4 q4 c% }: RNonetheless, we do not believe our patient is
7 w/ k7 ^; H5 s; M- u* I' @7 S+ Bgoing to experience any of the untoward effects from
/ F1 D4 k* R  p* B/ J) O8 Rtestosterone exposure as mentioned earlier because
# K! ?: O" Q7 K$ k& [the exposure was not for a prolonged period of time.
; f# L; A* E# }1 l8 EAlthough the bone age was advanced at the time of- _2 T8 W: |* e3 y( q
diagnosis, the child had a normal growth velocity at" w$ s6 w+ J8 _) Q. A
the follow-up visit. It is hoped that his final adult% r" E+ `- U2 T! Z* h- A
height will not be affected.. k+ u7 @; w- c4 Y+ `3 o, U
Although rarely reported, the widespread avail-! `( d  a9 K) J+ z0 q
ability of androgen products in our society may
7 H* x* J+ J3 L! Mindeed cause more virilization in male or female
4 O+ d3 i: N  ?6 |children than one would realize. Exposure to andro-
) @- h0 G( s( t' tgen products must be considered and specific ques-
0 u( ?5 y6 P' u) itioning about the use of a testosterone product or
) N1 r: ?( i! g9 ]% h0 b" Y( @gel should be asked of the family members during
- M, ]: r; e5 S1 z% hthe evaluation of any children who present with vir-
8 d# Q6 @* Z' Gilization or peripheral precocious puberty. The diag-
1 V% x4 @/ s, {0 \! ?2 l) Rnosis can be established by just a few tests and by8 \4 E) Q/ r( f4 C$ ^
appropriate history. The inability to obtain such a& m; q) I" z, O' l. s
history, or failure to ask the specific questions, may
) v& \7 A& D6 N( [4 o" bresult in extensive, unnecessary, and expensive
' w& v3 i9 `+ ~9 e4 X: yinvestigation. The primary care physician should be( T! w/ E- J" v& m
aware of this fact, because most of these children
' F+ k% H7 [9 L1 kmay initially present in their practice. The Physicians’
+ @; e2 z- M2 m; p9 eDesk Reference and package insert should also put a. E# u  u: J* m
warning about the virilizing effect on a male or5 ?& n- C; ^8 N
female child who might come in contact with some-& }; P6 H& h9 u. w9 n" n8 D& _7 l/ H
one using any of these products.
) f9 j- K( S$ H& y# M" Z8 u9 g( EReferences
. }  r) n6 d" B) |! m9 r6 m6 \1. Styne DM. The testes: disorder of sexual differentiation
4 l) U% G1 {2 Nand puberty in the male. In: Sperling MA, ed. Pediatric
. d. Y" N; i: k+ Y0 FEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;1 |# D; ^$ O4 L, b7 \2 w9 e" s' ]& T- s
2002: 565-628.
- K, ]+ M8 L+ M1 C5 D2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious- `# L5 w. L7 H- [4 C
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old7 E  i8 r" C7 ?" P
Boy Induced by Indirect Topical
6 Y0 Q; |+ Q, O9 J6 j; [7 dExposure to Testosterone
5 l* B3 p" m, I0 x! [4 SSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
. S5 z8 U$ m. u/ M6 E' D0 L4 Xand Kenneth R. Rettig, MD1
; G# v, ]' w8 }( |5 \0 ^Clinical Pediatrics4 \$ s5 D. a5 n( M  u
Volume 46 Number 6
) U: @, }& {/ O6 N& wJuly 2007 540-543: y7 K+ Q9 y; x
© 2007 Sage Publications
6 H' b3 F9 H( i7 [1 c10.1177/00099228062966516 O* n5 y& S1 A$ l* }. b) x
http://clp.sagepub.com
$ Q: c5 i* a, n# Z, a9 s; Whosted at
) y, t& H; _+ }8 X$ whttp://online.sagepub.com7 D. k6 {" C, K# h8 e, B2 G
Precocious puberty in boys, central or peripheral,6 i6 @3 @& m+ b+ ?% N2 b- w
is a significant concern for physicians. Central
: C! i% N# J2 r  \* E/ y5 f, Mprecocious puberty (CPP), which is mediated
6 ?) r) e! W3 i3 z. }8 W2 J; j4 gthrough the hypothalamic pituitary gonadal axis, has$ h& y! J+ k9 u
a higher incidence of organic central nervous system8 D3 D& X' @" e& A
lesions in boys.1,2 Virilization in boys, as manifested8 S1 C' N* N! H, }1 R+ c" _
by enlargement of the penis, development of pubic
9 A6 V9 {$ L6 o# l4 E' phair, and facial acne without enlargement of testi-* w7 y# r" h7 G) w
cles, suggests peripheral or pseudopuberty.1-3 We
0 C; A8 n& W6 H% O; E2 Ireport a 16-month-old boy who presented with the9 ]8 d' O5 b" Z; s9 w, L0 o
enlargement of the phallus and pubic hair develop-
% n6 E; h2 }5 h# Zment without testicular enlargement, which was due
- f! z$ ~( Q5 U. qto the unintentional exposure to androgen gel used by
' p( K$ G+ L9 w$ t! L: K" Kthe father. The family initially concealed this infor-) _9 A/ E" H8 B3 m' h0 s6 ?
mation, resulting in an extensive work-up for this
+ z0 d1 h' M1 p* I4 H- ~0 achild. Given the widespread and easy availability of
( q' _1 l) @* I: \1 etestosterone gel and cream, we believe this is proba-
, r# n4 }3 ~+ S! p  C9 E$ Q% Kbly more common than the rare case report in the
" C1 T! R7 f- ~0 F" B. ?literature.4+ m  J+ d5 e" z4 [
Patient Report. l( Q8 |7 N  u3 ~4 h. O' w9 {8 @
A 16-month-old white child was referred to the* a$ t. Z& P0 L- `- j" ^/ m3 Q( @2 P
endocrine clinic by his pediatrician with the concern5 \; A3 z- O& x5 f9 o
of early sexual development. His mother noticed
3 y* G2 W6 z* ^light colored pubic hair development when he was% z6 C# {  M" f0 e8 o2 e' T
From the 1Division of Pediatric Endocrinology, 2University of0 P+ Y6 B2 `: j4 y: g1 B
South Alabama Medical Center, Mobile, Alabama.
5 n% K: a5 D' I+ pAddress correspondence to: Samar K. Bhowmick, MD, FACE,
* T. m1 u" d9 f4 h' nProfessor of Pediatrics, University of South Alabama, College of2 o2 Z; s# n- u) ?; m+ Y9 D% U
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
9 S2 O* J% S. w8 M' Ke-mail: [email protected].
0 ]8 S: }2 D# pabout 6 to 7 months old, which progressively became3 k0 ?* r& o" F6 ]6 V
darker. She was also concerned about the enlarge-
( Q2 k) W2 _6 _* O/ q4 R  o# qment of his penis and frequent erections. The child; W0 Z/ g3 @' D( c
was the product of a full-term normal delivery, with
" ~: c" n" Z) D5 ra birth weight of 7 lb 14 oz, and birth length of
8 F8 @9 }# m8 g: N4 W7 [20 inches. He was breast-fed throughout the first year
6 x8 E6 ]- v3 c) Q) Qof life and was still receiving breast milk along with
% h# i& y: i8 R: N- Xsolid food. He had no hospitalizations or surgery,8 c" j# H* P! d, V. B( k
and his psychosocial and psychomotor development* P: H- x  d/ H. _
was age appropriate.. J+ w1 i. v; l; E6 R6 ~' v0 i' p; K7 h5 b
The family history was remarkable for the father,
7 ~# m5 u; N7 K, q# z- b7 twho was diagnosed with hypothyroidism at age 16,2 n1 d( p7 a  u
which was treated with thyroxine. The father’s
! b9 I1 N7 |' Theight was 6 feet, and he went through a somewhat# U$ f6 C! v, J/ g
early puberty and had stopped growing by age 14.
. R& P0 }7 k, u1 jThe father denied taking any other medication. The
2 K% ^& Y- G0 }: q" j, @child’s mother was in good health. Her menarche
9 J6 b  A" k) X  s" [/ i. twas at 11 years of age, and her height was at 5 feet
5 S! F* O6 R# Y: k. o+ V5 inches. There was no other family history of pre-
7 S2 o% H$ s: R! C- b; V3 ^cocious sexual development in the first-degree rela-. X$ e( O) P, W# F. Z
tives. There were no siblings.
& j2 R* Z4 m, w' lPhysical Examination2 ?' H0 A5 K1 g" w+ u  }
The physical examination revealed a very active,
. H5 X( V$ |! x+ _& r. l  p2 L3 ~playful, and healthy boy. The vital signs documented
8 M- i, W2 k6 d; la blood pressure of 85/50 mm Hg, his length was
2 S. m4 P( u) z0 M90 cm (>97th percentile), and his weight was 14.4 kg' N7 B8 v7 A7 v* B6 N. M
(also >97th percentile). The observed yearly growth- U1 {7 y. P8 R6 P% S
velocity was 30 cm (12 inches). The examination of% m  L5 n* |* n& }
the neck revealed no thyroid enlargement.' ?+ U. \2 o8 r) h( O
The genitourinary examination was remarkable for7 a! s2 W0 w6 D4 _; u4 \
enlargement of the penis, with a stretched length of
% M/ Z& n3 A( s; r8 M0 @8 cm and a width of 2 cm. The glans penis was very well
7 O8 y! ^. \3 l1 h) `developed. The pubic hair was Tanner II, mostly around
- o6 B! g' X$ F/ a. J9 X540' E2 z. Q1 Z) ~: z
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
4 G; G9 L0 E% s8 B4 O3 othe base of the phallus and was dark and curled. The
- l$ H' h: z9 m- h. Vtesticular volume was prepubertal at 2 mL each.
9 d. t! c$ J. B5 a) y5 rThe skin was moist and smooth and somewhat: O' d' V" t- B: Z
oily. No axillary hair was noted. There were no
, `# L9 l. T' e7 wabnormal skin pigmentations or café-au-lait spots.
& b5 v2 v  d9 d6 `9 E' A. \Neurologic evaluation showed deep tendon reflex 2+
1 Y5 ^1 ?. b, e# @; N# L. F" bbilateral and symmetrical. There was no suggestion% |- a5 ~9 h8 }$ C1 W
of papilledema.
3 p2 J$ v( r6 `) f& y) P0 B, I  }/ pLaboratory Evaluation1 q  u. a* k( ~6 \7 M' H
The bone age was consistent with 28 months by* _: u/ f' ]8 s' B" \& r7 ]
using the standard of Greulich and Pyle at a chrono-2 U7 g0 |1 E4 |/ F$ u
logic age of 16 months (advanced).5 Chromosomal
  C4 H  t' \+ R3 ekaryotype was 46XY. The thyroid function test  y9 p* T$ q4 j6 @
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
" o+ \" q0 a1 Hlating hormone level was 1.3 µIU/mL (both normal).
" \: W. c' W8 S2 K6 a' d  }The concentrations of serum electrolytes, blood( z( G% v( n5 z. \9 A! w0 F! T
urea nitrogen, creatinine, and calcium all were+ e5 L4 O6 F7 R
within normal range for his age. The concentration
- D2 s5 S3 q/ p) J( K  \7 C. i; nof serum 17-hydroxyprogesterone was 16 ng/dL1 T+ L, r1 g; q! T! \& U8 R. v
(normal, 3 to 90 ng/dL), androstenedione was 207 y5 R4 E$ l9 f# Q4 p: Y
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-9 x( g4 d9 W! B' M
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
& X7 r1 T1 k" y+ V- c+ t; q3 zdesoxycorticosterone was 4.3 ng/dL (normal, 7 to2 H$ s- ~8 q) X( Q& i
49ng/dL), 11-desoxycortisol (specific compound S)
$ j! X9 }2 c: M. b9 zwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-: \, i* t( _4 c7 z/ u; e5 U
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
. H5 h. y3 f& d8 g( mtestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
& y, ^: @% R; X/ W, j0 _and β-human chorionic gonadotropin was less than2 |" s/ |6 B" q2 [$ O
5 mIU/mL (normal <5 mIU/mL). Serum follicular. A0 d/ u; R% J( V$ |: ~5 j* I
stimulating hormone and leuteinizing hormone7 d: A9 ]3 S. c2 p, T5 \- |+ N& C
concentrations were less than 0.05 mIU/mL! V  w8 \% N- ~0 W+ m4 D
(prepubertal).
; F, A6 Z' p7 N7 F" y3 G4 V) z3 mThe parents were notified about the laboratory1 J" V! l* ~3 ]3 M7 I5 @
results and were informed that all of the tests were
- P7 J; _4 {0 F! K" Anormal except the testosterone level was high. The( p/ Z9 g* I5 ]2 p  y4 `! q
follow-up visit was arranged within a few weeks to
3 f5 z; c# i2 ?4 oobtain testicular and abdominal sonograms; how-' W9 t# G% x% {' i: M0 x
ever, the family did not return for 4 months.3 L. U$ N% ^: j# V- {7 g6 M
Physical examination at this time revealed that the
: U; d- g/ M* e& s' cchild had grown 2.5 cm in 4 months and had gained
* X9 t/ G% N6 h5 d  G2 kg of weight. Physical examination remained1 d: u4 E' J( `% Z9 _. U$ j
unchanged. Surprisingly, the pubic hair almost com-
: U6 w# o. B& }# P4 H" k" O& D& z/ Bpletely disappeared except for a few vellous hairs at9 V& n9 V1 O# @7 \% f$ n
the base of the phallus. Testicular volume was still 23 c4 e: j6 G/ l. {
mL, and the size of the penis remained unchanged.
3 n7 ^3 N# \) Q# {6 \: GThe mother also said that the boy was no longer hav-
: F2 M$ @: Y* s) K8 ying frequent erections.
  o% O# B- T& v; {* ~Both parents were again questioned about use of& e5 a) B% p/ t
any ointment/creams that they may have applied to$ m' I) l; ^$ S5 l% A
the child’s skin. This time the father admitted the: c& a( j4 a& ~( Y5 ]
Topical Testosterone Exposure / Bhowmick et al 541
4 P9 q8 ~! k9 |% B! i6 `4 D! Buse of testosterone gel twice daily that he was apply-2 w3 F$ P( n* ?6 ~) O
ing over his own shoulders, chest, and back area for% W1 e/ L: P% G3 h9 x1 z9 }* k
a year. The father also revealed he was embarrassed' m0 T. l7 ]1 K' r3 I, ^
to disclose that he was using a testosterone gel pre-5 G3 w5 l  E# k* \; I& Y
scribed by his family physician for decreased libido
! Y& L/ w- y- k2 u- x3 V% nsecondary to depression.
) G1 N; W  B1 [: q/ Z  vThe child slept in the same bed with parents.
2 ?; b% S. O. ^- C+ s; bThe father would hug the baby and hold him on his  |: d1 V8 R! X3 o& J) p
chest for a considerable period of time, causing sig-( y: Z4 ^7 _7 [2 a
nificant bare skin contact between baby and father.
) J- K8 W  f0 X9 [# e9 e' IThe father also admitted that after the phone call,
9 V- J% l. V6 C( b) ^* xwhen he learned the testosterone level in the baby" L( L9 p" Z/ @' D6 I7 ^6 b0 H( J9 N
was high, he then read the product information
; ^. I! `, C7 k! ~, W- O5 Lpacket and concluded that it was most likely the rea-
9 r3 O( }+ t7 ?1 s# k7 O+ yson for the child’s virilization. At that time, they0 U: d) k; `2 ]/ p
decided to put the baby in a separate bed, and the" \4 p: u8 c/ o( Z" I! `, ]0 Q
father was not hugging him with bare skin and had) Z8 A' x% `$ A1 c7 p
been using protective clothing. A repeat testosterone
8 u( c1 X5 @( V& K  b' Btest was ordered, but the family did not go to the
4 w5 D" [5 L2 c5 Z2 O; T9 b  A: ]laboratory to obtain the test.8 O4 E/ @, g4 L7 u- @
Discussion
9 D3 g- q& \+ }* ^2 |" KPrecocious puberty in boys is defined as secondary
" O! u, U5 U6 B6 m- ~: Hsexual development before 9 years of age.1,4: t6 U. ~+ S! B1 K! _
Precocious puberty is termed as central (true) when' i4 R+ d" X: G8 A; s" h* X
it is caused by the premature activation of hypo-$ Z2 y. d+ l' I
thalamic pituitary gonadal axis. CPP is more com-% d# \# t5 Z9 [. {* X
mon in girls than in boys.1,3 Most boys with CPP
  E* E5 D( w9 Z! {: _) y% lmay have a central nervous system lesion that is
+ f2 {% d, `9 R' Vresponsible for the early activation of the hypothal-
2 g( {# x, D- h" ]: k4 Zamic pituitary gonadal axis.1-3 Thus, greater empha-* C8 E# v9 N: B$ _
sis has been given to neuroradiologic imaging in
4 ^8 V' l) b" S& r; lboys with precocious puberty. In addition to viril-$ C; @6 J* P) o8 y6 {# i, Q! @
ization, the clinical hallmark of CPP is the symmet-
/ n) D( i% N# E; s3 G% Krical testicular growth secondary to stimulation by( U& K. @: S/ M* O
gonadotropins.1,3) q2 }$ ]6 B% ~3 w& h" C
Gonadotropin-independent peripheral preco-2 o& v0 m+ y, G! i' [; K
cious puberty in boys also results from inappropriate1 h6 F$ G$ k0 h
androgenic stimulation from either endogenous or/ J" M  ?) a1 r6 z' e
exogenous sources, nonpituitary gonadotropin stim-9 C& e1 p8 n: E. g+ W
ulation, and rare activating mutations.3 Virilizing& f4 I4 ^& I/ c( r
congenital adrenal hyperplasia producing excessive/ s% q  C# ~% a
adrenal androgens is a common cause of precocious
& v; j1 s! s- R( G. B1 m& Rpuberty in boys.3,46 |1 ?  j, S( [7 T
The most common form of congenital adrenal0 L. a# x8 v  _4 X6 v# c
hyperplasia is the 21-hydroxylase enzyme deficiency.; g9 N" z+ ^+ Z- l# s) ?# {& B" J
The 11-β hydroxylase deficiency may also result in, ^% }7 Z; @! B3 S! u3 a
excessive adrenal androgen production, and rarely,4 t" q5 N2 m8 B9 X8 O) l
an adrenal tumor may also cause adrenal androgen* l& L& V: B* o; B7 y
excess.1,3
$ r: p, e2 n2 e! w: j7 S+ lat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
& ?: l; d8 k! A542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
& U: a' z/ O/ kA unique entity of male-limited gonadotropin-9 t& _; n6 Y7 S+ ^6 p: J4 t# Q8 y, G
independent precocious puberty, which is also known
$ \* A  m9 n  Q& }$ Has testotoxicosis, may cause precocious puberty at a
) G! _1 e) K6 s9 Q1 I, qvery young age. The physical findings in these boys1 z, q. k  h; q/ ]( W6 i! Y, u
with this disorder are full pubertal development,- V6 I6 c" Z! c7 C& C* f7 V8 n0 T
including bilateral testicular growth, similar to boys
0 E+ F, q3 v8 o: X+ ]with CPP. The gonadotropin levels in this disorder
6 O- {0 m/ P0 oare suppressed to prepubertal levels and do not show. X1 ^9 L2 X$ h% U* v# }* a
pubertal response of gonadotropin after gonadotropin-7 w- B5 V' W" F/ e2 ^
releasing hormone stimulation. This is a sex-linked
4 U3 s( @& K( ?7 Hautosomal dominant disorder that affects only. m3 @% J) h# [
males; therefore, other male members of the family- j+ H" P; b5 n! v4 _7 t( O
may have similar precocious puberty.3
% F' X  }) @  S4 E! a: S5 M7 EIn our patient, physical examination was incon-
+ \6 M5 t8 d% [: rsistent with true precocious puberty since his testi-
2 o+ h4 Q7 V& R. N' xcles were prepubertal in size. However, testotoxicosis
' d  t9 R) E6 _8 o  gwas in the differential diagnosis because his father& O8 z' j3 O# I$ [" c
started puberty somewhat early, and occasionally,/ }6 K1 k: b0 `/ v9 O
testicular enlargement is not that evident in the  x& d" I$ g# \. ]3 J. f7 f
beginning of this process.1 In the absence of a neg-
7 G7 q) s9 q: ^) r/ M/ [& dative initial history of androgen exposure, our
; [9 W( Z+ e" M# Dbiggest concern was virilizing adrenal hyperplasia,9 J" A( O/ w' W. z3 @
either 21-hydroxylase deficiency or 11-β hydroxylase5 N; J# y& @0 @+ q2 X
deficiency. Those diagnoses were excluded by find-+ T- j  r* f2 w( \2 R: u
ing the normal level of adrenal steroids./ ~6 z# m: X7 m7 ^  G8 p
The diagnosis of exogenous androgens was strongly/ E! X; ?6 q3 {- v! l
suspected in a follow-up visit after 4 months because# Q; w- D) Z3 g
the physical examination revealed the complete disap-: H, a4 S5 F5 n( G, A  a8 D
pearance of pubic hair, normal growth velocity, and% c* x  q! x6 c8 l! |
decreased erections. The father admitted using a testos-. m  [+ w$ |' y" d
terone gel, which he concealed at first visit. He was% z9 ~. m+ j7 b6 s  K
using it rather frequently, twice a day. The Physicians’
6 C0 o) [  z' `Desk Reference, or package insert of this product, gel or8 R1 S% ?9 h& T+ S, ]
cream, cautions about dermal testosterone transfer to) b  h/ {9 K% {. o7 K
unprotected females through direct skin exposure.% L3 k. B+ j! ^' g+ M2 |
Serum testosterone level was found to be 2 times the/ K+ }' s0 g0 z
baseline value in those females who were exposed to
( E( L/ k; a" c* c4 A; d! Ceven 15 minutes of direct skin contact with their male. J6 q9 v: Q) u% @$ k
partners.6 However, when a shirt covered the applica-6 b- i( J9 o9 c, w
tion site, this testosterone transfer was prevented.% F( u0 N- X* M9 ~
Our patient’s testosterone level was 60 ng/mL,
# h% P6 w/ [. v! iwhich was clearly high. Some studies suggest that
6 X; o" D5 t; {8 V* }dermal conversion of testosterone to dihydrotestos-" |, l9 m5 r" V
terone, which is a more potent metabolite, is more
+ a4 e5 m- s1 K2 R+ c' s. S3 _active in young children exposed to testosterone- V- [. @' X8 g" K5 ^% D6 I
exogenously7; however, we did not measure a dihy-! ~% A3 i8 e' o6 e& U
drotestosterone level in our patient. In addition to% c# n5 A8 W6 k+ k
virilization, exposure to exogenous testosterone in2 ~4 [8 a; H* z
children results in an increase in growth velocity and0 U+ p5 b* e# j8 C6 u( L8 Y% Y: |4 F
advanced bone age, as seen in our patient.
+ W/ ]  ]: d8 a7 Y, d  a  h! QThe long-term effect of androgen exposure during
3 A2 p( g( @0 w7 ]8 cearly childhood on pubertal development and final
" y; a- Y: u3 s3 ^* d) badult height are not fully known and always remain( q; @. L$ \  P
a concern. Children treated with short-term testos-
$ R* P1 Z, ^* yterone injection or topical androgen may exhibit some7 Z6 b% J3 m  n6 q: @9 l" _$ @
acceleration of the skeletal maturation; however, after
! F; q1 s9 C7 R1 |5 T1 U8 Fcessation of treatment, the rate of bone maturation
3 j  C1 O+ G, Y; Y1 Ddecelerates and gradually returns to normal.8,9
; C9 |1 b& w6 p5 I9 C- V- o$ V* MThere are conflicting reports and controversy
! C' T' U/ Q2 D' uover the effect of early androgen exposure on adult
: j* e0 ~* b- Q% l$ G$ m/ Ypenile length.10,11 Some reports suggest subnormal  A: G4 u% q0 y
adult penile length, apparently because of downreg-
5 [1 u: n6 p% l# q2 ]( j* ~* zulation of androgen receptor number.10,12 However,. t- e1 T! t7 ^; Z; t
Sutherland et al13 did not find a correlation between* W6 q" @5 }: g! ^: J, q, ]3 V
childhood testosterone exposure and reduced adult
- a) \' V0 i3 |& q5 u8 ~penile length in clinical studies.
) m1 n  |0 d! j2 D! ONonetheless, we do not believe our patient is/ `# |, p7 P! b: z
going to experience any of the untoward effects from: W# O9 G! N+ {  ^( R! V; ~
testosterone exposure as mentioned earlier because
3 v- V1 J3 L( L5 \3 b6 Hthe exposure was not for a prolonged period of time.& l$ Y. p6 D  _# Z. J) o) R" c
Although the bone age was advanced at the time of- r. R. S! g& e  v5 N; W1 Q/ R* T8 {
diagnosis, the child had a normal growth velocity at
" S- a0 _" V; W. M3 M7 z1 `, I. qthe follow-up visit. It is hoped that his final adult
/ H( [  W1 T1 @* q; ^$ z- Uheight will not be affected.$ D( G+ N* _' s2 b
Although rarely reported, the widespread avail-! v" S: t8 a6 l
ability of androgen products in our society may0 p9 U, |; m  j$ h1 v& s
indeed cause more virilization in male or female, @: U3 Z7 |  C
children than one would realize. Exposure to andro-0 K( s4 z; B7 U3 f) ~
gen products must be considered and specific ques-% W7 Z( y( r5 A
tioning about the use of a testosterone product or) h' J1 y8 e, o6 U5 G! F% X  c
gel should be asked of the family members during4 c1 Q# E3 j" C
the evaluation of any children who present with vir-
9 g, H* L4 Y- C- milization or peripheral precocious puberty. The diag-$ l; }: X  z+ T; v
nosis can be established by just a few tests and by
! x. a8 ]+ s, z6 ^# Tappropriate history. The inability to obtain such a/ _7 N2 ]2 V$ O  z6 t7 p
history, or failure to ask the specific questions, may
$ w7 z4 r# h6 ?- W) {result in extensive, unnecessary, and expensive0 S# {- f" n7 }. o  O
investigation. The primary care physician should be
, ^3 N0 {4 f* Maware of this fact, because most of these children
3 i0 w* W8 O9 q  t5 Gmay initially present in their practice. The Physicians’# k% F1 d6 m/ O' t  A
Desk Reference and package insert should also put a
# Y6 m% g: ~7 X& v6 v8 K, Cwarning about the virilizing effect on a male or. I) C, V  n; S; V
female child who might come in contact with some-) Y6 H. _3 a* F2 i, o0 U$ k$ s7 f
one using any of these products.' E6 i, c; F/ a6 v# n  j! ^+ b
References$ i; m( A3 t* ?. y0 E- c. M
1. Styne DM. The testes: disorder of sexual differentiation
8 J: B, t8 q' Z0 Tand puberty in the male. In: Sperling MA, ed. Pediatric
: J# v$ _1 P9 B1 P8 `4 B( ZEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;" _2 H- R& L% ~
2002: 565-628.
3 J$ r1 f6 ?# J9 ?; v% \2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious* l) f/ @) n( g. P3 G8 X8 N  l
puberty in children with tumours of the suprasellar pineal
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感謝大大的辛勞分享!我會繼續在WK關注大大的文章!
發表於 2025-1-11 22:18:01 | 顯示全部樓層
女厕偷拍辅导班主任尿尿老师的逼很嫩还有一点
發表於 2025-1-17 16:31:39 | 顯示全部樓層
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4个什么样的?
發表於 2025-1-19 02:41:05 | 顯示全部樓層
" L+ v4 V4 m! e- R8 _/ n7 ^
精妙絕倫的精品,感謝啊!期待你更多更好的創作哦!
發表於 2025-3-8 22:04:50 | 顯示全部樓層
絕對的好貼!謝謝啊!逐字逐圖地看完這個帖子以後,我的心久久不能平靜,感恩啊!
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