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Sexual Precocity in a 16-Month-Old
( I& }2 Y, J1 R" q) TBoy Induced by Indirect Topical
. }5 p0 A: s" v% n( I$ rExposure to Testosterone' H6 J. ]0 ]- s; [/ z) d( v# w
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2) x. _/ D6 F4 q: J, F) C; D
and Kenneth R. Rettig, MD1) Z; \/ Z7 c( I! O9 o+ f8 K
Clinical Pediatrics
" O1 B) a5 K; X: [Volume 46 Number 6* e5 [. P' t7 [! a: M0 S* d/ D
July 2007 540-543
( K+ f7 N- [3 ~4 i/ G© 2007 Sage Publications
$ X9 M, z' j) i% x  v8 K10.1177/00099228062966510 u& o2 `5 B, s% Y! a4 k
http://clp.sagepub.com0 B3 ~/ [7 I% s" K5 H( ?
hosted at; N" a- N1 T9 {" U1 C. m
http://online.sagepub.com0 _0 C# c- G5 f. U5 Q: [& Q
Precocious puberty in boys, central or peripheral,
; `; ^9 P* R/ K6 \" W0 h# V- Iis a significant concern for physicians. Central
! t+ S+ D7 w6 ~. K; f- {precocious puberty (CPP), which is mediated9 M; g4 h* l' Q  M6 m
through the hypothalamic pituitary gonadal axis, has
8 q* ]; |  n7 C, Ja higher incidence of organic central nervous system
! S9 C6 W( s  `* k: f% klesions in boys.1,2 Virilization in boys, as manifested) l4 W" p4 R$ V. z
by enlargement of the penis, development of pubic" |/ {% L, @9 P+ K1 h
hair, and facial acne without enlargement of testi-$ {5 Y8 \, E" s" ?% T9 V8 r% Q/ z
cles, suggests peripheral or pseudopuberty.1-3 We
- S' x  l$ L8 U$ |" X4 Breport a 16-month-old boy who presented with the- ~  X* |" r9 @/ R  W: y5 |
enlargement of the phallus and pubic hair develop-
$ D9 D" p. |. Hment without testicular enlargement, which was due  G0 |, j, z- Y. ~& l
to the unintentional exposure to androgen gel used by- K; Z, d6 F  J" U/ `9 u2 z
the father. The family initially concealed this infor-* a& |* _. C( J% v0 F
mation, resulting in an extensive work-up for this2 B: B, n- q- N3 X- C
child. Given the widespread and easy availability of2 W+ h* a- [" ~) u
testosterone gel and cream, we believe this is proba-* H% M7 P) l& B1 s3 l2 r8 k' D
bly more common than the rare case report in the
$ w& C7 O- }5 D2 K8 aliterature.4
. B- n4 h0 D0 T3 ?8 aPatient Report7 K6 K  _# E# Q' B
A 16-month-old white child was referred to the2 L, D+ w. D1 P6 \8 }. c
endocrine clinic by his pediatrician with the concern; e' S! {$ s3 X& D% o8 E: e
of early sexual development. His mother noticed! x8 d% m0 m: s
light colored pubic hair development when he was
0 X( b8 x1 B2 t$ ?; q8 Z& w0 V& ]From the 1Division of Pediatric Endocrinology, 2University of
- f* {, o# A2 `- c5 uSouth Alabama Medical Center, Mobile, Alabama.+ z8 G5 T7 M0 Z2 q) i( `
Address correspondence to: Samar K. Bhowmick, MD, FACE,
9 c8 i! W2 ]* v) pProfessor of Pediatrics, University of South Alabama, College of+ \3 n) S, o7 J7 y
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
  b' M1 _* _, `1 Ve-mail: [email protected].) a) E) y- ]  [! s2 j
about 6 to 7 months old, which progressively became
0 ~1 m% ^' B& Rdarker. She was also concerned about the enlarge-( M" d! }! o; u
ment of his penis and frequent erections. The child+ q4 U! K1 T9 Z) M0 Z% N
was the product of a full-term normal delivery, with6 K8 j7 \" ?! o  t4 u5 j' Q9 ?9 c
a birth weight of 7 lb 14 oz, and birth length of; d9 c9 R+ w& E4 F
20 inches. He was breast-fed throughout the first year1 L6 b0 @7 X4 I" f
of life and was still receiving breast milk along with7 v% N/ ]& B5 N1 O# {+ K! z
solid food. He had no hospitalizations or surgery,
$ D) T& f8 \) Tand his psychosocial and psychomotor development
/ v  p' o2 Z% K  p$ {/ z, {4 |9 Gwas age appropriate.
7 M9 J# h' \7 W, G1 @2 }The family history was remarkable for the father,, W* R* h% `4 D' i; V
who was diagnosed with hypothyroidism at age 16,
! L9 F' n$ D9 Awhich was treated with thyroxine. The father’s
: ?' i7 n. J4 F) l0 `' F: b5 ?* j# Aheight was 6 feet, and he went through a somewhat0 g/ x) A+ }: G
early puberty and had stopped growing by age 14.1 f7 d% A- r( f# ?' r
The father denied taking any other medication. The! ~  T. a+ F3 A* ]
child’s mother was in good health. Her menarche- ?+ u& O9 T2 e' e
was at 11 years of age, and her height was at 5 feet
# y! l# L0 A; k$ W2 c! H5 inches. There was no other family history of pre-
. U1 g8 S2 z# g2 Hcocious sexual development in the first-degree rela-
, j  Q; F4 J7 [& z3 w0 Stives. There were no siblings.
% F9 Y: u. U' e; x: |0 E8 N* mPhysical Examination
8 E& l& W& Z8 y3 n! U0 HThe physical examination revealed a very active,5 C7 A! U; Q' M" v4 L8 B9 `. l* a
playful, and healthy boy. The vital signs documented
; p' G3 U# p. M7 f* Ea blood pressure of 85/50 mm Hg, his length was
4 ?7 a* N* e$ u' B% i7 M90 cm (>97th percentile), and his weight was 14.4 kg
; U" w" i7 r' I4 u: o) v' W0 Q0 p+ D(also >97th percentile). The observed yearly growth% x7 p$ N* n# Y3 g! ^
velocity was 30 cm (12 inches). The examination of. I* X( \& C9 e% K& x" `7 x% b! o
the neck revealed no thyroid enlargement.! s3 e% c, f9 ^2 ^8 B4 x
The genitourinary examination was remarkable for3 V! F' M7 a9 U" d* e8 g" P4 _' [2 G
enlargement of the penis, with a stretched length of5 `, p( \4 S: X3 m" s+ H
8 cm and a width of 2 cm. The glans penis was very well
  u6 |) i0 r$ [, [) ideveloped. The pubic hair was Tanner II, mostly around$ \0 e; `/ D0 b7 Q: R+ S
540
% v: }3 L# _, a# Y9 @" n5 e7 D# pat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from! t9 }4 V  R2 ^1 T* D! U9 l
the base of the phallus and was dark and curled. The
. a5 _( r0 I, i! R: {testicular volume was prepubertal at 2 mL each.
* n2 ?; e+ `1 W+ NThe skin was moist and smooth and somewhat- [& A+ \) u& q+ s: v& r( T
oily. No axillary hair was noted. There were no
( F3 E. U' h1 D% {abnormal skin pigmentations or café-au-lait spots.
8 b; x% [$ X3 E% [Neurologic evaluation showed deep tendon reflex 2+
/ l4 G: F. K* R  a. qbilateral and symmetrical. There was no suggestion
8 r8 H8 e2 R4 s$ g# h7 tof papilledema.: t& S9 A) K& }# f
Laboratory Evaluation6 x! x; H5 i2 [5 _2 d8 q
The bone age was consistent with 28 months by* p# c. Z3 x$ ~; B; r8 v
using the standard of Greulich and Pyle at a chrono-- `5 a0 T3 s/ T: j. d( _) ~' N
logic age of 16 months (advanced).5 Chromosomal/ W! |  H  h& K$ a- s2 S0 m- h
karyotype was 46XY. The thyroid function test8 B% l! e( Y2 J& g8 @3 }- P$ M
showed a free T4 of 1.69 ng/dL, and thyroid stimu-( b% R3 e# y+ e4 v- l6 L# M
lating hormone level was 1.3 µIU/mL (both normal).2 z% R  u  [% g  d
The concentrations of serum electrolytes, blood
0 X0 c) F% ~8 a0 ~* u; purea nitrogen, creatinine, and calcium all were
' ~5 ^1 T: J$ u& e! y- `9 r; \within normal range for his age. The concentration' T" S2 I# K, ]8 E1 _! N7 g
of serum 17-hydroxyprogesterone was 16 ng/dL
7 w8 G0 M7 s. S* b6 M+ Z6 x# }" G(normal, 3 to 90 ng/dL), androstenedione was 20
& I/ C& I  G2 y$ J* xng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
5 r( j9 j* j& R" |+ _3 e5 wterone was 38 ng/dL (normal, 50 to 760 ng/dL),
- }# v4 Z1 L, e1 K7 Y4 hdesoxycorticosterone was 4.3 ng/dL (normal, 7 to
) V* N& v& r# u1 b8 r1 V2 u4 s* Z49ng/dL), 11-desoxycortisol (specific compound S)2 B4 ?5 f7 p# ]( H9 @+ ?, L, T" r6 C
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-  V9 P7 p( @, k8 u. f: s
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
( i( T) Q1 e( i' E  n; t8 Xtestosterone was 60 ng/dL (normal <3 to 10 ng/dL),8 f! k/ f+ j, X* H' G0 x
and β-human chorionic gonadotropin was less than
% g  @8 a7 P) i5 l' l6 f5 mIU/mL (normal <5 mIU/mL). Serum follicular6 Q5 q0 P4 m9 a; E+ n
stimulating hormone and leuteinizing hormone
  T( T1 V* `4 ^, y2 Uconcentrations were less than 0.05 mIU/mL8 d1 W0 [/ R) u6 A  n+ c
(prepubertal).* x0 P6 H2 q- _, R+ w
The parents were notified about the laboratory8 j' S" F. n2 _$ X" b7 W
results and were informed that all of the tests were
1 X/ ~. [) j5 \normal except the testosterone level was high. The9 Q3 c9 G# a/ _# P% ]1 w! }+ Q' H1 Y$ i
follow-up visit was arranged within a few weeks to/ H. U2 l8 U9 i5 [# ^
obtain testicular and abdominal sonograms; how-
5 F5 H4 [" Z# e4 q% o, _8 \, aever, the family did not return for 4 months.# u8 {' g0 X. ^) s: p
Physical examination at this time revealed that the% C' O  c9 q' z
child had grown 2.5 cm in 4 months and had gained
& J- n0 r& L1 e) Q2 kg of weight. Physical examination remained
! P' E$ Q: W& Y* L3 ]- ^+ Hunchanged. Surprisingly, the pubic hair almost com-: K0 `% I0 x* S% v" K0 x1 l5 t' x0 R
pletely disappeared except for a few vellous hairs at5 k: ]4 K# X4 o4 S' k
the base of the phallus. Testicular volume was still 2
% P# c2 n0 t  u1 bmL, and the size of the penis remained unchanged.
: N3 _9 |2 ~+ aThe mother also said that the boy was no longer hav-
& l- s% n' w) u1 _1 o+ E6 J9 `) [ing frequent erections.! \& D- Q* u/ M4 }. O, q
Both parents were again questioned about use of* A; K' L$ ]2 K2 p- W8 H
any ointment/creams that they may have applied to
$ p: p. k6 e1 N& Q8 kthe child’s skin. This time the father admitted the
4 \  d: p* P% ^( y: |Topical Testosterone Exposure / Bhowmick et al 541
" q; R: n, m5 _5 Q0 X. Fuse of testosterone gel twice daily that he was apply-
+ n4 h4 f: T) ^6 [- ]. ?ing over his own shoulders, chest, and back area for
# \6 T6 ?2 y" R6 B( K( k/ ia year. The father also revealed he was embarrassed- Q- f1 v9 V1 G% }4 I
to disclose that he was using a testosterone gel pre-
& e; G2 r' p) Uscribed by his family physician for decreased libido
: S: a$ w/ e! `& [' o6 F( fsecondary to depression., ]3 Z) j& Q) \& T7 n# d6 m
The child slept in the same bed with parents.0 `3 p0 ~, {, A* z9 R, p; Y1 R
The father would hug the baby and hold him on his- u. z+ l1 c2 L9 E
chest for a considerable period of time, causing sig-
2 H2 I/ j/ T3 y1 i, |! _$ Wnificant bare skin contact between baby and father.( y: d3 o7 T& p( C: u% }
The father also admitted that after the phone call,
3 }: o+ N0 W6 F' ~5 g7 Nwhen he learned the testosterone level in the baby3 T4 q# T; M' P3 }4 e3 z" i
was high, he then read the product information
6 D3 Q" v. d& a& Q; jpacket and concluded that it was most likely the rea-
1 r* z8 t. O/ L5 |  zson for the child’s virilization. At that time, they2 R- n8 U1 R# T! M
decided to put the baby in a separate bed, and the7 i( w: z% U( G( ]' M& @
father was not hugging him with bare skin and had
' S8 N7 L& ~8 B; \( ebeen using protective clothing. A repeat testosterone
( _# e0 N4 P! Etest was ordered, but the family did not go to the7 |! o9 Y/ k5 @6 k4 `! E
laboratory to obtain the test.+ \1 Y3 \0 x+ Z6 X3 M6 _
Discussion) j! [3 |  u, L2 _! G6 p4 O
Precocious puberty in boys is defined as secondary+ _0 Z4 \1 [! a6 \
sexual development before 9 years of age.1,4
9 e( C. w& c0 vPrecocious puberty is termed as central (true) when* \; f. O7 v0 V& o% f% L
it is caused by the premature activation of hypo-- g/ n# |, }9 Y+ y% Q( I
thalamic pituitary gonadal axis. CPP is more com-
# A! }/ J0 g3 w% g9 Y8 Wmon in girls than in boys.1,3 Most boys with CPP
, R/ p4 m' p2 L% |4 a3 \may have a central nervous system lesion that is
7 i: v2 E' `& ~& x* }responsible for the early activation of the hypothal-
3 _+ u3 L6 q% Kamic pituitary gonadal axis.1-3 Thus, greater empha-5 d7 \' {6 H; g2 ~  D- `
sis has been given to neuroradiologic imaging in
- B( [  K0 f0 D& R; qboys with precocious puberty. In addition to viril-& D+ ~% R# K2 ]
ization, the clinical hallmark of CPP is the symmet-
+ M6 z1 H8 z! @9 Zrical testicular growth secondary to stimulation by
/ ]$ N8 ?! r2 [9 ugonadotropins.1,3
; u# w1 U# E4 s7 j$ y. ~, _) iGonadotropin-independent peripheral preco-. @7 P$ D& _, X; g  u
cious puberty in boys also results from inappropriate" [/ D6 L% d, g5 r/ L; V9 S" q
androgenic stimulation from either endogenous or0 E3 l. k6 O! [; v/ T$ k2 \! P
exogenous sources, nonpituitary gonadotropin stim-
7 k2 r) n/ E4 ^9 f: ]; F8 Hulation, and rare activating mutations.3 Virilizing
( l( S# x: b* o* S6 Pcongenital adrenal hyperplasia producing excessive
. S- E8 o6 n. M( f$ Y: `" @adrenal androgens is a common cause of precocious* |4 Z" O$ P# k9 z" L( C) O; f
puberty in boys.3,4
, m* [  o5 E4 i; Q, f* {: Q1 y: FThe most common form of congenital adrenal6 ]* D  q* ]* [2 Z- A
hyperplasia is the 21-hydroxylase enzyme deficiency.
; t1 Q2 E5 ?5 @The 11-β hydroxylase deficiency may also result in
/ |) O: S6 y' e! J. y3 G8 ~  [excessive adrenal androgen production, and rarely,
& g. |3 e( S3 ean adrenal tumor may also cause adrenal androgen
7 O$ J0 D0 y+ s" h, Yexcess.1,3
2 O, i$ A7 N: K3 \2 F  g# }" ?* nat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
3 B0 _% m2 u3 Y! g# g542 Clinical Pediatrics / Vol. 46, No. 6, July 2007: @7 f! Z6 V3 i7 f# w! H
A unique entity of male-limited gonadotropin-) O) ]) H' H% o% F6 j  i. x; K
independent precocious puberty, which is also known
8 z  G2 O& w' i8 B9 ~% }; s, gas testotoxicosis, may cause precocious puberty at a
. D6 z( ]4 Z0 g, l5 E# overy young age. The physical findings in these boys
4 W2 _4 P9 D% x% |1 c. x6 ewith this disorder are full pubertal development,
% P% k0 V; e3 |; F2 v$ Kincluding bilateral testicular growth, similar to boys
" M. V8 P( q8 X  Nwith CPP. The gonadotropin levels in this disorder
2 n0 n0 U& H0 k  a8 ~are suppressed to prepubertal levels and do not show7 A' U: j4 L0 }' W) W
pubertal response of gonadotropin after gonadotropin-) N- Z$ ?4 G- d! ]5 |8 ?& m4 i' i
releasing hormone stimulation. This is a sex-linked# v4 |5 h% T6 n8 Q
autosomal dominant disorder that affects only6 S! a0 k( e2 x2 N8 Y) W# y7 f
males; therefore, other male members of the family$ H/ q# b3 ?* K: y; v2 k
may have similar precocious puberty.3
0 o8 B" Y. o, F* QIn our patient, physical examination was incon-  K4 v5 U: ]+ p8 @9 R+ d2 E0 G9 q
sistent with true precocious puberty since his testi-
8 D) P) ~9 N0 v1 ecles were prepubertal in size. However, testotoxicosis
% U0 D7 \! _( a  `was in the differential diagnosis because his father1 L+ I/ r# F5 U" x2 e. U2 ]( z
started puberty somewhat early, and occasionally,8 @5 t" K" h1 v5 s4 y: b* {1 ~
testicular enlargement is not that evident in the* U/ V& ]3 j- E3 E, ], C8 D- I
beginning of this process.1 In the absence of a neg-, W: d5 H+ m9 A
ative initial history of androgen exposure, our
. d1 x4 g0 V. z, w9 M, E3 P9 jbiggest concern was virilizing adrenal hyperplasia,5 U6 ^" c/ }+ n5 [
either 21-hydroxylase deficiency or 11-β hydroxylase
$ ~3 B/ A6 g) ^) X/ x/ @( rdeficiency. Those diagnoses were excluded by find-
. h  ^/ u( I2 f2 v* Iing the normal level of adrenal steroids.6 G5 n! G' C% Q: w
The diagnosis of exogenous androgens was strongly
2 S& C3 \- M7 R2 h& `  i$ u: Osuspected in a follow-up visit after 4 months because2 y1 r6 s" D0 m# H/ J) |
the physical examination revealed the complete disap-
5 u% ?0 P$ `5 q- B# Qpearance of pubic hair, normal growth velocity, and( ~. a2 z! u( v' |/ _
decreased erections. The father admitted using a testos-
( ~+ i6 a# b- a4 L) i4 Dterone gel, which he concealed at first visit. He was5 F: D9 x1 M$ v7 [3 m4 G, o" E
using it rather frequently, twice a day. The Physicians’! f" h2 A1 Q1 U
Desk Reference, or package insert of this product, gel or: Q9 Q# m6 Q. l5 `. z" }! O
cream, cautions about dermal testosterone transfer to7 q6 E/ E2 V3 r! h2 ~. s
unprotected females through direct skin exposure.0 l1 o+ A' J5 g3 e
Serum testosterone level was found to be 2 times the5 i4 u& t, y5 v9 _
baseline value in those females who were exposed to
) F4 I! T9 a4 o2 l8 Leven 15 minutes of direct skin contact with their male  p6 i; I7 i2 S3 y7 v8 [; z( }2 O9 {
partners.6 However, when a shirt covered the applica-& N, a6 A1 X4 W, P- [% V
tion site, this testosterone transfer was prevented.; F' N& _. I9 x- V) A
Our patient’s testosterone level was 60 ng/mL,, }& F0 M/ x6 A
which was clearly high. Some studies suggest that5 ?9 D! f' [+ F: ]; O6 P
dermal conversion of testosterone to dihydrotestos-3 y, f: r( e2 B) o8 J) Y
terone, which is a more potent metabolite, is more6 m5 `  A/ A) P3 J6 l3 {/ o0 ], s
active in young children exposed to testosterone
3 y# L9 C( m+ U& E/ U. oexogenously7; however, we did not measure a dihy-: ?4 y! T2 v7 ?! z
drotestosterone level in our patient. In addition to' H6 \: b; r# O" p# U0 ^* M
virilization, exposure to exogenous testosterone in
. `, j/ |: ~. t; V% rchildren results in an increase in growth velocity and
- _! |/ q& `# i( }( Xadvanced bone age, as seen in our patient.
( r/ _, K. a6 e  ^The long-term effect of androgen exposure during
0 P+ e. l" E% i9 ~early childhood on pubertal development and final5 M  X) t  C: w2 k' p& [; ^+ e; o* w( b
adult height are not fully known and always remain& {( N3 @% a1 ?3 U5 ]7 |
a concern. Children treated with short-term testos-& [& A' V3 q- `" [( ~
terone injection or topical androgen may exhibit some
, c8 x% V5 J: x: }3 cacceleration of the skeletal maturation; however, after
1 z3 z- N5 d/ N4 U( ccessation of treatment, the rate of bone maturation
* q5 D: C- o3 F: c/ @2 i$ ~1 odecelerates and gradually returns to normal.8,90 a; b; V& [3 ?% C# P3 i
There are conflicting reports and controversy! \$ Q* d7 d* q7 O6 p( G
over the effect of early androgen exposure on adult2 t/ `: I7 `$ W+ |
penile length.10,11 Some reports suggest subnormal
* w2 o: s5 J) N; z1 a& U7 Vadult penile length, apparently because of downreg-& _% o0 ]- _" [/ K& }: N! Y
ulation of androgen receptor number.10,12 However,
' @$ w( @5 u0 b/ `" E2 rSutherland et al13 did not find a correlation between
$ j8 Z0 j( P# qchildhood testosterone exposure and reduced adult7 Q2 s# T4 S9 v4 [8 a+ h0 U8 f
penile length in clinical studies.7 h4 W* b: Q; z! a+ Q" p+ Y* {9 I% _) S
Nonetheless, we do not believe our patient is8 F+ ]! V* Z' a6 B+ K$ X. i
going to experience any of the untoward effects from
3 X2 S, O5 H! C" u8 Z0 {$ F- d2 Ttestosterone exposure as mentioned earlier because: ~8 J4 }$ A* A
the exposure was not for a prolonged period of time.
0 q6 _" g* m3 z8 F$ W( h# \. qAlthough the bone age was advanced at the time of# e; \9 ]  W- V- G- t8 Y7 |
diagnosis, the child had a normal growth velocity at
% q- Y% k" j/ ~) p8 Pthe follow-up visit. It is hoped that his final adult
3 U$ Q1 h( G9 `% Gheight will not be affected.
3 W8 Z9 P! q% C% W9 A6 NAlthough rarely reported, the widespread avail-
# g  N2 H7 _" {/ A7 n7 w3 Bability of androgen products in our society may; [: a, K6 J0 `6 D
indeed cause more virilization in male or female
& H/ V  ~1 W4 [7 X2 u' c' fchildren than one would realize. Exposure to andro-6 `/ p* w3 O  F7 E6 s% w; q+ f* p$ X
gen products must be considered and specific ques-% i4 ^9 P4 p6 M, Y" c
tioning about the use of a testosterone product or" [, m% _: P6 ^& p& F
gel should be asked of the family members during
6 B) F/ e% H# Q+ T- Ythe evaluation of any children who present with vir-& }  v' ]4 ~. n  o1 g% r" d7 d+ v- }! B
ilization or peripheral precocious puberty. The diag-- q+ m9 f% r; y* v1 W, W
nosis can be established by just a few tests and by
: Q. S* V% e, u$ M* Gappropriate history. The inability to obtain such a
# X5 a- Q& I6 {- K6 C/ j1 Khistory, or failure to ask the specific questions, may# l9 l, ^+ m4 S9 J8 I" P, X
result in extensive, unnecessary, and expensive
. ~) V$ j6 u$ rinvestigation. The primary care physician should be
& [2 c( f( n; ]# z* kaware of this fact, because most of these children
  B% R2 w/ e) g" wmay initially present in their practice. The Physicians’, Y; I7 W0 B  D* z9 p$ P
Desk Reference and package insert should also put a+ D0 g) \& @" C$ b, O+ F7 h
warning about the virilizing effect on a male or+ u) H. W) M! @- d& H' G0 }
female child who might come in contact with some-
, g# k* r, o6 K% g5 O* Yone using any of these products.' j5 F$ ?: n- v/ i9 }5 S$ q  _+ ^
References3 D; W9 P0 |6 V' |3 C# H' _* N
1. Styne DM. The testes: disorder of sexual differentiation
6 A) C! T4 n8 g+ J; Pand puberty in the male. In: Sperling MA, ed. Pediatric4 ^- g( v5 Q/ r7 D6 ?' a. ?
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;1 Q+ M# L. {( ]# n9 R/ `
2002: 565-628.
: k7 D' ?& X: K- C2 a2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious* H/ b( D8 q3 Y% ^$ F. ?0 |+ m
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
8 s- `# o# ^7 H* {; w5 k; SBoy Induced by Indirect Topical
  c% m+ a. g& G$ L7 Z  b# HExposure to Testosterone
( R9 f9 v4 T* mSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,21 F! D, m5 x: _" }3 {) P3 K3 K7 S
and Kenneth R. Rettig, MD1: K' h" |  D2 E, x+ F! p, T
Clinical Pediatrics% D: m. n9 ?1 S1 ?1 [: k+ ]
Volume 46 Number 6" _% l4 @- Z8 n  l- A: P
July 2007 540-543
: j; p' X5 h9 l7 _$ z© 2007 Sage Publications- B" k7 k7 N  q. [: [4 l
10.1177/0009922806296651, M7 B8 ~4 N' `5 A
http://clp.sagepub.com  v" g) O! k3 h/ u% a" s
hosted at
: j; T+ H% A9 x  [http://online.sagepub.com% u7 ^( ^9 B+ t$ g, L7 `
Precocious puberty in boys, central or peripheral,5 i2 Q) P/ t8 W  _# S- |2 \) ?% `
is a significant concern for physicians. Central' X% U# p/ c3 ?* E+ ]: _
precocious puberty (CPP), which is mediated. K+ M; J" T+ f+ g$ z
through the hypothalamic pituitary gonadal axis, has
6 E: r2 Y" x$ r! G2 X- @) ?a higher incidence of organic central nervous system! X5 [. z% Z  W6 h; A
lesions in boys.1,2 Virilization in boys, as manifested9 q4 O# K, L$ ?- g4 l9 ]' F
by enlargement of the penis, development of pubic$ m1 e- c" U# m2 V1 q' @
hair, and facial acne without enlargement of testi-( K1 {; S5 @, a% d
cles, suggests peripheral or pseudopuberty.1-3 We; r9 r" \# r3 w7 z+ U1 Q- N
report a 16-month-old boy who presented with the2 n% y4 @2 Q6 D7 F6 N
enlargement of the phallus and pubic hair develop-4 X0 Y4 K! w8 Y  @0 W* \
ment without testicular enlargement, which was due
. F2 K' f# x" `) Y# Ito the unintentional exposure to androgen gel used by3 M& ?7 R! k+ M+ {% d7 @2 }1 B1 H
the father. The family initially concealed this infor-
  P3 f# o  x, h& gmation, resulting in an extensive work-up for this/ @. Q2 @! Z5 G& I# p
child. Given the widespread and easy availability of
3 l( ^2 W, s8 \7 L% a6 Ctestosterone gel and cream, we believe this is proba-
8 a$ R# \! _$ b: q. mbly more common than the rare case report in the+ m, m3 ]: K- [$ s: S
literature.4
& M. ]* I- E% A8 M" |. a. `0 oPatient Report
- Z2 T. W6 c. w- O- a  TA 16-month-old white child was referred to the1 t- ?5 B7 ?: Y' X) p# f
endocrine clinic by his pediatrician with the concern
2 Z- C1 g/ S" g1 G7 h2 |of early sexual development. His mother noticed7 L; n' e% K( v% z* A4 h; M6 E
light colored pubic hair development when he was1 I2 s0 I( g2 O6 _. i7 D& c( k3 d
From the 1Division of Pediatric Endocrinology, 2University of
* u: O4 g1 t; zSouth Alabama Medical Center, Mobile, Alabama.! F5 i- n* k2 Y* X5 c) V
Address correspondence to: Samar K. Bhowmick, MD, FACE,+ R" h  z( o0 {; H0 b4 z
Professor of Pediatrics, University of South Alabama, College of
, O. M- p7 x% N  ?/ _+ gMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
- U0 D( s: N' r2 pe-mail: [email protected].
8 {' T; p0 f6 `( H, s% \5 Rabout 6 to 7 months old, which progressively became  \4 s9 z5 Z4 b: T
darker. She was also concerned about the enlarge-* T# s! ^2 l0 M1 K+ X- b/ {
ment of his penis and frequent erections. The child
. i' D3 b1 b8 Y  Kwas the product of a full-term normal delivery, with
4 g# S& F3 Y8 @5 @" ea birth weight of 7 lb 14 oz, and birth length of
+ I1 ~  ?/ F+ B20 inches. He was breast-fed throughout the first year
0 _0 i4 y+ J6 |& xof life and was still receiving breast milk along with9 R. [9 M) s0 r4 A
solid food. He had no hospitalizations or surgery,) L- _3 u7 }5 r! s0 b0 ~- }
and his psychosocial and psychomotor development
0 T, {$ d' _9 W2 m! l. m8 twas age appropriate.4 [/ e( g1 l% L9 f( e% e9 e
The family history was remarkable for the father,
" l) M+ o( x5 F6 z5 Z4 ~9 Fwho was diagnosed with hypothyroidism at age 16,4 z& {2 ?) [# A: f/ G- ~+ e
which was treated with thyroxine. The father’s* h9 J5 ~8 O) k; M0 P# Z1 M5 R1 v
height was 6 feet, and he went through a somewhat- S' V, q* k1 a! {' i' {
early puberty and had stopped growing by age 14.
; T1 k3 A, U( W. _  C; _The father denied taking any other medication. The
2 M3 @" ^5 f8 j3 }. @( P) Ochild’s mother was in good health. Her menarche; b2 z$ [) @: n4 c
was at 11 years of age, and her height was at 5 feet' I& q4 C8 i( d, ~! S
5 inches. There was no other family history of pre-
1 \; v' V2 L7 {7 u0 \: ?; o% Scocious sexual development in the first-degree rela-
4 z+ \1 p" m; gtives. There were no siblings.
# X3 u% m9 g# F) A0 b. g, T. ~* SPhysical Examination
# ^% Y& [1 }8 _3 h9 i2 A  C: f, WThe physical examination revealed a very active,
& ]  d* Z! }$ ?+ `playful, and healthy boy. The vital signs documented
1 T" ]; g7 j* F+ e! ^0 _a blood pressure of 85/50 mm Hg, his length was
( T& D- o- p6 l: P90 cm (>97th percentile), and his weight was 14.4 kg
! \7 u+ l- x+ C" Q! D(also >97th percentile). The observed yearly growth
2 J' r1 S2 r7 Z) k- G) Wvelocity was 30 cm (12 inches). The examination of
1 [# D+ s  Y& t$ [the neck revealed no thyroid enlargement.- U2 E% v/ k9 v1 t
The genitourinary examination was remarkable for
/ ~$ ]9 O" s+ I# d# E+ h+ ~3 S+ Denlargement of the penis, with a stretched length of
( D1 Y" e. e) Q9 Q9 R+ ^, o2 D8 cm and a width of 2 cm. The glans penis was very well
  {% Q  Y* P( L+ \) o9 adeveloped. The pubic hair was Tanner II, mostly around
) e$ D( m7 p" M* [; }540& V5 t: k$ I: z) }( f$ A& C
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from, H. m7 \7 [0 S% t3 W
the base of the phallus and was dark and curled. The" E! J. U- H! @7 N
testicular volume was prepubertal at 2 mL each.9 D4 }9 n* H. ^  D* `
The skin was moist and smooth and somewhat& [$ e+ `+ b8 d
oily. No axillary hair was noted. There were no
+ U# r; j+ Q7 w; Rabnormal skin pigmentations or café-au-lait spots.
/ L5 F. m! S2 I; }4 p% x9 u/ P6 NNeurologic evaluation showed deep tendon reflex 2+( g; q  C% V$ K
bilateral and symmetrical. There was no suggestion
  k4 l* F6 M# \9 Uof papilledema.
, t2 s+ f- j( W/ `) x9 D' S5 |) WLaboratory Evaluation
/ `" ~& ]4 ~$ X6 Q9 ?. TThe bone age was consistent with 28 months by) E" y5 ^( I5 s
using the standard of Greulich and Pyle at a chrono-
, n$ e2 P. {3 O6 f: c$ ~. S5 h/ d/ g2 A! \logic age of 16 months (advanced).5 Chromosomal. T" R" W7 R4 V
karyotype was 46XY. The thyroid function test
& a. F, ]" \) u# _( r6 t0 X' Dshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
+ u$ P3 }, d9 h6 a) a  z- xlating hormone level was 1.3 µIU/mL (both normal).
$ J9 k2 K9 |, u0 eThe concentrations of serum electrolytes, blood8 O$ |& [/ ]2 F" a# M* H3 u- a
urea nitrogen, creatinine, and calcium all were
. l$ O! p7 w& cwithin normal range for his age. The concentration: F5 W' G; r% W, m& R, \0 m
of serum 17-hydroxyprogesterone was 16 ng/dL% c! F3 V( M1 E% j1 l5 s
(normal, 3 to 90 ng/dL), androstenedione was 20
' [- \6 f% k2 ]8 _, Png/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
0 R% O( m( K4 N1 o- A! Gterone was 38 ng/dL (normal, 50 to 760 ng/dL),
: `! h1 k6 B' |. J# Q# jdesoxycorticosterone was 4.3 ng/dL (normal, 7 to( C& {5 W' p& Z7 r" T/ \1 l# P  r/ _3 @
49ng/dL), 11-desoxycortisol (specific compound S)3 i9 [- Q. K! s- Q  m
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-. {* s$ L/ t) v% Y
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total7 I8 n. s4 F# T* L' R
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),7 V9 K6 C4 c: l6 O0 M% ~% Q
and β-human chorionic gonadotropin was less than
; k. V5 I  P$ w5 mIU/mL (normal <5 mIU/mL). Serum follicular
" q9 x! X, V9 p, X; {stimulating hormone and leuteinizing hormone: d8 C% O' p; q5 L1 n3 q7 F+ W
concentrations were less than 0.05 mIU/mL: S3 R, M7 D  ]3 F/ z) G, ~& x
(prepubertal).0 W2 k& d. g0 D( a/ b8 s
The parents were notified about the laboratory. g- D) `# G" X" O# p' ?  q
results and were informed that all of the tests were  K. q  @* m7 l* @7 H
normal except the testosterone level was high. The
# W7 B: A. |4 b/ X6 x& S' R" }0 N5 ~; Q& m9 [follow-up visit was arranged within a few weeks to
) [5 A! }( ~! V1 u4 nobtain testicular and abdominal sonograms; how-6 D5 w0 V- `7 t1 W! K7 C$ u
ever, the family did not return for 4 months.
0 _& e7 ?* g" rPhysical examination at this time revealed that the" S) N0 B3 x( }  m. b' W
child had grown 2.5 cm in 4 months and had gained) C; }2 }  f9 Q# g4 t
2 kg of weight. Physical examination remained: Q( m' V6 {% l. l. i
unchanged. Surprisingly, the pubic hair almost com-8 s! V) I; ?5 k. I
pletely disappeared except for a few vellous hairs at
1 U5 ?6 w) E) }6 q& Wthe base of the phallus. Testicular volume was still 2
5 X, [0 y, m$ q) LmL, and the size of the penis remained unchanged.5 V& r4 a0 _; R) j4 }- k
The mother also said that the boy was no longer hav-
5 L6 ], H5 r, H5 E1 E: k- E$ Xing frequent erections.  V/ g; @2 Q* @( i3 ]
Both parents were again questioned about use of6 b, k$ C$ f) S7 K- J8 y+ D
any ointment/creams that they may have applied to1 m/ }+ w$ X4 ]6 c7 g- x3 N
the child’s skin. This time the father admitted the$ [$ l* `6 {* @+ D  n9 p
Topical Testosterone Exposure / Bhowmick et al 5414 C' O% L+ e( U1 `, [
use of testosterone gel twice daily that he was apply-$ p0 \8 o1 {; m' E$ `. s" t3 C
ing over his own shoulders, chest, and back area for
# V3 J! y0 o" S' \2 na year. The father also revealed he was embarrassed! o4 Y/ S, k6 s
to disclose that he was using a testosterone gel pre-
% j# p- \: [, D- R  c; B# rscribed by his family physician for decreased libido
: d, S, e2 @' v1 K/ dsecondary to depression.* J/ b5 d' Z* h; s( l0 e! u
The child slept in the same bed with parents.
& z+ ?5 m( q; E' JThe father would hug the baby and hold him on his# h- w5 \3 d4 l( n
chest for a considerable period of time, causing sig-
' F3 [/ R2 q9 g  F7 c' knificant bare skin contact between baby and father.
/ e4 P" g, L2 `# A6 i1 T; aThe father also admitted that after the phone call,6 Z" ?2 q: t: l, }
when he learned the testosterone level in the baby' O) q8 ^+ @5 k7 P& v# s0 F0 ?
was high, he then read the product information
/ q3 d" B) c: [1 Hpacket and concluded that it was most likely the rea-
& U& ]  K# @' s9 }0 I/ f0 h7 Nson for the child’s virilization. At that time, they
! ~) G: ^' {" sdecided to put the baby in a separate bed, and the
1 U6 f/ Y" O# Lfather was not hugging him with bare skin and had! `. Q8 H3 Y0 s0 q8 @* D
been using protective clothing. A repeat testosterone
7 A; L7 [4 A4 L1 Y: j% W( u1 ntest was ordered, but the family did not go to the- f8 i7 v$ T# X0 m( y  r
laboratory to obtain the test.
- A+ b- W/ L  i- TDiscussion
3 w. O$ H+ I. }! k; \Precocious puberty in boys is defined as secondary! S, t9 |2 _. I0 z; f& {$ H- y+ N
sexual development before 9 years of age.1,4
) B" t) H) M8 h2 e1 @$ C, r) ^Precocious puberty is termed as central (true) when
8 n( k7 L" e- K3 I  s/ Tit is caused by the premature activation of hypo-
1 }# F& o" g+ \4 @7 B: ythalamic pituitary gonadal axis. CPP is more com-5 z8 q$ y! {8 z1 m- r! v0 j
mon in girls than in boys.1,3 Most boys with CPP
0 c$ q* r9 c5 _0 J% T' Amay have a central nervous system lesion that is( ^+ I& |# v( N' K5 A
responsible for the early activation of the hypothal-/ D  L; y' T0 c5 X  @
amic pituitary gonadal axis.1-3 Thus, greater empha-7 k, i( _3 `( J% x
sis has been given to neuroradiologic imaging in
' ?) p' f  K! b4 gboys with precocious puberty. In addition to viril-# c. |) D9 x" D5 ^* D% f, g' x# t
ization, the clinical hallmark of CPP is the symmet-
; y, U# O( l! {8 U$ G% B' |rical testicular growth secondary to stimulation by
- v: U2 |# }0 s, ?% c$ xgonadotropins.1,3$ U1 [6 H9 P6 e+ S& m9 T; c
Gonadotropin-independent peripheral preco-
; y$ M/ b2 d4 V, ecious puberty in boys also results from inappropriate
8 f/ o& `$ z. y3 f& t& candrogenic stimulation from either endogenous or
$ W5 D) V; i, G5 l* jexogenous sources, nonpituitary gonadotropin stim-
' Y. h- b; t0 A& oulation, and rare activating mutations.3 Virilizing7 _& e% C$ Z2 Y! x: r- |
congenital adrenal hyperplasia producing excessive3 f. |" p6 L, v+ _
adrenal androgens is a common cause of precocious
) w. G, p- |; l! n1 w1 |3 Hpuberty in boys.3,47 G2 z+ S) s( F5 N
The most common form of congenital adrenal' y0 |- W9 ^6 n6 u- E! q
hyperplasia is the 21-hydroxylase enzyme deficiency.
/ T6 z& A  M7 h: j0 @5 TThe 11-β hydroxylase deficiency may also result in# L* k8 x/ g' s& D% D/ K
excessive adrenal androgen production, and rarely,
+ Y5 p: P9 l/ B. Xan adrenal tumor may also cause adrenal androgen
' t8 W7 `6 ?/ U+ H6 `8 k: rexcess.1,3
: b1 O! t3 Z+ N0 h, \6 uat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from6 S) A0 Q1 E1 Z
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
3 b% V# r" v: T! N5 uA unique entity of male-limited gonadotropin-
# A, H; t5 X2 Windependent precocious puberty, which is also known* u9 f9 n) y  U0 o1 k
as testotoxicosis, may cause precocious puberty at a( m. y2 D8 i0 n5 D9 X1 t. |# k8 _  {
very young age. The physical findings in these boys
1 l9 Y* [! k8 E) S$ {' Cwith this disorder are full pubertal development,
4 A; s& T' n$ M# r% o6 p; m2 sincluding bilateral testicular growth, similar to boys
/ B" V* T: P7 ewith CPP. The gonadotropin levels in this disorder3 f# _: {; p4 J. _+ B2 H$ y' K
are suppressed to prepubertal levels and do not show
5 y% @0 T7 b- F. H3 [; Fpubertal response of gonadotropin after gonadotropin-
3 ?% J! @& c, ureleasing hormone stimulation. This is a sex-linked3 b- ^8 L" Q& r, C. \; d
autosomal dominant disorder that affects only
! M4 e) O4 b3 ?( Lmales; therefore, other male members of the family
, W& h6 t; v4 Y6 Smay have similar precocious puberty.3
: y( u+ h/ B4 l2 X9 |" Z0 j- AIn our patient, physical examination was incon-& V4 J! P+ @5 F3 p
sistent with true precocious puberty since his testi-
  J) B7 \" a; k: `cles were prepubertal in size. However, testotoxicosis) P. J1 ^8 A; s( Y
was in the differential diagnosis because his father
/ Y8 [, l% q9 z! o# C5 r" o+ u! n3 {started puberty somewhat early, and occasionally,, L5 Y6 j9 y2 P9 e9 ]( ?" y4 D- x$ z
testicular enlargement is not that evident in the4 S3 w' B. t- n" X* x+ P9 C; O
beginning of this process.1 In the absence of a neg-9 W: {! o! e, n8 U4 W( g! z
ative initial history of androgen exposure, our5 _' ]/ t, `" m8 ^
biggest concern was virilizing adrenal hyperplasia,
. N  m' U' a" Z6 z9 h* l( Leither 21-hydroxylase deficiency or 11-β hydroxylase
* G8 R$ L& l  }deficiency. Those diagnoses were excluded by find-0 a. a- W8 w4 H, {$ D- C" z* B3 L; @
ing the normal level of adrenal steroids.
& O" s$ S* R3 bThe diagnosis of exogenous androgens was strongly
. _; p+ s4 h5 ^" fsuspected in a follow-up visit after 4 months because- A1 K; J7 M' c( a& C7 W3 }
the physical examination revealed the complete disap-/ k7 @8 e! s: T4 ~* |
pearance of pubic hair, normal growth velocity, and
6 }- w3 c% d  U" [decreased erections. The father admitted using a testos-4 Q! j8 ]  V5 V" B6 N: k
terone gel, which he concealed at first visit. He was
2 l, a0 U& d) ]9 @; W! ]using it rather frequently, twice a day. The Physicians’; Q* ^( I2 a) ]/ y
Desk Reference, or package insert of this product, gel or& C  K* |* t- l) W: ]3 q1 a6 Y/ P
cream, cautions about dermal testosterone transfer to
5 l7 a. \. A# V8 f; x) ^' cunprotected females through direct skin exposure.
3 N8 ]: k. ?7 D) ^; pSerum testosterone level was found to be 2 times the- z. H! |4 f* C0 ?& y7 _1 y
baseline value in those females who were exposed to
* F$ L" s5 ?) D7 |! s* x% g# q. C: t0 Eeven 15 minutes of direct skin contact with their male8 o( z" w6 z4 }5 w
partners.6 However, when a shirt covered the applica-  M0 y& G% |/ F  T$ E; X7 y& [
tion site, this testosterone transfer was prevented.( z, y9 \9 }; o! s# w
Our patient’s testosterone level was 60 ng/mL,
) U: {, {( A/ e1 Dwhich was clearly high. Some studies suggest that' b, v# f  N8 y
dermal conversion of testosterone to dihydrotestos-7 y' y. h) Z+ c- @+ M& e+ N0 _
terone, which is a more potent metabolite, is more
" o" e/ R2 D' nactive in young children exposed to testosterone
1 q3 i2 n3 \/ ~, @exogenously7; however, we did not measure a dihy-
  y5 {! [6 _5 ~0 R& Adrotestosterone level in our patient. In addition to
# O3 M& K/ B8 Evirilization, exposure to exogenous testosterone in8 X/ Y$ D7 b- h+ e
children results in an increase in growth velocity and
2 H" S2 F4 ]: H$ N( j  Cadvanced bone age, as seen in our patient.* S, I: h) I9 a: p$ |
The long-term effect of androgen exposure during/ _0 c8 }8 R6 j& {
early childhood on pubertal development and final* ?9 n( L4 M, A9 d$ N# A) k8 U
adult height are not fully known and always remain) }$ P* H0 `( g% i# q
a concern. Children treated with short-term testos-# x( j, ^$ D, X9 ~
terone injection or topical androgen may exhibit some
& r/ ~% K  n2 Jacceleration of the skeletal maturation; however, after
$ K8 ?* k+ h! Z2 O# b5 }cessation of treatment, the rate of bone maturation
5 d+ [3 F5 a5 _& Cdecelerates and gradually returns to normal.8,92 p, n! H' Z9 P; z# C% k
There are conflicting reports and controversy
6 [2 Q8 [1 d' ^) lover the effect of early androgen exposure on adult
/ R- w( I% x' v: y% X/ ^$ r' Kpenile length.10,11 Some reports suggest subnormal" z/ K, J! y- [; G% }3 f
adult penile length, apparently because of downreg-
- m: c; D7 c' {  gulation of androgen receptor number.10,12 However,
( X2 T% C% p0 Z9 o% K. lSutherland et al13 did not find a correlation between- B1 k0 R0 G: K+ ^: @
childhood testosterone exposure and reduced adult
5 Q( `* U' v! Spenile length in clinical studies., m4 B2 `; H' V' Y  d% `
Nonetheless, we do not believe our patient is
! w9 `. q1 K8 Egoing to experience any of the untoward effects from
1 ~$ ?/ I2 r5 h5 \( wtestosterone exposure as mentioned earlier because
" f5 \* ?% S- x' W& P4 N; A- pthe exposure was not for a prolonged period of time., y# D7 }; G: h7 A+ q5 L
Although the bone age was advanced at the time of
6 K. w  Y( S, |1 S( ]diagnosis, the child had a normal growth velocity at% ]: u0 Q9 u$ F
the follow-up visit. It is hoped that his final adult
5 J0 W5 j2 C. [$ \, ~height will not be affected.
( _4 s+ E0 y* t5 b! G3 VAlthough rarely reported, the widespread avail-! g" c; Q9 ^' \  e3 d' E* T& }
ability of androgen products in our society may% x7 L$ F5 Z& Y8 c4 S
indeed cause more virilization in male or female  t# H; {$ \8 X: w
children than one would realize. Exposure to andro-
3 }7 m: K7 {; V$ O+ X9 hgen products must be considered and specific ques-
% J2 b/ Z! m) T7 ^& \4 I. htioning about the use of a testosterone product or
) r  p. O8 d4 `# |+ u/ \0 [7 t8 Bgel should be asked of the family members during# `+ r# _/ C( r; a
the evaluation of any children who present with vir-
, y; q! F4 b/ x, L9 ]ilization or peripheral precocious puberty. The diag-
. h* _( ?, ]; s4 m  O! ~3 Y3 x- ?nosis can be established by just a few tests and by1 l( f3 _; P# Y$ x" I! J! w
appropriate history. The inability to obtain such a
% F9 W  m8 [$ {5 }& r6 ghistory, or failure to ask the specific questions, may
7 V1 n: m. v* ]. Jresult in extensive, unnecessary, and expensive) p. M' n0 z* t5 m
investigation. The primary care physician should be: s5 {/ n! Y2 v6 G( Q5 |
aware of this fact, because most of these children
$ S" q# R; }. o& @* ^! y! Lmay initially present in their practice. The Physicians’- o5 S# Z7 ?# P- I* ~$ A
Desk Reference and package insert should also put a
" x) D1 d# [$ ?6 o/ twarning about the virilizing effect on a male or% p9 e3 i8 }, g6 p; I
female child who might come in contact with some-
* m& X3 i5 ^8 A; D3 cone using any of these products.
& I; j6 S+ j# S* }2 i$ V8 FReferences: s7 m, B: K3 B# T) _0 _% W
1. Styne DM. The testes: disorder of sexual differentiation
( X' B. l5 l! Q/ ]and puberty in the male. In: Sperling MA, ed. Pediatric
- `; z4 g0 d) C. h$ FEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;! B$ v( b8 D7 U2 B/ X
2002: 565-628.
. o5 |) B- Y7 y$ ?; `2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
2 X1 I* b) ^) F3 w( l; y8 vpuberty in children with tumours of the suprasellar pineal
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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
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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
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
& H$ h1 |, @: v' `2 R/ ]7 n; K
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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