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Sexual Precocity in a 16-Month-Old4 K; ]$ z' [8 R& E% ]' X0 Q
Boy Induced by Indirect Topical
7 z- Z& V  c2 d% H  l8 _Exposure to Testosterone
- `2 t+ v6 i/ \* A) l( q1 z9 m  eSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
7 t7 k# z6 [8 C% Y& h1 B/ f$ x- uand Kenneth R. Rettig, MD1
0 Y3 Q) Z5 E8 b; x! a* L' o8 ?+ KClinical Pediatrics
# {# M" T" y9 h( m# ]5 X# Q' qVolume 46 Number 6
9 n) a6 V! {* f  {4 b' mJuly 2007 540-543
9 [( U3 {+ B8 g( w, S© 2007 Sage Publications
* a, E9 R- r+ U  n+ D10.1177/0009922806296651
- t2 {" J% O) b2 _$ E/ n" fhttp://clp.sagepub.com, O. V! }7 C& z$ D, @& [
hosted at& w' T4 ^, z) L. Y9 m* g
http://online.sagepub.com. D" c, c/ C2 _% F9 ]# W
Precocious puberty in boys, central or peripheral,$ R- W' ]) O" z5 Q- f
is a significant concern for physicians. Central
! B4 W6 D3 `5 a* M/ gprecocious puberty (CPP), which is mediated& K4 q4 q& n! ]9 J
through the hypothalamic pituitary gonadal axis, has
3 K% c: U( C: N& n: G# Aa higher incidence of organic central nervous system* L. h  _+ p4 V* l
lesions in boys.1,2 Virilization in boys, as manifested5 m' j3 q# b( O# M  W! K
by enlargement of the penis, development of pubic
/ m  {/ g3 g) S6 R5 Q& xhair, and facial acne without enlargement of testi-5 Z0 D/ @; t" O0 e. m9 B% Z
cles, suggests peripheral or pseudopuberty.1-3 We) w: r/ G5 }: ~7 `3 F6 r/ d% z& R
report a 16-month-old boy who presented with the5 j5 X; W& W7 ^$ S$ _+ o
enlargement of the phallus and pubic hair develop-
8 G2 r( l, F7 Y2 O0 g# Jment without testicular enlargement, which was due
7 h' t( l: R) w& u# |  B1 Cto the unintentional exposure to androgen gel used by
7 z: H/ u. z( [  l4 jthe father. The family initially concealed this infor-/ {3 k  r/ D) \0 D: J1 f
mation, resulting in an extensive work-up for this( }' e; m- a7 A; j+ W
child. Given the widespread and easy availability of6 a( `1 q6 ]3 ?, w/ {8 T  K1 [
testosterone gel and cream, we believe this is proba-
2 t1 I& N6 U6 xbly more common than the rare case report in the
; m& n' R4 D: h# \& ?literature.4/ z7 ~- t+ q8 u: D- R' q
Patient Report
% c; h: W4 n5 t, p7 OA 16-month-old white child was referred to the$ c* S% n! E8 y* x. T( g  E8 c
endocrine clinic by his pediatrician with the concern( P4 F- B  h1 ~' ?7 q
of early sexual development. His mother noticed
: Z2 \% M* M7 S4 e- v; glight colored pubic hair development when he was
5 I) E+ u/ ]4 h: {From the 1Division of Pediatric Endocrinology, 2University of" B1 U3 b4 l2 h% A# ?
South Alabama Medical Center, Mobile, Alabama.* y; w7 W4 O3 O7 |
Address correspondence to: Samar K. Bhowmick, MD, FACE,' V  n( Q4 F9 I- S
Professor of Pediatrics, University of South Alabama, College of
. v) {( L0 r- V  i2 M4 p4 v+ MMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;$ J4 z8 E5 F$ {8 o3 t
e-mail: [email protected].) }% l, m) s1 ~7 i5 _
about 6 to 7 months old, which progressively became: B* L+ A% R8 S! `3 u
darker. She was also concerned about the enlarge-
) U: R/ U6 D; _/ T7 H8 f! Bment of his penis and frequent erections. The child& d' d( d8 J( U
was the product of a full-term normal delivery, with) A* h/ Z( k- [- L6 h2 T
a birth weight of 7 lb 14 oz, and birth length of
; R3 r- u* K% q5 v5 a3 g4 \: [2 p20 inches. He was breast-fed throughout the first year% a+ l9 ~4 @0 X8 a! y1 a
of life and was still receiving breast milk along with1 ^+ e' i2 e4 e( A: ^
solid food. He had no hospitalizations or surgery,
2 A! V( j$ b9 T9 eand his psychosocial and psychomotor development3 ^/ [0 y) w+ b( i1 \+ M* z
was age appropriate.  \( W7 P" r& w$ Y9 E3 i7 p( T
The family history was remarkable for the father,- o/ j1 N, h6 q( C) l
who was diagnosed with hypothyroidism at age 16,# Z4 u0 x+ j) r8 @+ Z/ r. r
which was treated with thyroxine. The father’s
& ?  }* }2 n2 @4 O" M2 [" _height was 6 feet, and he went through a somewhat5 k' R: e+ e( w7 C: ~9 O8 l5 j
early puberty and had stopped growing by age 14.. F& R- {$ p) I3 I4 s- v) {
The father denied taking any other medication. The
2 m2 B' V8 s$ k; fchild’s mother was in good health. Her menarche+ p. E& U& Z5 x9 z, O1 D, q' r- h+ m
was at 11 years of age, and her height was at 5 feet
# ]2 L0 I$ q5 z2 b( }1 n3 z, f5 inches. There was no other family history of pre-. n- q, g/ B6 V
cocious sexual development in the first-degree rela-4 O# ^. k, p- f7 l
tives. There were no siblings.5 N9 A& t" Z. J/ w' x
Physical Examination- S% F! r) H; S3 O9 A6 N9 x4 E; J
The physical examination revealed a very active,
% J2 g( ]* A4 u7 [+ xplayful, and healthy boy. The vital signs documented
0 p% f- ?; x& a( C* T6 Ra blood pressure of 85/50 mm Hg, his length was
/ T& c6 S6 p6 O& o90 cm (>97th percentile), and his weight was 14.4 kg
) _8 F9 I: e! K3 Y; ^(also >97th percentile). The observed yearly growth
6 Z& h, D8 i, g) O# g, G8 C* lvelocity was 30 cm (12 inches). The examination of1 _" l# ^+ r8 N; [1 \8 ?5 |7 L, Z8 B
the neck revealed no thyroid enlargement." D& M; x7 L9 k  ]  M3 O! [8 `
The genitourinary examination was remarkable for) o. U- ~7 z4 ^/ _$ k6 E8 e
enlargement of the penis, with a stretched length of+ `& w3 A  s/ b& E. c( k: G! `
8 cm and a width of 2 cm. The glans penis was very well
. F( {* h$ n. B, w  `developed. The pubic hair was Tanner II, mostly around" W4 W* [" g6 I  q! ^! |. |( @
540
0 g# k1 E. |# A  B, i6 Gat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
; a2 y' V3 i/ pthe base of the phallus and was dark and curled. The
3 Y) [+ B) Q2 j! `- H& Etesticular volume was prepubertal at 2 mL each.
9 ]7 \4 j; H- }; ~( b/ o$ G) s) eThe skin was moist and smooth and somewhat
- T3 E: z2 T8 W/ Y, a" Woily. No axillary hair was noted. There were no
7 _7 `9 @: a  E- V8 c# ]& }abnormal skin pigmentations or café-au-lait spots.# i% b- c/ e3 q& r) j+ ?
Neurologic evaluation showed deep tendon reflex 2+
  _6 G9 J5 T3 e3 d/ rbilateral and symmetrical. There was no suggestion
& m9 i4 a* b9 R" @- c. Dof papilledema.
: m; V* U; {; ^( _7 bLaboratory Evaluation
- }. t: }2 K/ E9 n) f* V- uThe bone age was consistent with 28 months by
9 A( A# w% g7 y6 f$ rusing the standard of Greulich and Pyle at a chrono-- K! W3 ]) l: Y7 i
logic age of 16 months (advanced).5 Chromosomal
7 G) e* \4 s) [1 Y/ [/ [karyotype was 46XY. The thyroid function test* s/ A" T3 b' [9 r4 B& [
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
1 q1 ?5 `( J2 G5 y' Blating hormone level was 1.3 µIU/mL (both normal).
5 I8 l8 n- r! R1 k; @' GThe concentrations of serum electrolytes, blood
- `; u: k/ K& @urea nitrogen, creatinine, and calcium all were
4 B; {, S  o. R! T* _9 z' S% @within normal range for his age. The concentration
# Y: r% ?* o4 h0 N4 D$ q( }+ {of serum 17-hydroxyprogesterone was 16 ng/dL; p2 y$ O, Z% ^, d; |4 ~
(normal, 3 to 90 ng/dL), androstenedione was 20
: ^7 C, s7 ^6 r2 Z: a. n# \( B& T: png/dL (normal, 18 to 80 ng/dL), dehydroepiandros-/ N" |% W" t; h/ {9 Z2 u
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
# x* i, _/ l, ~& _- O7 M) ~desoxycorticosterone was 4.3 ng/dL (normal, 7 to
% i, M7 C& A# Z" ?0 d49ng/dL), 11-desoxycortisol (specific compound S)
0 ^% U7 R* ]* c5 hwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-0 x) K3 N9 Z8 S( ]- w" c
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total* f/ H  }/ H5 y, U) h8 y7 t$ o
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),0 s# A% M6 ?0 P( T
and β-human chorionic gonadotropin was less than, L) A2 ~  X; E( A5 D
5 mIU/mL (normal <5 mIU/mL). Serum follicular
6 K( S% _! g! c+ kstimulating hormone and leuteinizing hormone
0 E: ?. @) @7 o2 zconcentrations were less than 0.05 mIU/mL5 `9 y( j9 w' c6 V
(prepubertal).
6 P5 z5 ^) l7 d! q% QThe parents were notified about the laboratory6 @' L! [2 Z. L* N
results and were informed that all of the tests were2 x! J5 C) ]+ G# B8 i4 m$ Q
normal except the testosterone level was high. The" h1 H" `% ]/ G  d2 Y" F
follow-up visit was arranged within a few weeks to
! K, r( P* o: o; mobtain testicular and abdominal sonograms; how-& g' p. n( ~2 K0 V2 C8 U( K* L
ever, the family did not return for 4 months.) \8 M1 b) k5 C' B
Physical examination at this time revealed that the
+ z8 }# v; N: o6 b; M* |child had grown 2.5 cm in 4 months and had gained
3 s3 t* x+ `0 c2 kg of weight. Physical examination remained
. Q6 H# w" r7 w/ v8 aunchanged. Surprisingly, the pubic hair almost com-
' q' t: B4 C- M  B* L! m# n0 n; cpletely disappeared except for a few vellous hairs at" X# c& W  {6 M* r
the base of the phallus. Testicular volume was still 2
5 P, \. q+ b$ F5 F; x3 nmL, and the size of the penis remained unchanged.) C2 d7 M# _7 X
The mother also said that the boy was no longer hav-4 v" m7 r% U# W) H1 L
ing frequent erections.2 m4 `+ G# A% x  V
Both parents were again questioned about use of
. z. `% [' H/ b8 g/ V5 T/ S- Aany ointment/creams that they may have applied to
! a3 V! Y) O# @the child’s skin. This time the father admitted the
) ?' T( ?( w1 l/ u9 \9 ETopical Testosterone Exposure / Bhowmick et al 5414 B0 u# ?+ E. B, r( r5 R
use of testosterone gel twice daily that he was apply-
( N) V( r- L- t* Eing over his own shoulders, chest, and back area for! j8 H9 J7 R; m$ k% |) ^" a
a year. The father also revealed he was embarrassed
' }+ H' z% ]0 n; X0 tto disclose that he was using a testosterone gel pre-
' b( Q. _4 {8 j$ {scribed by his family physician for decreased libido/ `; D5 V8 Q& W: t5 {0 i4 }
secondary to depression.' k5 D4 k. k' k, e9 Z, u" k* G& g
The child slept in the same bed with parents.
; B1 q+ T9 K4 u% P+ l! v: P6 _The father would hug the baby and hold him on his
: r+ n2 B4 W% w, M( T6 l- Gchest for a considerable period of time, causing sig-
/ v0 f) ^8 r6 y. {7 anificant bare skin contact between baby and father.
% e' E; J% x5 c% i) O+ W* qThe father also admitted that after the phone call,% t& C& M4 r8 w& J& E
when he learned the testosterone level in the baby
. v$ @' {" j3 B1 B$ Z6 X- ~was high, he then read the product information
! h) b9 P. \$ z5 F* epacket and concluded that it was most likely the rea-: ]) X* x9 U3 x% P
son for the child’s virilization. At that time, they
$ X. [6 S( B6 a; odecided to put the baby in a separate bed, and the
0 |- v4 A, v7 n6 ?- w- U* A6 bfather was not hugging him with bare skin and had. \2 Y$ r: w. `3 U# G2 p# N0 L2 I! w
been using protective clothing. A repeat testosterone; M; a4 \) }1 D3 \$ p* }( t
test was ordered, but the family did not go to the4 Q6 Z3 f2 J( t, Y  Y
laboratory to obtain the test.; `# i+ B9 y6 ~
Discussion6 D0 X* z6 J; K- j* i/ |! M
Precocious puberty in boys is defined as secondary
% R8 z/ N( y& V& P- Asexual development before 9 years of age.1,4
8 P0 `, J  v1 n# \' f$ zPrecocious puberty is termed as central (true) when( k5 k0 |. G& z4 B# e$ q' K- S0 u
it is caused by the premature activation of hypo-2 r0 G( i! c! W/ u7 |
thalamic pituitary gonadal axis. CPP is more com-
& f4 o7 o. _" Bmon in girls than in boys.1,3 Most boys with CPP: I7 X0 |* p; a" s( x+ }
may have a central nervous system lesion that is
/ U3 E3 m, ]* E" t0 i4 eresponsible for the early activation of the hypothal-
, r( c. F+ w1 K" _amic pituitary gonadal axis.1-3 Thus, greater empha-
( T$ r7 U% G- b/ `, gsis has been given to neuroradiologic imaging in
! C& C* A  Z" w# oboys with precocious puberty. In addition to viril-
' g: O! {! r6 F8 nization, the clinical hallmark of CPP is the symmet-
2 \! f; l' v6 i8 W2 ]- C7 krical testicular growth secondary to stimulation by/ }9 ~- n9 E) \( _
gonadotropins.1,3
: {; G7 H- Q2 O  z) I8 GGonadotropin-independent peripheral preco-
8 j  ~- r+ Z: K8 ]0 y0 F. M* E4 ~cious puberty in boys also results from inappropriate
" w0 b1 [1 D; p- x0 u  Landrogenic stimulation from either endogenous or0 u; |# I% p5 J& O3 Z5 Z3 n
exogenous sources, nonpituitary gonadotropin stim-
, w% U$ G& a" l' G1 w; L. vulation, and rare activating mutations.3 Virilizing
% U7 R3 E  ]$ ]1 W1 Vcongenital adrenal hyperplasia producing excessive
7 F2 b) P1 N( H2 Z" fadrenal androgens is a common cause of precocious* t: N. G" v# D
puberty in boys.3,4, ~& R8 a9 R  Q6 z: R5 [* D
The most common form of congenital adrenal
$ g( e8 i  P; w+ Xhyperplasia is the 21-hydroxylase enzyme deficiency.* J7 O; f8 c+ ^( |
The 11-β hydroxylase deficiency may also result in
/ @# I  N, f4 _6 R3 `: h/ p" jexcessive adrenal androgen production, and rarely,7 t3 e# `  J& I
an adrenal tumor may also cause adrenal androgen
: b4 ^2 _" f1 V  p6 f, Xexcess.1,3! x$ t5 S. G) @/ z6 J2 T
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
& O7 }' A5 [$ {. T: Z( G4 e542 Clinical Pediatrics / Vol. 46, No. 6, July 20071 Z5 `2 ?- c: u9 n8 Y, ^
A unique entity of male-limited gonadotropin-
8 h  k8 V- h4 Q+ s0 i# d2 e) qindependent precocious puberty, which is also known4 w) d. W6 P! z" y9 b* ?* n
as testotoxicosis, may cause precocious puberty at a
& `7 [. }$ D* e, Rvery young age. The physical findings in these boys
& E( U# `/ S- p* y7 \5 M( lwith this disorder are full pubertal development,: s$ @4 K0 J1 j4 R
including bilateral testicular growth, similar to boys. a/ v" C7 I; T
with CPP. The gonadotropin levels in this disorder
2 h4 ]7 ^& n2 X* [3 Lare suppressed to prepubertal levels and do not show" ~8 t/ L' k  Y9 G
pubertal response of gonadotropin after gonadotropin-$ E- L3 c; p! s4 T2 F" Y6 \- G
releasing hormone stimulation. This is a sex-linked
- v3 E- A$ t  \1 Tautosomal dominant disorder that affects only$ t' a4 {" ?1 e3 }" D
males; therefore, other male members of the family
5 o8 @& g# e1 A! wmay have similar precocious puberty.3
( O) |7 g2 C0 w( g5 IIn our patient, physical examination was incon-+ D9 n0 _% z* [/ ~" a3 T: d* U
sistent with true precocious puberty since his testi-; ^  m8 h1 m$ X
cles were prepubertal in size. However, testotoxicosis6 K  v% f. a7 F% f( u8 l) L
was in the differential diagnosis because his father6 B) A, v0 U% a  m0 b; M
started puberty somewhat early, and occasionally,
: T* n- k- ^3 k) z# rtesticular enlargement is not that evident in the5 F% @4 L3 |1 P1 _
beginning of this process.1 In the absence of a neg-2 U. A( e% o2 j4 j* p1 @7 J& Z
ative initial history of androgen exposure, our
2 @# W& K( ~: Q- {biggest concern was virilizing adrenal hyperplasia,
; N, f1 A4 W3 u. v, W" ~either 21-hydroxylase deficiency or 11-β hydroxylase1 D9 o, U9 ~* }1 m
deficiency. Those diagnoses were excluded by find-
( V& C" B3 A; \* s1 Qing the normal level of adrenal steroids.
. i+ s* \: g' H/ ~" @/ BThe diagnosis of exogenous androgens was strongly
. ]9 t& k' M/ k; qsuspected in a follow-up visit after 4 months because% o' I& \9 N- a: `' u5 t+ Q
the physical examination revealed the complete disap-, k" e0 b# }% P4 a
pearance of pubic hair, normal growth velocity, and) w5 N* f; q4 ?7 q( ?: w/ s. ?5 z3 z
decreased erections. The father admitted using a testos-
# L: ~* A4 Z9 dterone gel, which he concealed at first visit. He was
1 `( f' O( U$ U, q8 W7 e- k. u' b: t  qusing it rather frequently, twice a day. The Physicians’
" F8 U' F+ |  `7 ?' JDesk Reference, or package insert of this product, gel or
" i. ~& X2 H7 ~7 _cream, cautions about dermal testosterone transfer to
7 F, K4 p( k' F6 zunprotected females through direct skin exposure.
( m- |- N+ H& s5 J2 _Serum testosterone level was found to be 2 times the
# m: G2 [+ p6 }) W5 k4 [baseline value in those females who were exposed to
! P! `& l7 U$ V4 Deven 15 minutes of direct skin contact with their male
# n, R/ @+ F# b3 {" T4 f* ppartners.6 However, when a shirt covered the applica-
( e4 a  K& X9 g5 u' dtion site, this testosterone transfer was prevented.% Y- S+ |7 }9 |
Our patient’s testosterone level was 60 ng/mL,
9 H# w9 A! A( X' y" L8 ?which was clearly high. Some studies suggest that
) [9 d9 G5 E6 K7 |* M4 ^! Cdermal conversion of testosterone to dihydrotestos-
& q$ s1 O: o" T5 P/ qterone, which is a more potent metabolite, is more
- _- t  x" M+ @1 e2 n( cactive in young children exposed to testosterone" h! K3 B: @( k( G
exogenously7; however, we did not measure a dihy-/ a5 a' @( u2 I; n) O
drotestosterone level in our patient. In addition to9 w) @$ A# g& f: Y6 E$ H; G# y
virilization, exposure to exogenous testosterone in
" d7 Y# a, k- }8 o2 Pchildren results in an increase in growth velocity and
0 z+ [4 [, o' }, d- c; t, @advanced bone age, as seen in our patient.
  `3 g' P& B8 O4 S$ }7 _$ ^8 }The long-term effect of androgen exposure during. r# I  B/ H% K: s8 P' B
early childhood on pubertal development and final
; [& }# w9 j: a$ o$ Y* b+ [/ f3 A* zadult height are not fully known and always remain% ?, S( f, G7 E% P
a concern. Children treated with short-term testos-( a( Q0 \, H0 E: t$ Z" v
terone injection or topical androgen may exhibit some
$ _* f. b, w: F4 vacceleration of the skeletal maturation; however, after
6 ]8 j! l7 s& ^9 F) X  Jcessation of treatment, the rate of bone maturation
+ E1 g* z6 w0 N+ H8 Udecelerates and gradually returns to normal.8,9+ Y( g7 U! y7 r4 ^. N, O
There are conflicting reports and controversy
3 `0 }- ]/ i9 ?+ w! xover the effect of early androgen exposure on adult
6 E* O' f0 O/ |penile length.10,11 Some reports suggest subnormal
$ {/ t- j' {- cadult penile length, apparently because of downreg-
) G" O! H- w* j+ Y  s' Tulation of androgen receptor number.10,12 However,
3 P3 g' G! M/ ]5 Q4 A% \+ ^4 FSutherland et al13 did not find a correlation between0 u* Z: d) ?6 Q1 E$ C6 ~
childhood testosterone exposure and reduced adult
0 l. u' u( ?: p0 c9 @penile length in clinical studies.
; |) g$ _4 @& U' h4 B+ g1 tNonetheless, we do not believe our patient is
- Q* z6 x+ m- r) i0 p' F7 @1 G% _4 E! ^going to experience any of the untoward effects from( ^3 [. m: T0 z' Y, s
testosterone exposure as mentioned earlier because
' }2 A6 I- P0 H" Y( m3 x: A+ zthe exposure was not for a prolonged period of time.
4 {  [: t- `: \" [+ J) V  E3 i" kAlthough the bone age was advanced at the time of+ h" i% l, t) P; ?
diagnosis, the child had a normal growth velocity at2 _4 ?! U8 Z, b, z8 E" U4 {9 A8 k
the follow-up visit. It is hoped that his final adult8 b; p" m4 u& h  g% D1 T
height will not be affected.
. Q( Y3 Q& z0 P0 ~Although rarely reported, the widespread avail-
0 f3 f2 F  y- f3 o& \' kability of androgen products in our society may
/ L: O) q- h  E. Z6 \* Bindeed cause more virilization in male or female; ?9 W" m- t- q2 w0 H
children than one would realize. Exposure to andro-# W/ Z. a  s* a/ t+ y! j/ ~+ R. W
gen products must be considered and specific ques-5 G9 k9 n' L4 {. b+ E- [
tioning about the use of a testosterone product or" v; h0 l! I1 o- j6 f# O. e) B0 _% g
gel should be asked of the family members during/ C+ t. E. d0 p
the evaluation of any children who present with vir-
4 z- _, v1 L& Filization or peripheral precocious puberty. The diag-
8 W  M% [9 U4 l: I6 S# gnosis can be established by just a few tests and by4 p% O4 d8 R4 V% \
appropriate history. The inability to obtain such a2 T5 B8 T! W8 w4 y5 _$ t, X# B8 b
history, or failure to ask the specific questions, may
& G6 X) B4 V$ H6 i2 |/ Mresult in extensive, unnecessary, and expensive
) `8 ]4 G2 [- h. V. x1 z+ |3 Tinvestigation. The primary care physician should be
6 n, G$ q4 c6 d. i5 iaware of this fact, because most of these children
, N$ t* ^" K7 n) K: T5 bmay initially present in their practice. The Physicians’( B7 {) g4 Q0 G2 Q0 j& z
Desk Reference and package insert should also put a
) ?4 ?. B* ]4 r' n' I* }0 zwarning about the virilizing effect on a male or' F" E% y0 u. b) T
female child who might come in contact with some-% ?5 T+ F$ `4 B/ E9 X' {
one using any of these products.
! j- q; N0 S' u1 C. kReferences
2 ?8 W4 j3 S$ t/ E1. Styne DM. The testes: disorder of sexual differentiation* \8 U' k' ~0 l
and puberty in the male. In: Sperling MA, ed. Pediatric, `: D- D0 y4 E; W# j
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
/ y% s) C$ A% P1 _: |* Q) H& @2002: 565-628.
2 {/ f3 C' }+ G0 T2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
6 y7 F/ e3 `+ y: Dpuberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
) J9 }7 h9 b( b' [$ LBoy Induced by Indirect Topical1 Q. [( J! Z+ T9 @
Exposure to Testosterone
6 J5 a! }5 g/ z% H; BSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2* T, r; ~' {+ g" W% z) V! I
and Kenneth R. Rettig, MD18 u3 w2 [4 L6 r/ E, c
Clinical Pediatrics  ~  ^& u. X8 ?( O: E0 B* D9 ]! k$ K
Volume 46 Number 67 v2 N4 @9 h& @8 t: c
July 2007 540-543
0 s' n* n2 }2 }% S. t2 c3 H8 s© 2007 Sage Publications
. Y7 A7 Y" l: ^; R- `10.1177/0009922806296651
! I  z- w( B* q0 D, I  I* Hhttp://clp.sagepub.com2 r4 c9 K8 a5 H; F/ a( w
hosted at
: D+ H0 w* w; R7 A+ Uhttp://online.sagepub.com
) {" ]7 R3 M* I3 l* P4 {" p5 jPrecocious puberty in boys, central or peripheral,7 v2 j- b2 H0 y* K$ K7 i
is a significant concern for physicians. Central
# o; n. h. q5 @: V4 yprecocious puberty (CPP), which is mediated
3 p" p- v* w+ A& Uthrough the hypothalamic pituitary gonadal axis, has
9 d8 v" ?( p. p6 {- Aa higher incidence of organic central nervous system
+ i! S$ U- T! `  S  U4 Glesions in boys.1,2 Virilization in boys, as manifested/ k- g* H4 }, V" _! m7 o
by enlargement of the penis, development of pubic
# v3 D+ y# }$ C/ Z- k, f" J5 T7 Nhair, and facial acne without enlargement of testi-
/ c* ], s, B2 G+ e6 ]2 Jcles, suggests peripheral or pseudopuberty.1-3 We
1 e9 B5 c& x) Qreport a 16-month-old boy who presented with the7 {, P$ h1 p4 d" ?# R9 t) r# S
enlargement of the phallus and pubic hair develop-
- \- _0 t' c. R8 q, s" |5 |( cment without testicular enlargement, which was due3 N+ u) ?' B6 q% @+ Y7 Z) c
to the unintentional exposure to androgen gel used by
. @% }" x/ ?/ q' z# ^$ wthe father. The family initially concealed this infor-
; |( l  b1 ?- G' n$ G+ N5 K2 ]mation, resulting in an extensive work-up for this8 z! U% Y& i" [9 T2 O. `3 x
child. Given the widespread and easy availability of
3 i5 U+ R# T9 g. k9 itestosterone gel and cream, we believe this is proba-
2 N# b1 B' G3 o$ |. g8 Z, sbly more common than the rare case report in the
/ Z+ a' P5 a2 ~literature.4( q4 O! B7 F# B8 d
Patient Report
/ L* i, w) e8 a  q: h8 p5 c2 C: {A 16-month-old white child was referred to the, t& \4 _+ J$ ~" }  E
endocrine clinic by his pediatrician with the concern: A3 O3 M: g, c5 Y8 p( u
of early sexual development. His mother noticed
) Y' i8 e! x0 U5 f' r1 ^light colored pubic hair development when he was
- Y" Q4 U3 ?+ m0 t. v, U7 l& zFrom the 1Division of Pediatric Endocrinology, 2University of
4 X% O- v: ?2 P! O4 p. u! iSouth Alabama Medical Center, Mobile, Alabama.
8 U7 _. A% {4 I! P+ r# q/ _Address correspondence to: Samar K. Bhowmick, MD, FACE,/ V% c/ }6 c( t2 b
Professor of Pediatrics, University of South Alabama, College of
5 q5 I4 H) y$ Y% c/ I& @6 tMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
- d8 a+ |& l$ I  J+ X, _6 B9 @& L' se-mail: [email protected].+ c7 ]" P3 A# W" e6 \1 q; D
about 6 to 7 months old, which progressively became; _' f2 o2 ]  U: F0 y, _) E; z
darker. She was also concerned about the enlarge-
# n/ T/ Z, C2 x* O6 c9 e- Y( r' x  Hment of his penis and frequent erections. The child) K" M: q* C/ X
was the product of a full-term normal delivery, with
) F1 X: R6 ]1 a8 M: P/ x% R5 Ma birth weight of 7 lb 14 oz, and birth length of
/ p1 c0 U& ]: _0 e# E) A20 inches. He was breast-fed throughout the first year
0 q( O) i) G' K2 J1 F- ^of life and was still receiving breast milk along with
9 s+ n) B0 B0 ]1 Y. c' m' Vsolid food. He had no hospitalizations or surgery,  T- M. Q! P0 C3 T; @& |
and his psychosocial and psychomotor development1 @% p; e6 w8 [- Y$ E% `, o) q
was age appropriate.9 @' \6 c% [* x8 ^: ~3 @
The family history was remarkable for the father,
, T) [3 k3 v; ?' N- }5 e( R. awho was diagnosed with hypothyroidism at age 16,: Z) O8 J7 G4 o1 {) I& R
which was treated with thyroxine. The father’s9 D* R( T8 j# k4 i- o
height was 6 feet, and he went through a somewhat& C; F& i, {- A6 |
early puberty and had stopped growing by age 14.
5 l( L9 I9 Q( [2 j, B4 uThe father denied taking any other medication. The: U1 m% J2 M" [7 e; A8 q
child’s mother was in good health. Her menarche
( f- \& Z" @" t8 `" }( @1 cwas at 11 years of age, and her height was at 5 feet; z% G$ _, ^! Y+ K! n! \0 i
5 inches. There was no other family history of pre-- F9 w: {4 K. V% `7 R/ C& i5 P' a  K
cocious sexual development in the first-degree rela-: z0 A$ C2 d( ?6 |7 G/ A3 b
tives. There were no siblings.9 @; `, k0 J4 `& U" h; ^
Physical Examination/ F5 p8 i) ?& w3 ]. x5 C. c
The physical examination revealed a very active,& _/ X- j' I2 C$ r2 p5 y
playful, and healthy boy. The vital signs documented, ^/ T6 Y+ [0 p4 t  P
a blood pressure of 85/50 mm Hg, his length was3 L* {; [, S$ y( e; a6 X/ i
90 cm (>97th percentile), and his weight was 14.4 kg6 Z4 h, Z) p# Y4 m' e2 h
(also >97th percentile). The observed yearly growth2 q8 r( g, L  l" J/ y
velocity was 30 cm (12 inches). The examination of; O% y. q9 k) w) T3 m$ b
the neck revealed no thyroid enlargement.8 W4 {. b, d" W+ R- J, C# l; j1 Z9 Z' T
The genitourinary examination was remarkable for! v* k9 z( X# G: V3 ?
enlargement of the penis, with a stretched length of+ ^6 n' h, {' a/ f  p. \; A1 [
8 cm and a width of 2 cm. The glans penis was very well
* V% f; n, `% Z( edeveloped. The pubic hair was Tanner II, mostly around
1 s4 X/ B, Q* I" y540
/ M! G* x) n+ Xat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
4 _! L1 k# @' _/ k$ cthe base of the phallus and was dark and curled. The
. e& T+ ?( a& `4 _testicular volume was prepubertal at 2 mL each.* o+ {3 l2 K/ P; `
The skin was moist and smooth and somewhat
8 x+ z+ h# \! _7 b# g8 \- [oily. No axillary hair was noted. There were no
8 l1 j  O0 b+ e- y& t. Iabnormal skin pigmentations or café-au-lait spots.4 m7 C( ~4 _$ s
Neurologic evaluation showed deep tendon reflex 2+
% m  x% M4 Z! h. `4 {bilateral and symmetrical. There was no suggestion6 q& d* K$ T" j
of papilledema.
( L/ p* E3 ~0 o$ uLaboratory Evaluation# }1 Y( U3 d8 S* |2 e
The bone age was consistent with 28 months by
( @( A. {+ `8 ?1 Vusing the standard of Greulich and Pyle at a chrono-" U7 g7 s# o$ g! m. F
logic age of 16 months (advanced).5 Chromosomal' a# ~( F* n  z) D1 d
karyotype was 46XY. The thyroid function test
: S. y# }  g9 s# `0 q: _showed a free T4 of 1.69 ng/dL, and thyroid stimu-
- h) e3 v4 h# B6 r6 G1 |8 @+ Ylating hormone level was 1.3 µIU/mL (both normal).! t4 m$ ]* s& Q; D6 h
The concentrations of serum electrolytes, blood
/ R: t& l% g, v3 @+ s1 gurea nitrogen, creatinine, and calcium all were2 B  {( B" G9 u$ o2 ~. m# D' K. C
within normal range for his age. The concentration
9 k" K* @5 z. _  H2 l7 jof serum 17-hydroxyprogesterone was 16 ng/dL
/ a/ v; a3 c6 G& W(normal, 3 to 90 ng/dL), androstenedione was 200 F; z  g6 j0 q, S$ _2 v! M
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-6 t! w, R( b0 F# j
terone was 38 ng/dL (normal, 50 to 760 ng/dL),& r( u/ k" M% d* q
desoxycorticosterone was 4.3 ng/dL (normal, 7 to+ n. q, T+ s7 R4 v, y3 L
49ng/dL), 11-desoxycortisol (specific compound S)/ A, q  n$ c* h0 [$ K* M. C" C
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-5 M6 `* U* o! x2 O6 s
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total8 x1 N8 L+ E# Y5 q0 O
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
$ w! f# V, V+ Z) C7 s# ~and β-human chorionic gonadotropin was less than# V, P4 m/ B4 s9 o6 Z% c
5 mIU/mL (normal <5 mIU/mL). Serum follicular
4 M( U2 w) k% x5 R9 ]stimulating hormone and leuteinizing hormone. A8 R3 z2 P+ l' o4 N  N: }
concentrations were less than 0.05 mIU/mL
3 A  {: f; s6 N5 ~(prepubertal).
' W: j/ f3 R( C' r% kThe parents were notified about the laboratory
5 l9 M" u' H% W7 j; q+ O# T, H2 Bresults and were informed that all of the tests were
; D& y/ r! K1 l$ {7 a8 `) v* \normal except the testosterone level was high. The2 T# u$ n# K5 j: o* |
follow-up visit was arranged within a few weeks to) O+ }" Q+ o9 Q' B" ?; g$ F4 D
obtain testicular and abdominal sonograms; how-
+ t+ {& t1 Q' v( lever, the family did not return for 4 months.0 P% Z) i  B0 E% ?
Physical examination at this time revealed that the  n$ ]" D3 M# S
child had grown 2.5 cm in 4 months and had gained' `5 H8 M1 |- r7 @2 L& j
2 kg of weight. Physical examination remained
/ ]6 s2 P8 |9 T- z/ Tunchanged. Surprisingly, the pubic hair almost com-
1 a, t9 k/ G3 {4 u, Q) x2 d; I  Vpletely disappeared except for a few vellous hairs at
( z5 `* |7 z8 \4 J/ o. g. I3 A/ lthe base of the phallus. Testicular volume was still 2
% B# T, z) U: V3 H9 D3 ImL, and the size of the penis remained unchanged.
; M$ r; `" l1 w% O8 e: bThe mother also said that the boy was no longer hav-% d3 L$ f7 O2 `- i" u& B! Y4 E
ing frequent erections.% p: V! N- T7 T" R) @+ Z3 `0 O
Both parents were again questioned about use of# ^0 @. R/ A! Q& l
any ointment/creams that they may have applied to9 u7 t/ P! R7 D# R$ J  l- [! [
the child’s skin. This time the father admitted the/ o. G# w" w, D4 M% P3 I, _  m7 g
Topical Testosterone Exposure / Bhowmick et al 541
& r! L( a& }- ?* J( L9 g! @; suse of testosterone gel twice daily that he was apply-
/ z$ [2 H! |1 I& R; G! j% r! iing over his own shoulders, chest, and back area for
7 k7 m2 G7 S& L: \; i' ia year. The father also revealed he was embarrassed; y- Y( g. a, \$ q+ H2 U, U% H
to disclose that he was using a testosterone gel pre-* l9 X; S+ K- s" W# d
scribed by his family physician for decreased libido1 i6 H/ K7 g: M8 j3 E' @6 I6 a
secondary to depression.
+ \2 ], Q* V( Q* rThe child slept in the same bed with parents.
+ S+ L# P4 X. C2 [The father would hug the baby and hold him on his
$ e1 ~+ X" \3 t9 x  g4 A% gchest for a considerable period of time, causing sig-* y) l/ Y: S" F# w% D$ Y4 Z* {# J
nificant bare skin contact between baby and father.
8 X. z7 F' u" ], qThe father also admitted that after the phone call,% p' A3 n. Q1 C( l5 b4 s) _
when he learned the testosterone level in the baby2 V4 F) e. x) }! n
was high, he then read the product information
' G+ E  M% ^: V5 x  t! k/ Ypacket and concluded that it was most likely the rea-  U6 t$ ?+ ~# H& S$ `& r: c- s
son for the child’s virilization. At that time, they
1 l) k/ j# S0 Y9 M, |decided to put the baby in a separate bed, and the
% \4 ]& n( p) P# {4 W9 a8 N5 Y+ N1 lfather was not hugging him with bare skin and had  F' L, x5 L( z$ C) ^7 W
been using protective clothing. A repeat testosterone
0 r9 n; e' R9 R% n2 U& V" V$ dtest was ordered, but the family did not go to the
( L3 l* r. e1 _1 ?# m7 J! b; j3 dlaboratory to obtain the test.
, u. V& ?9 y3 MDiscussion
& P. n; P5 I+ t9 GPrecocious puberty in boys is defined as secondary
' f1 R7 o1 v4 w- f- a  bsexual development before 9 years of age.1,4- }. ?$ ^' q2 M8 C& o1 [& v
Precocious puberty is termed as central (true) when
( y2 Z. Z8 u9 T- `  ?- Zit is caused by the premature activation of hypo-& w- u5 B+ w; Y! f7 ?2 x+ U
thalamic pituitary gonadal axis. CPP is more com-
& E$ t+ @! h8 x5 V' H& Gmon in girls than in boys.1,3 Most boys with CPP
3 ?  k  k  S/ V0 ^may have a central nervous system lesion that is
2 T% Y- |; P$ O6 p/ Q5 h- sresponsible for the early activation of the hypothal-$ [. _1 V9 J0 y9 u$ Y5 N# m
amic pituitary gonadal axis.1-3 Thus, greater empha-
2 P1 x8 y" g2 T1 Psis has been given to neuroradiologic imaging in6 s: f- g) ^0 R9 A$ I" C
boys with precocious puberty. In addition to viril-1 Q! [5 J5 `6 j0 e
ization, the clinical hallmark of CPP is the symmet-
( m" w- R5 K; g# K" Trical testicular growth secondary to stimulation by
4 S+ ~8 |% {' n/ Z, \; Ggonadotropins.1,33 {0 o( f# I6 x
Gonadotropin-independent peripheral preco-
3 {+ H; {7 Y: Q; t0 H7 lcious puberty in boys also results from inappropriate
- j4 T' V. V7 X/ v5 nandrogenic stimulation from either endogenous or
" x, b2 @# T6 ^' Fexogenous sources, nonpituitary gonadotropin stim-
& a2 N( q* v- a- v/ G, S- n* G( tulation, and rare activating mutations.3 Virilizing2 j" q: C' R  s) O. n" V
congenital adrenal hyperplasia producing excessive" r7 C$ E0 ^2 C8 f" Z
adrenal androgens is a common cause of precocious1 h8 }$ D& i' u+ Z1 G
puberty in boys.3,4# m! z8 y" K* \
The most common form of congenital adrenal
, c: O7 d- H( V/ _0 Vhyperplasia is the 21-hydroxylase enzyme deficiency.1 F) R$ R9 q% q' O
The 11-β hydroxylase deficiency may also result in
) e! c* S. M8 f1 V/ nexcessive adrenal androgen production, and rarely,& P, w8 s0 S$ Z# T
an adrenal tumor may also cause adrenal androgen
, W& o& J9 L2 `7 {3 oexcess.1,3
( \& {8 ^% b6 T1 Eat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from$ d8 T5 M$ _  e) x
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007+ G8 l/ G3 c8 F* O( Q2 P
A unique entity of male-limited gonadotropin-5 L/ \/ _" B* w" `6 g) p
independent precocious puberty, which is also known2 c7 |6 x/ O6 x% S! I
as testotoxicosis, may cause precocious puberty at a
) P5 D+ R' [2 T) J/ f1 |4 S( Xvery young age. The physical findings in these boys
% Z9 T% D. |8 I( Kwith this disorder are full pubertal development,7 Z1 U9 n6 i$ D
including bilateral testicular growth, similar to boys* w, @* {0 M: q1 C/ W2 u, d# y
with CPP. The gonadotropin levels in this disorder2 h$ a$ n, p2 Z& V' J* M5 R5 a
are suppressed to prepubertal levels and do not show7 `! s- }- X9 ]! T: n5 j, `
pubertal response of gonadotropin after gonadotropin-6 f+ X; R* t/ D) [' ]
releasing hormone stimulation. This is a sex-linked
, p$ [: d+ W) E: pautosomal dominant disorder that affects only1 [( ^, x4 Z6 Z# K) ?1 P' G
males; therefore, other male members of the family
% t: d$ l8 D8 Y0 M3 T+ @may have similar precocious puberty.3
! D( x- J: j5 Z& F3 w8 C% X; ]In our patient, physical examination was incon-
) B0 |! P) r2 e+ ^2 @7 |1 N/ B1 |sistent with true precocious puberty since his testi-# e/ K) f2 h: v  Y
cles were prepubertal in size. However, testotoxicosis
  ~1 S- g  b+ a: A4 Lwas in the differential diagnosis because his father& c" A4 p% Y* n5 P( C
started puberty somewhat early, and occasionally,) P1 A, ^5 c+ k3 x- ?! J7 `, J
testicular enlargement is not that evident in the
, S8 b; X2 m% O1 [beginning of this process.1 In the absence of a neg-& f, k* L2 d2 U0 d& v& r. R
ative initial history of androgen exposure, our) q0 j* N5 g% \* I* Y
biggest concern was virilizing adrenal hyperplasia,) D/ b5 E0 v8 G& Z! ]
either 21-hydroxylase deficiency or 11-β hydroxylase
0 {& p7 l9 J/ f4 j2 Q! pdeficiency. Those diagnoses were excluded by find-5 E0 a2 j/ _( [+ s9 w, G
ing the normal level of adrenal steroids.
2 c+ t$ p% m& G8 zThe diagnosis of exogenous androgens was strongly* x. \! [- N9 K* U9 X3 z- f+ d
suspected in a follow-up visit after 4 months because
/ v8 R9 Q  m/ o! c; zthe physical examination revealed the complete disap-
9 M3 ?% `" X# b! }pearance of pubic hair, normal growth velocity, and
/ l: @  |$ K3 adecreased erections. The father admitted using a testos-
2 ?+ Q0 p7 P* W% F" b5 `* b  Pterone gel, which he concealed at first visit. He was$ W* r, }$ y2 }" N8 }
using it rather frequently, twice a day. The Physicians’
) M' D. Q& Q2 s* E& |Desk Reference, or package insert of this product, gel or
! A/ [, @- o9 R7 T% B% u4 q  Acream, cautions about dermal testosterone transfer to
0 u& k2 U8 H# T% Zunprotected females through direct skin exposure.
* L" x, K, |, j* J; a1 ~Serum testosterone level was found to be 2 times the
1 O$ B( C! _8 Ybaseline value in those females who were exposed to/ x& }! [3 P- A# L0 ^/ g: ]
even 15 minutes of direct skin contact with their male5 ?$ e% P* k6 S2 k7 B
partners.6 However, when a shirt covered the applica-
! H) V# Z! {, m8 i5 T$ t; ition site, this testosterone transfer was prevented.
1 [7 z3 P9 ~* C+ LOur patient’s testosterone level was 60 ng/mL,  d& D, \  |" ^. |" {- k
which was clearly high. Some studies suggest that
- ]5 `5 E8 o% ]% L8 odermal conversion of testosterone to dihydrotestos-1 v" `& D+ Z4 Y+ Z) ~$ H
terone, which is a more potent metabolite, is more
8 r0 h9 j) Z$ l( \active in young children exposed to testosterone; {: |& T/ w$ f9 d7 i4 F
exogenously7; however, we did not measure a dihy-% t8 n7 X/ Z$ {! F) ?: P2 x
drotestosterone level in our patient. In addition to
0 U& V3 |. Q5 p* ivirilization, exposure to exogenous testosterone in
: r' O1 P' X& Z1 G. c3 Kchildren results in an increase in growth velocity and
" I, w9 }7 n6 V% [, e& q# p8 Xadvanced bone age, as seen in our patient.
- l$ p$ }" K: c9 F5 E$ ?( bThe long-term effect of androgen exposure during
' b& O+ v, j* a4 Nearly childhood on pubertal development and final
/ G+ ?, |$ J! |% t6 xadult height are not fully known and always remain) ~) x+ w" d; i3 S; [) Q8 U
a concern. Children treated with short-term testos-; e/ H  K! ^# [0 X9 c5 [- f+ ]
terone injection or topical androgen may exhibit some
3 X6 U; m0 T; V. x7 S, L. Dacceleration of the skeletal maturation; however, after2 \! K" e5 J6 @' c: M
cessation of treatment, the rate of bone maturation
$ T! D" W; ^& ^1 H' |. b9 }decelerates and gradually returns to normal.8,9
( ~& R8 V# J: A9 X% O+ v5 z2 W- f, lThere are conflicting reports and controversy
9 W' F6 k. x0 T2 lover the effect of early androgen exposure on adult4 e% K1 k& a2 b! v9 `
penile length.10,11 Some reports suggest subnormal
" j5 G; w( s3 }adult penile length, apparently because of downreg-
) |" K( e' o" i9 g1 k2 n$ v: Y1 {; oulation of androgen receptor number.10,12 However,9 W/ M" x' U7 x! x; i  Y% u2 [2 ?
Sutherland et al13 did not find a correlation between
$ @6 D! l. h  Y# u3 W) echildhood testosterone exposure and reduced adult
; q6 L. c  G1 y) t- ]$ w% rpenile length in clinical studies.3 |2 K/ F2 }6 q/ K
Nonetheless, we do not believe our patient is! D( X' o0 W3 w4 {: u6 U
going to experience any of the untoward effects from1 R8 M" `7 U/ A
testosterone exposure as mentioned earlier because' S5 y0 J2 x- Y7 |0 v, t* f! P
the exposure was not for a prolonged period of time.6 @7 t* ~$ @% S- W1 e% ~9 `( m/ Z
Although the bone age was advanced at the time of/ q4 O. z8 [# d1 Q$ p9 W
diagnosis, the child had a normal growth velocity at
+ \/ ]# T4 P) ]/ wthe follow-up visit. It is hoped that his final adult
, ]! U3 F  X& R7 S% Gheight will not be affected.
+ I+ p) \1 k& vAlthough rarely reported, the widespread avail-5 T: V  k# D" O
ability of androgen products in our society may9 U# u+ ~8 ^7 v0 a0 Z$ N
indeed cause more virilization in male or female
& S! W2 q+ ?4 _) J' y: Mchildren than one would realize. Exposure to andro-2 p9 S& X1 A8 Z+ [9 N& y- v& n3 ~& O
gen products must be considered and specific ques-
( v9 x9 G! q6 j# {2 Utioning about the use of a testosterone product or
4 K) m0 @8 y. U: ngel should be asked of the family members during
3 L. j4 E& b& o6 P# `the evaluation of any children who present with vir-+ L  R4 B) Q- Z0 \' z$ q
ilization or peripheral precocious puberty. The diag-
/ ~2 h0 y/ w- M. J& g. Inosis can be established by just a few tests and by
' d3 V7 ?1 u0 K3 I4 F# Y) X, pappropriate history. The inability to obtain such a8 T8 y3 o  E3 i8 w
history, or failure to ask the specific questions, may8 f: X9 W0 {0 l( [* {
result in extensive, unnecessary, and expensive
9 D7 \5 [5 P# T' ]& j$ Tinvestigation. The primary care physician should be! u* k( y- F+ {' U
aware of this fact, because most of these children2 z; z  c# e8 ]0 D3 x& q' b/ g0 B0 W
may initially present in their practice. The Physicians’( b- o5 B% Y) |7 U5 V+ v, I# }
Desk Reference and package insert should also put a
0 U6 M8 c3 S+ ?% e- L3 |  g  ^warning about the virilizing effect on a male or
0 P1 u* [( Y- s- E& Hfemale child who might come in contact with some-+ A: g, F8 p- I4 n. Z
one using any of these products.
/ u1 i+ v/ y& Y; u, dReferences) M: H& [5 k9 L" J
1. Styne DM. The testes: disorder of sexual differentiation2 q9 ^. X3 i) n( u; z) \' E8 T2 }
and puberty in the male. In: Sperling MA, ed. Pediatric( p6 k( }. k& n! @
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
2 [# e. Y* X8 g5 B8 ^" u$ J: Q2002: 565-628.
' d4 R& M7 z4 e6 l( E4 `6 z% x" A2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious7 @0 p" A$ t- V3 z/ z& z
puberty in children with tumours of the suprasellar pineal
發表於 2025-1-7 21:59:43 | 顯示全部樓層
這個我收藏了!謝謝分享!WK的資源越來越豐富,這少不了大大的辛勞!
發表於 2025-1-10 10:43:39 | 顯示全部樓層
VIP精品區,資源無限好賺金任務區,輕松賺金幣
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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

$ v! q; u0 E1 h- z8 d4 U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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