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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
. @4 v9 a& n9 F' ^  E7 d; cBoy Induced by Indirect Topical  m8 B6 c  M/ _* k& [
Exposure to Testosterone  d! x7 d* r- |/ A5 S
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,28 O7 z( O5 N9 U! A( S; c
and Kenneth R. Rettig, MD1; d. m# q5 Q8 c
Clinical Pediatrics( F7 x+ x9 e1 K- p  C2 z* r
Volume 46 Number 64 W6 u; A4 H7 D
July 2007 540-543
3 K, q: W5 a. Y© 2007 Sage Publications# R; @$ [# ]2 R% u/ M
10.1177/0009922806296651
$ @' d: z1 M4 a' khttp://clp.sagepub.com/ h5 r# c/ R( N$ t$ k/ R2 p
hosted at9 z% u7 A5 |/ _1 X5 L- N
http://online.sagepub.com
9 M# V. b8 @* j/ bPrecocious puberty in boys, central or peripheral,
; `: t* Q- {9 Uis a significant concern for physicians. Central
) r# ]" {2 M* Hprecocious puberty (CPP), which is mediated
2 Y8 @# l: @5 [' Z, r0 bthrough the hypothalamic pituitary gonadal axis, has$ o. p8 l: Q$ L0 c7 |
a higher incidence of organic central nervous system& U% W1 U4 u3 T; x  c" C" J
lesions in boys.1,2 Virilization in boys, as manifested
9 ^3 i. m  ~) }9 g: rby enlargement of the penis, development of pubic
& K! V. d. O8 s& P) G# dhair, and facial acne without enlargement of testi-* C; F0 K& N! n' L; m
cles, suggests peripheral or pseudopuberty.1-3 We
" \4 p& q. H8 W$ `4 I6 y9 U$ z3 }report a 16-month-old boy who presented with the
( N/ g# n: k+ m" Q& g9 Jenlargement of the phallus and pubic hair develop-5 h; x1 x- ~. L7 ^' f1 N2 E
ment without testicular enlargement, which was due
9 r4 n% e" ~3 X! l% _% Fto the unintentional exposure to androgen gel used by
7 K8 n  l! v6 z+ Cthe father. The family initially concealed this infor-
! o5 G; _, ^0 p* C& vmation, resulting in an extensive work-up for this
$ o5 n. {5 ~  f+ q- ~7 [child. Given the widespread and easy availability of7 z/ S( U; [4 s  q* i! n& X  Q6 v: l
testosterone gel and cream, we believe this is proba-
" M8 `" f/ W/ ^/ Mbly more common than the rare case report in the
% n& p2 A2 g: a& |2 Yliterature.43 ^( }5 w7 V, c7 l: n
Patient Report
0 i' S9 d: U% QA 16-month-old white child was referred to the! z# }' ?" q- l& E7 K/ p
endocrine clinic by his pediatrician with the concern) R0 v& q' T8 q* y! |& q
of early sexual development. His mother noticed
& N5 k$ b9 H4 \& e8 Rlight colored pubic hair development when he was
/ h) h) \! h! C8 x! OFrom the 1Division of Pediatric Endocrinology, 2University of
# q2 s( x7 O/ eSouth Alabama Medical Center, Mobile, Alabama.
" H) r$ l. t2 d  B- F& ^Address correspondence to: Samar K. Bhowmick, MD, FACE,2 |3 C! N/ i' p
Professor of Pediatrics, University of South Alabama, College of: W" f7 ~/ z- i/ b
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;* F0 q% V/ o8 \# `7 A
e-mail: [email protected].7 u/ D- d6 I, y: T4 b7 }
about 6 to 7 months old, which progressively became1 }) k8 y0 Y2 O. J& I
darker. She was also concerned about the enlarge-3 S# [5 j, T& M4 a+ l  T4 S( H6 H
ment of his penis and frequent erections. The child- ]% ?& T/ L/ ^) i' j8 T
was the product of a full-term normal delivery, with- V  U0 a7 @* }0 }. N! F
a birth weight of 7 lb 14 oz, and birth length of. E0 m: M0 c  o4 i0 ^6 O- _
20 inches. He was breast-fed throughout the first year: C& L2 ?0 k/ V. z3 g! W7 ^
of life and was still receiving breast milk along with
/ A* Y$ D; I, O# B0 `+ rsolid food. He had no hospitalizations or surgery,: Q4 K  B; p' x* I; E# f
and his psychosocial and psychomotor development; q" l# J9 h# R9 ]+ L, a
was age appropriate.
; Q, e9 }3 |7 hThe family history was remarkable for the father,6 F2 k, n: R7 ^1 z2 ]
who was diagnosed with hypothyroidism at age 16,
# N# L% k! ]8 D! ewhich was treated with thyroxine. The father’s
! K+ H, V3 ~7 M. N# V9 s7 I* n2 iheight was 6 feet, and he went through a somewhat
; j+ Z( \+ \+ _& searly puberty and had stopped growing by age 14.7 t; H# |' r7 }4 L/ T
The father denied taking any other medication. The
! _3 u/ L, U( P+ q. s: z4 Wchild’s mother was in good health. Her menarche
4 \( y1 M. J, O" hwas at 11 years of age, and her height was at 5 feet( I6 F/ ~: U6 P8 k/ ?
5 inches. There was no other family history of pre-4 E/ b- R5 Y- j4 T0 X$ N
cocious sexual development in the first-degree rela-
& ~0 ~; G0 Y) utives. There were no siblings., @! r4 A- ?8 \& Q( q' s: J/ _4 E
Physical Examination# @$ B3 X* z9 J
The physical examination revealed a very active,
6 R8 w1 H1 B/ w& B5 j4 Dplayful, and healthy boy. The vital signs documented# Y/ B& S: Q* I+ o9 O6 G* U% a
a blood pressure of 85/50 mm Hg, his length was7 p' V3 {  w$ V* \# |; I/ v6 e- S
90 cm (>97th percentile), and his weight was 14.4 kg7 F- K7 ]/ \: z8 e$ z' `; z( s+ Q
(also >97th percentile). The observed yearly growth
) [/ U: D7 N, ?" Qvelocity was 30 cm (12 inches). The examination of
0 x* f8 M6 Q1 k- G( j; V6 Fthe neck revealed no thyroid enlargement.6 \5 j8 ~  f: R4 Y; z
The genitourinary examination was remarkable for
$ O: f4 ?1 s3 ienlargement of the penis, with a stretched length of
% J. ^4 G8 J2 n0 ^$ @6 I4 g8 cm and a width of 2 cm. The glans penis was very well
. f% {, C  Q2 w9 }4 R, S  k+ ddeveloped. The pubic hair was Tanner II, mostly around# A" w7 L/ D) k) `* D  ~
540
: P; e. e  s% f8 K6 B) L! gat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from% c) c7 n1 g5 O( J
the base of the phallus and was dark and curled. The
. Q/ H0 t0 e3 I. p5 z" ztesticular volume was prepubertal at 2 mL each.
2 x  B3 f8 h& ]0 qThe skin was moist and smooth and somewhat4 T9 j: R+ Z; j% W3 Y8 q2 X; {
oily. No axillary hair was noted. There were no
  U3 [/ E  C* N5 V! n$ Labnormal skin pigmentations or café-au-lait spots.
+ d7 o$ A) V6 V3 \+ r& w9 lNeurologic evaluation showed deep tendon reflex 2+
; u8 m: E0 z1 h, E+ Xbilateral and symmetrical. There was no suggestion
: o* O$ W0 ]+ k' b) C% v# Hof papilledema.
$ Q) o: D; @% a4 zLaboratory Evaluation3 w5 M! g: t6 c# B
The bone age was consistent with 28 months by9 N% E8 ~* c% O
using the standard of Greulich and Pyle at a chrono-
4 y% F3 U; `: Z& y4 m3 a8 Jlogic age of 16 months (advanced).5 Chromosomal! P) ~; C# p+ ^/ h' Q
karyotype was 46XY. The thyroid function test+ s8 `! F6 X7 z& U' g  }/ a
showed a free T4 of 1.69 ng/dL, and thyroid stimu-5 _0 ?* p. b$ R
lating hormone level was 1.3 µIU/mL (both normal).
- v1 i' t7 s( GThe concentrations of serum electrolytes, blood
, w: T+ t) e- _urea nitrogen, creatinine, and calcium all were$ F. B: d- w! ^9 F! D) I. d3 Q
within normal range for his age. The concentration: \7 @& c" W: {& x* K' h
of serum 17-hydroxyprogesterone was 16 ng/dL
( a9 ~2 v- C: a2 K  o) D(normal, 3 to 90 ng/dL), androstenedione was 20! @4 G& H, G1 b; r- O4 ?
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
' I7 O! v8 D# o, Kterone was 38 ng/dL (normal, 50 to 760 ng/dL),
& w2 P$ t* v. F  T: {. R" Y9 `6 ?desoxycorticosterone was 4.3 ng/dL (normal, 7 to; Q1 B" d' y/ t% Q8 `
49ng/dL), 11-desoxycortisol (specific compound S)
6 b; |. r. k! dwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
: Y9 \" U  I! v. b2 Utisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total1 a* ^: m0 _, i( V4 D# Y8 Z! ^, W7 b4 Q
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
2 M' h9 y) L" ]. Z2 F- O7 S" Xand β-human chorionic gonadotropin was less than
, Z5 j- c3 w& ~7 W! @6 Z, V5 mIU/mL (normal <5 mIU/mL). Serum follicular
2 l% O# g6 L7 L5 w- b2 estimulating hormone and leuteinizing hormone
7 y! x3 U, |2 fconcentrations were less than 0.05 mIU/mL" A& y8 J3 |; R9 a
(prepubertal).1 S6 a/ u& Z! F; l6 _0 [2 L+ b
The parents were notified about the laboratory" `# ~% {7 u6 K* {6 O
results and were informed that all of the tests were  \8 _- f7 A! _8 ~
normal except the testosterone level was high. The" c. x' l# S* X
follow-up visit was arranged within a few weeks to
# c" v: B$ I; b" g' t9 f  Pobtain testicular and abdominal sonograms; how-2 ?+ a6 w% V8 j; s$ |0 d4 j
ever, the family did not return for 4 months.
" u: N4 m" r* c: ?1 T' o2 cPhysical examination at this time revealed that the* D/ W/ ^" v7 @7 U
child had grown 2.5 cm in 4 months and had gained
6 I# A% X' g) u  i& m: O( y$ z2 kg of weight. Physical examination remained" _- H& N9 l0 S; ^. c/ p) v; C! K
unchanged. Surprisingly, the pubic hair almost com-7 I# E' C  I- T2 J' N
pletely disappeared except for a few vellous hairs at
/ e$ t0 d: P5 R* `9 e# O# M( Q- Y2 [the base of the phallus. Testicular volume was still 2
4 _9 v% F4 `2 J; u7 S" wmL, and the size of the penis remained unchanged.  O, J/ _* G  Q% O& B  P
The mother also said that the boy was no longer hav-) w5 C7 @6 _/ d" Q
ing frequent erections.
7 ~" _/ _! y# Q- j5 e! xBoth parents were again questioned about use of
5 K# ]* K9 v! M- j) b; Lany ointment/creams that they may have applied to) J0 ]" e% f7 s' q( ^+ }1 g+ a
the child’s skin. This time the father admitted the- `) M% c  T% @# U
Topical Testosterone Exposure / Bhowmick et al 541; [! a* k: g) _6 y: g7 J6 m0 S  H/ A
use of testosterone gel twice daily that he was apply-$ L4 @" j; Y% |# \& T
ing over his own shoulders, chest, and back area for6 b2 R0 G  O6 Z0 k7 C
a year. The father also revealed he was embarrassed
% x9 q/ H- k+ X7 @" sto disclose that he was using a testosterone gel pre-
0 W- i3 a4 ]' c( O0 Q* }- u: bscribed by his family physician for decreased libido
: P( l0 t$ r2 ?: L" g8 isecondary to depression./ h! X5 P" `; I8 \# Z. {
The child slept in the same bed with parents.6 q8 s6 d8 P9 }
The father would hug the baby and hold him on his
  t5 {% M& d; `; ^% u3 C  ^4 x+ [, schest for a considerable period of time, causing sig-
$ c4 j" [6 {! b7 ^nificant bare skin contact between baby and father.
) A; m: r. e) h- aThe father also admitted that after the phone call,0 j2 D2 c) a  B/ g
when he learned the testosterone level in the baby! x5 {  L) Y+ T( H5 p" a
was high, he then read the product information8 |2 k: G5 \2 T) }' K
packet and concluded that it was most likely the rea-
7 r6 v$ }& ~/ s6 Q; ~2 E8 Gson for the child’s virilization. At that time, they
( ?3 p! _% X. L5 G( L9 Mdecided to put the baby in a separate bed, and the2 ?5 \# z! O7 f/ ]! |- o
father was not hugging him with bare skin and had
8 R' x, ]2 i8 L6 {0 ibeen using protective clothing. A repeat testosterone; ^6 v, H9 @& R+ _4 ?+ ]
test was ordered, but the family did not go to the
! C0 l: u5 F& g: H3 V- P  g4 Qlaboratory to obtain the test.8 b8 v9 ~3 ^3 M# W1 g
Discussion0 s. u# W# m2 V6 d. k2 e
Precocious puberty in boys is defined as secondary
7 ?* u/ A6 p- ^sexual development before 9 years of age.1,4
' g; A" \" y, I$ {Precocious puberty is termed as central (true) when
! r1 s4 p/ ~$ Tit is caused by the premature activation of hypo-
- P, @" x# }  f1 Q# pthalamic pituitary gonadal axis. CPP is more com-
4 C( U; s) K9 ?$ h# ?mon in girls than in boys.1,3 Most boys with CPP
- N3 j+ B/ c$ R2 y' fmay have a central nervous system lesion that is
  F$ a; e- ]0 b; D4 Rresponsible for the early activation of the hypothal-8 i+ O/ s8 y3 H
amic pituitary gonadal axis.1-3 Thus, greater empha-& Z. q9 V9 [3 d
sis has been given to neuroradiologic imaging in
* {0 m" x. u( {- H6 b. Q" Zboys with precocious puberty. In addition to viril-6 ?% Q+ d  r) Q! o
ization, the clinical hallmark of CPP is the symmet-8 D) r. n3 Y! b/ U8 \
rical testicular growth secondary to stimulation by( d4 _0 y0 z/ |6 J. h
gonadotropins.1,3( @1 }+ }6 \# [( V
Gonadotropin-independent peripheral preco-& o# S8 B$ R$ ^  u* t0 k% q3 b
cious puberty in boys also results from inappropriate
: a9 w  a  l; k0 Tandrogenic stimulation from either endogenous or5 I" P+ u$ P' e; O, S
exogenous sources, nonpituitary gonadotropin stim-7 {! H* k- ^1 v7 F
ulation, and rare activating mutations.3 Virilizing" G: K1 O3 V" m8 g& ~) q
congenital adrenal hyperplasia producing excessive. V8 ]4 d; Q5 L  W3 e
adrenal androgens is a common cause of precocious
, I4 a4 Q! n1 a% O2 ?1 N7 b$ o. Npuberty in boys.3,4
+ s: s* m4 x  i8 `$ z9 Z, C$ T; ^The most common form of congenital adrenal
& h; O6 z9 _; u5 A" ohyperplasia is the 21-hydroxylase enzyme deficiency.
3 b: s3 e4 v( e2 c# Z3 t5 ]/ a/ NThe 11-β hydroxylase deficiency may also result in* ?8 [/ k1 `9 {( u  U$ y$ }
excessive adrenal androgen production, and rarely,8 Y4 r4 ?; r% w. _$ f8 H! l- _# o
an adrenal tumor may also cause adrenal androgen$ g4 Y% B! l3 t9 w0 G3 P8 i
excess.1,3
7 M& ~- K2 H/ m- K0 }, O& _/ {: pat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from8 Y$ R: m6 ^4 `* b
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007; x# @3 p  m% S7 L% c( ?4 I
A unique entity of male-limited gonadotropin-0 y7 b+ I/ }5 F2 s6 P3 e4 a
independent precocious puberty, which is also known
7 M8 ?' E, i/ W5 l6 z/ Nas testotoxicosis, may cause precocious puberty at a
6 _1 O2 I" J- e2 [5 Zvery young age. The physical findings in these boys
* V& U+ g# e  j- _$ e4 X0 nwith this disorder are full pubertal development,8 ?& t- y6 B* C; t
including bilateral testicular growth, similar to boys$ q5 w+ b2 T* z% S
with CPP. The gonadotropin levels in this disorder
: h7 s( r" T9 @4 I% F; Uare suppressed to prepubertal levels and do not show! o" u. y( t/ z. x: f+ t& w' m
pubertal response of gonadotropin after gonadotropin-9 H, y1 ]: F4 N; T) n6 k; J
releasing hormone stimulation. This is a sex-linked
( ?6 }- ~+ ^4 u' Y, C! L( O# Nautosomal dominant disorder that affects only
( w0 Q3 b2 e' i* xmales; therefore, other male members of the family3 h: Z. F( A) D( n. n/ R( S. _1 R
may have similar precocious puberty.3
" ]4 ~4 c# |, D( dIn our patient, physical examination was incon-
$ X+ [( E$ I" D1 K, ~sistent with true precocious puberty since his testi-' Y$ c" j" w0 R. f% B, Q/ ~
cles were prepubertal in size. However, testotoxicosis9 Y' o3 L3 G' ?( Q
was in the differential diagnosis because his father' Y/ ]' g& A" y
started puberty somewhat early, and occasionally,
: {1 r; O0 ^4 h% F  `testicular enlargement is not that evident in the! G9 [) O: {3 \! v2 J
beginning of this process.1 In the absence of a neg-
0 F. l4 L, ^) P) Sative initial history of androgen exposure, our
& D- ^4 U% s- `8 E$ `( k; Abiggest concern was virilizing adrenal hyperplasia,% U! M+ Z1 A; o1 `6 D4 }- y3 ?
either 21-hydroxylase deficiency or 11-β hydroxylase
7 S! `9 B6 {' X3 M( _4 s! V* zdeficiency. Those diagnoses were excluded by find-* K3 g! o+ W: r
ing the normal level of adrenal steroids.8 x9 v7 x; R  z3 C3 u( q6 @' Q& U" Z% R5 k
The diagnosis of exogenous androgens was strongly
/ w3 O3 A* ?  S# f* W* i6 o: m- ysuspected in a follow-up visit after 4 months because/ U9 d, w% y& T4 v5 J
the physical examination revealed the complete disap-" V/ ~; V! y; R8 ~8 E0 a. r
pearance of pubic hair, normal growth velocity, and
7 T$ |7 Z1 ?7 mdecreased erections. The father admitted using a testos-% R$ N# G* k2 A) h/ b* B
terone gel, which he concealed at first visit. He was
8 @0 a6 H! r: A: b4 ^$ ?+ n& H& Cusing it rather frequently, twice a day. The Physicians’
7 T/ }. h; `8 d. `* K! D4 i6 N1 p4 LDesk Reference, or package insert of this product, gel or
' s# o# z4 x* I# h6 ^cream, cautions about dermal testosterone transfer to- P- h, O' W( B5 X& O' c
unprotected females through direct skin exposure.
% {' h/ g9 M; ASerum testosterone level was found to be 2 times the- {* ^' z0 R+ s7 |: N
baseline value in those females who were exposed to7 {- F. ]2 E. ~4 a+ C' N
even 15 minutes of direct skin contact with their male
, I6 D: P% V! Zpartners.6 However, when a shirt covered the applica-
; F) F7 B' P  ]( R: Etion site, this testosterone transfer was prevented.
8 X% h; v( b2 n  P. y, lOur patient’s testosterone level was 60 ng/mL,' Q- {1 N4 H) E8 j7 o/ E
which was clearly high. Some studies suggest that
+ T# G- f( J2 R/ a- q/ w! Idermal conversion of testosterone to dihydrotestos-
- Y$ _8 |4 G. F0 A0 Vterone, which is a more potent metabolite, is more
5 a( i/ h- |# Gactive in young children exposed to testosterone
  s/ E) F  W, @# t5 U  j. Zexogenously7; however, we did not measure a dihy-% R* ]: O: p. ?9 I& u
drotestosterone level in our patient. In addition to; B  d3 x: n& R4 t+ y
virilization, exposure to exogenous testosterone in# P3 G! R4 K" L4 P6 S. B
children results in an increase in growth velocity and
' I; c) C) Q0 p. S$ Q, oadvanced bone age, as seen in our patient.
: p6 y6 o! E4 j# |. L% }1 aThe long-term effect of androgen exposure during
) u4 {7 v) E. j, j& Bearly childhood on pubertal development and final
6 \3 C3 D1 E3 y$ Padult height are not fully known and always remain
0 Q0 R; K0 ~8 s/ `a concern. Children treated with short-term testos-2 T' N0 m" h, A* {) S- M
terone injection or topical androgen may exhibit some7 l1 w4 I/ X6 g7 P
acceleration of the skeletal maturation; however, after
* i9 o9 U$ f7 [cessation of treatment, the rate of bone maturation
/ \5 ]8 p+ z1 }3 ~decelerates and gradually returns to normal.8,9
5 B2 [/ H9 l9 B2 {/ c( IThere are conflicting reports and controversy0 p2 e8 |" _8 P/ K9 g- R
over the effect of early androgen exposure on adult
! G' b/ u& h5 P- [3 z. fpenile length.10,11 Some reports suggest subnormal' p- O) W: y# k* L- ?" y. }! {' a
adult penile length, apparently because of downreg-
7 ]2 V' ^4 L; q4 w+ Rulation of androgen receptor number.10,12 However,
, `# R7 h. l6 m7 ASutherland et al13 did not find a correlation between# v, ^- k3 m! G$ x7 H6 @$ A" a
childhood testosterone exposure and reduced adult! c* A% k! U0 w; E
penile length in clinical studies.2 ~/ @! k: a& H% l4 T  W' P
Nonetheless, we do not believe our patient is
" e, m; _+ `& s( ~going to experience any of the untoward effects from% i/ b: B9 k4 V4 b
testosterone exposure as mentioned earlier because3 ^! ^2 v4 s" z7 l
the exposure was not for a prolonged period of time.' f" S1 q& }/ H( b
Although the bone age was advanced at the time of; r# ~8 M! T4 j, R0 l: t( J2 N
diagnosis, the child had a normal growth velocity at/ h3 n! U! l$ O
the follow-up visit. It is hoped that his final adult# {3 ]- s' ]/ H* X
height will not be affected.
9 w4 P1 }7 O4 U8 @Although rarely reported, the widespread avail-
( G- f8 Y& Y3 Qability of androgen products in our society may( \; e5 R% `' o% ~9 R) v
indeed cause more virilization in male or female0 y) ?7 |5 l6 H$ G# J
children than one would realize. Exposure to andro-5 H+ V$ _' j: W; c
gen products must be considered and specific ques-
+ Z: _) }& ]" C1 Y# Rtioning about the use of a testosterone product or
' V5 v5 D3 p0 T4 s2 Xgel should be asked of the family members during
" c  c/ r) O7 `% ?the evaluation of any children who present with vir-$ ?" q  u  |; H. W. {
ilization or peripheral precocious puberty. The diag-0 b4 p, V  j$ O. j8 I# X( _; n
nosis can be established by just a few tests and by
# _& u& Q& y  x' u" ?* J* b3 W4 o( `4 dappropriate history. The inability to obtain such a
" I" U  y5 t2 F1 |history, or failure to ask the specific questions, may' U+ X$ r! U% \
result in extensive, unnecessary, and expensive
! A2 O9 }. D( }2 H  K! K4 ]investigation. The primary care physician should be
. I1 M7 h6 H, p7 i4 t# d) A! Caware of this fact, because most of these children
' c2 v* U0 E* k# F) S' mmay initially present in their practice. The Physicians’0 N0 j7 w; W+ K4 f- E; Y# i: h
Desk Reference and package insert should also put a
5 G& |2 F: i0 z) twarning about the virilizing effect on a male or" A# U4 t) Q' O0 p% H" C
female child who might come in contact with some-
2 H( d2 W" H* Oone using any of these products.) u6 Y( @5 x; d) W
References% M& V* L8 a/ O; n
1. Styne DM. The testes: disorder of sexual differentiation' R  R& \" V7 O; s
and puberty in the male. In: Sperling MA, ed. Pediatric! T# }* p5 n3 \) s$ m- ?( I% [. F
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;/ u! T- c& ]! c+ D1 y
2002: 565-628.& ^' u; z# m+ P5 I
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious/ d* t2 ^  g# I4 _: U4 [+ Y
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
6 {! v" J9 \  tBoy Induced by Indirect Topical5 k4 A  D1 G( \+ d. }
Exposure to Testosterone
( O. o& s$ R* [' r& h7 i# y+ hSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
7 l. P- n: X. f! ~: D+ Fand Kenneth R. Rettig, MD1
( {8 c9 t' w& v: C6 Q/ q3 DClinical Pediatrics8 B9 r# S5 l2 X4 v
Volume 46 Number 6* ~- ]2 u* B- ]: m0 G
July 2007 540-543
8 f6 X) A" K* G9 O% a! J% T( n+ y© 2007 Sage Publications
7 l& ^* @# ~6 m10.1177/0009922806296651+ M6 H+ d1 V6 J8 T
http://clp.sagepub.com% V3 y+ [8 T0 d9 l# Q
hosted at2 G* H5 O- r1 G7 B
http://online.sagepub.com
$ K, h, _+ v% h: oPrecocious puberty in boys, central or peripheral,
5 {# ~' [+ E0 ?1 U/ v2 yis a significant concern for physicians. Central
5 h. k6 ]4 s4 m5 b9 e' Wprecocious puberty (CPP), which is mediated
$ U, g8 {- d) ethrough the hypothalamic pituitary gonadal axis, has. p, C7 W$ D2 W) s) p& t  `6 I
a higher incidence of organic central nervous system6 U2 O' ~) W7 Q
lesions in boys.1,2 Virilization in boys, as manifested
8 w+ \, F7 y0 M7 C# L& T) {by enlargement of the penis, development of pubic
% i# {5 U9 p+ ^% Z% _hair, and facial acne without enlargement of testi-& O4 u6 l; q6 x; O
cles, suggests peripheral or pseudopuberty.1-3 We- ?: U3 Z  t; l1 A% f  j
report a 16-month-old boy who presented with the
& N- @9 W7 `- [enlargement of the phallus and pubic hair develop-! O/ @; Z1 E8 z/ i: g6 ^/ l
ment without testicular enlargement, which was due
' k4 t1 i' T& n- B1 v; Eto the unintentional exposure to androgen gel used by
+ t- V- t% s. \' [( [5 m3 Z! Nthe father. The family initially concealed this infor-
, N7 a7 B. Z1 m; y. W! Ymation, resulting in an extensive work-up for this
! a/ `! l% @* K7 g; Vchild. Given the widespread and easy availability of3 S' t* h6 T1 K( Y
testosterone gel and cream, we believe this is proba-
9 h; i! i( i3 ^5 d  fbly more common than the rare case report in the
% C8 a/ m0 K( n% [& c5 zliterature.46 X9 D7 X/ g" D3 v9 P; L
Patient Report- C1 U1 `2 C: W/ F
A 16-month-old white child was referred to the
& L9 r+ s: {6 F! P7 Wendocrine clinic by his pediatrician with the concern: M' S2 M! D' c/ `  G9 E2 y  M
of early sexual development. His mother noticed
; a% K- V& ~2 P  [; M0 slight colored pubic hair development when he was
; Z8 ~0 V, I0 p- f3 ?From the 1Division of Pediatric Endocrinology, 2University of# L) m' c1 }, d' u+ ?3 H
South Alabama Medical Center, Mobile, Alabama.
7 [% g# d3 d, T' D* g$ X8 Q3 GAddress correspondence to: Samar K. Bhowmick, MD, FACE,. u$ ~% E2 t/ v3 B* Z
Professor of Pediatrics, University of South Alabama, College of" M- W1 J5 {* @7 ~
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;3 s6 g( ~$ b  P# d
e-mail: [email protected]./ k% P4 [5 D; I" X6 }
about 6 to 7 months old, which progressively became
: v. B! e! w/ w8 W" x: ]$ Odarker. She was also concerned about the enlarge-% o' i- H) h6 |% s3 Q  v
ment of his penis and frequent erections. The child
* j8 Q0 E9 r. e% wwas the product of a full-term normal delivery, with
; a$ }. V% C9 ^9 N/ m- Ea birth weight of 7 lb 14 oz, and birth length of
% e" e$ {* G; r20 inches. He was breast-fed throughout the first year. t+ i% e: m; W7 u7 z
of life and was still receiving breast milk along with
# q1 {) {$ K& m5 g! P5 \7 ^solid food. He had no hospitalizations or surgery,
6 w: c3 t! A5 e  n$ W( S2 Jand his psychosocial and psychomotor development7 w. b# ]$ e. S' b  Q0 Q' s
was age appropriate.0 t3 V0 v7 R3 K! E
The family history was remarkable for the father,
' v2 L2 x9 A( f( O# R% q$ A1 Awho was diagnosed with hypothyroidism at age 16,
, E6 U$ M0 P" mwhich was treated with thyroxine. The father’s4 A. g! i- l( i* e- A
height was 6 feet, and he went through a somewhat
+ i. {- l; D7 d7 k% [5 Aearly puberty and had stopped growing by age 14.
/ v" Z) K4 j$ IThe father denied taking any other medication. The: v$ H# U2 R, a* f
child’s mother was in good health. Her menarche% ^; I, v, ~' u
was at 11 years of age, and her height was at 5 feet! X$ W- r4 {+ X3 C0 p1 R
5 inches. There was no other family history of pre-
2 _8 J2 A" I% Ecocious sexual development in the first-degree rela-
+ U+ z: d# k7 K  Qtives. There were no siblings.
/ Z) v( Y2 S" p  b3 e: ?Physical Examination( J% p( K( F0 Q& n& x
The physical examination revealed a very active,
; S; Z+ ?4 B/ Lplayful, and healthy boy. The vital signs documented5 W) I5 \  q1 y7 n& A
a blood pressure of 85/50 mm Hg, his length was) p+ u0 M3 D& ]) ]4 ?+ I
90 cm (>97th percentile), and his weight was 14.4 kg
# I3 Y$ h8 y! Y3 V(also >97th percentile). The observed yearly growth
; S3 o. W1 @, t* n0 n! Xvelocity was 30 cm (12 inches). The examination of
/ }/ P! ~# w" q0 Z7 C* H: h3 Lthe neck revealed no thyroid enlargement.1 [8 g7 Q, {3 H0 P4 H
The genitourinary examination was remarkable for, ]+ z' k7 u; j+ z; ~: I! h0 R
enlargement of the penis, with a stretched length of& V- V5 P4 L7 g  [' J5 _1 m- x1 }
8 cm and a width of 2 cm. The glans penis was very well
5 g$ z9 T- r& s& @9 _3 X0 `developed. The pubic hair was Tanner II, mostly around
6 ], V# f) t& K9 M  M540
, A0 E" }8 `$ Y3 k- ^at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
: B7 X) J. N3 L% c0 _( x: _the base of the phallus and was dark and curled. The8 t- q1 }  v- w4 [
testicular volume was prepubertal at 2 mL each.
3 F6 Y4 V4 @. U8 M( w6 IThe skin was moist and smooth and somewhat9 F) Q4 i: n: m$ V
oily. No axillary hair was noted. There were no
9 {- i# D4 u" V* M. X) Habnormal skin pigmentations or café-au-lait spots.
' W6 x5 t9 ]; KNeurologic evaluation showed deep tendon reflex 2+
6 A( E4 C/ I0 Q0 I2 y  ~bilateral and symmetrical. There was no suggestion
! h( @2 R9 [9 O8 R, n; W" oof papilledema.
9 V6 O! m, B! h) k% R3 FLaboratory Evaluation
% z. F4 T" h& u. VThe bone age was consistent with 28 months by
) s0 k1 G9 ~( J8 D. `using the standard of Greulich and Pyle at a chrono-
6 ~' r1 p+ A( l9 j  R7 flogic age of 16 months (advanced).5 Chromosomal# A4 F7 p1 u6 l4 ^, N
karyotype was 46XY. The thyroid function test- ]5 `8 T$ I+ L) }; A
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
0 k0 a- r5 F2 c9 l5 ?) Slating hormone level was 1.3 µIU/mL (both normal).  n( I; j4 d7 P7 i1 I) |
The concentrations of serum electrolytes, blood- j. p% I! `" s6 _* o
urea nitrogen, creatinine, and calcium all were) n0 R" l% z6 x
within normal range for his age. The concentration
$ M' H! w+ Z8 n( q- Cof serum 17-hydroxyprogesterone was 16 ng/dL% r7 l# S+ Q+ ?1 [
(normal, 3 to 90 ng/dL), androstenedione was 20
! B  h1 P4 s" J- _0 v. R; I7 [1 Wng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
6 w' B6 `% q5 k  G. x8 T( ?terone was 38 ng/dL (normal, 50 to 760 ng/dL),
4 d0 \: H2 W( p# Z; l' A, E( r6 S1 ydesoxycorticosterone was 4.3 ng/dL (normal, 7 to
: {: \* ^# u8 D8 p6 ~7 S49ng/dL), 11-desoxycortisol (specific compound S)
$ j& P# t9 r! T) Qwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-3 x- w& V+ I7 C
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total4 }) i& T( D" g& G; K
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),, N" O7 l! q6 k+ [0 i
and β-human chorionic gonadotropin was less than
& a0 v4 @8 q1 {  m$ V7 u5 mIU/mL (normal <5 mIU/mL). Serum follicular
7 s0 q' [) Z+ Qstimulating hormone and leuteinizing hormone7 Z& p9 }: s% g8 J& X/ X% p
concentrations were less than 0.05 mIU/mL6 ?3 z3 Z! B0 G3 y
(prepubertal).
( `5 C7 S7 K% k: T( o8 b) hThe parents were notified about the laboratory0 N8 G# g- ]& B6 d$ w; u
results and were informed that all of the tests were; H2 A( Z/ |4 a+ A6 M3 G7 w
normal except the testosterone level was high. The& c- d. D- b; n  k+ _: ]# n
follow-up visit was arranged within a few weeks to% |& o/ ]# \# ?$ P' R! R5 a
obtain testicular and abdominal sonograms; how-4 Y6 `9 b' i5 m$ }
ever, the family did not return for 4 months.( l- L& c8 O0 x  b
Physical examination at this time revealed that the
. x. c! z! c. o# h- K: Zchild had grown 2.5 cm in 4 months and had gained
8 Q6 E1 n0 F# @/ Q2 kg of weight. Physical examination remained4 n: Y+ H2 _; q4 A% }
unchanged. Surprisingly, the pubic hair almost com-
, f2 N' `& L* w" Lpletely disappeared except for a few vellous hairs at
# i7 N9 f7 A2 y3 S( N, E3 Mthe base of the phallus. Testicular volume was still 26 e& b, F5 b5 h
mL, and the size of the penis remained unchanged." ~( g3 T- _3 Q5 T6 n/ i
The mother also said that the boy was no longer hav-
: i! X/ y" b8 c" G: E) u7 Ting frequent erections.. w4 y4 \! O5 ]0 x; p. o4 y
Both parents were again questioned about use of
' }8 ?( d; v+ A& m4 b4 M. ?8 cany ointment/creams that they may have applied to* R* H3 e( K& A4 Y% o% ~8 m
the child’s skin. This time the father admitted the
. j7 o) V# v" D/ gTopical Testosterone Exposure / Bhowmick et al 5412 k# ~/ @" y  O2 ]$ c1 z+ L
use of testosterone gel twice daily that he was apply-# f& l, n% b$ s) q: C; R
ing over his own shoulders, chest, and back area for
. w. ^5 x: v5 k- wa year. The father also revealed he was embarrassed
" y; I0 R- K7 _5 J( r4 pto disclose that he was using a testosterone gel pre-  ^: K! Z) w& v+ E" W8 {2 y
scribed by his family physician for decreased libido
3 `% G: w  q1 n9 W2 o5 Lsecondary to depression., n0 ?& k! S% h% D/ |4 s
The child slept in the same bed with parents.
+ n) V6 m) \' r0 @The father would hug the baby and hold him on his
" Y  g5 O2 a$ D8 I+ `# hchest for a considerable period of time, causing sig-
5 `9 ]3 M$ |; {! Z6 Enificant bare skin contact between baby and father.% Z1 X8 `4 y6 O. ^
The father also admitted that after the phone call,
! b' L, \4 ?* swhen he learned the testosterone level in the baby
  g* L' N" ]# W% c+ s+ fwas high, he then read the product information# C  d# P# G2 ^/ F# G) D
packet and concluded that it was most likely the rea-# Z2 r# h  ]! Y$ \3 s4 R" B
son for the child’s virilization. At that time, they; F4 C5 ~' ~$ S/ b7 s
decided to put the baby in a separate bed, and the, z1 l* ?! l3 V8 U8 x  ]* H8 L
father was not hugging him with bare skin and had4 o# b  [7 o) W4 _, `. }% E/ u2 Y
been using protective clothing. A repeat testosterone' e/ }2 ^; l/ k' {; T6 G) M4 g4 B
test was ordered, but the family did not go to the7 m6 E4 D/ r+ h* X, B+ J
laboratory to obtain the test.. ^4 U" \9 `0 m5 \1 g; l
Discussion
! ]' |! l# e, Z) m4 ~- v3 }9 YPrecocious puberty in boys is defined as secondary6 W8 T7 B6 Z/ A8 j
sexual development before 9 years of age.1,41 u+ Q4 N. h/ Y
Precocious puberty is termed as central (true) when
) R$ l8 Z) N/ [+ Oit is caused by the premature activation of hypo-1 ^9 h" J! L' o0 R5 q
thalamic pituitary gonadal axis. CPP is more com-7 p, n) o# m8 O5 T
mon in girls than in boys.1,3 Most boys with CPP9 _! T, \5 C$ I" h7 Y& t
may have a central nervous system lesion that is. c+ Y/ ]2 H$ _0 @: F
responsible for the early activation of the hypothal-
1 c6 d' G: m+ g7 wamic pituitary gonadal axis.1-3 Thus, greater empha-9 G  {2 A0 N0 Y
sis has been given to neuroradiologic imaging in
$ n. \& [! ~  Q- b; @boys with precocious puberty. In addition to viril-3 e) u. k6 I$ Z) P0 w# g2 t6 k
ization, the clinical hallmark of CPP is the symmet-
3 d: {+ c* o& [1 O) Wrical testicular growth secondary to stimulation by" V$ ^! Y3 s$ _  t8 i7 z
gonadotropins.1,3
6 l, y2 v4 N1 YGonadotropin-independent peripheral preco-
' H4 w* Q( i) q1 G8 ucious puberty in boys also results from inappropriate
* _2 E7 [# W: t, ]0 F+ q! Gandrogenic stimulation from either endogenous or" y3 H) I! B' _
exogenous sources, nonpituitary gonadotropin stim-
5 L3 V3 I2 {3 m& _. b2 S2 `ulation, and rare activating mutations.3 Virilizing/ K( E; F. W4 f7 q' Y
congenital adrenal hyperplasia producing excessive
7 a9 e( v4 t( k- x0 d8 aadrenal androgens is a common cause of precocious
) W, N( Z3 R6 c; A% |$ Fpuberty in boys.3,4! e( u) K, d7 Z) y, f1 \/ t; t
The most common form of congenital adrenal8 o& a- a. L) ~5 S* D
hyperplasia is the 21-hydroxylase enzyme deficiency.! L* E; ~% w$ p5 R
The 11-β hydroxylase deficiency may also result in
. F% H; h" Q" {: n. e/ _excessive adrenal androgen production, and rarely,: Q/ H5 v5 G  @# K# P9 I1 b% [  s
an adrenal tumor may also cause adrenal androgen! T1 O. B7 d$ L
excess.1,3
: J/ V. C! ]5 H0 u# G3 t* bat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
" C7 x: ]! ], s" m0 b/ s( v. Q* h' o) e542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
8 e5 f& M. P# n0 `* W9 d$ c' tA unique entity of male-limited gonadotropin-
' x" h+ X# a: z- gindependent precocious puberty, which is also known
7 j0 o3 ^5 ~' @" S. l6 Has testotoxicosis, may cause precocious puberty at a
7 w, D- y; {1 y: @! Ivery young age. The physical findings in these boys
2 [4 o3 r2 u) I$ N( i/ h# b( |with this disorder are full pubertal development,( p3 O- Z0 O# O) t
including bilateral testicular growth, similar to boys
/ Z# s9 i9 h6 Z8 `) Z0 Xwith CPP. The gonadotropin levels in this disorder) t1 l. d- H* G3 A9 ~9 Y0 o
are suppressed to prepubertal levels and do not show7 |! p6 w: X1 T: X
pubertal response of gonadotropin after gonadotropin-. t, J2 ?& A8 f* ?$ p
releasing hormone stimulation. This is a sex-linked2 P7 K# Y/ R3 n) P* s
autosomal dominant disorder that affects only* T6 C9 t+ B9 N5 p
males; therefore, other male members of the family5 C7 M/ s5 z: X! s' Z7 U% K4 k
may have similar precocious puberty.3. m8 j( o1 G+ z& y8 C7 u" V
In our patient, physical examination was incon-7 ?, v' H$ ?7 [$ W8 s" e7 A) [
sistent with true precocious puberty since his testi-4 g) K) L5 j0 J7 v
cles were prepubertal in size. However, testotoxicosis* U5 G0 f8 p5 M( G/ Q$ i3 m3 `
was in the differential diagnosis because his father9 ?* ]& C! N& D9 ]) K- |1 n
started puberty somewhat early, and occasionally,
6 d+ X6 s5 d2 n4 X0 Btesticular enlargement is not that evident in the
$ l) j* ]6 S, \: wbeginning of this process.1 In the absence of a neg-
% U  R, c( B) _; y; x# J5 Hative initial history of androgen exposure, our
1 A, j1 v0 c# hbiggest concern was virilizing adrenal hyperplasia,# t  d- p- a) C) l
either 21-hydroxylase deficiency or 11-β hydroxylase
" {2 [4 @' m8 A/ l; Y7 W; e5 `deficiency. Those diagnoses were excluded by find-$ ]. n' e8 u' {3 q2 w9 @9 r+ ^
ing the normal level of adrenal steroids.
7 ~8 P' L5 l, ?4 O. xThe diagnosis of exogenous androgens was strongly
9 S7 a+ v' K+ Z5 r! o. jsuspected in a follow-up visit after 4 months because
" R4 v; O- n5 v- v* i) Kthe physical examination revealed the complete disap-
& W& @, z' ?" w: `pearance of pubic hair, normal growth velocity, and3 N6 Z. ~/ u% k. Z: E2 u' E6 q* s. l
decreased erections. The father admitted using a testos-- w) j" {- d, r3 ^& A5 ?& L
terone gel, which he concealed at first visit. He was0 d! e& ~  k3 ^0 h, c: w
using it rather frequently, twice a day. The Physicians’! v) N! ]+ n2 ~* G2 `
Desk Reference, or package insert of this product, gel or
5 W! j# q, b# Y/ scream, cautions about dermal testosterone transfer to
; w. m1 K; C' H- |# w5 l5 l% hunprotected females through direct skin exposure.
5 f& ?  X& f( p! \: hSerum testosterone level was found to be 2 times the
% B+ C0 H% J1 fbaseline value in those females who were exposed to# {0 L% w& p4 c
even 15 minutes of direct skin contact with their male
6 {1 y# C  Z# O2 |+ h7 Apartners.6 However, when a shirt covered the applica-: R: }$ j8 \3 ~" n' S% ~% z
tion site, this testosterone transfer was prevented.: k% ^! U% C8 _5 E1 @$ T/ Y: R
Our patient’s testosterone level was 60 ng/mL,/ e8 y( U. R4 E
which was clearly high. Some studies suggest that
% p8 h' Z$ ?' L, D9 \2 R- i, C) tdermal conversion of testosterone to dihydrotestos-
$ L7 ^2 P0 Y9 [$ oterone, which is a more potent metabolite, is more
. x1 v* R: R% hactive in young children exposed to testosterone
3 I: ^( Y( [' q' D3 Texogenously7; however, we did not measure a dihy-% O0 j) A# a6 l- ~, L) j, I; A
drotestosterone level in our patient. In addition to. r# G+ q1 f6 `0 C+ M& ]2 T
virilization, exposure to exogenous testosterone in
1 |5 X+ u9 l8 Schildren results in an increase in growth velocity and8 U' x8 J& L, ~3 j7 x) w: I
advanced bone age, as seen in our patient." _; P0 l  u8 w  V3 I
The long-term effect of androgen exposure during- D3 D! l% w7 @* b) G% N& c
early childhood on pubertal development and final
. m8 N  a6 n- b* F' c9 t& T2 madult height are not fully known and always remain
! |: z: S6 y" Aa concern. Children treated with short-term testos-
/ ]( P& f$ x" O9 |terone injection or topical androgen may exhibit some/ ~' W- b) H$ ~
acceleration of the skeletal maturation; however, after9 J1 w( {) ]+ q# h3 k
cessation of treatment, the rate of bone maturation8 Z% o8 R# X2 b. \" e
decelerates and gradually returns to normal.8,9
+ _7 E2 W9 ?3 ]; XThere are conflicting reports and controversy
5 H8 X5 b8 e! R# }, u. ^4 Nover the effect of early androgen exposure on adult9 c2 [  W0 T' d( M
penile length.10,11 Some reports suggest subnormal" u" C8 w. k( K% u2 S
adult penile length, apparently because of downreg-4 H  G! ]$ ^/ g) ^9 |* X# }) N( U
ulation of androgen receptor number.10,12 However,6 Q7 k8 M3 x5 P/ X9 j9 B/ Y
Sutherland et al13 did not find a correlation between2 w4 `, W+ `3 n9 R
childhood testosterone exposure and reduced adult
  _* A9 m* l7 C' s. bpenile length in clinical studies.
# F2 h, y& B4 n  WNonetheless, we do not believe our patient is
5 x: }7 b) \; H5 ~+ Jgoing to experience any of the untoward effects from) z: \% y" k1 N/ d6 ~, W& u! P* i
testosterone exposure as mentioned earlier because/ b3 i- r! C9 Q+ i) t3 s1 }$ X! A: ^; t
the exposure was not for a prolonged period of time.- k# V" @" G0 ^/ N  c
Although the bone age was advanced at the time of  @. P$ K& t# q# s( S5 r
diagnosis, the child had a normal growth velocity at- Z/ S2 ^# Y  W; I) j* V
the follow-up visit. It is hoped that his final adult
$ W1 n. S- `! b( R3 C& {height will not be affected.
. f# E) t$ Z0 |0 [: X% b- I0 W6 \Although rarely reported, the widespread avail-
2 h6 v0 q' p$ k2 M6 Tability of androgen products in our society may! }( [* D$ o( E9 H/ ]
indeed cause more virilization in male or female
: n  A! J: T: d2 d. ^( c+ }& C  j0 bchildren than one would realize. Exposure to andro-4 k2 a8 q8 C2 I/ W3 D  H
gen products must be considered and specific ques-
/ E. L: I$ o( d% r& N, Ntioning about the use of a testosterone product or' O) t. O. S6 A" T3 @' _2 Q
gel should be asked of the family members during
# f  U0 M; `: n( K7 Dthe evaluation of any children who present with vir-
6 @  n! k) X7 @7 k- x  l5 y/ qilization or peripheral precocious puberty. The diag-: h+ H7 A9 B/ W+ J& ]
nosis can be established by just a few tests and by4 o- O! q9 g' @& ~
appropriate history. The inability to obtain such a! ?/ Z4 S4 {# {" j4 u' W
history, or failure to ask the specific questions, may
( M. ?* t" ?" aresult in extensive, unnecessary, and expensive8 d/ F' I& `1 y8 j  l5 [$ z. j
investigation. The primary care physician should be
8 Q! Y. V: E2 \# A; t& p; j. caware of this fact, because most of these children4 b( d! I4 z& h0 ^6 D& j0 j( [
may initially present in their practice. The Physicians’
( |/ `6 |* M4 Y3 y7 U+ _, ]5 M9 pDesk Reference and package insert should also put a3 g& ^" S0 a9 U1 J* D% |6 u) t
warning about the virilizing effect on a male or
1 w) w' m% P% z3 H) P. y% R3 q9 jfemale child who might come in contact with some-- V7 M6 Z: @: h: v
one using any of these products.1 @6 m- H0 f) b2 d9 r& C& T
References: }3 F2 {. y6 i0 _, I/ a5 w
1. Styne DM. The testes: disorder of sexual differentiation- Y7 W' j5 s: m3 P: r% J& W- n
and puberty in the male. In: Sperling MA, ed. Pediatric- b$ D' d( Z4 b2 B2 V& o2 ~
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
  l7 ^' n0 n) p% y8 o; e5 F2002: 565-628.; K% z; e1 d/ |) r' f( i8 R
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious( k  e; ^( [+ m- b/ W; }
puberty in children with tumours of the suprasellar pineal
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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

0 C$ S, w% N% u# u0 h- o0 E1 m/ b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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