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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/ d6 W( C8 X! L3 m% J; A
Boy Induced by Indirect Topical
( R, w- E- P' @2 n% vExposure to Testosterone
% Y2 ]: i& A  w. tSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,21 j: h# e9 b% s+ g
and Kenneth R. Rettig, MD1
, M) L- V* I5 S$ H# z0 WClinical Pediatrics# ~9 ?2 z  V* }( C" m1 W
Volume 46 Number 6
6 \8 r& U$ y% Z) U( W8 [July 2007 540-543
; c; W: Q8 }: h5 R6 {$ K© 2007 Sage Publications
) P% I* C! i0 t" B& d10.1177/0009922806296651/ E- c6 u& K; O" @# Q
http://clp.sagepub.com/ \4 q7 N% _+ F7 U
hosted at
: w5 I; y; K, P+ l, ^" Phttp://online.sagepub.com
. T4 P* A9 ~0 F2 v4 ^Precocious puberty in boys, central or peripheral,& R0 g7 i* h- ]" |
is a significant concern for physicians. Central- H7 T, Z  I1 `6 K
precocious puberty (CPP), which is mediated
. M7 z# s+ U0 @: {$ N) }through the hypothalamic pituitary gonadal axis, has9 X1 }- r) U6 g# L# O- F7 _+ t5 j( l
a higher incidence of organic central nervous system
9 N# r1 S: S' B* o/ Q$ ilesions in boys.1,2 Virilization in boys, as manifested
8 B, _1 l7 p! O6 ]/ ^by enlargement of the penis, development of pubic
4 n& N* ~2 x8 chair, and facial acne without enlargement of testi-
: o# [, ~2 C$ U! |. V" K; tcles, suggests peripheral or pseudopuberty.1-3 We
. T( u1 F; N$ Preport a 16-month-old boy who presented with the
2 V5 U' s4 `8 _) Genlargement of the phallus and pubic hair develop-7 B! c5 ?. c  ?2 i9 Z
ment without testicular enlargement, which was due  d- e4 j, J3 `# ^; X) s$ M
to the unintentional exposure to androgen gel used by2 O/ g) W+ Q" O
the father. The family initially concealed this infor-
2 w$ }4 N+ e1 H4 |, Cmation, resulting in an extensive work-up for this1 e: q% c4 M$ `; G5 k. A* q- e
child. Given the widespread and easy availability of
# y6 g- o4 C  Otestosterone gel and cream, we believe this is proba-& A% v: h9 ?; i/ i; I; X- O, ~
bly more common than the rare case report in the. ~, i, a. u8 B& u- h5 Q- ?
literature.4
% e8 F: O% N0 ?- Z! m3 |7 ^7 tPatient Report- `. C. c" b) \, ?
A 16-month-old white child was referred to the
$ d" G' u1 p& \6 v/ Q4 d; @endocrine clinic by his pediatrician with the concern
% a( H: J9 f3 w( N) bof early sexual development. His mother noticed
- |  `/ E5 j6 ^% M9 A" B% y1 n7 E: klight colored pubic hair development when he was
3 m- m, I3 W/ V( `, f  N! x& _From the 1Division of Pediatric Endocrinology, 2University of# [  c# Q: b$ e' t1 g0 l
South Alabama Medical Center, Mobile, Alabama.
  y6 g8 M% l8 H# o: O& O1 U4 kAddress correspondence to: Samar K. Bhowmick, MD, FACE,2 s8 I% {) K3 P
Professor of Pediatrics, University of South Alabama, College of
( ~' ?  |! S/ D; GMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
5 h, |) s% A0 ]# z# U' k+ h0 te-mail: [email protected].
* ?) ^( [% u8 @% _about 6 to 7 months old, which progressively became' a9 k* n& d9 T8 @
darker. She was also concerned about the enlarge-4 U4 T  y$ Z) |, `
ment of his penis and frequent erections. The child8 s* j$ w7 M8 H. `8 m0 Q2 P
was the product of a full-term normal delivery, with
' h( W/ w5 G$ w$ `2 Ua birth weight of 7 lb 14 oz, and birth length of5 x% L* q9 L3 ]" Q
20 inches. He was breast-fed throughout the first year6 Z8 r7 I" ?: r+ z+ h! x
of life and was still receiving breast milk along with
  j2 T7 A8 ~+ A: asolid food. He had no hospitalizations or surgery,
& D/ g& f& n' s4 A) R9 Sand his psychosocial and psychomotor development0 p5 c& ?( M; I3 l$ Z1 Y* F0 T7 J2 p
was age appropriate., S6 U* o, U# l( [
The family history was remarkable for the father,% B+ |7 l( w8 y, t5 T* q
who was diagnosed with hypothyroidism at age 16,2 }" D& H2 ^- s
which was treated with thyroxine. The father’s
4 a# C/ o) d4 F1 N5 Eheight was 6 feet, and he went through a somewhat8 O8 R' @' D+ n6 k' t
early puberty and had stopped growing by age 14.2 C# @3 g  j4 }
The father denied taking any other medication. The  {6 R* V& Q3 T
child’s mother was in good health. Her menarche
3 O& {  o7 I9 r" p* w- m; V+ v! ?was at 11 years of age, and her height was at 5 feet1 M9 |$ g. `- q% H. |2 Y  l0 P
5 inches. There was no other family history of pre-
" [; C7 |0 E. d$ A5 `$ P6 Z0 jcocious sexual development in the first-degree rela-
. X3 l& P. l9 ^2 H& ytives. There were no siblings.9 D$ w3 [" s) g/ h2 Q& w
Physical Examination
8 Y' ^8 [8 z0 }  K8 s$ t' lThe physical examination revealed a very active,3 p/ f/ L* V' Z5 L* K) Q, s# B
playful, and healthy boy. The vital signs documented
  N8 a6 L# ?5 ]a blood pressure of 85/50 mm Hg, his length was
; U& u7 B* O0 N6 @. D90 cm (>97th percentile), and his weight was 14.4 kg, f4 V0 w& @5 a8 j
(also >97th percentile). The observed yearly growth  A- J* V) g& b6 `  R# _, M  ^& `
velocity was 30 cm (12 inches). The examination of
* n! _4 I* q1 W, e" @: R* Dthe neck revealed no thyroid enlargement.0 I. U) s' {% ]) |3 N+ a
The genitourinary examination was remarkable for% ]& ?2 S, N' s6 y
enlargement of the penis, with a stretched length of& Y" w  y! g( [" }4 O) A9 B
8 cm and a width of 2 cm. The glans penis was very well( ~, \9 ~; P9 |+ q+ I* t! d8 [" M& m% }
developed. The pubic hair was Tanner II, mostly around% l3 m+ E) b0 ]* B; H9 j$ @! @
540
# b8 A/ F/ a! V& ?( _at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
- n' B6 f: q) \# v) G3 }the base of the phallus and was dark and curled. The
5 L4 q' q$ S/ g6 d" M6 W- l8 k9 ctesticular volume was prepubertal at 2 mL each.
8 j. k) ^' _) A' j9 aThe skin was moist and smooth and somewhat7 }1 i# i% W5 i7 ^' V. y
oily. No axillary hair was noted. There were no8 x2 h1 e8 o, N2 {6 M
abnormal skin pigmentations or café-au-lait spots.
5 C( y, v2 w: H4 R& MNeurologic evaluation showed deep tendon reflex 2+- _, F; H( t5 x5 b
bilateral and symmetrical. There was no suggestion1 ?% d1 B7 S  b% H$ Z
of papilledema.% h: ]1 g  O. h+ M, S" c6 r* q
Laboratory Evaluation
3 ^0 m% a1 a" o5 j0 _1 o% }The bone age was consistent with 28 months by
& E! O9 j$ q4 B. j" F, h% tusing the standard of Greulich and Pyle at a chrono-
4 Y3 i' x* |! n& J; Qlogic age of 16 months (advanced).5 Chromosomal2 Z: G/ l8 w# m9 W
karyotype was 46XY. The thyroid function test
  a/ `! r9 J* c, r& Kshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
4 H& u8 K) |+ ]0 A) Alating hormone level was 1.3 µIU/mL (both normal).9 h! R9 I1 h# Y/ S3 j
The concentrations of serum electrolytes, blood
  Q7 f! e& m0 }" V' C1 q0 A. @3 nurea nitrogen, creatinine, and calcium all were) g9 N/ }+ c, d
within normal range for his age. The concentration7 P# F, Q- |% c! L' N; a
of serum 17-hydroxyprogesterone was 16 ng/dL
$ u9 Y6 Q5 P6 Y: K, K( c(normal, 3 to 90 ng/dL), androstenedione was 20: l& x8 ]( a6 B% q
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
. P! Q4 o2 i" O1 c% H7 N' ~terone was 38 ng/dL (normal, 50 to 760 ng/dL),
4 `& }" X  y3 x* `# W3 tdesoxycorticosterone was 4.3 ng/dL (normal, 7 to
( M6 a) D5 t" n( ~49ng/dL), 11-desoxycortisol (specific compound S)# O' E. e/ u0 Y6 \  ]- ^9 t
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
0 N7 h. v( ]7 C+ w- Ytisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
7 e1 c6 B; t/ s* }- w( |8 vtestosterone was 60 ng/dL (normal <3 to 10 ng/dL),( K* M* y5 _+ g- v+ ]
and β-human chorionic gonadotropin was less than! m) M9 u! B  p
5 mIU/mL (normal <5 mIU/mL). Serum follicular
9 s# e  q2 a4 }stimulating hormone and leuteinizing hormone
# W( c' Q. B5 `& k: A. A+ Y6 X8 @concentrations were less than 0.05 mIU/mL4 `' }% W( M  E5 ~
(prepubertal).) _, Z3 v0 R4 a  P  t* _* n4 G! @' a
The parents were notified about the laboratory
9 \& ?5 U8 ^6 W2 l: b7 Nresults and were informed that all of the tests were" s  J$ Y; b" ^2 ^' |% V* p0 o% G
normal except the testosterone level was high. The
, [' P) Z4 z& {5 Zfollow-up visit was arranged within a few weeks to
/ k7 |  r+ X4 nobtain testicular and abdominal sonograms; how-: x6 x8 [2 }7 c6 j
ever, the family did not return for 4 months.' q4 Y- B( u7 ?7 G2 U
Physical examination at this time revealed that the3 G! Q6 c' {7 \! e2 R0 P+ f
child had grown 2.5 cm in 4 months and had gained
% r1 W+ b9 q! n3 j/ ]2 kg of weight. Physical examination remained9 n7 C7 y2 C$ q  n: t% W
unchanged. Surprisingly, the pubic hair almost com-
0 l0 O4 @/ h  o- J& Zpletely disappeared except for a few vellous hairs at
" A: f: O3 J) X" Y) e- X% Mthe base of the phallus. Testicular volume was still 2
8 b! B  a! f2 M: N# P; \& }  zmL, and the size of the penis remained unchanged.
5 C2 [2 v6 N$ q# RThe mother also said that the boy was no longer hav-' C( Y4 B: v5 X  E2 T* y6 _
ing frequent erections.- h) y. m0 n* M: L( Q; R" A
Both parents were again questioned about use of
6 j+ |3 H0 f4 p7 T0 }. R  xany ointment/creams that they may have applied to' Z" x! t. M) a5 e; i, A
the child’s skin. This time the father admitted the
: P& B! M/ `3 \' u5 e/ o" `Topical Testosterone Exposure / Bhowmick et al 541
( }8 q0 G, L& V' r! F9 fuse of testosterone gel twice daily that he was apply-
; s* V& e* z3 u7 a! _1 Fing over his own shoulders, chest, and back area for9 P' A' U+ x1 {- V9 |" `( E
a year. The father also revealed he was embarrassed
4 c4 i" c4 x1 k! T+ _: mto disclose that he was using a testosterone gel pre-
; `1 k& ?7 T9 vscribed by his family physician for decreased libido0 l7 e9 [  n* V8 ?
secondary to depression.
' p& s! @" }6 G1 CThe child slept in the same bed with parents.. \# O5 r$ K3 i  C8 S( h3 ~, L
The father would hug the baby and hold him on his
5 g- ~& c3 w7 G: L) w! Ychest for a considerable period of time, causing sig-! _( b' I+ d: y1 i2 x& n8 Y, ?* ]* R$ P
nificant bare skin contact between baby and father.
4 U9 f  w6 S& kThe father also admitted that after the phone call,
1 \* }, V* O$ g* V4 e7 p1 r; qwhen he learned the testosterone level in the baby
" I. M; L4 j" H9 v& I: [was high, he then read the product information
2 r0 F, T& l# s+ }( T; @! S5 Y6 Y& M5 [packet and concluded that it was most likely the rea-! x$ u# ?. M- I9 o9 F, `
son for the child’s virilization. At that time, they
6 I  T7 f8 [$ sdecided to put the baby in a separate bed, and the
- p7 N0 }, D9 w, [+ y1 a/ Zfather was not hugging him with bare skin and had3 v- ]- W$ C" E
been using protective clothing. A repeat testosterone6 e2 W) }5 O1 i1 K  Z, z6 s% x
test was ordered, but the family did not go to the, n; z3 f1 o2 x: M/ A' |
laboratory to obtain the test.3 k' R) I! u# l2 H& [
Discussion0 e( S0 e* r  z/ E# z# N& g
Precocious puberty in boys is defined as secondary
  s, F% f5 z) [8 Psexual development before 9 years of age.1,4: |$ y+ S' s4 F8 L; d& ]. d
Precocious puberty is termed as central (true) when- z/ J2 ?, T4 N! t- ^7 K6 @
it is caused by the premature activation of hypo-; l2 K/ T3 u! }; y
thalamic pituitary gonadal axis. CPP is more com-& G/ A3 L" R. s8 K; N; r
mon in girls than in boys.1,3 Most boys with CPP* n* ^- {9 _7 ~# \* d; t
may have a central nervous system lesion that is
$ _. ~. Z9 E. @, w2 {0 {: {responsible for the early activation of the hypothal-
7 X3 e0 j- J' m. R! famic pituitary gonadal axis.1-3 Thus, greater empha-
* h/ C' p; T! t3 rsis has been given to neuroradiologic imaging in& Y: y% A- ^- W% B& x6 U: o
boys with precocious puberty. In addition to viril-
, {% E3 M2 x2 zization, the clinical hallmark of CPP is the symmet-
9 w) w+ m  T" p! I! Brical testicular growth secondary to stimulation by
% j+ `- Z* R7 a: Ggonadotropins.1,3
6 B& c( W2 }0 m  F+ C; yGonadotropin-independent peripheral preco-
6 K2 i8 _, v; mcious puberty in boys also results from inappropriate
! H! Y" [1 [# {: W8 randrogenic stimulation from either endogenous or
, O: g+ C+ K# O# t8 q7 Iexogenous sources, nonpituitary gonadotropin stim-3 D& D+ K- C7 _  q6 G: q$ Z7 N
ulation, and rare activating mutations.3 Virilizing
% r: }; z! V) c- L9 H1 U4 i# icongenital adrenal hyperplasia producing excessive
: P4 Q4 d) B- H8 Iadrenal androgens is a common cause of precocious
" o# C" S3 r- Gpuberty in boys.3,4
# t6 b5 d0 _8 @; z: rThe most common form of congenital adrenal
4 R2 J+ \0 D/ y9 o9 ^hyperplasia is the 21-hydroxylase enzyme deficiency.
* m: \" \5 m- c( o+ d& t9 aThe 11-β hydroxylase deficiency may also result in
9 d2 k2 h4 [! M: e: Y: oexcessive adrenal androgen production, and rarely,
" W5 B9 f- |( Xan adrenal tumor may also cause adrenal androgen: b, r+ N; a* ?) T' b8 h- D6 D
excess.1,3/ R$ Z4 N; Z& K/ y  |, G3 v3 |8 E
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from9 q  [1 V! H; R, }" a! w  c  C4 n
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
+ a- i' c) M6 h8 H$ \0 Y$ k! jA unique entity of male-limited gonadotropin-
, ~! ~0 p5 p0 C! M$ Gindependent precocious puberty, which is also known0 _# [' N+ `; D6 k  F
as testotoxicosis, may cause precocious puberty at a% s6 Z' d; A/ J
very young age. The physical findings in these boys; d7 c2 ]6 w1 A( O
with this disorder are full pubertal development,; \/ @9 R+ t/ Y' ?
including bilateral testicular growth, similar to boys2 y8 ]' n8 {( K6 J( v8 y( y
with CPP. The gonadotropin levels in this disorder
: y1 m' A5 ?" l% uare suppressed to prepubertal levels and do not show
) w, e: L5 }$ t" }5 O; }. apubertal response of gonadotropin after gonadotropin-
' m. S, i# w( ~9 A) areleasing hormone stimulation. This is a sex-linked. t$ C# J" Q$ `% f2 C3 }$ N9 t' i7 e+ r) p
autosomal dominant disorder that affects only
: `% x; X, v/ ]' Tmales; therefore, other male members of the family
# R' U# g/ G/ {7 e, L7 }* h9 W; g4 Jmay have similar precocious puberty.3
( g. Q# p: e% T# LIn our patient, physical examination was incon-
+ h" L# n* U, ?/ ~7 Ssistent with true precocious puberty since his testi-; \. u; o; R5 L, T# E, T0 B6 j+ L1 L
cles were prepubertal in size. However, testotoxicosis
5 I; U! d$ s# Nwas in the differential diagnosis because his father
5 l3 g/ t! h  Ostarted puberty somewhat early, and occasionally,
- O" Y4 V2 B0 w2 C/ N0 @testicular enlargement is not that evident in the
! L# D& v6 u3 D8 H6 a/ Q' Hbeginning of this process.1 In the absence of a neg-
1 r2 k* c, s- eative initial history of androgen exposure, our' t9 _8 o" r% w) w
biggest concern was virilizing adrenal hyperplasia,* _, P: q' x; ^$ C" A4 J
either 21-hydroxylase deficiency or 11-β hydroxylase
3 t% f  Y7 ^* p. e! r- w( z4 p* ^deficiency. Those diagnoses were excluded by find-& h+ U: |. ~- A" P1 y/ S
ing the normal level of adrenal steroids.
6 a/ E! t- U" c7 s) m$ B) x' zThe diagnosis of exogenous androgens was strongly
+ a4 p* f0 |- G2 dsuspected in a follow-up visit after 4 months because6 R9 z' X3 k6 p
the physical examination revealed the complete disap-
0 s. I/ w) f$ Upearance of pubic hair, normal growth velocity, and
; d7 j/ v  A' e* rdecreased erections. The father admitted using a testos-( T& x4 ]! m5 F- s" f+ C9 l
terone gel, which he concealed at first visit. He was) G! w# ?8 c1 p" E3 |- J+ o
using it rather frequently, twice a day. The Physicians’" F6 j! W6 r6 r+ @5 E$ q
Desk Reference, or package insert of this product, gel or
8 S2 L: B, D/ ^" L4 v' |cream, cautions about dermal testosterone transfer to$ j1 T7 K/ x6 Q* C
unprotected females through direct skin exposure.4 k. J' B2 b! v* K! L/ G4 p
Serum testosterone level was found to be 2 times the: r6 K. P2 G. B
baseline value in those females who were exposed to
- d. ~1 V8 d. Qeven 15 minutes of direct skin contact with their male0 i: n. H9 V' C' z' K' `* J/ Z  r
partners.6 However, when a shirt covered the applica-
; S4 m5 H' V3 X' J, J4 @tion site, this testosterone transfer was prevented.; V8 S9 j' i6 c
Our patient’s testosterone level was 60 ng/mL,
% ~$ ]7 C  t8 V% \2 G' m0 pwhich was clearly high. Some studies suggest that
. H! X; _) Q' M4 v, Adermal conversion of testosterone to dihydrotestos-
) F! O& q- L' D' }, B0 F/ `3 ?7 Iterone, which is a more potent metabolite, is more
$ u% }& @+ `- tactive in young children exposed to testosterone0 f* w( y2 S4 t; w( J8 `
exogenously7; however, we did not measure a dihy-
' w( N- S# l5 N8 e- o: }" o* edrotestosterone level in our patient. In addition to
, x7 e6 q7 f% J# e0 t) {, Vvirilization, exposure to exogenous testosterone in$ f2 z; Y5 b+ B4 F# J
children results in an increase in growth velocity and
% g" h* H0 P1 ^5 Q& r9 q8 l$ }advanced bone age, as seen in our patient.+ \8 F! K. j% n! e
The long-term effect of androgen exposure during6 R% u, Z: F1 ~+ x* ~$ i
early childhood on pubertal development and final
& s# g5 ^% @, zadult height are not fully known and always remain
; z0 f! n7 k- j: h/ P9 ba concern. Children treated with short-term testos-
- G7 `. p! Q  ]0 E! R' g9 dterone injection or topical androgen may exhibit some1 `6 W' G+ S# {0 i( ~* A& M2 H
acceleration of the skeletal maturation; however, after
% P8 j! q2 s* k* m4 |cessation of treatment, the rate of bone maturation
2 b5 w7 J3 G7 C6 C4 ^0 tdecelerates and gradually returns to normal.8,94 e9 r4 E* A( v
There are conflicting reports and controversy
7 `1 z3 v1 ?3 B* X6 h) l: R  vover the effect of early androgen exposure on adult/ v& T" a4 n+ J/ `
penile length.10,11 Some reports suggest subnormal3 u8 m. ~2 p, g
adult penile length, apparently because of downreg-4 H  {+ j. c2 M* {! j! X7 f
ulation of androgen receptor number.10,12 However,/ c7 f7 P2 P; a) C( d
Sutherland et al13 did not find a correlation between1 {5 H  x+ a& O
childhood testosterone exposure and reduced adult
) `' H, G" F7 gpenile length in clinical studies.. b0 k  @( |4 _! [: Q
Nonetheless, we do not believe our patient is
. b- Y0 _# P& m  T) x- L: i. Fgoing to experience any of the untoward effects from9 Z1 t4 t' w7 O) S6 q
testosterone exposure as mentioned earlier because$ H* X1 f( w) W  k0 D3 p* z
the exposure was not for a prolonged period of time.! X5 }. z' `6 A' K- C# F& {6 r1 }
Although the bone age was advanced at the time of
) B9 h8 ?8 A% @8 Ldiagnosis, the child had a normal growth velocity at$ c1 @7 K0 t8 f/ m  A2 o
the follow-up visit. It is hoped that his final adult! P- t, K1 y7 s: g, A
height will not be affected.5 i0 k& `  o& J8 z) n2 e3 ~& w' x9 A4 s
Although rarely reported, the widespread avail-
  Q6 I1 R' Y3 D3 ?ability of androgen products in our society may7 e6 s. l0 @  }
indeed cause more virilization in male or female
6 J8 y( T8 y, J# nchildren than one would realize. Exposure to andro-3 e1 _" }5 h. [- Q
gen products must be considered and specific ques-
! i& t5 x' f) t8 c( otioning about the use of a testosterone product or: A. S1 }* b- ^( p3 w' ~! P
gel should be asked of the family members during2 w" \3 A/ @8 P
the evaluation of any children who present with vir-8 a& d$ V* E6 Z: n
ilization or peripheral precocious puberty. The diag-
, }) h0 y' W& ?6 cnosis can be established by just a few tests and by6 y# w% N  @3 e4 W; t2 h
appropriate history. The inability to obtain such a+ s8 D7 V' f, T  V
history, or failure to ask the specific questions, may
! E$ r! W+ {, s7 |6 ^# sresult in extensive, unnecessary, and expensive
9 W% [/ P8 @5 D1 J9 ninvestigation. The primary care physician should be1 D/ @" Y) x% d/ ]/ J! F
aware of this fact, because most of these children
  X% A. O5 [) l2 emay initially present in their practice. The Physicians’
7 L! H6 H3 p2 K3 {: K' r3 SDesk Reference and package insert should also put a
6 ]3 X. {$ G$ a2 w+ F7 ^& ^warning about the virilizing effect on a male or
$ N9 {8 N& _0 Y1 Afemale child who might come in contact with some-
, _" u) e) p: n8 k  e7 ~one using any of these products.
5 `) T4 }7 X, c1 hReferences
7 i# |& @& i: b7 z0 t8 k5 L8 I1. Styne DM. The testes: disorder of sexual differentiation1 _, `0 B: b- p6 a
and puberty in the male. In: Sperling MA, ed. Pediatric( Q1 D! z  L7 T2 Z$ K) s8 ]3 {
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;$ N5 @( F2 n/ C5 e
2002: 565-628.2 _! `. z$ T8 }  o" D
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
3 _: c  W/ `9 ^% Z) y; Opuberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old$ a8 \. c4 b# c9 Y
Boy Induced by Indirect Topical& F" b( D4 A6 ?6 J7 d
Exposure to Testosterone
2 n: u1 k- }" o) HSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
6 R8 ]2 \2 I# G3 U3 b0 eand Kenneth R. Rettig, MD1
4 |  Z, h4 z& L0 fClinical Pediatrics6 N1 ?/ ~8 k* c$ k# c; T9 i  h
Volume 46 Number 6
. e  c8 _: K$ Z, ]$ E/ IJuly 2007 540-543
- g+ @/ m! L; H: E) H: \© 2007 Sage Publications
9 e9 x7 v8 u" G# N" i0 @10.1177/00099228062966514 g2 u, l4 l  f8 ?, n" c" f
http://clp.sagepub.com
; j  d7 m- w4 V% \( xhosted at$ z  ~; ]* [( h7 {
http://online.sagepub.com
3 Z8 s1 _, m! |3 _! i' G/ `Precocious puberty in boys, central or peripheral,6 r( |8 ~1 e- K3 b
is a significant concern for physicians. Central: `" x; ?( H  I0 N! M' W
precocious puberty (CPP), which is mediated. r# G) H3 `" l
through the hypothalamic pituitary gonadal axis, has+ T# X4 D8 h, j" S' P2 u9 F4 y# e
a higher incidence of organic central nervous system" g6 q( c' f3 f. Y8 G- z- p
lesions in boys.1,2 Virilization in boys, as manifested* }5 j: G) Q% ]# B  e* v! |
by enlargement of the penis, development of pubic
8 c: _. _4 v$ W) ]hair, and facial acne without enlargement of testi-
. Q3 b( _! p4 ~( ^3 r7 T0 icles, suggests peripheral or pseudopuberty.1-3 We; @& b6 o) r7 l/ T
report a 16-month-old boy who presented with the
5 D& {7 s1 E5 }( Eenlargement of the phallus and pubic hair develop-
* `' M6 `, Q0 l& K% xment without testicular enlargement, which was due
5 t5 A) U# X& p) o( a$ _% Rto the unintentional exposure to androgen gel used by3 w9 G6 a6 L6 \/ ~
the father. The family initially concealed this infor-$ W, x7 x+ Q2 \2 }8 K3 {" O5 l2 T- w
mation, resulting in an extensive work-up for this
1 c* B' x2 }# c% R  X* P3 T9 S' tchild. Given the widespread and easy availability of
4 ^$ ]5 b% `; _# |- Dtestosterone gel and cream, we believe this is proba-  C! a  g6 Y& l5 s: z; C8 R
bly more common than the rare case report in the% |" g9 q$ M0 j- U+ w4 p
literature.4
3 i7 j8 ^0 }7 G- `5 CPatient Report
3 b' @: h1 e: _* DA 16-month-old white child was referred to the3 G: F7 S- r% v1 r
endocrine clinic by his pediatrician with the concern! T( c# \) p2 x1 }0 f# H
of early sexual development. His mother noticed
& R* R3 }9 [7 F- R( }) hlight colored pubic hair development when he was$ O9 v9 _% Y: R; `
From the 1Division of Pediatric Endocrinology, 2University of
& U0 D$ ^) z9 j' @South Alabama Medical Center, Mobile, Alabama.8 G- [' W5 ~3 s# r/ S% d8 T! O8 a
Address correspondence to: Samar K. Bhowmick, MD, FACE,1 A# ?0 U  j- i' z5 A' k) ^# @7 e
Professor of Pediatrics, University of South Alabama, College of
8 G+ b5 v$ G* U' @4 M6 B( e4 }+ u5 R: GMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;4 z- r# g- s, H. L
e-mail: [email protected].
: t4 a& o3 N! B- P" Kabout 6 to 7 months old, which progressively became1 k8 M9 M/ J* @. c
darker. She was also concerned about the enlarge-
2 n: C/ u' M: a* w  W9 ument of his penis and frequent erections. The child
0 ~6 |* w# g! `: O/ G) G8 f! l, xwas the product of a full-term normal delivery, with
& j5 V" @* @5 z* _a birth weight of 7 lb 14 oz, and birth length of/ X& D) E3 a- @0 s% e3 ?/ J* R6 @3 g
20 inches. He was breast-fed throughout the first year
) h+ C" v5 r6 N9 G! A+ d# ?( E8 k6 Mof life and was still receiving breast milk along with: o. F; S2 a3 l
solid food. He had no hospitalizations or surgery,
! K0 B" ]3 K; m. {$ Uand his psychosocial and psychomotor development
  c( @: E/ Y+ V: pwas age appropriate.2 A: n8 G2 B$ J2 B% {7 q
The family history was remarkable for the father,: E) j7 ~+ O4 l1 h( x
who was diagnosed with hypothyroidism at age 16,
1 d8 i* Y" j: {4 Y% rwhich was treated with thyroxine. The father’s
' ^% {7 e1 a6 r3 e% c* lheight was 6 feet, and he went through a somewhat7 [* h' [; ~6 z
early puberty and had stopped growing by age 14.( C: }  F/ _, J" _! e" j/ t
The father denied taking any other medication. The
! }* f9 m* |% i& X* Y" r/ Gchild’s mother was in good health. Her menarche( J: @! @, ^, \
was at 11 years of age, and her height was at 5 feet
; n  E6 i0 U9 U9 F6 m# n( t5 inches. There was no other family history of pre-4 g3 n1 l+ F! j  u( E
cocious sexual development in the first-degree rela-
2 W+ _* l; p; E( gtives. There were no siblings.
1 K' F& H! T3 n+ ~. wPhysical Examination
9 f  s. h( r% Y, _) K# sThe physical examination revealed a very active,0 M" x( g1 F; G" {$ u( o
playful, and healthy boy. The vital signs documented! |' b3 {4 k/ q# [8 w0 J
a blood pressure of 85/50 mm Hg, his length was! C) n- h8 N2 H, ~9 M  @8 z
90 cm (>97th percentile), and his weight was 14.4 kg7 e- z4 L) n3 j5 H
(also >97th percentile). The observed yearly growth! A( o: U" s" ]+ g3 m7 i. ]9 ^
velocity was 30 cm (12 inches). The examination of
* F2 n2 O( j4 m4 d* zthe neck revealed no thyroid enlargement.. u  P! ?8 E5 P6 q6 x2 k# R
The genitourinary examination was remarkable for
4 ]+ T0 `4 j( h2 l) ?enlargement of the penis, with a stretched length of1 j9 p! h- x; g* H1 @4 y1 d
8 cm and a width of 2 cm. The glans penis was very well6 D$ U4 g4 Z' m. o: y: z, S
developed. The pubic hair was Tanner II, mostly around3 X3 I  Z8 |9 i. E
540
" b% _# q4 ^  H% Jat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from1 G  V5 k4 |8 J
the base of the phallus and was dark and curled. The  c) I* a5 a' N/ G2 Z% \! ?  _
testicular volume was prepubertal at 2 mL each.
. d) `: u$ a& P/ K; v$ qThe skin was moist and smooth and somewhat) W% }5 \2 a3 A5 G+ k( W
oily. No axillary hair was noted. There were no* [9 Z# G- C2 ^. k  ~
abnormal skin pigmentations or café-au-lait spots.7 K8 u3 \- q7 ~8 V
Neurologic evaluation showed deep tendon reflex 2+! Z& R3 {) O# U; O
bilateral and symmetrical. There was no suggestion
( q! P/ V$ z$ g( M9 tof papilledema.! O2 u( \# {' T% ~# O7 M! @
Laboratory Evaluation
& F( V; ~, }: }: @The bone age was consistent with 28 months by, S5 `! ?7 Q2 x
using the standard of Greulich and Pyle at a chrono-. \" v& y0 U. d- {4 e0 {4 o* n+ D
logic age of 16 months (advanced).5 Chromosomal
/ h+ d9 h4 M* f* b  skaryotype was 46XY. The thyroid function test% [  Z/ e  @. L1 O. d* B
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
7 {7 b$ j8 d: |# ]% F4 G/ e3 ~4 w0 wlating hormone level was 1.3 µIU/mL (both normal).' v+ Q: J: X; s6 I! _
The concentrations of serum electrolytes, blood* _) l7 b3 Z! d( l& J( W1 c
urea nitrogen, creatinine, and calcium all were( @8 W1 C. I5 c: @. o
within normal range for his age. The concentration
/ q# X& [, P, _+ j4 Hof serum 17-hydroxyprogesterone was 16 ng/dL4 O; j/ f9 R2 m! b
(normal, 3 to 90 ng/dL), androstenedione was 20: j3 U8 g6 A6 s7 G0 E/ @& E
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-  @2 Q) }! o7 n6 o3 L+ ~5 u; x. t6 @
terone was 38 ng/dL (normal, 50 to 760 ng/dL),. U4 j, O% H4 i8 N+ I8 B
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
0 O8 {* M* N7 @8 [! |  o5 S49ng/dL), 11-desoxycortisol (specific compound S); {8 v' i' c0 B* O/ w, K9 H2 L
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-) k3 y2 p/ O- t& v2 R8 [/ j- f
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
2 u+ Z4 k- }7 Q4 \2 v: ttestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
( ?. V$ _* ^6 z. R. ], w1 G% tand β-human chorionic gonadotropin was less than
2 G& n4 {5 B1 i7 H( f, S( Z5 mIU/mL (normal <5 mIU/mL). Serum follicular
7 _5 b6 `! O6 X0 s6 gstimulating hormone and leuteinizing hormone% L2 u  r+ K0 Z. m) h) \6 t; O
concentrations were less than 0.05 mIU/mL
. y9 F) i7 l7 S' G(prepubertal).
& I$ x+ C+ k( aThe parents were notified about the laboratory- ^, _9 |) J& a" ]2 T! ]
results and were informed that all of the tests were
5 E8 f* J* p" W: z; G' [( H- d8 Vnormal except the testosterone level was high. The
; y4 |$ `8 I8 {; o! l! ufollow-up visit was arranged within a few weeks to
* F/ @! {* {0 n0 D* k! p1 {obtain testicular and abdominal sonograms; how-3 c# o  E* [/ N. W) @. r
ever, the family did not return for 4 months.. ]2 \% R* h. g
Physical examination at this time revealed that the
& `$ k* m# A! p$ Vchild had grown 2.5 cm in 4 months and had gained0 U( _5 K0 N+ u9 V9 _
2 kg of weight. Physical examination remained
) p" H9 x4 b$ U1 o3 c- J; |0 munchanged. Surprisingly, the pubic hair almost com-' L7 K! v( s( L4 C# ~6 v9 a
pletely disappeared except for a few vellous hairs at
$ u  G0 A9 o4 ?' A' ithe base of the phallus. Testicular volume was still 2' y: f1 v  P8 H$ o6 B  v2 K
mL, and the size of the penis remained unchanged.
0 G  Z. ?* u# F- kThe mother also said that the boy was no longer hav-
- r9 o# {5 k" e8 H  F5 D5 Ping frequent erections.8 l2 c5 h% s0 O
Both parents were again questioned about use of
3 t8 P( q+ K1 t/ Z( xany ointment/creams that they may have applied to; w$ @# f! V3 e
the child’s skin. This time the father admitted the
! P$ b. X+ x4 p' ]+ t* hTopical Testosterone Exposure / Bhowmick et al 5417 U" _% P+ `6 B+ V. W
use of testosterone gel twice daily that he was apply-
; W3 a2 Y- A2 }9 w$ B7 l. qing over his own shoulders, chest, and back area for
- G+ ^' [5 n+ e7 e* m1 oa year. The father also revealed he was embarrassed! s, H/ ]" a5 Q4 x% Y" L# R# E) }
to disclose that he was using a testosterone gel pre-6 D- s6 A1 v! Q( T4 [5 I
scribed by his family physician for decreased libido
& n$ x% U$ Q8 i! y8 ]' csecondary to depression.
; n, H' N  d5 l' b  ZThe child slept in the same bed with parents.
! `4 F& x  `( J. z! i  K* z+ v( W& YThe father would hug the baby and hold him on his
* W7 i9 w! h6 _- h2 i! _* R# Gchest for a considerable period of time, causing sig-, Y/ e% s3 b# y* Q- s9 c
nificant bare skin contact between baby and father.
4 X2 x5 [4 v- u% kThe father also admitted that after the phone call,  O4 `0 a7 d) j! b0 L% o
when he learned the testosterone level in the baby8 _( L% u: k5 W: p* z  o5 d
was high, he then read the product information0 {1 a1 W- d; `/ d( y: s' e( l
packet and concluded that it was most likely the rea-
4 H# Q/ \8 Q+ M2 d3 ~son for the child’s virilization. At that time, they) T3 i% z( {3 J
decided to put the baby in a separate bed, and the
: \' t6 S7 H& q1 Mfather was not hugging him with bare skin and had
. n5 X' l4 z3 V; c6 R% ~been using protective clothing. A repeat testosterone
# z+ u* Q. [  r2 j+ Stest was ordered, but the family did not go to the$ f+ R5 ^5 W# i
laboratory to obtain the test.
3 z9 ?- k1 N6 J( ^# X. yDiscussion% W" j0 y6 i- l& U, C
Precocious puberty in boys is defined as secondary  n. u6 p. D/ _" Z0 f) e9 \* Y# O7 m
sexual development before 9 years of age.1,4
0 z' q6 e& Z$ qPrecocious puberty is termed as central (true) when8 l  j' Q3 N  V: Q
it is caused by the premature activation of hypo-
! u3 C, ~* h# ?- }' Zthalamic pituitary gonadal axis. CPP is more com-4 o* d9 T. k4 `& G2 r3 i( P5 D
mon in girls than in boys.1,3 Most boys with CPP1 k; x3 r$ n% d0 E# p1 g% C
may have a central nervous system lesion that is$ K" e8 h+ C7 I, v. C
responsible for the early activation of the hypothal-
* t& o! r6 E( S. e# q2 h4 q9 Qamic pituitary gonadal axis.1-3 Thus, greater empha-
! t% j! q) o! B5 u8 _4 f( b, W" Ssis has been given to neuroradiologic imaging in) a( h' n- X/ h4 m
boys with precocious puberty. In addition to viril-5 u) C, D. B1 s# Q" g
ization, the clinical hallmark of CPP is the symmet-
9 n; l  P2 Q  I: N: ?  Q- [: Urical testicular growth secondary to stimulation by
4 @: n: u; I+ P( }gonadotropins.1,37 O, \2 Q: u/ F+ ~! b+ n
Gonadotropin-independent peripheral preco-$ ~- Z9 M9 Z# i+ t
cious puberty in boys also results from inappropriate+ q/ Z. t! U5 M8 A
androgenic stimulation from either endogenous or1 I& E& G1 W- @
exogenous sources, nonpituitary gonadotropin stim-
& B$ }6 v) ]9 _4 L; R% k- oulation, and rare activating mutations.3 Virilizing  a, \; ?+ a1 B$ Q$ N$ q
congenital adrenal hyperplasia producing excessive; D0 Y  m/ J$ v
adrenal androgens is a common cause of precocious/ p! N! O" j& I8 \
puberty in boys.3,4
3 H1 F; u# u' A6 |2 F9 c1 ]The most common form of congenital adrenal( c1 q% S- V. @
hyperplasia is the 21-hydroxylase enzyme deficiency.
0 S# Q  f& M/ A: {  UThe 11-β hydroxylase deficiency may also result in) b& d+ u$ G3 r- D; c5 l; W2 D
excessive adrenal androgen production, and rarely,
+ W7 [9 o0 k" san adrenal tumor may also cause adrenal androgen: @0 [9 i- |7 m" Z' C7 Z
excess.1,3
" {7 D# v) |" a5 n5 B1 Cat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from; G; d% F. M7 U# X
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
+ T. |& r$ _+ ~8 e5 H, y7 B' BA unique entity of male-limited gonadotropin-
+ l) W9 a' P# y: H$ [" i# cindependent precocious puberty, which is also known! z  S8 O& x1 W- O( H1 V
as testotoxicosis, may cause precocious puberty at a
4 B& D  y/ e; [9 Nvery young age. The physical findings in these boys
2 \4 m% w% G0 ]7 @$ V0 uwith this disorder are full pubertal development,: {6 ?! T4 t" }9 l1 a/ g4 W
including bilateral testicular growth, similar to boys
, F- e& c8 n& fwith CPP. The gonadotropin levels in this disorder
* {+ ~% G# R$ d2 h0 j0 eare suppressed to prepubertal levels and do not show( ?& |* u$ [+ i9 T( {2 v$ e; B
pubertal response of gonadotropin after gonadotropin-9 V. [  C2 n5 E4 ?/ ?: b0 _
releasing hormone stimulation. This is a sex-linked# i$ c/ r( f! M, ^
autosomal dominant disorder that affects only0 `) j+ K+ M; J+ r  {
males; therefore, other male members of the family4 ^7 x$ C/ Z7 D, ~& x6 K& W
may have similar precocious puberty.3
8 n; X/ V) v) s' S6 z6 aIn our patient, physical examination was incon-: c0 f! U0 r2 F7 _* u+ |
sistent with true precocious puberty since his testi-
, h+ t8 W% P- i- r% f3 o2 Pcles were prepubertal in size. However, testotoxicosis" [6 ]' t2 T" d; |6 u
was in the differential diagnosis because his father
, F3 `8 w8 S1 @4 w# |started puberty somewhat early, and occasionally,
; e* F! a+ r/ I8 \4 @testicular enlargement is not that evident in the
8 o( F: j! \0 S! m* }6 f4 n/ {beginning of this process.1 In the absence of a neg-/ k* V' x, X" E  V$ ^) V% a
ative initial history of androgen exposure, our7 o$ R$ p0 Q! b: ]1 w6 N, |& f3 z& s
biggest concern was virilizing adrenal hyperplasia,
, K# l1 |2 D1 xeither 21-hydroxylase deficiency or 11-β hydroxylase
* k3 B$ o1 a/ g. v$ sdeficiency. Those diagnoses were excluded by find-
* e0 y8 @) V8 Q' ~4 Wing the normal level of adrenal steroids.6 z6 A& L* g' _; I- p
The diagnosis of exogenous androgens was strongly% t* A5 ?6 H& h8 B
suspected in a follow-up visit after 4 months because7 i8 h0 b7 [# b7 `! R- S$ i( L
the physical examination revealed the complete disap-  [3 Y) b5 a+ ~6 R2 Y
pearance of pubic hair, normal growth velocity, and
; X# g, j( l0 U1 l4 F6 Fdecreased erections. The father admitted using a testos-
3 b7 N" t: k3 Eterone gel, which he concealed at first visit. He was1 _( i, ]0 X, K- l
using it rather frequently, twice a day. The Physicians’
; R1 `5 {1 C: Y* \# K& bDesk Reference, or package insert of this product, gel or$ K/ v# l3 j8 L- o
cream, cautions about dermal testosterone transfer to& o9 d. m+ B( y9 h9 n
unprotected females through direct skin exposure.
& m0 m/ k/ P/ x$ \8 @Serum testosterone level was found to be 2 times the1 g+ y2 T. }+ g6 W  z" w
baseline value in those females who were exposed to' O4 _- y0 T1 D; p1 Y1 A3 [
even 15 minutes of direct skin contact with their male5 _6 [2 {8 k5 D1 _9 T
partners.6 However, when a shirt covered the applica-
& G/ `' O! d. ztion site, this testosterone transfer was prevented.
1 V) Y$ ?2 \& ]! e* |6 s0 dOur patient’s testosterone level was 60 ng/mL,
, n+ B4 j, i6 l2 N( gwhich was clearly high. Some studies suggest that
% L: p; _, k* {- A! \! U* F9 |2 x1 n( qdermal conversion of testosterone to dihydrotestos-( y! h$ V: M% I) I
terone, which is a more potent metabolite, is more. P( H, k0 J1 e0 G; \
active in young children exposed to testosterone
. B8 l$ Y* [5 L+ L) N9 O# rexogenously7; however, we did not measure a dihy-& v8 g4 D3 J0 a, u
drotestosterone level in our patient. In addition to
- X- Z# b  e7 [2 v1 k* ]virilization, exposure to exogenous testosterone in( ~+ a: k5 i5 U- t$ \. l, z# n" W
children results in an increase in growth velocity and6 K. P! _$ `* W/ E5 B
advanced bone age, as seen in our patient., q, }2 o) N# C1 v! l
The long-term effect of androgen exposure during
# W' G6 ^: D/ K3 ^early childhood on pubertal development and final( l+ x) y) u" z* k
adult height are not fully known and always remain% o. V1 N, Q3 }3 s" m' u
a concern. Children treated with short-term testos-
: ?9 ~3 T- c$ p4 s2 {# }; hterone injection or topical androgen may exhibit some
: U% ~  T) N3 r6 `  v* T6 Lacceleration of the skeletal maturation; however, after
. Y" p# {9 w# m) \. p( bcessation of treatment, the rate of bone maturation$ Z; B* z: q" L9 N- ]$ y
decelerates and gradually returns to normal.8,9
: M# C: |. I2 Y* c  iThere are conflicting reports and controversy
6 v, g/ ^/ @3 u4 b- `+ ?, A. Q3 Zover the effect of early androgen exposure on adult4 e4 r, H0 S% u" T5 X% a
penile length.10,11 Some reports suggest subnormal
+ ?- M. _& L; P# @, w+ Tadult penile length, apparently because of downreg-% @' I. S$ w5 T/ d& T
ulation of androgen receptor number.10,12 However,
# m( F/ y  x* l: q! j6 LSutherland et al13 did not find a correlation between
7 K& i; `2 H$ u: r8 m# V" vchildhood testosterone exposure and reduced adult
* o+ P" N' Y6 o) O' ppenile length in clinical studies.
5 t# N8 c4 P0 _' A' I1 f- q7 uNonetheless, we do not believe our patient is
) U' F: W- @6 T1 i+ Ugoing to experience any of the untoward effects from9 k( J7 A4 h* G8 T4 b
testosterone exposure as mentioned earlier because
) S$ \( i1 j, u5 Fthe exposure was not for a prolonged period of time.
: g! j" O7 n* K; M$ EAlthough the bone age was advanced at the time of* p2 z( r' C0 P( S' P2 s) z' v
diagnosis, the child had a normal growth velocity at
8 J1 R+ X. |; zthe follow-up visit. It is hoped that his final adult, [) C$ @) W4 D6 V6 E4 K! q* W
height will not be affected.8 s! F7 A( s  W9 ~+ X
Although rarely reported, the widespread avail-
  ]5 V& W9 n4 Q  [0 B' P8 Z! @ability of androgen products in our society may
+ k+ x4 b. z( F4 W& _9 N$ R  d; uindeed cause more virilization in male or female
, P' O% g# x( `  g0 r' ichildren than one would realize. Exposure to andro-" }& a' ]( e) W. {% a% k% A
gen products must be considered and specific ques-% D# Q. i1 n! z
tioning about the use of a testosterone product or$ Z0 H0 ]' S6 \. h' _
gel should be asked of the family members during
$ B" H2 Y4 \  q; o9 @% O; S9 Bthe evaluation of any children who present with vir-
! m; f/ z# E) {# {& g  w( xilization or peripheral precocious puberty. The diag-$ \  R7 n6 W8 [$ L& f+ {+ F
nosis can be established by just a few tests and by
- F& e2 t  ~3 z) Jappropriate history. The inability to obtain such a
  ^; W' R" h! U$ m% }7 K  K5 ohistory, or failure to ask the specific questions, may' ~3 ]6 G! e8 G9 v; W+ A
result in extensive, unnecessary, and expensive, H" Q4 _7 `$ {: u/ W" r! a
investigation. The primary care physician should be  z8 w4 M- i/ U* B/ @+ [
aware of this fact, because most of these children
3 l9 E4 y4 u, T* Gmay initially present in their practice. The Physicians’3 C2 u$ J1 ]1 A9 ~$ O" p/ z' n6 V
Desk Reference and package insert should also put a- l/ z7 _4 d+ u: s
warning about the virilizing effect on a male or  V  W9 Z3 ^5 M0 A
female child who might come in contact with some-
8 z7 Q3 P$ p& D: d' Lone using any of these products.6 p4 u( Y9 Q0 f3 u/ q+ p4 F
References
; W: X# t2 I+ Y1. Styne DM. The testes: disorder of sexual differentiation
% ?' n) m: H, i1 a8 |1 A- Uand puberty in the male. In: Sperling MA, ed. Pediatric
/ S/ T) p2 G2 A7 ~" T2 p0 d. rEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;: l+ X  Z3 R  L" d+ J  @/ y
2002: 565-628.: l8 ?) j2 N5 q7 X! f
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
0 E0 V$ l: r4 I. Dpuberty in children with tumours of the suprasellar pineal
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感謝大大的辛勞分享!我會繼續在WK關注大大的文章!
發表於 2025-1-11 22:18:01 | 顯示全部樓層
女厕偷拍辅导班主任尿尿老师的逼很嫩还有一点
發表於 2025-1-17 16:31:39 | 顯示全部樓層
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
" T  G# P7 R9 q; @9 V+ U- |5 `
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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