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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-Old0 n% j2 v9 p/ W8 Q" N# O
Boy Induced by Indirect Topical
9 d! Q+ @: u8 V8 H4 zExposure to Testosterone# E8 D1 N% I) A' v2 Z
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2% U, b# ^9 Z- W" z
and Kenneth R. Rettig, MD1' |3 v$ r' x. G8 N- _/ g- X
Clinical Pediatrics
5 i, u, s4 V' B, F3 m2 G/ FVolume 46 Number 6% t1 r& h% g; W/ ^( I
July 2007 540-543+ E5 e8 a: [% D8 V
© 2007 Sage Publications
0 l8 B  A3 E, I0 n10.1177/0009922806296651
: K# f  C, e) k: E8 C* ~http://clp.sagepub.com4 _& q" w3 ?- ^: d$ U+ q, y
hosted at$ c) m: [; [5 ~$ _: M# Q3 v; Z
http://online.sagepub.com
+ H, _/ G: C) P- \' [& fPrecocious puberty in boys, central or peripheral,6 }4 z  C  `7 o2 J: }3 U5 ?. F
is a significant concern for physicians. Central
" W4 G- S5 ~, r1 V& lprecocious puberty (CPP), which is mediated
* C& M4 w' o+ i+ U- Mthrough the hypothalamic pituitary gonadal axis, has
7 Z6 s+ C& b# K) K/ Xa higher incidence of organic central nervous system
  [4 [0 N8 V% i6 i8 W2 v5 alesions in boys.1,2 Virilization in boys, as manifested
/ V8 l  ]  k/ r4 aby enlargement of the penis, development of pubic
! s" k- w. o. W- [$ ?hair, and facial acne without enlargement of testi-
& ^2 `. X( U4 N) z( R! Ccles, suggests peripheral or pseudopuberty.1-3 We1 W' V1 F3 A  S5 o& X) m8 X+ \
report a 16-month-old boy who presented with the
* }2 a- ^- L  ]& {enlargement of the phallus and pubic hair develop-8 j$ f% M0 m5 s9 ?. [- {' }+ B4 i
ment without testicular enlargement, which was due
. R) W& A: x) Wto the unintentional exposure to androgen gel used by
# p  n& a1 f) V, ~1 @& ^5 J; fthe father. The family initially concealed this infor-
" y- f0 ^/ d8 e( W3 N- kmation, resulting in an extensive work-up for this
6 y' Y, v9 ^; [9 G) wchild. Given the widespread and easy availability of
+ ^- y; H" R1 P7 }, n7 |* I5 ntestosterone gel and cream, we believe this is proba-, c& Q6 L/ i- Q
bly more common than the rare case report in the
" ~# r# L) S  E5 v( x% R+ Aliterature.4
  N% l: b% _  PPatient Report
+ Q# m1 R. W- {1 }! J2 RA 16-month-old white child was referred to the1 I! w6 E/ ~3 v$ v0 r* n
endocrine clinic by his pediatrician with the concern2 k3 X* x7 B5 K! j& a
of early sexual development. His mother noticed/ F5 O- [3 I) |1 [+ Q1 _; z, a
light colored pubic hair development when he was, M" l! `0 x& B/ V
From the 1Division of Pediatric Endocrinology, 2University of
& S6 \$ N5 Q- j2 {# b7 ZSouth Alabama Medical Center, Mobile, Alabama.: _* S! |# d" [0 {1 C9 q" B
Address correspondence to: Samar K. Bhowmick, MD, FACE," @" j- X0 C- D  Q
Professor of Pediatrics, University of South Alabama, College of6 j& Q) U) H- \- m" }7 p5 q3 G! x
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
5 ~  x% c' ^2 v- Ue-mail: [email protected].
4 f. l4 k4 t6 G3 Habout 6 to 7 months old, which progressively became& z. ~* Q/ c: K: V" O
darker. She was also concerned about the enlarge-9 H% d$ w+ B/ |4 B5 ^
ment of his penis and frequent erections. The child. }, D2 }' t6 s# y; M$ E3 r3 b1 E
was the product of a full-term normal delivery, with* Q) M2 \, u1 u: _' i( ^! b: }: L8 _0 p
a birth weight of 7 lb 14 oz, and birth length of; V3 C& Z6 ]+ @3 M: i6 V% E6 ~$ g
20 inches. He was breast-fed throughout the first year, H: w, ~, m! P- s) ?' u7 c
of life and was still receiving breast milk along with4 B3 `6 ~3 ]) G9 S
solid food. He had no hospitalizations or surgery,. y) e' H- r8 f
and his psychosocial and psychomotor development! T0 h. D2 H# w- e, G
was age appropriate.. L2 u1 t8 K8 }. K! h, J$ M
The family history was remarkable for the father,- V4 l7 V" j9 D2 j( ?
who was diagnosed with hypothyroidism at age 16,% b3 E  `- t0 ^2 ]) e9 m
which was treated with thyroxine. The father’s
- g% _1 x; n8 A9 _9 H# L* vheight was 6 feet, and he went through a somewhat
: D; I' W+ i4 E8 w# Q; Hearly puberty and had stopped growing by age 14.8 n4 u3 `! ~) X8 S2 n- p
The father denied taking any other medication. The
3 D& {5 l) h9 i! hchild’s mother was in good health. Her menarche. }4 I  b% }& W' Q4 [% E' R) I' M
was at 11 years of age, and her height was at 5 feet/ A5 u: Q" z8 F: C2 I3 |
5 inches. There was no other family history of pre-
0 j4 t' R9 m! [cocious sexual development in the first-degree rela-
  \' k4 R! w( f5 o$ f& ?tives. There were no siblings.
3 R  `. Y9 K5 i, L$ t7 E7 g- k  vPhysical Examination, N; f9 @. {3 J$ Y8 w# j3 p
The physical examination revealed a very active,2 \3 w1 c+ A( _/ v3 J
playful, and healthy boy. The vital signs documented( K: d7 n1 V8 O9 X
a blood pressure of 85/50 mm Hg, his length was! p4 P* P9 J3 V5 s. B1 B
90 cm (>97th percentile), and his weight was 14.4 kg
6 z/ g- V8 N" ]/ o, i2 H(also >97th percentile). The observed yearly growth* O9 G1 K8 C, U' R
velocity was 30 cm (12 inches). The examination of8 s5 r2 @2 p7 h' a% U
the neck revealed no thyroid enlargement.# g3 w. f" H' T% N
The genitourinary examination was remarkable for! S1 R( k- E& f; w) T
enlargement of the penis, with a stretched length of
6 n1 @5 }8 P7 k6 s" d8 cm and a width of 2 cm. The glans penis was very well6 J' J, ]" ?7 ^$ D, Z
developed. The pubic hair was Tanner II, mostly around
2 X$ |" v) {; }5401 H  E* ~3 u, z( d  J& h" F
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from' Q  S! S# Q: h  ^) O) a) p
the base of the phallus and was dark and curled. The! Z; h  T7 S8 i
testicular volume was prepubertal at 2 mL each.: q7 U. [& D3 _8 f
The skin was moist and smooth and somewhat, c8 s% F  `0 l% ^3 d
oily. No axillary hair was noted. There were no
  n+ }5 z& ^* u: H3 d2 Iabnormal skin pigmentations or café-au-lait spots.
3 G  m8 A/ \- r8 p! [Neurologic evaluation showed deep tendon reflex 2+/ A, F* J* d4 \" J" H# \7 ~4 i
bilateral and symmetrical. There was no suggestion
( i, k' D5 }, a, tof papilledema.5 P$ w( Z6 E# h- h: e
Laboratory Evaluation# E. p8 G7 P! U( P$ _9 M" v, }& N
The bone age was consistent with 28 months by1 E( V) q& @% C# v% c4 M& x7 ?
using the standard of Greulich and Pyle at a chrono-
9 ]. U: |2 f/ c8 p2 F3 llogic age of 16 months (advanced).5 Chromosomal7 o0 {/ P" m, D: e6 w' N
karyotype was 46XY. The thyroid function test
9 C1 l* _' k8 _: I2 O/ Pshowed a free T4 of 1.69 ng/dL, and thyroid stimu-! X2 C4 K% T" p1 A
lating hormone level was 1.3 µIU/mL (both normal).
* X% p6 [- ~2 x' c# T# Y* tThe concentrations of serum electrolytes, blood
# m$ x' K3 e! v3 ?; ~, Burea nitrogen, creatinine, and calcium all were
. Z+ _+ d' [* Q4 J  iwithin normal range for his age. The concentration: J! s9 \% h  P- d) r$ R$ [# M% ]
of serum 17-hydroxyprogesterone was 16 ng/dL7 [1 M$ X) s7 |  g4 ]& X
(normal, 3 to 90 ng/dL), androstenedione was 20( i( [- j, X7 n- a/ }" l8 t
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
8 F( e0 u7 m( s5 n# r+ kterone was 38 ng/dL (normal, 50 to 760 ng/dL),3 ~) b/ W  |( J1 f/ ?+ I: k
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
  Y& V  |$ H/ x, v49ng/dL), 11-desoxycortisol (specific compound S); I* B) b; x/ r9 r& j
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
6 I8 I7 ]$ {3 e/ \' m. l7 G) gtisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total5 O+ _, {! a. N: S6 p
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),) b1 d% i* z7 R7 }
and β-human chorionic gonadotropin was less than1 R3 j/ I) h+ J5 a% \& ?2 W
5 mIU/mL (normal <5 mIU/mL). Serum follicular
8 I; j) L7 C: estimulating hormone and leuteinizing hormone
1 A% w1 X/ `$ d* C' g( |concentrations were less than 0.05 mIU/mL
- x# h% q0 t* z( e/ R(prepubertal).
  e) y4 m3 D9 R, d3 nThe parents were notified about the laboratory
$ `1 b- m/ Z  q: n4 F3 G1 z6 zresults and were informed that all of the tests were
- }$ p( F- t4 X- E4 \& F2 Ynormal except the testosterone level was high. The
' J; h( q6 _" Bfollow-up visit was arranged within a few weeks to
. A" s0 J5 B: e. y" gobtain testicular and abdominal sonograms; how-. t; H% \, B& v+ t' _
ever, the family did not return for 4 months./ P/ _6 Y7 X' S8 q9 B
Physical examination at this time revealed that the
% l; q% U8 p9 o8 V) {child had grown 2.5 cm in 4 months and had gained" o3 z, [" c: y' p, |7 m, k
2 kg of weight. Physical examination remained
# D9 V/ d3 E/ q; p6 t* Q: Q( Z0 _unchanged. Surprisingly, the pubic hair almost com-
% o1 S: R. G) W, E+ L$ upletely disappeared except for a few vellous hairs at
5 K' Q* U- B" M7 J  gthe base of the phallus. Testicular volume was still 2; N2 Q) g% B+ r( E: W+ h
mL, and the size of the penis remained unchanged.% u1 \3 x: i3 Y& Q6 W( W/ E
The mother also said that the boy was no longer hav-
* k6 d) e7 {  Y: Sing frequent erections.; ]: g6 }5 r2 o+ {+ [8 L5 x$ a
Both parents were again questioned about use of) }2 Q/ `9 j. p% Z
any ointment/creams that they may have applied to
& M/ f$ V" o# u. `1 ~) {3 Tthe child’s skin. This time the father admitted the* ?4 ^7 B( w7 O1 [2 S4 `6 t
Topical Testosterone Exposure / Bhowmick et al 5411 V6 O6 ~0 Y4 P0 J0 k' l5 `
use of testosterone gel twice daily that he was apply-
% N: @8 ?5 h( F. }8 S5 Ning over his own shoulders, chest, and back area for
: k1 y" B/ P8 @: xa year. The father also revealed he was embarrassed
) D' @8 f8 y4 f9 Z3 Uto disclose that he was using a testosterone gel pre-
. b1 q4 j% U7 _5 a: P/ h+ w6 }scribed by his family physician for decreased libido
  b% t4 K  j1 o) g" e& J5 isecondary to depression.
& Z- W$ i, E' H) Y# }7 @The child slept in the same bed with parents.1 r% x7 q* f- E1 z* e3 C
The father would hug the baby and hold him on his
! x7 N3 z% J$ S' p& tchest for a considerable period of time, causing sig-
' A8 s3 D$ V$ Pnificant bare skin contact between baby and father.
3 x8 o) z6 F) Q: H! G' H  [/ xThe father also admitted that after the phone call,
$ ~' a$ x8 x  f+ hwhen he learned the testosterone level in the baby/ O, I( _2 u9 l7 ]0 K2 M
was high, he then read the product information0 F% J, `8 l4 c" V$ X
packet and concluded that it was most likely the rea-6 U  @2 n2 ~. g( V2 o8 N
son for the child’s virilization. At that time, they
+ R, d. j2 B. @. O6 G4 A" Xdecided to put the baby in a separate bed, and the
5 l1 I/ U* @1 }  q- ?father was not hugging him with bare skin and had5 ?" r2 [; M7 \
been using protective clothing. A repeat testosterone
! |# [/ r3 P( M& W; ]& t) `test was ordered, but the family did not go to the
* Z6 D/ v" V9 i# n& Claboratory to obtain the test.
' A2 F. q" g7 r1 j/ k) EDiscussion
4 H9 \6 u& s. c; ]Precocious puberty in boys is defined as secondary
8 k  ]7 X4 p5 |% E& `! l3 V0 K: s5 jsexual development before 9 years of age.1,4) }) c- u$ `' c% q6 s
Precocious puberty is termed as central (true) when
  Q4 W& q0 Y4 M) g) J& t, ]! kit is caused by the premature activation of hypo-1 F3 w) s8 P, M
thalamic pituitary gonadal axis. CPP is more com-
' Y1 O  Q" K6 J( C0 b5 l! umon in girls than in boys.1,3 Most boys with CPP
1 W) |! |0 W5 L; ~3 q% j5 N( xmay have a central nervous system lesion that is; f/ Y3 Q+ e8 \: {$ Z* z/ F
responsible for the early activation of the hypothal-+ D# W. R# \; r; l' H
amic pituitary gonadal axis.1-3 Thus, greater empha-6 I3 h, J: u8 Z5 W; A" s
sis has been given to neuroradiologic imaging in
7 H+ f3 R9 o6 Q* O  rboys with precocious puberty. In addition to viril-
" \3 n# z3 H$ l, R' ?4 r2 {" _1 iization, the clinical hallmark of CPP is the symmet-
* S0 \2 ~" ~$ q* ^rical testicular growth secondary to stimulation by
1 f) E; I0 Z/ n. \' R" Y( hgonadotropins.1,3
6 C# P; Z) o; `/ s( m) SGonadotropin-independent peripheral preco-
7 F# j6 ]  p/ A$ g# R' M; icious puberty in boys also results from inappropriate
  q0 h& u% `1 S/ m; mandrogenic stimulation from either endogenous or
, K) ?" g" n9 @1 [" Z- t9 M% `exogenous sources, nonpituitary gonadotropin stim-( |1 S+ e6 a/ c* C+ w5 f
ulation, and rare activating mutations.3 Virilizing# O: r& k  R8 ]  f
congenital adrenal hyperplasia producing excessive
8 h0 f& n  l. \* L" U  wadrenal androgens is a common cause of precocious
- v- V0 X$ n# o& b) u4 J3 R# apuberty in boys.3,4
1 ^: U) x: L6 YThe most common form of congenital adrenal
3 s* Q' M$ |+ Q% J; Bhyperplasia is the 21-hydroxylase enzyme deficiency.2 j6 X  @* Z, x* L! R3 J
The 11-β hydroxylase deficiency may also result in! l9 {2 g# A3 w7 H- z
excessive adrenal androgen production, and rarely,
8 a% R" i5 K6 A0 I1 x6 Zan adrenal tumor may also cause adrenal androgen
/ n* J: R2 q3 l; Y9 G9 `excess.1,3) ]# f" K/ r' p- m$ ^$ ]4 E
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
4 P+ K1 x2 h% w* ^542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
5 J% E% ]' x) ~: T' aA unique entity of male-limited gonadotropin-$ x  s+ G2 O  U
independent precocious puberty, which is also known- \' B5 @0 r; l. h: _
as testotoxicosis, may cause precocious puberty at a9 p* [& n0 \) [
very young age. The physical findings in these boys
. k; _1 V. A( r" O0 i7 h: W+ R' F7 ~with this disorder are full pubertal development,
2 d: A8 A$ `4 @% l9 _6 cincluding bilateral testicular growth, similar to boys( F  U# f7 y9 o$ r3 C* h
with CPP. The gonadotropin levels in this disorder
; A2 a1 e* ~5 X$ `5 V+ care suppressed to prepubertal levels and do not show
; F% R! n  V% j- _pubertal response of gonadotropin after gonadotropin-
2 t8 \0 }& ^2 e2 [5 \* n& _7 t% j# Creleasing hormone stimulation. This is a sex-linked( j4 G9 _- E6 O) Y: f
autosomal dominant disorder that affects only
" u' k! O  N1 @4 k2 {males; therefore, other male members of the family5 _% D: E+ s7 M7 X, G% o
may have similar precocious puberty.3
, u: R' a8 K# D+ c- b" ]8 y5 k0 eIn our patient, physical examination was incon-
, @9 u4 D; Z+ _2 z) Xsistent with true precocious puberty since his testi-
* `+ p) D( R; v4 wcles were prepubertal in size. However, testotoxicosis) ]0 }" @# ^: ?" n0 o8 g9 ]
was in the differential diagnosis because his father
' O. V% b1 W! k- R+ p1 dstarted puberty somewhat early, and occasionally,% s/ ]4 Z7 e$ |/ M! M0 q3 M' f$ X: y
testicular enlargement is not that evident in the
: `1 F* m) |( V$ m  n# Ibeginning of this process.1 In the absence of a neg-4 i" f: }& m* E# C6 B5 d
ative initial history of androgen exposure, our
( v9 t2 q% S+ a, p4 Z" G- g# Q3 hbiggest concern was virilizing adrenal hyperplasia,0 z$ S) H# Z, L# W7 ~: R
either 21-hydroxylase deficiency or 11-β hydroxylase
* |9 F6 p- [5 rdeficiency. Those diagnoses were excluded by find-
; |! s4 c( e9 G2 m; a$ h# Wing the normal level of adrenal steroids.( C8 S1 j( i* _4 k& {% [* J
The diagnosis of exogenous androgens was strongly
: F6 v& }/ {( {+ d% Tsuspected in a follow-up visit after 4 months because
/ F  {& ]( H' C. @0 y* G+ Tthe physical examination revealed the complete disap-
% Y' y$ b4 M* p' spearance of pubic hair, normal growth velocity, and
' C3 J1 G# V6 ~* w  ndecreased erections. The father admitted using a testos-
6 \, R1 C% j8 e. z. A4 U/ Iterone gel, which he concealed at first visit. He was
; z* S& h9 X3 x, P" S+ i$ kusing it rather frequently, twice a day. The Physicians’
$ q9 B7 q- Q$ p2 `: b  w+ G5 F: A. qDesk Reference, or package insert of this product, gel or0 T; z& }+ [8 `5 n
cream, cautions about dermal testosterone transfer to
! V% I" c( H( N  @! Hunprotected females through direct skin exposure.8 f1 N0 w: k2 x* I/ C7 l1 p
Serum testosterone level was found to be 2 times the: Y5 i4 W4 F8 a& `2 \0 [
baseline value in those females who were exposed to
+ E9 F- h& @' _) Ueven 15 minutes of direct skin contact with their male; y5 M" }4 q. n( D- y1 x3 ~
partners.6 However, when a shirt covered the applica-
* R: n7 }, K3 S: {5 ntion site, this testosterone transfer was prevented.
; n" q) R/ m# IOur patient’s testosterone level was 60 ng/mL,( o, P8 O0 O5 l+ p
which was clearly high. Some studies suggest that
+ b& ~& J" J7 G" Kdermal conversion of testosterone to dihydrotestos-1 h- J* B5 [. }# z6 }6 I
terone, which is a more potent metabolite, is more' n) j7 D" ^: v/ Z
active in young children exposed to testosterone& ^9 c( A( s2 C8 T
exogenously7; however, we did not measure a dihy-
. [8 N$ F# }7 A# r5 q( B: r) Qdrotestosterone level in our patient. In addition to
9 x1 p- r  |( [  _- d4 G4 M7 f+ avirilization, exposure to exogenous testosterone in% p# L' x5 P, ~
children results in an increase in growth velocity and
. E! S. G; P& T: C# ?advanced bone age, as seen in our patient.
+ l6 A' K- Z" s1 WThe long-term effect of androgen exposure during
7 G2 |; k" V- u: r! vearly childhood on pubertal development and final
- V  l* Z: D9 p, {% [adult height are not fully known and always remain! `) a$ ]! I0 T1 P( P! J
a concern. Children treated with short-term testos-. H8 o" i) {5 M& `) _* C
terone injection or topical androgen may exhibit some9 w, E' S0 w" c1 W5 F3 H
acceleration of the skeletal maturation; however, after: P# Y( K/ y  \, {
cessation of treatment, the rate of bone maturation
  n' B! X3 S* C; Adecelerates and gradually returns to normal.8,9
" ?9 F1 P: N4 e! B) z8 o3 w  bThere are conflicting reports and controversy5 u6 \1 D. G7 ?, ~6 r! [% E. `
over the effect of early androgen exposure on adult1 n4 ~6 [0 j: X$ E" T8 l) u7 a4 U4 C
penile length.10,11 Some reports suggest subnormal
* {+ v. I* [5 T% M0 _; _; yadult penile length, apparently because of downreg-% K. n* `( `; T# y+ R, A' I9 L
ulation of androgen receptor number.10,12 However,
4 C3 C% o* W+ C8 @Sutherland et al13 did not find a correlation between
) _! d9 |3 y) Y! g- r% achildhood testosterone exposure and reduced adult
$ _0 n5 v, _. ~5 [, @% kpenile length in clinical studies.
6 x# P1 E+ Y  sNonetheless, we do not believe our patient is  k6 b" U, b3 I+ C, J2 O5 R' x
going to experience any of the untoward effects from% e. R, M6 S! [3 a, o
testosterone exposure as mentioned earlier because" `( P6 S, g, M/ O
the exposure was not for a prolonged period of time.2 L  ]* r8 {4 C& Y" j( R
Although the bone age was advanced at the time of
; g1 N2 _: B; Y8 Sdiagnosis, the child had a normal growth velocity at
) {$ O$ O$ D8 x3 u/ u( Sthe follow-up visit. It is hoped that his final adult
" n6 W2 [0 u0 E7 [" H& T( oheight will not be affected.8 e$ [- ?) W! B/ e+ P/ J
Although rarely reported, the widespread avail-" f; z6 E! O2 L5 I+ L
ability of androgen products in our society may0 e$ R' l: e7 X, U
indeed cause more virilization in male or female
& S/ Z: B- c1 d. i0 K) \3 Echildren than one would realize. Exposure to andro-+ c7 S1 R( \% W, K* ^, m
gen products must be considered and specific ques-, Z3 Z- f$ \5 A+ k; V& i
tioning about the use of a testosterone product or
+ {* _; x( W1 f" X1 T1 ~5 C# V" Tgel should be asked of the family members during
2 P8 H, G; M: k0 {. Mthe evaluation of any children who present with vir-
. L4 J2 A: P/ O/ Z( tilization or peripheral precocious puberty. The diag-
- m: R1 q- d6 g$ Y: Y) [1 e; R) i" }nosis can be established by just a few tests and by. u! E4 b. S2 Q! w
appropriate history. The inability to obtain such a
5 y* c1 U+ o2 j; a+ ghistory, or failure to ask the specific questions, may) ^) F2 k6 `' ~0 v
result in extensive, unnecessary, and expensive" l& H+ N& D; {: s* ^: S6 a2 \
investigation. The primary care physician should be
( X$ V2 k  {5 Faware of this fact, because most of these children
$ X$ c' V: P, t. s7 {( Nmay initially present in their practice. The Physicians’- d( ?: {8 K5 c1 u
Desk Reference and package insert should also put a
1 Z( C/ {2 X* ?, k' Zwarning about the virilizing effect on a male or3 q$ \7 W" ^. A( \$ o8 E5 [+ E/ n
female child who might come in contact with some-+ g* y7 W6 n9 G5 Y
one using any of these products.
, a0 W" G8 l3 _1 @References
$ T4 Y# K4 N$ m6 L- n6 h; X1. Styne DM. The testes: disorder of sexual differentiation
- Z1 K- [( r! x& K! j+ v4 Dand puberty in the male. In: Sperling MA, ed. Pediatric
  o0 q, \7 u8 sEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;1 m. X; Z( b( I* J
2002: 565-628.# l' z3 o  e! w6 G: V, E
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious  z+ u" {& x  T+ o4 e1 ^  Y4 o2 U
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old2 M* M1 M" f* R, _
Boy Induced by Indirect Topical
$ ^4 _: D. F9 k9 K% c% k6 c: O* V2 t7 XExposure to Testosterone
4 Z! m2 _6 a! r" v  _( pSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
0 n  H$ `7 u5 J3 Xand Kenneth R. Rettig, MD1, L% L+ a8 C3 ?- R
Clinical Pediatrics
% w7 R  c. f5 j; @6 G; SVolume 46 Number 6
, p8 U' N0 h, c% J3 VJuly 2007 540-543! q; }4 Q  }: o2 M# ^
© 2007 Sage Publications
1 d! u- P& h/ R( Z1 M0 T7 M- R6 e: M4 S10.1177/00099228062966516 b/ R8 T& N, W* O* X, l
http://clp.sagepub.com! {5 t; u/ L" [+ L7 [9 v
hosted at1 |: |3 E* F( P- q, }
http://online.sagepub.com
" y; _$ Q' y! @3 U) yPrecocious puberty in boys, central or peripheral,5 c8 e& x7 f# ]6 _
is a significant concern for physicians. Central
( o# {# k" L1 r+ E" q5 U# Aprecocious puberty (CPP), which is mediated; J; X) @5 a  k. n! y9 e
through the hypothalamic pituitary gonadal axis, has
$ G* [. b" ]! j* o/ ^, ca higher incidence of organic central nervous system/ _6 J  k. w1 B6 U0 G0 ]8 ?
lesions in boys.1,2 Virilization in boys, as manifested: l$ l9 Q' }  t. p
by enlargement of the penis, development of pubic4 k  O# h; b: G8 m2 o
hair, and facial acne without enlargement of testi-
5 A* d* H' c8 X0 Rcles, suggests peripheral or pseudopuberty.1-3 We5 P' X( d  u7 o) `" `' d+ m
report a 16-month-old boy who presented with the
+ S: P0 H1 b" k1 h- O) @) w* Wenlargement of the phallus and pubic hair develop-4 u+ \2 O% O5 E
ment without testicular enlargement, which was due+ y2 X: p3 {! l) O
to the unintentional exposure to androgen gel used by
2 W$ M7 P9 h8 S5 i( z5 dthe father. The family initially concealed this infor-% F1 E& a% E- C0 ~7 }; E2 }/ w
mation, resulting in an extensive work-up for this
1 A' K& v/ N8 r: C) U% Hchild. Given the widespread and easy availability of
2 b  c- W5 o- R, X+ d! x6 u8 u) stestosterone gel and cream, we believe this is proba-
' i# b$ z1 W, i5 V7 J( e9 ^; vbly more common than the rare case report in the
) X- M6 `8 @* E: _literature.4  \8 y# |1 j+ |$ z! t+ T, E. G+ @
Patient Report
$ M9 m, [" V+ HA 16-month-old white child was referred to the
  L) r' @" W. i2 N) Nendocrine clinic by his pediatrician with the concern
7 \6 q! I/ c! P2 m$ d# uof early sexual development. His mother noticed5 K& D" f8 Y, G# G- c+ Y. |  x
light colored pubic hair development when he was
1 n; f: R9 e1 G6 C5 CFrom the 1Division of Pediatric Endocrinology, 2University of
/ [+ C, u5 p% z3 `South Alabama Medical Center, Mobile, Alabama.( ^; L" a# j3 }& x! d4 ]2 C
Address correspondence to: Samar K. Bhowmick, MD, FACE,3 f$ m# u' g8 D" b9 K
Professor of Pediatrics, University of South Alabama, College of
4 |- [( L) `8 U0 i7 K" PMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;7 P& `; c+ d0 F2 h' d) C  q
e-mail: [email protected].
8 `; G5 c" F- a5 o; |/ N' |8 s+ Xabout 6 to 7 months old, which progressively became
" r# B+ A8 p9 R- p; P  b: Udarker. She was also concerned about the enlarge-
# x  g3 ~$ z" h# H6 B! V: dment of his penis and frequent erections. The child9 q0 c8 n; |  D1 k
was the product of a full-term normal delivery, with
  a* t( ?- G9 {" t& ~# ea birth weight of 7 lb 14 oz, and birth length of5 K1 g" W' Z' N2 {* d: S3 K- X" s& C
20 inches. He was breast-fed throughout the first year
& M/ y& j5 v2 Z6 y% gof life and was still receiving breast milk along with9 H2 H0 ]- Z, f7 q2 T
solid food. He had no hospitalizations or surgery,1 ?" j7 d6 }9 i
and his psychosocial and psychomotor development5 ]3 J6 e! F1 |4 n# E7 ^! G
was age appropriate.: N" T/ Y, D3 V% I
The family history was remarkable for the father,' L0 ?% f3 j- n+ c/ G2 `( Q
who was diagnosed with hypothyroidism at age 16,3 P8 ]" k! I6 o; K8 b9 j
which was treated with thyroxine. The father’s' L8 U6 W. n1 Z  m
height was 6 feet, and he went through a somewhat' V9 Z8 A3 {. o
early puberty and had stopped growing by age 14.
6 d: x% u/ G, U: fThe father denied taking any other medication. The
) C. _8 i) ?5 x8 ichild’s mother was in good health. Her menarche
1 _6 G; b. ^1 c6 vwas at 11 years of age, and her height was at 5 feet4 Q/ I4 e9 V  w( z" C0 }1 G
5 inches. There was no other family history of pre-
4 |' {; @7 h6 X. J2 S$ qcocious sexual development in the first-degree rela-
2 c  ?$ m- v2 m7 jtives. There were no siblings.  Z& s7 r# N) |1 P' _* B6 l
Physical Examination
6 ~# }" c) r( j3 I+ KThe physical examination revealed a very active,2 [' N; `6 {5 [* A  g
playful, and healthy boy. The vital signs documented4 t/ K$ b9 E3 |8 }
a blood pressure of 85/50 mm Hg, his length was
# v! C: O6 N+ o: B- d+ v% X$ a. }90 cm (>97th percentile), and his weight was 14.4 kg
, H$ @6 n0 a' c(also >97th percentile). The observed yearly growth
3 X  f9 c3 S9 gvelocity was 30 cm (12 inches). The examination of7 ?* s; a! \; Y+ c
the neck revealed no thyroid enlargement.
9 |* u4 P% e- ?: W; }3 m( OThe genitourinary examination was remarkable for! d7 c9 u) D& l1 x
enlargement of the penis, with a stretched length of; W& o, W2 Q  [* z2 b
8 cm and a width of 2 cm. The glans penis was very well
  A3 a$ B2 V0 ?0 }% V1 Tdeveloped. The pubic hair was Tanner II, mostly around
( N( M$ K2 N* Q4 W9 W) `! |540  t% i" e% a$ w- T# c) n) Q$ N
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from! n! W9 o/ j! ]+ `& W( ~
the base of the phallus and was dark and curled. The
; v  c$ B% w. C! Htesticular volume was prepubertal at 2 mL each.
% H# j: [: y, Y3 ?% T' _; v5 fThe skin was moist and smooth and somewhat9 l& R2 _: z: v& Q# H% T
oily. No axillary hair was noted. There were no
8 ^8 H  \/ Z$ I- p. j* Iabnormal skin pigmentations or café-au-lait spots.+ f% R7 k: `5 t+ ]$ x/ D
Neurologic evaluation showed deep tendon reflex 2+
9 M0 \+ U0 a" ~. y( \bilateral and symmetrical. There was no suggestion
% [# g$ Z8 E' a) k# m, f" b  {of papilledema.9 n1 Q% u5 s& K5 x# T6 [
Laboratory Evaluation3 X$ j/ o7 X/ I
The bone age was consistent with 28 months by
8 t# f* p1 c% o: G0 }' Husing the standard of Greulich and Pyle at a chrono-4 D& h" N0 a& I: Z* q
logic age of 16 months (advanced).5 Chromosomal
4 W( F* p; k8 w% Y) dkaryotype was 46XY. The thyroid function test
  J3 t2 t9 M! m& D2 I6 Q: Ishowed a free T4 of 1.69 ng/dL, and thyroid stimu-
# R& C3 O9 w0 A8 V* E7 f; j" r( t/ [lating hormone level was 1.3 µIU/mL (both normal).
; h) k" Y1 h( r! sThe concentrations of serum electrolytes, blood
1 e8 P2 Q! i) z' Xurea nitrogen, creatinine, and calcium all were& J. U3 _4 D8 f! _* P4 @' Z
within normal range for his age. The concentration
2 e$ G1 J  j" r1 `0 y+ F" w% Xof serum 17-hydroxyprogesterone was 16 ng/dL9 V) f8 Z# s7 l+ }
(normal, 3 to 90 ng/dL), androstenedione was 20
% x' }  Z, ?6 s# v3 b5 Ing/dL (normal, 18 to 80 ng/dL), dehydroepiandros-% ~6 a; a3 v2 f- M" W$ T
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
  c. H: j, F) |+ E# Odesoxycorticosterone was 4.3 ng/dL (normal, 7 to% \% C- k9 S6 o! d
49ng/dL), 11-desoxycortisol (specific compound S), T( i- P  K$ _. }; e# L/ N- D
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-. H) x9 s' [6 i! ]
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
5 x# S* c) Y4 [8 t$ @: [testosterone was 60 ng/dL (normal <3 to 10 ng/dL),8 Y$ k. p0 J9 W; t
and β-human chorionic gonadotropin was less than  G! c2 C7 v6 @7 M2 A5 e4 t" G2 x3 I
5 mIU/mL (normal <5 mIU/mL). Serum follicular+ f# S7 Z; G( |7 g* I
stimulating hormone and leuteinizing hormone& }) P/ t1 W7 M  h$ Z
concentrations were less than 0.05 mIU/mL" A; Q% ]9 V$ w/ J- s" h/ m8 N
(prepubertal).; m  M% i5 f& v7 i. Q3 R+ x: u
The parents were notified about the laboratory
9 I7 i/ P4 _- ^% B* H4 F5 yresults and were informed that all of the tests were0 [& e# D; l0 l8 I
normal except the testosterone level was high. The3 I2 j4 L  j. S$ C' E* z
follow-up visit was arranged within a few weeks to
1 z5 Z5 @2 ~1 c" n* B- K% ?obtain testicular and abdominal sonograms; how-
, Z" C; l# T- b* r6 Oever, the family did not return for 4 months.9 O" h  _4 T  Y. W- Q- g
Physical examination at this time revealed that the
3 I  ~- J( A6 R; C+ ~% gchild had grown 2.5 cm in 4 months and had gained5 Z/ j5 e4 v/ H: d" _
2 kg of weight. Physical examination remained
2 m" c5 g  ^( ?/ k# G' dunchanged. Surprisingly, the pubic hair almost com-
  Z# D& a  l2 S2 F, X2 }' epletely disappeared except for a few vellous hairs at
# ?4 L: `' [$ ~3 Sthe base of the phallus. Testicular volume was still 2
% S" I1 m# W2 y7 c' a/ w; AmL, and the size of the penis remained unchanged.
& M6 u& `4 j. W1 Y9 a) z" C/ GThe mother also said that the boy was no longer hav-
5 m* l1 Y( {4 T1 D) p( u* w% Bing frequent erections.1 R* B$ I0 U* r, h  s
Both parents were again questioned about use of9 {5 ^, t6 ^4 i1 \
any ointment/creams that they may have applied to
1 q$ l: M2 t0 hthe child’s skin. This time the father admitted the
2 B: X3 b4 ]" aTopical Testosterone Exposure / Bhowmick et al 5417 e6 y% m  s! D2 I- v3 h
use of testosterone gel twice daily that he was apply-
+ H5 A3 u4 S/ W: D0 }% e. @ing over his own shoulders, chest, and back area for; e) Q& Z; \$ }! d
a year. The father also revealed he was embarrassed) `0 M/ Z, E4 \% F* j
to disclose that he was using a testosterone gel pre-3 b8 [/ E) K; I1 k0 F; b3 i# B
scribed by his family physician for decreased libido
, B# O) G) Y0 ]" Z4 c* ]% \secondary to depression.6 o2 V1 _- f/ p1 a. o! `0 m' f
The child slept in the same bed with parents.
- N: r5 ]. H: A+ BThe father would hug the baby and hold him on his
- @" O. |7 `* S1 t* [, Q' @$ echest for a considerable period of time, causing sig-
6 w# M1 x$ f( k  C$ B% Vnificant bare skin contact between baby and father.
3 f3 p  D- ~7 D  b9 q- OThe father also admitted that after the phone call," O/ z: L: _4 g7 t: ?6 }
when he learned the testosterone level in the baby
: A, Q. h( O, n# V2 owas high, he then read the product information. m( b0 ]" S* q# X7 e1 `) \) F: W
packet and concluded that it was most likely the rea-1 }6 e. W& \" X" u( l
son for the child’s virilization. At that time, they2 B6 q9 i; R, {0 O
decided to put the baby in a separate bed, and the! M! _3 y7 B  C8 g( V% B
father was not hugging him with bare skin and had
3 i6 V) F/ m& X$ m* F, W  ibeen using protective clothing. A repeat testosterone
# S( y; Z! I2 M5 l1 @; ^test was ordered, but the family did not go to the
% L6 x$ U& O% F9 Mlaboratory to obtain the test.
" e  t+ w) A2 MDiscussion
  R' |# b1 J0 S% u; u6 Y+ WPrecocious puberty in boys is defined as secondary
9 Q) ?3 M: X. q9 A/ tsexual development before 9 years of age.1,4
) K! I& x; D& _/ OPrecocious puberty is termed as central (true) when
, \9 v) [9 B! i' yit is caused by the premature activation of hypo-
6 K& L) o. `; d) F* J* rthalamic pituitary gonadal axis. CPP is more com-
0 K# `* U2 K* u7 r  J5 ymon in girls than in boys.1,3 Most boys with CPP, }5 {( `6 j! H
may have a central nervous system lesion that is
; p0 G) A7 [4 s9 F- Iresponsible for the early activation of the hypothal-) _/ A0 a" {% c; \' F
amic pituitary gonadal axis.1-3 Thus, greater empha-
0 e$ a& C: Z' z/ S4 s# J  Osis has been given to neuroradiologic imaging in: x% R! |# ^! g7 A4 j
boys with precocious puberty. In addition to viril-
( U4 u; \$ M8 }ization, the clinical hallmark of CPP is the symmet-
3 h# K: U2 e+ ^rical testicular growth secondary to stimulation by8 T) O% d$ k0 F( z- V5 ~# d
gonadotropins.1,3
% M, y; ]+ j+ X" w& u& }Gonadotropin-independent peripheral preco-
) |* Y& O2 G+ Y$ l) n; }& [; zcious puberty in boys also results from inappropriate
2 J4 n( M& l7 L# z1 kandrogenic stimulation from either endogenous or
0 w$ V/ Q$ n2 S6 n2 M7 @exogenous sources, nonpituitary gonadotropin stim-' Z# E) c& x% H: k/ K! u
ulation, and rare activating mutations.3 Virilizing
; A2 T. G5 I% ^' z3 Ncongenital adrenal hyperplasia producing excessive- y! `2 N" I0 c
adrenal androgens is a common cause of precocious- P2 o/ L9 G  B5 `$ E
puberty in boys.3,4) R" a$ f( U# b2 x% b# b5 E3 i
The most common form of congenital adrenal* q9 q- J  ~$ _& ^  y
hyperplasia is the 21-hydroxylase enzyme deficiency.4 Y  a# v- r. {2 A- |
The 11-β hydroxylase deficiency may also result in" M4 `# ~7 z1 w8 Q8 s1 h: V. t
excessive adrenal androgen production, and rarely,% r* D! _9 M7 ]! N' ]% h  {4 Y5 U
an adrenal tumor may also cause adrenal androgen3 [+ r1 W; J, i9 S
excess.1,3/ ]7 }; [2 S, Q, s
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from, d0 H) u; ^( Q! W( n+ h3 k8 u2 @
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007, c* H, l% \$ k+ g; Q
A unique entity of male-limited gonadotropin-. ^& |' x" G3 ~
independent precocious puberty, which is also known+ @& ]; e2 }! P4 f
as testotoxicosis, may cause precocious puberty at a
8 Y3 r  x# N: b% ^very young age. The physical findings in these boys/ H0 i4 l# R+ G
with this disorder are full pubertal development,
. _: \6 o# t; B5 T( M, s! Gincluding bilateral testicular growth, similar to boys
: q* t6 R) k; Z; ~' w( ^% zwith CPP. The gonadotropin levels in this disorder- R/ E) z; M+ X2 @, ]" h0 F
are suppressed to prepubertal levels and do not show) ?/ w* `) {7 w7 \
pubertal response of gonadotropin after gonadotropin-$ l  m& U" K* c! X, O. U! y
releasing hormone stimulation. This is a sex-linked
0 w/ \% {0 k3 F4 K3 Vautosomal dominant disorder that affects only
8 G! k/ O  l) X$ Wmales; therefore, other male members of the family' h: ~6 d6 V/ b) W
may have similar precocious puberty.3
; `/ B5 X* u9 u: I/ i8 gIn our patient, physical examination was incon-- X1 q+ i' \; o/ m
sistent with true precocious puberty since his testi-9 @, e# x- J7 w! s: a
cles were prepubertal in size. However, testotoxicosis- ~4 H7 J" G5 ~. K  v
was in the differential diagnosis because his father5 s4 q' v: I5 ?* o& q" y
started puberty somewhat early, and occasionally,$ q  w! Y7 X1 t6 x4 b% K
testicular enlargement is not that evident in the
. A9 B9 a. I( e% n9 N5 f3 wbeginning of this process.1 In the absence of a neg-
  Y7 h# e3 x9 sative initial history of androgen exposure, our
% m9 X' p8 K8 a) t; ^7 z" P! Mbiggest concern was virilizing adrenal hyperplasia,
1 u/ U0 P& {/ D* B& oeither 21-hydroxylase deficiency or 11-β hydroxylase
: c! _7 k" A: h- \0 N% Xdeficiency. Those diagnoses were excluded by find-6 `8 c( ]* P& \0 ?9 Z1 e4 K
ing the normal level of adrenal steroids.
* z2 Z% {1 b8 Q% ]+ _! ?  ?& H3 oThe diagnosis of exogenous androgens was strongly$ e% H& T1 h' F- \
suspected in a follow-up visit after 4 months because/ D  j' G2 T2 A9 m# K; w
the physical examination revealed the complete disap-  a5 J3 p: p2 A3 ^6 F
pearance of pubic hair, normal growth velocity, and1 d2 h( [% B0 s' X; a5 R# q% }, z
decreased erections. The father admitted using a testos-8 s' i; Q' u6 ~- N
terone gel, which he concealed at first visit. He was
6 Q; K0 b" b9 X. z9 I, D( T; V# C/ Iusing it rather frequently, twice a day. The Physicians’1 L6 F. ^/ j# e: ~9 k
Desk Reference, or package insert of this product, gel or
0 `, {& d0 I8 s8 `( t) c0 ?cream, cautions about dermal testosterone transfer to) [* }* @) `" P! m3 T
unprotected females through direct skin exposure.
# A  B7 t) G% I* @, pSerum testosterone level was found to be 2 times the6 p4 k8 }  ~$ u3 f( A
baseline value in those females who were exposed to
3 D% h* o- @! G; Geven 15 minutes of direct skin contact with their male1 u: y$ m* J) [. C% C
partners.6 However, when a shirt covered the applica-
+ g. q& `; A( o$ e$ [  M4 P/ Gtion site, this testosterone transfer was prevented.) w0 b3 Q& I. Z* Q1 S5 z0 m
Our patient’s testosterone level was 60 ng/mL,
4 g! k$ \1 `6 Y- A# Gwhich was clearly high. Some studies suggest that2 O9 a5 r# u: s2 H  u; {2 _1 @& X
dermal conversion of testosterone to dihydrotestos-# s+ h$ _! N; U
terone, which is a more potent metabolite, is more
- m( y. N1 V: ~8 j6 R" a$ p# O/ y3 aactive in young children exposed to testosterone" V% E! m) P" f  N! p  H
exogenously7; however, we did not measure a dihy-
6 T- k7 e2 H' n) Qdrotestosterone level in our patient. In addition to
4 D8 H( A! a6 z2 {virilization, exposure to exogenous testosterone in
& w5 b0 b. x+ W0 ochildren results in an increase in growth velocity and
9 |1 P1 A5 S6 ^: I% ^advanced bone age, as seen in our patient.
1 e& O! S7 \1 yThe long-term effect of androgen exposure during
; ?4 U& Q& e3 j! Bearly childhood on pubertal development and final
2 X) o; a8 a4 n( R; B3 T8 F; Aadult height are not fully known and always remain7 z5 ]3 X& O% V, S" _
a concern. Children treated with short-term testos-; k0 Z7 E+ O$ u, |% L
terone injection or topical androgen may exhibit some$ p9 i" G# |( H4 m# ?; s7 O( `% E
acceleration of the skeletal maturation; however, after: a) m  }! y  q$ i) Z2 Y
cessation of treatment, the rate of bone maturation6 V5 s, f* M, W4 K* \
decelerates and gradually returns to normal.8,98 |! N1 w2 J. g3 |7 D
There are conflicting reports and controversy- c9 W* d+ p2 z8 W* \- S2 c- C+ @0 S
over the effect of early androgen exposure on adult
4 m8 B! I9 {  x. v" ~1 qpenile length.10,11 Some reports suggest subnormal
+ d5 y( r; w- m: R' Radult penile length, apparently because of downreg-
6 k% F& d( M' }: G- c8 xulation of androgen receptor number.10,12 However,$ T' ~% I$ p8 {4 t( \% m  @: v
Sutherland et al13 did not find a correlation between1 c$ d1 X# z7 n' R$ A  t" B
childhood testosterone exposure and reduced adult6 _- q* Q/ H' B
penile length in clinical studies." l9 V* o& F7 h+ L8 R
Nonetheless, we do not believe our patient is
1 P# S& ]9 j2 Z9 ^! ]5 rgoing to experience any of the untoward effects from% ]: k- E0 Y& `8 s
testosterone exposure as mentioned earlier because6 z  N5 Y. q! i  q
the exposure was not for a prolonged period of time.
5 t( Y. A* K" |8 V- m. RAlthough the bone age was advanced at the time of, Y- o/ X! G8 K: [9 ?2 i# ?0 s& }& m
diagnosis, the child had a normal growth velocity at
, y( C. j( x- c4 T% @3 athe follow-up visit. It is hoped that his final adult$ o) H% X3 V9 U% G
height will not be affected.
0 c% d" h( f, k0 H" T( bAlthough rarely reported, the widespread avail-! V& K2 M/ n. q- n- a) }
ability of androgen products in our society may
! K% \, B8 |( i2 _/ H. b; S" ?8 ^indeed cause more virilization in male or female1 @( v, N% r; g4 g$ v* N7 n6 H" K' Q
children than one would realize. Exposure to andro-5 |4 c0 o* g) _5 S
gen products must be considered and specific ques-( n% R  S8 n: X! \, ^5 O
tioning about the use of a testosterone product or4 W( a7 n& k4 d0 V" }
gel should be asked of the family members during
6 I9 M& ?: i1 E* o1 w6 F7 Pthe evaluation of any children who present with vir-
) J! v8 ]0 f- x* p( M! q2 }# Tilization or peripheral precocious puberty. The diag-
  l% }) B8 e' a9 n3 W" l1 u1 I* qnosis can be established by just a few tests and by$ D* g( X9 G9 {4 S1 t% r, ]- Z
appropriate history. The inability to obtain such a( G  j7 Q3 T/ p# b& R
history, or failure to ask the specific questions, may
4 [% a2 w6 Z" m, l% A) Kresult in extensive, unnecessary, and expensive
. m0 f8 G) d. q3 ]investigation. The primary care physician should be$ O3 m3 J* ~% {; e
aware of this fact, because most of these children
$ M! Y% N0 r- q! T3 [may initially present in their practice. The Physicians’
! t& g) \" N3 ]2 e, W5 h: cDesk Reference and package insert should also put a' b# o- ^9 i: f: z# J
warning about the virilizing effect on a male or3 V7 c& P* |  \" a6 y7 Q
female child who might come in contact with some-
: g( m. Q0 L% aone using any of these products.
' o& X' z/ X0 `9 h2 XReferences
4 i) V: X# R8 a" t4 @1. Styne DM. The testes: disorder of sexual differentiation
! |: @2 \; H+ D5 h! `: ?and puberty in the male. In: Sperling MA, ed. Pediatric+ Q2 K/ m- _. b, ?0 C% l
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;( u1 c3 L9 N6 F2 |3 E0 M! J2 S1 D
2002: 565-628.
  p. X  M0 ]. Q8 o$ r; n* ~2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious9 [6 @* f# V, W; S7 H
puberty in children with tumours of the suprasellar pineal
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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
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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

- s, @& A( ?& F+ w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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