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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
9 c3 f( P; _6 Z( O% h/ lBoy Induced by Indirect Topical# L0 ]6 c3 `4 g9 i9 o# s
Exposure to Testosterone  ?4 S3 O* T5 @6 q$ ~; j, E8 |; U
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2, L9 b5 Z$ W7 u3 `' V; B' Y/ V- R
and Kenneth R. Rettig, MD1
; u+ \) q- n, aClinical Pediatrics# h( l0 x# C1 _# O
Volume 46 Number 6
6 X4 o# I! B  h# x9 D& AJuly 2007 540-543; R/ _1 Y- h( L5 t
© 2007 Sage Publications5 u, C+ Y6 w6 Y) g, g( L5 k6 |
10.1177/0009922806296651
* a# ]9 A4 T  }9 Xhttp://clp.sagepub.com7 F# Q' ], n8 D) Z* ?) z
hosted at& w2 S4 ^0 c: D/ H6 K& U  i" {
http://online.sagepub.com& j& W4 w& O4 \. x
Precocious puberty in boys, central or peripheral,
' p/ k/ Y/ v, w8 g, D5 tis a significant concern for physicians. Central& N0 c1 V$ Y6 n% Z2 {
precocious puberty (CPP), which is mediated6 ^0 U/ H6 V  j4 I
through the hypothalamic pituitary gonadal axis, has
7 t+ z  }" A. h  o% p. [! q2 v' ya higher incidence of organic central nervous system
5 U, _8 n. K' T5 z( ?  C( R' l" @lesions in boys.1,2 Virilization in boys, as manifested* [2 C; q- K& i+ q, j4 r. T
by enlargement of the penis, development of pubic
  p& o& _1 v. v( y& c" Shair, and facial acne without enlargement of testi-
5 Y0 X) o6 F) j. G" H3 `$ lcles, suggests peripheral or pseudopuberty.1-3 We1 i9 X* q/ g- T
report a 16-month-old boy who presented with the
% [5 \8 I9 }7 {" o+ `9 ]enlargement of the phallus and pubic hair develop-
" _7 ~6 e. ?3 H2 a& zment without testicular enlargement, which was due
( I5 ]# C* u: p- u9 Rto the unintentional exposure to androgen gel used by
+ p! K5 s7 y  |; n$ Kthe father. The family initially concealed this infor-' H) `1 k8 s5 ]: {6 \
mation, resulting in an extensive work-up for this$ F9 [* d2 n8 o' ^( d. t
child. Given the widespread and easy availability of5 y2 o* j/ G' `: J5 F) b
testosterone gel and cream, we believe this is proba-/ z- x8 S5 T1 I
bly more common than the rare case report in the
2 O1 g0 }0 ?2 L: f7 o3 V+ @literature.49 v; |9 [& R* [. c6 J
Patient Report
6 _) e+ m2 m) q5 o. ~A 16-month-old white child was referred to the
' @/ u3 h  O) _endocrine clinic by his pediatrician with the concern
( Q8 y$ V+ \5 p% C" Iof early sexual development. His mother noticed
1 @+ E$ P0 i% b. Z& \1 r6 \. |light colored pubic hair development when he was
. ]" O& q4 B6 }% ]" W) LFrom the 1Division of Pediatric Endocrinology, 2University of% L$ e& Z/ j# r9 s0 \' W
South Alabama Medical Center, Mobile, Alabama.% G- J; B9 _* q3 s1 n
Address correspondence to: Samar K. Bhowmick, MD, FACE,
) m' @: J) @& L3 g0 iProfessor of Pediatrics, University of South Alabama, College of  @  G5 V/ e2 N2 M. M' c8 K9 H
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;+ N' l1 e& @& S: ]
e-mail: [email protected].- l" R! o. t% ]
about 6 to 7 months old, which progressively became1 H* [5 b/ [) ?( [9 D
darker. She was also concerned about the enlarge-
. r) c6 v% m# i" Wment of his penis and frequent erections. The child
  s3 @- f. s7 p4 \: n6 s) Kwas the product of a full-term normal delivery, with
/ e0 |0 x. p6 ]a birth weight of 7 lb 14 oz, and birth length of& _7 N9 k" A3 d; k
20 inches. He was breast-fed throughout the first year
" k) n0 ]8 P2 k! J& Z/ aof life and was still receiving breast milk along with
5 r7 |! R/ Y1 V' e% zsolid food. He had no hospitalizations or surgery,1 s# @7 Y* W+ m5 |3 [
and his psychosocial and psychomotor development* t8 u) U) z- h6 h, Q, I! L! h
was age appropriate.
; u; z$ ~; P) {1 E8 D3 M6 r7 TThe family history was remarkable for the father,% C# o8 C8 z2 L& S+ u& D- d
who was diagnosed with hypothyroidism at age 16,8 A. B' b9 T6 K+ n
which was treated with thyroxine. The father’s
3 E3 {: S, d' V4 fheight was 6 feet, and he went through a somewhat
( u! }9 ]) q3 e" wearly puberty and had stopped growing by age 14.% }/ }& ^' O5 K$ n- w8 T) m0 l5 h' _
The father denied taking any other medication. The1 t: o! U6 k' k# `; W0 C
child’s mother was in good health. Her menarche
5 |0 \; X9 l7 O  C+ uwas at 11 years of age, and her height was at 5 feet) _7 I6 w2 n' n6 f+ f) U, V3 m' A
5 inches. There was no other family history of pre-$ I" n) v* N& p% I) r
cocious sexual development in the first-degree rela-
  d! Z2 j5 Y" }: ^' Ktives. There were no siblings.3 N( P: @% P9 f# ~
Physical Examination
0 k4 U: h" J" W7 z4 tThe physical examination revealed a very active,5 T2 Y/ e* Q2 B3 H0 l- x" `. P
playful, and healthy boy. The vital signs documented/ h  B! e* R2 A  o/ {! f2 d1 N
a blood pressure of 85/50 mm Hg, his length was
2 s  |+ C# T1 E8 p1 z- }0 _/ ?( ~7 E90 cm (>97th percentile), and his weight was 14.4 kg1 P2 |, p+ |( D6 H, }. ~
(also >97th percentile). The observed yearly growth
- p7 [! M* i( T  `' f5 a3 x' Uvelocity was 30 cm (12 inches). The examination of/ D" H' [) \, N5 ^9 g7 [
the neck revealed no thyroid enlargement.  x  N1 T7 n+ [- H! B
The genitourinary examination was remarkable for- q1 a4 W3 W# h4 y8 q5 U- V; c
enlargement of the penis, with a stretched length of' {( Z2 w2 i3 k& ]
8 cm and a width of 2 cm. The glans penis was very well0 {# T8 ?- h' b% b+ A
developed. The pubic hair was Tanner II, mostly around
7 m. [9 u. s7 S* A, K5402 |- u3 _: S: K; @
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from  Y  Z2 k$ {+ c; K2 G" ^( i
the base of the phallus and was dark and curled. The
# v. a' c! _+ Z; \* b# wtesticular volume was prepubertal at 2 mL each.- ~5 Q. \) S) K3 h. O3 p; Q
The skin was moist and smooth and somewhat
# F  H+ W8 X' v* o: c7 Q; ^oily. No axillary hair was noted. There were no
+ _% _1 c& L! R0 kabnormal skin pigmentations or café-au-lait spots.; r5 t5 m" l4 p- C- u
Neurologic evaluation showed deep tendon reflex 2+
# c" [$ X! ~8 u3 obilateral and symmetrical. There was no suggestion
& u! R" g7 b, i/ o8 Xof papilledema.1 m8 ?% p+ F1 ?! [( |# g; M1 s
Laboratory Evaluation% U+ x9 c  w3 ^
The bone age was consistent with 28 months by, H. P4 g- L8 K' w
using the standard of Greulich and Pyle at a chrono-
& Z' T, V% H9 q0 u& g9 J8 F+ ologic age of 16 months (advanced).5 Chromosomal
$ R1 g6 z0 Y- a- m) }karyotype was 46XY. The thyroid function test% {0 o/ x. y# i9 b0 K
showed a free T4 of 1.69 ng/dL, and thyroid stimu-/ e6 S7 ?1 |9 Y3 R& t! c
lating hormone level was 1.3 µIU/mL (both normal).
. Q9 i% s! l0 C1 \& MThe concentrations of serum electrolytes, blood
! E9 n4 F6 Y! a/ E/ iurea nitrogen, creatinine, and calcium all were6 ?; M3 v5 N6 o7 W8 s% P
within normal range for his age. The concentration
  l. L2 }2 E$ e* U5 Dof serum 17-hydroxyprogesterone was 16 ng/dL6 g" k: l# Q! n* A% U* e. T! E
(normal, 3 to 90 ng/dL), androstenedione was 20
# V; w3 g# M* A% [4 g& t! Sng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-+ u# C: L/ ]& @, j* m2 Y1 R
terone was 38 ng/dL (normal, 50 to 760 ng/dL),' @+ L0 S$ }4 X( C: S- @$ m
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
, ?) G( |2 N7 H9 F0 N1 W7 M49ng/dL), 11-desoxycortisol (specific compound S)% T9 t" M' a+ l3 |" T
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-% O5 c, b3 m7 h. p* J/ S
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total$ g/ A2 x7 z: a2 T% P- A
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
5 W! B4 \: c2 \and β-human chorionic gonadotropin was less than
/ l$ K: Z- \$ w0 w, B( s+ {6 {3 Q6 A5 mIU/mL (normal <5 mIU/mL). Serum follicular5 J8 K% v, a# X3 B
stimulating hormone and leuteinizing hormone
" p5 W: J7 [) W- ~  Qconcentrations were less than 0.05 mIU/mL
2 T( m7 T  A$ }(prepubertal).) `. |, W9 `' G
The parents were notified about the laboratory' P. H2 [& }+ Z2 u
results and were informed that all of the tests were
. `* q0 V# h; k& i$ Y4 Qnormal except the testosterone level was high. The
) n7 a% D, l, [8 b) K; ]follow-up visit was arranged within a few weeks to* I" [/ P* d1 r' m; {
obtain testicular and abdominal sonograms; how-
$ ^8 b$ q$ @& R3 F- K$ mever, the family did not return for 4 months.* L3 q2 b( i- b: A! u
Physical examination at this time revealed that the
* C0 `. M( u- Y' D. zchild had grown 2.5 cm in 4 months and had gained2 B" p& F! |! A" f
2 kg of weight. Physical examination remained1 D, U7 f/ a7 `1 v
unchanged. Surprisingly, the pubic hair almost com-: s/ r6 I) e( X0 W" A# {
pletely disappeared except for a few vellous hairs at9 X, a1 _6 S3 `# d% V! z
the base of the phallus. Testicular volume was still 25 ^# [& p& S  B- S/ z; V
mL, and the size of the penis remained unchanged.
2 w9 m( Q( ~# w2 HThe mother also said that the boy was no longer hav-
9 ]! [; T. S$ |/ ]3 ?$ zing frequent erections.
& r, Y+ w* }6 A0 T" t1 LBoth parents were again questioned about use of7 B7 [  t0 ?% M
any ointment/creams that they may have applied to
0 v7 X2 T+ b+ c( _; R( jthe child’s skin. This time the father admitted the' P2 `/ T: ?' e( _" e
Topical Testosterone Exposure / Bhowmick et al 541; G0 D* ]9 P0 q/ j0 ?+ ^. w- T# c
use of testosterone gel twice daily that he was apply-
/ Q1 X9 J) o" J% `' b; W- \# Ging over his own shoulders, chest, and back area for
" D6 F7 D" n& W& \/ n! I4 Ja year. The father also revealed he was embarrassed
' L/ x; {% }% p% u6 }* Qto disclose that he was using a testosterone gel pre-
% U0 v4 P# k0 \scribed by his family physician for decreased libido0 s, ^; U. I1 Z7 V  w+ }; s
secondary to depression.5 _$ Q2 V! f& }
The child slept in the same bed with parents.) g( I1 C2 t- N+ }
The father would hug the baby and hold him on his0 f5 e- Q' V) i1 V/ s
chest for a considerable period of time, causing sig-! p0 Z) Y& `6 q$ @0 |% @
nificant bare skin contact between baby and father.
6 ]/ v6 \) w2 f# N) R! @The father also admitted that after the phone call,' `+ n( v# G7 x
when he learned the testosterone level in the baby+ r' ~- d/ r' o; _
was high, he then read the product information, r% O# y, j' x! Y
packet and concluded that it was most likely the rea-# S5 z" H& x: a$ u% B
son for the child’s virilization. At that time, they1 P, C# x" r5 k" g* c/ q
decided to put the baby in a separate bed, and the1 c$ Y( ?5 z* ?' }, T  c) z4 M
father was not hugging him with bare skin and had8 N' Q: F+ }* j. W. k
been using protective clothing. A repeat testosterone
6 ~; O- z8 i+ [9 `% M" Vtest was ordered, but the family did not go to the# X+ Q" k; |- `
laboratory to obtain the test.
6 U6 m$ u0 d4 i' N. hDiscussion; u; W9 H3 [0 ^2 }% n& y
Precocious puberty in boys is defined as secondary& \3 t( h& l- ?: t! ^" B
sexual development before 9 years of age.1,48 e4 F7 X# S6 L" e
Precocious puberty is termed as central (true) when
& g6 O' Q  {8 C0 n: [! V+ \it is caused by the premature activation of hypo-- D2 d! L: ~6 f, [7 h8 I
thalamic pituitary gonadal axis. CPP is more com-  C' B( G# K9 d4 V6 U" h- f
mon in girls than in boys.1,3 Most boys with CPP
( y' L) y. k* T! imay have a central nervous system lesion that is
! s7 d0 U0 F) N9 d$ presponsible for the early activation of the hypothal-
/ c& z. P9 l) }5 b* q# r+ l, eamic pituitary gonadal axis.1-3 Thus, greater empha-
0 v  j4 r) U$ X6 {' Ysis has been given to neuroradiologic imaging in/ c) g  j) t  K
boys with precocious puberty. In addition to viril-
& h$ ]1 G& c& K5 }ization, the clinical hallmark of CPP is the symmet-$ l: i" f, _4 m
rical testicular growth secondary to stimulation by
( P* X" d# H3 {7 b3 _gonadotropins.1,3$ W! G. J( }" o: K3 O: m  L3 }
Gonadotropin-independent peripheral preco-
. ]; `" C0 H' [cious puberty in boys also results from inappropriate
; ^3 \$ e- w/ P1 N: \5 \# A. Zandrogenic stimulation from either endogenous or
5 \0 @2 s% [/ C0 y9 U" s) T! Fexogenous sources, nonpituitary gonadotropin stim-! s+ y, u/ d4 m9 Y' |
ulation, and rare activating mutations.3 Virilizing8 G' d) v8 J, O
congenital adrenal hyperplasia producing excessive
$ z* }2 X. |  q2 Y5 O5 W7 oadrenal androgens is a common cause of precocious9 }! r# N! E6 B6 {1 z+ _& j. Q
puberty in boys.3,4
8 U- n; y0 D, @, e: V, KThe most common form of congenital adrenal
# u: \, o4 }: w* ~& u4 Yhyperplasia is the 21-hydroxylase enzyme deficiency./ i! i* W; M' H- M0 M9 o4 b; p
The 11-β hydroxylase deficiency may also result in+ w% v2 ]* I# X9 N
excessive adrenal androgen production, and rarely,
7 W& m* X3 o5 ^* ~$ zan adrenal tumor may also cause adrenal androgen
, N# C4 R5 a2 E6 _, Jexcess.1,3
& K8 R# L) T8 aat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
, j3 B) W  t9 o542 Clinical Pediatrics / Vol. 46, No. 6, July 20072 u( C' x7 j0 V& m  X
A unique entity of male-limited gonadotropin-
& n- g8 S" l( A  Y4 pindependent precocious puberty, which is also known* C4 s0 ]# n3 D
as testotoxicosis, may cause precocious puberty at a
3 H  e6 z+ y0 B/ Q& Hvery young age. The physical findings in these boys( c1 o+ A( t) p2 S' Q3 R' J
with this disorder are full pubertal development,/ E/ J1 S. Y) E/ x# R8 C$ m
including bilateral testicular growth, similar to boys6 A( |. t* S7 ]' x1 V
with CPP. The gonadotropin levels in this disorder
8 T7 i1 o; r) L& E3 w4 iare suppressed to prepubertal levels and do not show
, z* o1 E0 B2 f' r& K( Rpubertal response of gonadotropin after gonadotropin-
' h# C* ]. x- C" o& B% W6 creleasing hormone stimulation. This is a sex-linked
/ I2 _: S8 }4 M" D+ C# Kautosomal dominant disorder that affects only; l4 k5 [  t, h
males; therefore, other male members of the family
& v/ v0 c9 r9 emay have similar precocious puberty.3
# o3 {# R  F) ?- Q6 o3 e" HIn our patient, physical examination was incon-
( a+ `/ L; k8 o" n" A) gsistent with true precocious puberty since his testi-
% D# g) m; G: z; \5 Bcles were prepubertal in size. However, testotoxicosis
7 B& s9 j: M9 E8 k2 O) T/ H8 ewas in the differential diagnosis because his father
. r* o6 G9 d. n  [started puberty somewhat early, and occasionally,+ U8 a( y% E3 |( g6 d1 e
testicular enlargement is not that evident in the" X$ y% c1 ~% x* h
beginning of this process.1 In the absence of a neg-( R8 c& E- q: y7 b! N: [$ I
ative initial history of androgen exposure, our
& @8 b2 }+ z) S& d9 p0 sbiggest concern was virilizing adrenal hyperplasia,
) v. Z% D: P5 T$ O6 Reither 21-hydroxylase deficiency or 11-β hydroxylase
( m( S  }# x$ ?' k% V0 jdeficiency. Those diagnoses were excluded by find-
; }9 d9 w  q' i# e9 ~, M* ?ing the normal level of adrenal steroids.- C: H* F* e0 D) V4 r) |7 f
The diagnosis of exogenous androgens was strongly) @9 J# z: L- K& {2 Q
suspected in a follow-up visit after 4 months because
/ W3 c5 G' s' jthe physical examination revealed the complete disap-0 c$ a# i- b, D  T' Z  d3 o( p  C
pearance of pubic hair, normal growth velocity, and. u1 x1 [1 p/ [! N) v! ~
decreased erections. The father admitted using a testos-
* E! D+ t" l- }; ]8 J- ^terone gel, which he concealed at first visit. He was5 O* z7 x  h8 E) Z
using it rather frequently, twice a day. The Physicians’
% n- W! V3 S! a/ MDesk Reference, or package insert of this product, gel or
( N: l& L. W  i' rcream, cautions about dermal testosterone transfer to
; J! A! b7 \; v& J% }( ?+ E* {: ]unprotected females through direct skin exposure.* p9 D' Z) a: V
Serum testosterone level was found to be 2 times the
/ {: h& {6 ]# ], ?3 N* Mbaseline value in those females who were exposed to
" C3 D" Y0 I& x- _2 L6 Geven 15 minutes of direct skin contact with their male
1 P. x6 L$ o  l% K% b* Opartners.6 However, when a shirt covered the applica-
; v$ l9 V1 O" _4 E3 {tion site, this testosterone transfer was prevented.: d3 O' I+ |; p3 K
Our patient’s testosterone level was 60 ng/mL,! ~: K% |" N4 l6 P
which was clearly high. Some studies suggest that
7 T+ q- d" q. `7 A% a$ Adermal conversion of testosterone to dihydrotestos-
$ y8 S! ~( H" u- e' iterone, which is a more potent metabolite, is more
/ a: K: h" y+ @active in young children exposed to testosterone
; \  _& K0 Y  ]exogenously7; however, we did not measure a dihy-4 L" [. @2 e* l) I$ \( b4 w
drotestosterone level in our patient. In addition to( J( ~- P1 B3 e: K5 N$ Z
virilization, exposure to exogenous testosterone in
& F; z2 ]. N; e7 C2 ?children results in an increase in growth velocity and
6 |2 b6 k) E4 d2 i( |# kadvanced bone age, as seen in our patient.
( s7 o, K) J1 ^! ^9 n: X7 a- VThe long-term effect of androgen exposure during
$ l, |6 H  A! k6 J: B. y4 Gearly childhood on pubertal development and final
2 {3 E0 v# C5 L1 T/ |" g; uadult height are not fully known and always remain; U0 ^/ v& N2 E$ E  G
a concern. Children treated with short-term testos-
2 w# ?3 |4 U, F3 R1 mterone injection or topical androgen may exhibit some( q+ h$ i! N6 _5 k0 Y3 g  Z6 G
acceleration of the skeletal maturation; however, after
9 ?* p" i# u9 ]. ocessation of treatment, the rate of bone maturation
4 ~0 ]9 u& f- }# X: B; wdecelerates and gradually returns to normal.8,9
' B! ]8 e% p6 E5 B" TThere are conflicting reports and controversy
6 q, P( f7 w, P, H( E! ], Z+ hover the effect of early androgen exposure on adult
  A2 l( L5 [- F5 Z3 rpenile length.10,11 Some reports suggest subnormal
% o% ?) ]; n3 kadult penile length, apparently because of downreg-
& J/ {7 P5 |4 @) p, D, x9 [) Culation of androgen receptor number.10,12 However,
9 V. _2 `; w  }6 [* m' J5 GSutherland et al13 did not find a correlation between
, c, u4 h* K3 F/ a/ @, J+ \* Zchildhood testosterone exposure and reduced adult
9 o+ d$ X: C: ^2 O: ppenile length in clinical studies.
7 v+ R( l5 S" G; S. c( [, rNonetheless, we do not believe our patient is
3 J) x, v5 Q' c! l; q' @going to experience any of the untoward effects from8 M/ o2 ~8 {9 z- s8 V
testosterone exposure as mentioned earlier because3 s, M2 v7 \' F# V
the exposure was not for a prolonged period of time.
1 G% l! e$ U" L$ f! w( ~+ OAlthough the bone age was advanced at the time of9 e+ I( M$ R& |" |. d  B" `
diagnosis, the child had a normal growth velocity at
4 C' a; N) u0 J( P2 S8 ^( s) D" Dthe follow-up visit. It is hoped that his final adult9 B5 K/ Z& `, L0 X# l# M( P4 b$ Y
height will not be affected.
* M/ q( b! H4 H& N8 I# oAlthough rarely reported, the widespread avail-
7 n7 [. Q& N# a7 B5 k1 dability of androgen products in our society may
6 L8 [1 I) T7 I8 k1 Rindeed cause more virilization in male or female
) I2 w0 E) ~$ ~children than one would realize. Exposure to andro-0 Z' ?3 M7 V- }8 C$ C
gen products must be considered and specific ques-6 y; C+ Q8 t" M  f) `
tioning about the use of a testosterone product or
! X3 q- ^0 Q. L5 [: s  Igel should be asked of the family members during+ ]% e6 `( `- I, ~8 f
the evaluation of any children who present with vir-
: C4 r1 U, p# u: {4 c6 Z9 {9 Cilization or peripheral precocious puberty. The diag-1 u- b9 j" Q+ v/ b8 c/ Q
nosis can be established by just a few tests and by+ S; S( h( Y5 w" ^! M. O$ h
appropriate history. The inability to obtain such a# i4 U, O2 L% D  J# I( L( N
history, or failure to ask the specific questions, may" l  z5 x/ N2 @* c+ o3 C5 I  Z% A
result in extensive, unnecessary, and expensive
" z9 B3 S: E9 O( R4 T) Z9 |5 A3 xinvestigation. The primary care physician should be
2 Q5 s5 \% x) ?9 [1 _" y2 xaware of this fact, because most of these children" o* F; x/ }  _  C- q! o- z6 K
may initially present in their practice. The Physicians’( P* x# v, [  j' w* v; t
Desk Reference and package insert should also put a9 @2 }' k1 f1 o' \4 ^0 s
warning about the virilizing effect on a male or
# o# |) W4 R+ E2 }5 u6 Tfemale child who might come in contact with some-5 B2 i! U( `- V
one using any of these products.
. O: o! o! q+ _+ v0 AReferences3 U4 ?- D6 \4 l1 `4 M$ s3 n
1. Styne DM. The testes: disorder of sexual differentiation
' P. N* i" r% [' aand puberty in the male. In: Sperling MA, ed. Pediatric( f  D. ^* }  S* e" o0 W8 b/ I
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;2 \6 T) k! m2 n: F9 K- I* K
2002: 565-628.- k$ [9 u2 f: ^
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious2 e+ l0 I* N' p( Y2 a9 q' c6 ^2 J
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
8 p* L7 j. I1 i% o8 kBoy Induced by Indirect Topical
) w' k3 [# V, V0 w+ dExposure to Testosterone% [) p5 \' b, @" U: _) @
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2+ g  B; u2 E% M' Z  o( z0 R
and Kenneth R. Rettig, MD11 q, J& u1 X  Z& i+ B1 o! v3 O
Clinical Pediatrics
6 a9 Q+ P! `# [# S2 Q# M" d% |3 yVolume 46 Number 6; |/ j4 |* ^+ G. o7 ]& K
July 2007 540-543! y: U9 R; G' J* v- P4 [% G' `7 `
© 2007 Sage Publications
1 D5 @6 ^& F) Q$ N10.1177/0009922806296651
. A. ?) e$ ^3 {3 o7 Ghttp://clp.sagepub.com# `. S$ u% g. J5 q
hosted at) ?; j2 K  }9 ~% @6 q- \
http://online.sagepub.com3 h$ l: H! `! C2 D2 e- q
Precocious puberty in boys, central or peripheral,7 ^% E- U3 K: C
is a significant concern for physicians. Central
5 T  U8 S; @" b4 K6 i" [) O- H, B( eprecocious puberty (CPP), which is mediated
0 d( i4 C) g# D! F# S' Q/ pthrough the hypothalamic pituitary gonadal axis, has
% i6 `0 }- c! W+ p5 aa higher incidence of organic central nervous system+ R; @4 n  q; S
lesions in boys.1,2 Virilization in boys, as manifested
9 J4 I  L' h1 t, @5 Tby enlargement of the penis, development of pubic7 z% x+ F# m4 S' B' l" c
hair, and facial acne without enlargement of testi-' o4 v- H0 {2 j
cles, suggests peripheral or pseudopuberty.1-3 We
7 h, t" ?  L* G) V8 {report a 16-month-old boy who presented with the
" O: n  ?8 R% o: {enlargement of the phallus and pubic hair develop-) h7 [" G9 L" z
ment without testicular enlargement, which was due
# H! x. |) r( r8 d6 W8 ito the unintentional exposure to androgen gel used by7 Z/ u) y( E! \3 D7 C  n
the father. The family initially concealed this infor-
8 t2 q6 Z5 h5 [* `mation, resulting in an extensive work-up for this% ]' ~" k* O9 a' C# a
child. Given the widespread and easy availability of' g1 }2 y2 W  W" O% C; V
testosterone gel and cream, we believe this is proba-7 I" a% u' b. t, g, U( x( u, A
bly more common than the rare case report in the2 @/ N5 F) M3 W4 M% L% c
literature.4( }- B3 E3 r! u( b. p
Patient Report
" k2 l1 R" g) \1 xA 16-month-old white child was referred to the
+ `9 R: W9 u/ _( mendocrine clinic by his pediatrician with the concern/ N: F6 X- G6 \, C3 S. {2 j
of early sexual development. His mother noticed
7 j& `" l! I( W2 f" q/ a' w( q, slight colored pubic hair development when he was
7 k2 q; I6 A: O6 s5 M# o$ o: @From the 1Division of Pediatric Endocrinology, 2University of: {' {# b9 A$ v( D' N
South Alabama Medical Center, Mobile, Alabama.5 a8 E, E( X8 _! ?/ d2 r
Address correspondence to: Samar K. Bhowmick, MD, FACE,
5 P, V1 P) Y/ k- e9 T. m: q7 Z9 v6 [Professor of Pediatrics, University of South Alabama, College of' Z7 O' T1 o+ A0 p0 s
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;) K/ |+ ?4 c3 V7 Y1 K* R% w" f
e-mail: [email protected].
9 u2 K! a/ f' G0 b" X0 P* habout 6 to 7 months old, which progressively became
% M% Z8 G$ D' r3 X% N; [1 M" A4 Cdarker. She was also concerned about the enlarge-
: z8 v% D6 s  @4 \, U7 Y6 Nment of his penis and frequent erections. The child
! e, _2 `* Y2 ?& C& C  @/ H' Pwas the product of a full-term normal delivery, with
! _+ i1 ?# d, @a birth weight of 7 lb 14 oz, and birth length of; M# ~: z. {+ k( D3 A6 `2 G9 Q$ b
20 inches. He was breast-fed throughout the first year# u  ?% h/ }+ r" e; `
of life and was still receiving breast milk along with* {  v; [; P4 o" |+ y
solid food. He had no hospitalizations or surgery,
- L( g! g, `/ Z4 N6 V/ nand his psychosocial and psychomotor development
# P: P1 c( z- n# v/ j7 \( Bwas age appropriate.! s& q2 M( `0 l. K7 ?
The family history was remarkable for the father,: Q" K5 K" A7 {  w6 [* L
who was diagnosed with hypothyroidism at age 16,. Y! H% }- X0 i, x  k
which was treated with thyroxine. The father’s
2 V! v8 N1 S4 \. t- D! Kheight was 6 feet, and he went through a somewhat
  J+ ~8 J. {+ G  ]7 kearly puberty and had stopped growing by age 14.) ?' z' m( p% E$ s( a) r
The father denied taking any other medication. The
9 A. Q* {, k& a- O8 P% o( m: xchild’s mother was in good health. Her menarche. ]2 W$ P, a. E. ~
was at 11 years of age, and her height was at 5 feet4 J' B! o2 I4 e' y8 C
5 inches. There was no other family history of pre-
+ |5 K2 n" ]" |4 Rcocious sexual development in the first-degree rela-4 O8 S, _/ n. [
tives. There were no siblings.
1 e& a1 Y: j; A' ?. CPhysical Examination
% G! u  R2 j5 ~The physical examination revealed a very active,) s: d' w6 @' z2 k
playful, and healthy boy. The vital signs documented
- B0 W6 T& x9 Q7 P4 }5 N$ ya blood pressure of 85/50 mm Hg, his length was2 H$ g- k1 i  ?% M# M. U
90 cm (>97th percentile), and his weight was 14.4 kg) Y! F; |( r4 s( g: F( E
(also >97th percentile). The observed yearly growth: Q4 Q' r( g% k  |: R
velocity was 30 cm (12 inches). The examination of3 t" A& r2 }8 Q. v8 O
the neck revealed no thyroid enlargement.7 x: \8 _4 g9 m( [% D+ k$ s' |
The genitourinary examination was remarkable for6 M' k( T, A3 C5 _) g4 u  E
enlargement of the penis, with a stretched length of1 {( p5 t3 g: Z4 V& ^
8 cm and a width of 2 cm. The glans penis was very well
; [4 T* s5 U/ h% d# r2 u5 qdeveloped. The pubic hair was Tanner II, mostly around9 J+ L: Z& u  N7 I, }( K9 p
540
# y5 ~; K) E% {6 K  t  Yat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
% u$ j, ?1 V. c0 R. R: [$ ?. y* ?the base of the phallus and was dark and curled. The5 u1 U7 i4 P1 B0 K
testicular volume was prepubertal at 2 mL each.2 g: d& H2 T; K2 K. J5 R6 T$ _$ k
The skin was moist and smooth and somewhat: k4 s( L! T- b$ [1 A$ \& w( x9 V
oily. No axillary hair was noted. There were no
, A2 F! z, y; E# [) d: k* ~abnormal skin pigmentations or café-au-lait spots.# ]  w  W0 [8 ?% K$ ?/ Q: j
Neurologic evaluation showed deep tendon reflex 2+
* n+ q# f3 R8 m& x$ ^bilateral and symmetrical. There was no suggestion% c8 z, F3 p4 T  H3 u- K. F+ D
of papilledema.
* P9 V' j: j2 y5 l. y1 ALaboratory Evaluation4 d  k4 ?5 t! R& S1 n! Z3 ^: ^
The bone age was consistent with 28 months by
% f/ F+ W( a' s, fusing the standard of Greulich and Pyle at a chrono-
( J2 x! t7 {7 y7 D0 Ologic age of 16 months (advanced).5 Chromosomal# h+ N% \& K4 b/ L) k5 w' |
karyotype was 46XY. The thyroid function test% q" j; K: o2 T/ |8 T
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
4 f3 }1 d; L4 H) M$ _% alating hormone level was 1.3 µIU/mL (both normal).0 G& J7 ^# W9 r6 f
The concentrations of serum electrolytes, blood4 y$ x  O4 ]: o, k. b+ n
urea nitrogen, creatinine, and calcium all were% N6 e; d3 B+ O+ z; W) i, S
within normal range for his age. The concentration# P* j3 R! h6 c- k8 ^8 D
of serum 17-hydroxyprogesterone was 16 ng/dL
) l$ u5 N7 a6 x& y4 g9 X/ b(normal, 3 to 90 ng/dL), androstenedione was 20  S1 {& a& y  H; F( ]  s* T" {: X
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
+ s- k5 b; M, G, |terone was 38 ng/dL (normal, 50 to 760 ng/dL),# B. N4 A" {. ]) u
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
/ q3 a" A6 y- [* Q8 z! f% h49ng/dL), 11-desoxycortisol (specific compound S)
3 W9 a; |. j& F* [) P) }; |. W1 Ewas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
) E. i" y- U$ V5 G( Ztisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total% ]- f1 u' |4 v6 K4 e, d
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),7 P! {. h4 u' A2 X8 v- h! _/ p+ I
and β-human chorionic gonadotropin was less than
: d  W  m$ F8 |2 E9 L' W" r5 mIU/mL (normal <5 mIU/mL). Serum follicular
  @& P! o  c* T2 {stimulating hormone and leuteinizing hormone
' E( g  S/ R+ [' ^concentrations were less than 0.05 mIU/mL
) Z0 C3 \) l5 J" }7 D. Q(prepubertal).' i$ `7 }' ~) X6 F4 _( ?5 \. p
The parents were notified about the laboratory
7 a* M1 l' p8 j$ P9 i+ k- Dresults and were informed that all of the tests were
2 y7 v" N7 n- f  ]normal except the testosterone level was high. The
: ^; o. p7 l* \follow-up visit was arranged within a few weeks to9 H( x9 f* T7 r$ q3 R# r: b3 H
obtain testicular and abdominal sonograms; how-
& g0 U: J6 j" ~; r/ \: ~2 \$ Gever, the family did not return for 4 months.
9 n5 D* |, X9 v7 S/ g# iPhysical examination at this time revealed that the5 J+ F; s3 V1 N4 [- _$ L7 ]) U- [
child had grown 2.5 cm in 4 months and had gained& s, l% R3 p' l6 R! g7 B; c. B: X
2 kg of weight. Physical examination remained  h% X! U* h* D, A6 }( K+ ~
unchanged. Surprisingly, the pubic hair almost com-
0 }  J8 K6 J4 npletely disappeared except for a few vellous hairs at& T" X* M( ^- i
the base of the phallus. Testicular volume was still 20 n0 e" p; j" N
mL, and the size of the penis remained unchanged.
0 g" F$ {+ ?6 D8 P( [0 _+ ZThe mother also said that the boy was no longer hav-9 G$ \* J- C/ \
ing frequent erections.* L9 \  w8 S7 _, H$ d# ^
Both parents were again questioned about use of
: D/ n1 D/ [. x0 d: {! ~any ointment/creams that they may have applied to" G8 O/ ?7 |5 I! I, D. i
the child’s skin. This time the father admitted the5 \0 S, T' n3 T3 t& {/ t7 }9 F
Topical Testosterone Exposure / Bhowmick et al 5418 C/ L2 l+ F* W
use of testosterone gel twice daily that he was apply-3 m8 k2 X5 D! J) s) h
ing over his own shoulders, chest, and back area for
# V2 Y9 n* c, Q+ K; r8 c0 Fa year. The father also revealed he was embarrassed
( N+ j7 u2 u; O" dto disclose that he was using a testosterone gel pre-
' W) K0 z" Y  A+ qscribed by his family physician for decreased libido0 D/ D1 O! [. S1 }
secondary to depression.# p" Y6 U$ U* N  K
The child slept in the same bed with parents.3 V) \' f7 t, K
The father would hug the baby and hold him on his. ^+ [( \" i2 f
chest for a considerable period of time, causing sig-
( J+ `" w4 y2 V3 q% ?0 xnificant bare skin contact between baby and father.
# c$ N6 J7 H! v6 W# ~9 T5 g7 m4 pThe father also admitted that after the phone call,
/ K" U" I; Z9 G2 r- a) {* rwhen he learned the testosterone level in the baby
; P* g, c- j; Q$ j0 [1 z1 gwas high, he then read the product information0 A8 N4 m  m( R, Y* {
packet and concluded that it was most likely the rea-
( g$ ~7 x* f7 g& U5 A' ?' N2 i+ \son for the child’s virilization. At that time, they
. q& f. B% m. ~decided to put the baby in a separate bed, and the
% f6 Y/ h+ [8 Kfather was not hugging him with bare skin and had
# M+ J, P' Q: X7 f/ fbeen using protective clothing. A repeat testosterone
# K6 \/ k8 L7 @+ k$ N3 itest was ordered, but the family did not go to the, N  a- D+ U1 {+ m/ D
laboratory to obtain the test.
, m, F# D  X, x9 q1 Q; F! dDiscussion
0 }/ S; f7 h/ v2 i9 UPrecocious puberty in boys is defined as secondary
( {, a9 v7 N* u8 n3 vsexual development before 9 years of age.1,4
$ y; C% z, k6 SPrecocious puberty is termed as central (true) when, c" V+ X! l% S# q3 x
it is caused by the premature activation of hypo-3 T% r( [0 d) y* o. m
thalamic pituitary gonadal axis. CPP is more com-
8 \* A! q% F1 [9 [9 gmon in girls than in boys.1,3 Most boys with CPP3 |' V* J2 y4 T( _$ Z0 w$ ?
may have a central nervous system lesion that is
+ }# b% \# a# E2 iresponsible for the early activation of the hypothal-
8 F+ z7 x0 |7 v' T% ]amic pituitary gonadal axis.1-3 Thus, greater empha-3 `% z& Y3 A+ ]6 w" n
sis has been given to neuroradiologic imaging in
& X0 l0 Z1 n# D" ?9 k) `5 q* bboys with precocious puberty. In addition to viril-  h- p# G% n" o
ization, the clinical hallmark of CPP is the symmet-
1 l" S6 Y, M" e3 V0 ~rical testicular growth secondary to stimulation by& S* J& z# A. l2 v9 G
gonadotropins.1,3
, t- g4 ]9 x& D' @! d- EGonadotropin-independent peripheral preco-- r) [) O; a: ^* ^% o, H+ y
cious puberty in boys also results from inappropriate
2 }  A4 f! x4 R4 J( ~$ landrogenic stimulation from either endogenous or
8 W& I/ ]' n: [3 a! L" @exogenous sources, nonpituitary gonadotropin stim-  T" T; v3 G  Z
ulation, and rare activating mutations.3 Virilizing
- L0 k' V1 G8 _  R; Z* U% qcongenital adrenal hyperplasia producing excessive
* P/ k. p7 S' J' Z* p! _! g, Zadrenal androgens is a common cause of precocious3 e7 [( ?0 M) \2 p2 x! y0 h5 |, \' n
puberty in boys.3,4# s: ?% e! T! P) _4 g
The most common form of congenital adrenal1 k! u) f. I) }
hyperplasia is the 21-hydroxylase enzyme deficiency.0 \0 i; N5 _$ Q7 A# V4 O5 I; q. _0 H" O- P
The 11-β hydroxylase deficiency may also result in& y' d! A0 v8 N( {' }
excessive adrenal androgen production, and rarely,
) M0 `/ a. e* f& _1 Q9 Van adrenal tumor may also cause adrenal androgen
: |* p; n( P; v/ {5 Uexcess.1,3. c/ O. e# N" W4 w! o; k" N
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
. P' H1 y. ?4 V( c* S; R) t542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
. q/ y1 ]1 j8 c! I( EA unique entity of male-limited gonadotropin-
2 I5 J: Z7 e8 R- G, findependent precocious puberty, which is also known* k/ F' t0 u! H" k4 y& z" \( h
as testotoxicosis, may cause precocious puberty at a
5 ^+ {# A/ l* nvery young age. The physical findings in these boys
: ]# d& K! y  i4 ?. Lwith this disorder are full pubertal development,
( z; w" S4 ~6 ^5 V2 A2 Vincluding bilateral testicular growth, similar to boys
  T0 W, ]+ f/ X7 K1 W4 Awith CPP. The gonadotropin levels in this disorder  J2 _  D3 _" [& H2 U* t" G: Z8 y+ Q& \
are suppressed to prepubertal levels and do not show
! C6 _5 [& k0 f7 h8 X- K7 \* u) Gpubertal response of gonadotropin after gonadotropin-
. k. T% z! H+ p! q6 @releasing hormone stimulation. This is a sex-linked
$ {0 p4 u" }, K. g% Fautosomal dominant disorder that affects only
- k8 n9 t# k+ C# l& D/ H" Z% Zmales; therefore, other male members of the family% b$ _$ Y6 y& v+ m
may have similar precocious puberty.3
+ ^( Q" K5 N: F$ I! \: jIn our patient, physical examination was incon-: P0 m. f1 S1 `  m2 k% c
sistent with true precocious puberty since his testi-" W& |5 t4 G8 t- R9 J9 O) L
cles were prepubertal in size. However, testotoxicosis
- V# S) D0 R. `3 H  swas in the differential diagnosis because his father' n3 i, C% s. g6 B  h7 X
started puberty somewhat early, and occasionally,
. S# j. p$ V! o) [0 Atesticular enlargement is not that evident in the, y! e) x. e2 n, I3 K+ D* P3 [: O
beginning of this process.1 In the absence of a neg-: y% x! \- q. d, ~
ative initial history of androgen exposure, our
! T3 A9 t& U+ K4 \8 ^; d  q7 dbiggest concern was virilizing adrenal hyperplasia,
& q- Y- G% {& r5 y  leither 21-hydroxylase deficiency or 11-β hydroxylase
1 V& J. ~) Y3 j. S# Ydeficiency. Those diagnoses were excluded by find-! k& p3 h" E+ d
ing the normal level of adrenal steroids.7 p/ A3 d& k4 ~, |3 l" s  X! m
The diagnosis of exogenous androgens was strongly
6 \" i( U% U9 ^  K( N6 lsuspected in a follow-up visit after 4 months because" K) P& k  A+ V1 K  \/ c
the physical examination revealed the complete disap-
: h3 U9 ~2 c6 N  w4 x0 U% n2 v, apearance of pubic hair, normal growth velocity, and$ i/ k2 d/ R$ t, u0 Q6 x
decreased erections. The father admitted using a testos-) g7 e. r( Q& v& g% P! }& W9 j
terone gel, which he concealed at first visit. He was( W8 r( Y" {$ e( Z5 p0 \2 h+ S
using it rather frequently, twice a day. The Physicians’
& ]" k, Y6 r/ TDesk Reference, or package insert of this product, gel or( X/ F: B2 X! K8 ]
cream, cautions about dermal testosterone transfer to7 ?8 U+ J8 [& N. k( G
unprotected females through direct skin exposure.
) H) T; v% K( T, B* D3 V( h; _Serum testosterone level was found to be 2 times the1 ?2 B9 }: f0 K
baseline value in those females who were exposed to
4 N5 [9 J5 j2 O  Meven 15 minutes of direct skin contact with their male! @7 \' w9 O% Z4 q/ E7 S# `/ H
partners.6 However, when a shirt covered the applica-
2 Y8 ~+ S, M) o9 Stion site, this testosterone transfer was prevented.; k6 h, {& `6 y' V0 \6 n3 `
Our patient’s testosterone level was 60 ng/mL,% P# k) r5 M% I  ?4 S1 @
which was clearly high. Some studies suggest that
4 i) M1 j% ]0 ~  f% P  Idermal conversion of testosterone to dihydrotestos-0 h% O+ c. [& \) A
terone, which is a more potent metabolite, is more$ S8 u  E( V; C- ?$ i/ c7 K
active in young children exposed to testosterone7 @5 K0 T3 v+ _* u0 V
exogenously7; however, we did not measure a dihy-: Z. ]7 R$ C; G
drotestosterone level in our patient. In addition to/ q; F# F% o9 a
virilization, exposure to exogenous testosterone in
3 \% w, ]$ x( c4 R9 ychildren results in an increase in growth velocity and  g7 }9 p  D! t* Y6 T& E2 p+ n
advanced bone age, as seen in our patient.& Y( D% A& d9 P( z5 N+ t& g
The long-term effect of androgen exposure during
1 y1 U2 A1 E  j, c" searly childhood on pubertal development and final/ O# k) ]8 R; D! t( x
adult height are not fully known and always remain; I' p5 p; m& X' _! n1 r* q
a concern. Children treated with short-term testos-
2 H9 k! L6 h/ C# e( X% B5 i  @terone injection or topical androgen may exhibit some/ H/ M/ b6 B1 G* _: v
acceleration of the skeletal maturation; however, after: L. _+ |( @' F+ Y; Q' T3 V7 q
cessation of treatment, the rate of bone maturation
% F- z& @# m" z) I% udecelerates and gradually returns to normal.8,9& B  a2 M; \: g7 d
There are conflicting reports and controversy
$ g  F2 G& K' N- T6 a( Oover the effect of early androgen exposure on adult
+ r+ t+ N0 K, y  Cpenile length.10,11 Some reports suggest subnormal  _6 a+ q5 N4 M* A
adult penile length, apparently because of downreg-: l6 L' Z: F( d
ulation of androgen receptor number.10,12 However,! E' \1 v3 h) _1 r8 T
Sutherland et al13 did not find a correlation between3 M% c& ^3 W2 V* N& W1 [7 t
childhood testosterone exposure and reduced adult1 `( c3 _2 M3 ^1 i9 R& U! \) v$ s
penile length in clinical studies.
* P1 f9 M  W9 t6 z" w  CNonetheless, we do not believe our patient is
+ ~' n, N. `0 R+ W. F. ~" Qgoing to experience any of the untoward effects from( g# ]+ _4 p1 [+ g1 F7 \
testosterone exposure as mentioned earlier because4 z7 L1 n! @5 V
the exposure was not for a prolonged period of time.
( z! j# J+ H" R  s3 e3 `2 e/ OAlthough the bone age was advanced at the time of
# X( K. S* H% q( }' @! {9 b+ m+ tdiagnosis, the child had a normal growth velocity at1 e4 @& w% a2 ~2 I$ z$ Q7 B+ z5 }
the follow-up visit. It is hoped that his final adult
0 H3 q* w6 V. ~, L9 Vheight will not be affected.
) V, J; o" q5 Q" v+ ?' |8 dAlthough rarely reported, the widespread avail-
, v+ u' }( _+ d1 c, kability of androgen products in our society may. I- X. w7 \( a. S( o8 e
indeed cause more virilization in male or female
7 R1 m4 x- R. x; K3 N3 Ichildren than one would realize. Exposure to andro-0 F5 c( r/ l: Q* X) [! S
gen products must be considered and specific ques-" j7 ?+ I+ R8 C
tioning about the use of a testosterone product or1 y0 {3 n3 r3 P) b
gel should be asked of the family members during: Q, {8 e' l( k9 \! i* F
the evaluation of any children who present with vir-& ^" m# h0 j' J$ k- Q$ ^+ {* w8 f
ilization or peripheral precocious puberty. The diag-  i6 [4 g3 y4 f- N9 N
nosis can be established by just a few tests and by
3 O( m2 B0 @! S# {appropriate history. The inability to obtain such a/ o2 _: s6 @, g
history, or failure to ask the specific questions, may
0 p) f$ K# d- P( }result in extensive, unnecessary, and expensive6 N8 X) }6 D: s! {
investigation. The primary care physician should be2 N' ?& R" i# d6 Y+ x
aware of this fact, because most of these children# m$ i5 B( ]  M# B; m9 ^
may initially present in their practice. The Physicians’+ a, W" |5 W& `
Desk Reference and package insert should also put a' D7 z8 c9 c; V0 p. z% [% @
warning about the virilizing effect on a male or
$ d5 a+ ?+ K  R% lfemale child who might come in contact with some-
8 ~7 y5 `4 e% ~5 vone using any of these products.
# ^( ~. X+ s* N2 y$ ^/ h5 nReferences
5 [0 `3 D- o6 `3 k4 T! U/ n' q1. Styne DM. The testes: disorder of sexual differentiation  y7 s# @; h; X9 ?* g
and puberty in the male. In: Sperling MA, ed. Pediatric' d4 h/ S+ l( g7 M0 O
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;& @, a7 N* O) S) R
2002: 565-628.
% X& W  }3 d+ s* T3 m' b, x% ]2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
6 S6 G' f) n  X/ Y( |9 W+ s, Hpuberty in children with tumours of the suprasellar pineal
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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
. F9 r0 a6 f8 L8 c& C! G7 {9 K$ g% h
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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