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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
+ R/ U+ {6 h% Q; [Boy Induced by Indirect Topical! u( v7 _1 X7 K" J7 k( y
Exposure to Testosterone4 }) g- A3 w0 {9 d
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2! m; F7 D! B$ z
and Kenneth R. Rettig, MD1
2 Q5 T: v! N& UClinical Pediatrics
6 L& U: R" \* ?7 L. v: G" B8 WVolume 46 Number 6$ H! w/ ]8 ], H' l2 C
July 2007 540-543
( |% g: M/ Y/ \: s2 t7 J© 2007 Sage Publications
/ @6 |4 K! W# Z' L& g" V10.1177/0009922806296651. s) M& F4 ?0 a: k9 U) y
http://clp.sagepub.com6 Z% r0 ?3 t/ a! r) d
hosted at& a6 \/ Y0 d6 C6 j' k
http://online.sagepub.com& D: ^! A" c" J; a! x
Precocious puberty in boys, central or peripheral,
* l4 z2 Z) q7 n- v, ois a significant concern for physicians. Central
, e6 O" L* b5 C7 |) s9 `precocious puberty (CPP), which is mediated) N- i6 A0 O/ q9 C4 ^
through the hypothalamic pituitary gonadal axis, has" k; l* V. b# {- J# v1 i
a higher incidence of organic central nervous system# d/ j/ }- V2 h6 B0 b, s  I
lesions in boys.1,2 Virilization in boys, as manifested/ x# G4 G3 e' k1 n3 V+ c( d
by enlargement of the penis, development of pubic/ }& U( U3 b/ f! D9 f2 r
hair, and facial acne without enlargement of testi-; T' M: ^2 J3 j$ c/ }* O% p5 d7 H; z
cles, suggests peripheral or pseudopuberty.1-3 We- h' U( h; ]- I+ F5 s5 {- y$ y
report a 16-month-old boy who presented with the) v) d  @' A# H# W% g
enlargement of the phallus and pubic hair develop-
- o/ F+ X5 V1 s1 fment without testicular enlargement, which was due5 A% m& H; y0 e- q) ^! Y3 T( Y6 ~
to the unintentional exposure to androgen gel used by
  M6 l: \+ a4 N0 h( cthe father. The family initially concealed this infor-
$ d* W0 K9 U% ?$ amation, resulting in an extensive work-up for this
- l4 C1 y* k3 c6 U4 q! E  Ychild. Given the widespread and easy availability of
% `" G+ d# v1 z9 [1 x% A" Ptestosterone gel and cream, we believe this is proba-
/ R/ |% D; M& |2 \( Y5 w! hbly more common than the rare case report in the& k2 t4 \- B( W, L
literature.4
% R- r0 B+ L& h  QPatient Report: B$ I2 T5 ]" t5 O" E2 i( O& l
A 16-month-old white child was referred to the" W3 u; k! b  O
endocrine clinic by his pediatrician with the concern
4 W, s7 _/ G; P! G7 ?' Gof early sexual development. His mother noticed
3 E/ x. }, B/ v$ C2 @light colored pubic hair development when he was4 R# R: U1 f1 w9 L7 Z4 H
From the 1Division of Pediatric Endocrinology, 2University of
9 y; w9 h  v0 X  H0 aSouth Alabama Medical Center, Mobile, Alabama.0 P( S; O5 q  x
Address correspondence to: Samar K. Bhowmick, MD, FACE,
2 N0 d$ `# w1 A% r5 i3 ZProfessor of Pediatrics, University of South Alabama, College of  N8 j# C# W# S  i" d9 u
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
2 V; Z9 ~0 H. R6 B" b$ x7 M) se-mail: [email protected].& u  @# Z4 G4 G  H8 M
about 6 to 7 months old, which progressively became
# x1 M, A2 H: ]darker. She was also concerned about the enlarge-2 Q: u$ G* F# ~$ [% y
ment of his penis and frequent erections. The child( `  N" c+ f+ y7 q
was the product of a full-term normal delivery, with
" I) M9 F  K+ Wa birth weight of 7 lb 14 oz, and birth length of
* l. F, G3 u6 z% }20 inches. He was breast-fed throughout the first year, M) ?* S- f6 F: ~+ @, N: ^
of life and was still receiving breast milk along with9 C2 a- ]2 L! V' |  F) S
solid food. He had no hospitalizations or surgery,* o8 I5 x( r' g* Z' S( G
and his psychosocial and psychomotor development
) @/ K. Y* P. c% A3 {& ywas age appropriate.
* ^- h/ B0 d8 a3 Z. XThe family history was remarkable for the father,4 E+ f3 o1 v/ p+ z
who was diagnosed with hypothyroidism at age 16,% c; w- P) Z# O: g8 k3 r
which was treated with thyroxine. The father’s7 v0 f+ X+ m, S6 n2 T
height was 6 feet, and he went through a somewhat
$ J8 E: C" R# }% n. W8 d  Nearly puberty and had stopped growing by age 14.
, h5 \) ]& G* f, \- s4 kThe father denied taking any other medication. The3 U8 b/ k! E/ t& D. Z3 u8 D5 o
child’s mother was in good health. Her menarche
8 n3 J) m( `1 G! ?4 X" kwas at 11 years of age, and her height was at 5 feet
% {. o; n2 R3 j# V5 inches. There was no other family history of pre-
' a: E8 W$ L  K1 z: vcocious sexual development in the first-degree rela-
) k  w' m' c; q5 G/ B8 _7 dtives. There were no siblings.
/ n8 N& C) l* O- Y0 B: WPhysical Examination
3 j+ @4 f3 x( YThe physical examination revealed a very active,3 B& a. n$ `: b
playful, and healthy boy. The vital signs documented
: N- c" B+ b7 v) ?a blood pressure of 85/50 mm Hg, his length was, z, D' P4 q( G( C7 i: J4 \% _
90 cm (>97th percentile), and his weight was 14.4 kg
$ r" [* S/ A" E2 M! k- S: H(also >97th percentile). The observed yearly growth; g  R# |$ J4 P( t2 D: M
velocity was 30 cm (12 inches). The examination of6 S" T# z* j: G& W* B, I
the neck revealed no thyroid enlargement.& m9 c; d1 N) e, y3 y
The genitourinary examination was remarkable for4 U2 e+ y5 ]& z6 r3 E) E: Y" E
enlargement of the penis, with a stretched length of
0 A4 s# f7 V: s! R, o' W8 cm and a width of 2 cm. The glans penis was very well" Q6 b. g+ B) ~" |; E; ~5 u
developed. The pubic hair was Tanner II, mostly around& o3 W' T; w# |  i1 S
540" Q. G. b+ s3 z+ ]
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from& b) R9 I1 q4 s. v. K, J: c
the base of the phallus and was dark and curled. The
" h  o4 O9 V' d$ Ttesticular volume was prepubertal at 2 mL each." f) K) ^8 w, u3 N5 c6 C) V# R, E
The skin was moist and smooth and somewhat4 I$ p& _2 h5 O
oily. No axillary hair was noted. There were no
4 f$ f$ j/ d0 Uabnormal skin pigmentations or café-au-lait spots.
1 X: E; S) @, X+ q) QNeurologic evaluation showed deep tendon reflex 2+
- y8 K0 G) X, L1 w- L/ K$ Pbilateral and symmetrical. There was no suggestion
6 E! S9 K5 l. I. m) _) Dof papilledema.2 k$ a, `# }% ^3 O8 d& o6 K5 v) C% E
Laboratory Evaluation# C0 e* T& c# o
The bone age was consistent with 28 months by
; h# w- ?' h! m+ p8 Ausing the standard of Greulich and Pyle at a chrono-
" _* Z/ {, ?  W  M, Alogic age of 16 months (advanced).5 Chromosomal
# l. {3 Q2 B% ~1 k2 z* S* a3 Ikaryotype was 46XY. The thyroid function test$ f% o1 v, o$ k; V" ?- s5 z
showed a free T4 of 1.69 ng/dL, and thyroid stimu-- S& E, D) V! _: c! Y
lating hormone level was 1.3 µIU/mL (both normal).
/ M9 E$ w- S! [& G$ E! OThe concentrations of serum electrolytes, blood+ B3 E+ ~! u! j% y& o
urea nitrogen, creatinine, and calcium all were
4 R/ n4 M# X% gwithin normal range for his age. The concentration: c2 d: h6 u! e8 U, Z" N
of serum 17-hydroxyprogesterone was 16 ng/dL
- K2 m1 p3 N7 }(normal, 3 to 90 ng/dL), androstenedione was 20
, g% T9 d5 h4 |/ N+ a( rng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-% ^/ K0 ^. P$ p  j9 }3 H
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
- e2 @4 X. P: J6 X% Sdesoxycorticosterone was 4.3 ng/dL (normal, 7 to
7 N! f* U8 L0 w* {49ng/dL), 11-desoxycortisol (specific compound S)+ A7 U1 D4 u# k' Y) X+ V3 b
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
# s) `* [! Z# W2 r' o7 Ltisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
) B  L6 M" f4 ttestosterone was 60 ng/dL (normal <3 to 10 ng/dL),1 y$ W( g" h: A' m7 Q7 T  d
and β-human chorionic gonadotropin was less than) d+ K) t, g4 T& E3 v
5 mIU/mL (normal <5 mIU/mL). Serum follicular' W0 E- J$ e5 K) d4 J  o" ~( [
stimulating hormone and leuteinizing hormone
. x# j" ^; b; A# o& \7 ^concentrations were less than 0.05 mIU/mL7 p2 J. k  F) `3 G- P
(prepubertal).% @0 M- M. l2 [2 L3 ]3 V8 d
The parents were notified about the laboratory& G% d4 f  N& D  k
results and were informed that all of the tests were
$ V; u$ ]- ?, S8 h# Cnormal except the testosterone level was high. The9 K2 q$ `( ~; r
follow-up visit was arranged within a few weeks to2 U$ m: I# p7 W4 [3 T9 _2 M
obtain testicular and abdominal sonograms; how-
8 s- F, M1 ]" O2 ?8 s4 F+ @ever, the family did not return for 4 months.
7 N  p* z( m6 B$ m% i! C$ c0 s/ uPhysical examination at this time revealed that the0 D3 y, z+ G$ C$ R3 }
child had grown 2.5 cm in 4 months and had gained. v4 I( y. `# {2 r. i. m
2 kg of weight. Physical examination remained
, [# o, [, x6 Z, J: Uunchanged. Surprisingly, the pubic hair almost com-
/ T5 ?2 O/ I/ p, _; Q7 U! \pletely disappeared except for a few vellous hairs at6 G3 m% C- `+ i3 ?7 F
the base of the phallus. Testicular volume was still 2
* N1 p# N4 [5 B4 ?. {; {mL, and the size of the penis remained unchanged.
2 T- ?' V; J& t2 d# J6 W+ z; W" ~6 tThe mother also said that the boy was no longer hav-
/ R9 R3 u7 U! j8 Sing frequent erections.
: B" R: S2 C6 z- fBoth parents were again questioned about use of( g+ \( G7 I, o$ S4 W# O
any ointment/creams that they may have applied to
( F3 E! S! L+ U% Tthe child’s skin. This time the father admitted the
4 D: L; X5 [) ?+ S: F: V+ Q; s6 RTopical Testosterone Exposure / Bhowmick et al 541
, a" l- h6 a3 I, e" D( M$ Ouse of testosterone gel twice daily that he was apply-
$ h9 C5 g) t* {. C+ q! ying over his own shoulders, chest, and back area for+ n  P$ ^) b8 a) k
a year. The father also revealed he was embarrassed
; @' |1 n7 B$ x* b% R* kto disclose that he was using a testosterone gel pre-# @/ u" q. U  c0 _1 D  F
scribed by his family physician for decreased libido
4 Z* D( y$ R: }1 n" J. z3 \secondary to depression.
$ C8 {9 k+ q1 \! P6 k+ xThe child slept in the same bed with parents.* D( n( f4 ?8 X8 X$ }/ W& ?7 E/ d
The father would hug the baby and hold him on his5 G% Z  B$ d9 }- x" i" D
chest for a considerable period of time, causing sig-' y. g& G( ]6 x  U, a5 M
nificant bare skin contact between baby and father.
( T2 D8 a7 M" T' lThe father also admitted that after the phone call,/ N0 V5 h/ L4 p% ^
when he learned the testosterone level in the baby
. `: c- g( ^5 J& ~/ Vwas high, he then read the product information) Y6 B2 {& M8 M" p: q
packet and concluded that it was most likely the rea-5 L! c& D6 w# \
son for the child’s virilization. At that time, they2 @) Y2 b+ ]( x2 l, ~0 ?% x
decided to put the baby in a separate bed, and the: ]! F) ~  Z! u0 p
father was not hugging him with bare skin and had9 c* N' d2 y% A) c: W+ z7 M
been using protective clothing. A repeat testosterone
, m3 Q: T! v9 ?7 O4 a. gtest was ordered, but the family did not go to the
& h7 \) X( B' g- N3 `laboratory to obtain the test.
1 R8 K9 G2 D8 t* h0 KDiscussion
+ N/ c; K8 B: R1 J/ e' M) }3 qPrecocious puberty in boys is defined as secondary+ o. |+ g/ k* N4 j$ F: T$ O- c0 q& T
sexual development before 9 years of age.1,42 H& y( C, z! m
Precocious puberty is termed as central (true) when
& U5 A0 a" V  e( D1 F/ Q% B8 Sit is caused by the premature activation of hypo-
; L0 E% [3 u& U/ vthalamic pituitary gonadal axis. CPP is more com-7 p+ ?  L9 b5 o' k! M  F$ @
mon in girls than in boys.1,3 Most boys with CPP( }" B3 ^1 P. J4 P. _0 V
may have a central nervous system lesion that is
1 d, Y/ K# D3 t0 ^9 O6 N. Xresponsible for the early activation of the hypothal-* V  D, Z/ u7 B0 k' }% [
amic pituitary gonadal axis.1-3 Thus, greater empha-5 g# \2 b' H$ y* @4 j6 q( W# s
sis has been given to neuroradiologic imaging in1 w0 A+ C3 Y/ t9 @3 Q$ l- _
boys with precocious puberty. In addition to viril-! V; q& X1 a; |) M8 x* m
ization, the clinical hallmark of CPP is the symmet-! F- ~& p0 U; Z
rical testicular growth secondary to stimulation by3 C2 U4 X7 b  F" R6 s6 L2 ~' y8 F
gonadotropins.1,39 m7 \( K# K, y' b, `& ^
Gonadotropin-independent peripheral preco-6 b) b1 X6 H8 C
cious puberty in boys also results from inappropriate
' o# X0 i/ p& iandrogenic stimulation from either endogenous or- r1 |2 R8 @+ P- D
exogenous sources, nonpituitary gonadotropin stim-
  G- _8 |0 o2 ~& S* Mulation, and rare activating mutations.3 Virilizing# Y; n  T( B! G$ I
congenital adrenal hyperplasia producing excessive- ^3 a& z/ ?# a; @& d
adrenal androgens is a common cause of precocious
9 ^7 m' X1 U8 T1 Npuberty in boys.3,4( v* f) c# c# N3 u+ x- i
The most common form of congenital adrenal8 R6 B6 r5 U% s6 @: w& C
hyperplasia is the 21-hydroxylase enzyme deficiency.1 l+ U6 v1 f; h  R
The 11-β hydroxylase deficiency may also result in
: b2 D1 a, H  cexcessive adrenal androgen production, and rarely,: D1 k& G7 r6 ?) |: B" h
an adrenal tumor may also cause adrenal androgen
# }7 T5 P# q3 Cexcess.1,30 Q1 t- @" O/ \* i+ z# D% A3 E+ O
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
. _8 L+ O# O0 V: L542 Clinical Pediatrics / Vol. 46, No. 6, July 20079 L( y9 k6 J* u# X& g$ ~/ T
A unique entity of male-limited gonadotropin-9 b, K. ]( j% j5 I* a; K
independent precocious puberty, which is also known6 {% I! Y$ @6 T- w, O8 W  o
as testotoxicosis, may cause precocious puberty at a( T+ M/ k% M5 N4 V$ f5 j
very young age. The physical findings in these boys
0 A9 }1 U. D4 N/ F0 i. n$ S; Wwith this disorder are full pubertal development,/ P) {4 d5 F! x2 j
including bilateral testicular growth, similar to boys
8 k1 x0 @# W  K$ U& ^  e; Twith CPP. The gonadotropin levels in this disorder
6 }/ R8 f% V# Y( dare suppressed to prepubertal levels and do not show" u7 Z2 X  I0 ?3 p6 l' Q
pubertal response of gonadotropin after gonadotropin-
0 B/ o5 Y( K/ B6 C9 X/ W8 |releasing hormone stimulation. This is a sex-linked: c9 L8 ?2 ?2 d! T( {5 M2 X
autosomal dominant disorder that affects only3 ?4 Z; I* _' L9 e: L  I3 D- C3 G
males; therefore, other male members of the family
  r( y3 n, h/ Tmay have similar precocious puberty.3
# @! i4 [: l5 cIn our patient, physical examination was incon-
" n$ F/ i- b4 X6 |* Y& G3 I5 Xsistent with true precocious puberty since his testi-9 R( d9 Y, k# h  m4 h. Q
cles were prepubertal in size. However, testotoxicosis8 S) h1 `$ H3 F
was in the differential diagnosis because his father0 z) |" i2 C" O0 F- V
started puberty somewhat early, and occasionally,0 d+ T$ J; C! \  P; O! y
testicular enlargement is not that evident in the* l9 C1 q( o1 J# v. _
beginning of this process.1 In the absence of a neg-
! h2 Q. v. Y0 ?5 i7 m/ N" ~# _ative initial history of androgen exposure, our4 K! i2 k8 l  k2 o# @8 A) y/ z
biggest concern was virilizing adrenal hyperplasia,
% F, Y( g% I! S" jeither 21-hydroxylase deficiency or 11-β hydroxylase
% j+ J) @9 W7 L" Tdeficiency. Those diagnoses were excluded by find-
$ E& W, Y7 J% ding the normal level of adrenal steroids.
5 P0 W  S. ^# U# c% X1 B: |The diagnosis of exogenous androgens was strongly
9 a- j! s" w: f# G2 Osuspected in a follow-up visit after 4 months because* w4 f* f( R! X# O
the physical examination revealed the complete disap-: U6 j: H/ O. e* p4 X
pearance of pubic hair, normal growth velocity, and
& g" _4 B- n+ {! I6 r+ p4 Bdecreased erections. The father admitted using a testos-+ `9 i  a' A3 H( h, _
terone gel, which he concealed at first visit. He was& q$ `" {7 \* \2 A: Y5 @! d! H9 c
using it rather frequently, twice a day. The Physicians’
5 F$ [% ]7 r( W( l9 FDesk Reference, or package insert of this product, gel or
0 s" T8 W& E; R- Y) U5 c: m5 t" Kcream, cautions about dermal testosterone transfer to* h9 k* T7 z4 E7 q/ e1 L. a
unprotected females through direct skin exposure.
) s) T% K9 \+ S2 ?6 r. K0 B/ fSerum testosterone level was found to be 2 times the. d1 s9 V) [" @
baseline value in those females who were exposed to9 d# b4 t8 H7 v7 V* V3 z" W( {( N
even 15 minutes of direct skin contact with their male  S& ]9 O0 j, T$ {+ O
partners.6 However, when a shirt covered the applica-
; j. d. \" l# xtion site, this testosterone transfer was prevented.
0 V) J9 G, [- {. Z4 m5 hOur patient’s testosterone level was 60 ng/mL,
4 X. L3 m& g# n2 `which was clearly high. Some studies suggest that% N4 `2 ~# F2 m, `/ H; c: A
dermal conversion of testosterone to dihydrotestos-" `3 p6 |2 k: f' b
terone, which is a more potent metabolite, is more0 o: ?. K7 N- k8 h. ^
active in young children exposed to testosterone& H1 x- l) L. I6 L* U
exogenously7; however, we did not measure a dihy-2 }+ D& z8 ]7 N; S9 a- g) b
drotestosterone level in our patient. In addition to
- N/ F5 h# a# p5 b; n' W+ J8 {virilization, exposure to exogenous testosterone in/ T6 G  j* O8 l, V0 k
children results in an increase in growth velocity and  }7 h% e7 _* U
advanced bone age, as seen in our patient.
( u; s2 r& R  q1 G2 k: I. ]2 WThe long-term effect of androgen exposure during
8 N: ]$ d: E  d$ n* d: tearly childhood on pubertal development and final) K% V  X* v7 S1 }* @  [
adult height are not fully known and always remain
& Q  Z5 [6 Y4 X$ ?, s! ea concern. Children treated with short-term testos-( k3 c0 X5 o* `* t' q; t
terone injection or topical androgen may exhibit some
6 j4 r1 v6 ]1 N' l' Z  W7 B% d9 lacceleration of the skeletal maturation; however, after4 G' n' i) i' W6 ]3 d. X
cessation of treatment, the rate of bone maturation
* S5 m; k6 m0 o! sdecelerates and gradually returns to normal.8,9/ Z: L/ B# L. y% T) P4 L
There are conflicting reports and controversy. S& Y9 M: v* p2 F8 B
over the effect of early androgen exposure on adult4 |( C' V  z5 {9 g
penile length.10,11 Some reports suggest subnormal& b7 t# x2 f1 W" ^" v
adult penile length, apparently because of downreg-
" o) H; G* [5 I4 Z& lulation of androgen receptor number.10,12 However,) {, d+ w! M6 |! R# O
Sutherland et al13 did not find a correlation between) E. X! r( e& B1 O5 ?5 H
childhood testosterone exposure and reduced adult
  w" w4 K* ?& q4 `" rpenile length in clinical studies.
& Q3 l3 ^) L# CNonetheless, we do not believe our patient is
2 W/ R  ~" k% j5 _1 |& l% u" Pgoing to experience any of the untoward effects from
6 v# d7 \, l/ f# l% o7 ?4 Rtestosterone exposure as mentioned earlier because  j; i5 s/ w9 h: V+ o
the exposure was not for a prolonged period of time.% D% j. J7 a- _' ~! m8 q7 _3 D7 _
Although the bone age was advanced at the time of3 p1 D$ {; p$ O
diagnosis, the child had a normal growth velocity at
/ v  c% R$ E( H. J0 V, othe follow-up visit. It is hoped that his final adult
( \4 U. k# t6 q! Y. c# z5 I& Rheight will not be affected." j5 S3 a$ T  a! r% I, }
Although rarely reported, the widespread avail-2 H5 }" c; N, k; P7 m8 [
ability of androgen products in our society may
; Y6 p+ e, ]: [6 m/ l9 Dindeed cause more virilization in male or female
6 L6 a. Y. v/ V1 h! tchildren than one would realize. Exposure to andro-1 R$ L0 g6 i7 Q" ~1 C' U
gen products must be considered and specific ques-
: w( P) ?/ g7 r: `6 \, xtioning about the use of a testosterone product or
) l+ ~1 Q, q. Y9 j: c( \gel should be asked of the family members during
1 d4 Y; R! @. ?& W5 C' ethe evaluation of any children who present with vir-! m- ^. ?2 I( U
ilization or peripheral precocious puberty. The diag-
$ n5 x# B' J3 vnosis can be established by just a few tests and by
& W+ d% m, ?. t* Q! W7 `0 U' |appropriate history. The inability to obtain such a7 E( r2 {8 M; S( Y3 c
history, or failure to ask the specific questions, may
+ [, v" r0 l& d3 sresult in extensive, unnecessary, and expensive+ D2 ]& Q) B4 u9 L/ y3 ^; G
investigation. The primary care physician should be4 f  e. L  z3 p3 C, w6 L
aware of this fact, because most of these children3 C5 c: C* U* h9 p
may initially present in their practice. The Physicians’
6 D& H' ]$ b1 f% M; Z* iDesk Reference and package insert should also put a' a3 l' w& U7 \9 z: T
warning about the virilizing effect on a male or
9 e+ w6 B) A# U: Bfemale child who might come in contact with some-
; p; f. E. q# y3 G( n; x) @one using any of these products.! f& L6 T$ S0 b0 L! N3 x5 k
References4 _! l' ]5 l" R3 Q' o) \' x' H
1. Styne DM. The testes: disorder of sexual differentiation
$ v, u/ P0 W6 ]1 o) j9 R: Fand puberty in the male. In: Sperling MA, ed. Pediatric/ M% B. b$ l; X8 e
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
" F' [7 V0 w" u! \# c2002: 565-628.
/ b1 `1 Y4 B0 D# b" L/ w2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
( s: r! L( J* c- \) }puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
/ O* @% _5 [+ @; VBoy Induced by Indirect Topical
; _3 t) ]* `" v3 q, aExposure to Testosterone/ I) i% A" g; H' D/ S
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
# y7 Y" @& b9 v9 ]$ [and Kenneth R. Rettig, MD1
2 Z3 O/ {" C' ?; m  c7 ZClinical Pediatrics
' h0 B$ t) ]5 F; WVolume 46 Number 6) D6 _# @! Q# j4 J, L* N/ P
July 2007 540-5436 W: ?5 K6 C' T+ K
© 2007 Sage Publications
8 w% i4 i0 V8 d  v# O/ d2 c10.1177/00099228062966510 m5 {% [4 ^) _6 H  I
http://clp.sagepub.com
' L1 E$ d6 b  N: P8 f  U( _1 Lhosted at
  i( y  q/ @( F4 F# Nhttp://online.sagepub.com9 Z( F' E* [% \2 b8 g
Precocious puberty in boys, central or peripheral,
7 Z5 w1 c  X& F: F1 h; Ais a significant concern for physicians. Central
- d7 D7 H; j2 O8 S4 Xprecocious puberty (CPP), which is mediated1 c2 |6 R% R0 Z( P, @
through the hypothalamic pituitary gonadal axis, has
, U  q& W; x/ p5 ka higher incidence of organic central nervous system
# J0 c; R1 \7 F! llesions in boys.1,2 Virilization in boys, as manifested
1 Q' C) N7 T& Rby enlargement of the penis, development of pubic9 z( c; i  I; t0 e3 }: c7 f
hair, and facial acne without enlargement of testi-( A* C3 I" [" g! X; n$ H
cles, suggests peripheral or pseudopuberty.1-3 We( \+ U; O) e& |
report a 16-month-old boy who presented with the
# p9 n4 e8 b: X5 fenlargement of the phallus and pubic hair develop-
+ r# C7 x8 `, w6 fment without testicular enlargement, which was due" c3 q0 P6 p! Z$ ?1 F( e. P
to the unintentional exposure to androgen gel used by
1 ]5 h$ b. C% R& Y. T* Pthe father. The family initially concealed this infor-4 A4 E4 @" A1 I0 m8 O
mation, resulting in an extensive work-up for this2 Z- n9 h6 |6 d4 b  |0 l5 \+ R  v9 O
child. Given the widespread and easy availability of
7 L/ n3 I0 k+ |' ?6 f6 Z, ]' U0 Dtestosterone gel and cream, we believe this is proba-
' O+ S6 R8 g3 z  I$ x, D5 L% {; G, Jbly more common than the rare case report in the
3 o, `/ ?; N4 {! t9 [literature.4
( w( o% [: J: V" tPatient Report
9 ?6 \1 [9 ~: m4 |# v/ @  hA 16-month-old white child was referred to the( E- K! X( o# e2 p. n" p& q6 x
endocrine clinic by his pediatrician with the concern( J  T. O" |5 x1 }8 H( E: U& d8 j
of early sexual development. His mother noticed4 U8 I6 d- a3 w
light colored pubic hair development when he was
- e* I. |) W8 P% k9 q- TFrom the 1Division of Pediatric Endocrinology, 2University of* t( [) p# I0 Q" E5 G5 m
South Alabama Medical Center, Mobile, Alabama.# J' T6 `: {: C5 [0 m/ }0 g1 L) ?$ Q
Address correspondence to: Samar K. Bhowmick, MD, FACE,
7 s: r$ B$ {: F6 {2 y' GProfessor of Pediatrics, University of South Alabama, College of
) J, R5 X0 P9 _9 W) x+ N1 ZMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
  F' z$ t, M6 k0 v6 E! Q) Fe-mail: [email protected].0 i! j  W9 \5 u+ ?( y5 K- L
about 6 to 7 months old, which progressively became* t- d5 o, x4 V! `" y. j" g4 ]
darker. She was also concerned about the enlarge-/ g8 R# ?9 R/ y7 n( W: q7 ]6 Q9 C
ment of his penis and frequent erections. The child
: u' J) O4 Z: R5 qwas the product of a full-term normal delivery, with
9 `5 q# U) ~1 l/ ca birth weight of 7 lb 14 oz, and birth length of/ k- _# H) @2 ?) Q4 Y
20 inches. He was breast-fed throughout the first year" W3 d* b- z( e7 z
of life and was still receiving breast milk along with
1 M- y) h, N* {solid food. He had no hospitalizations or surgery,
  k( e# ^/ Q3 @and his psychosocial and psychomotor development" p9 j" b: o( J$ Y
was age appropriate.9 x% _2 y: C) J& R
The family history was remarkable for the father,
  s  I/ o: N. m6 |/ lwho was diagnosed with hypothyroidism at age 16,
9 x4 ]; \6 o* c: r6 y9 y  l2 xwhich was treated with thyroxine. The father’s
6 z: P3 C3 V7 P( `height was 6 feet, and he went through a somewhat
3 a* o, \- G& r* L1 c0 b7 Bearly puberty and had stopped growing by age 14.# V0 O' ]5 C& E3 {
The father denied taking any other medication. The
) R3 ]4 E* |5 Q; Ichild’s mother was in good health. Her menarche8 W* n3 w0 p. i5 T4 n1 r; c
was at 11 years of age, and her height was at 5 feet
3 L# F: j% n1 X* Q+ ?5 inches. There was no other family history of pre-
3 P/ t3 K& Z0 }  r% d( Ccocious sexual development in the first-degree rela-
: ^5 e5 k0 M6 f. a1 |5 P/ Q  X; Btives. There were no siblings.
9 K5 ]1 r: ], ^9 O4 v# [% LPhysical Examination
0 p/ a) G6 X9 K. nThe physical examination revealed a very active,
4 \, M4 d1 U' G+ t% K# pplayful, and healthy boy. The vital signs documented& t$ O9 w% K9 Y2 g, R- Z4 s
a blood pressure of 85/50 mm Hg, his length was- [' H8 t' a' i+ c& Q
90 cm (>97th percentile), and his weight was 14.4 kg
: p: k$ V& P" G3 {2 I(also >97th percentile). The observed yearly growth  d3 ?5 A8 @5 [- `2 ^- x
velocity was 30 cm (12 inches). The examination of8 E4 A% o: \0 ]# r/ l# N
the neck revealed no thyroid enlargement.! k0 o" ]5 C2 @$ x: b- j# O# n
The genitourinary examination was remarkable for# t( X$ m( D- r6 q$ C
enlargement of the penis, with a stretched length of
# K8 j( S) o, Q* v8 cm and a width of 2 cm. The glans penis was very well5 G5 ]7 S. e- ]+ o$ ~
developed. The pubic hair was Tanner II, mostly around
) v! Q7 G5 _) k) N4 _; B3 ^/ e% ?5401 s& J" N& i6 m! B. S
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
! \& w6 O- n3 _8 T1 \the base of the phallus and was dark and curled. The
( D# }; @3 U# b: o+ I$ P2 s1 f4 `4 Ptesticular volume was prepubertal at 2 mL each.6 T$ W* Z. {& o( V4 c- m, ~
The skin was moist and smooth and somewhat
. m: N6 j  S- l. B4 Poily. No axillary hair was noted. There were no
3 j! f3 |1 M# t, Zabnormal skin pigmentations or café-au-lait spots.
5 }/ Q1 }) p) R6 C# ?Neurologic evaluation showed deep tendon reflex 2+
- T; F& C  @3 |% z- {bilateral and symmetrical. There was no suggestion7 @& {9 g: ]; {, n- x! U& ]% s+ P
of papilledema.# N% R# f8 r9 O; z/ p& ~
Laboratory Evaluation
! U( ]* v8 p! S$ s! H: h' |The bone age was consistent with 28 months by
$ c& n5 R% W. E3 P6 D( wusing the standard of Greulich and Pyle at a chrono-
9 ?* C: a1 G- q9 Jlogic age of 16 months (advanced).5 Chromosomal
' T; X7 u2 X2 a* r' Hkaryotype was 46XY. The thyroid function test7 z6 i& P0 ]8 _0 t# G2 P
showed a free T4 of 1.69 ng/dL, and thyroid stimu-8 c1 o- f' K: O* ~
lating hormone level was 1.3 µIU/mL (both normal).
) _  M, O' W4 g- Y4 c" GThe concentrations of serum electrolytes, blood& j! g7 h! y: X# k; q
urea nitrogen, creatinine, and calcium all were4 I; P4 Y$ e; C; |. n* B+ k
within normal range for his age. The concentration
5 ^7 h0 Z6 z! T0 v; }of serum 17-hydroxyprogesterone was 16 ng/dL# J  B# F" Q5 z7 [- Z
(normal, 3 to 90 ng/dL), androstenedione was 20
. e" C) e. V# t7 t: |  g9 Ing/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
0 V  b& \! W2 y* l1 W3 n$ Sterone was 38 ng/dL (normal, 50 to 760 ng/dL),8 ]4 z1 I( a9 Q0 g& W9 _" K
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
7 G/ y4 m* A7 i( U% Q: _9 m49ng/dL), 11-desoxycortisol (specific compound S)
7 B  l( _" P; D3 F  f( Vwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
! o8 E: X# x* ^0 h# a0 |tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
/ F" C( J1 ]& r4 u; r- Ktestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
& q/ w! @9 ^. `0 ~- f  Pand β-human chorionic gonadotropin was less than
3 C; \9 Q, f7 ?% \- S5 mIU/mL (normal <5 mIU/mL). Serum follicular
0 W3 |6 ]+ c% H* ]! jstimulating hormone and leuteinizing hormone8 s! b- @+ v* B# r& D( C
concentrations were less than 0.05 mIU/mL7 P! q4 V( L2 d5 o
(prepubertal).
7 G$ V" f2 D' r- `/ T7 aThe parents were notified about the laboratory+ T$ F  }1 x% N% ?. J0 }( g* a
results and were informed that all of the tests were- j% H% n+ \! p: d+ t' f' o
normal except the testosterone level was high. The
" v- J; e' a+ @, l6 S; d$ Qfollow-up visit was arranged within a few weeks to- m9 \9 A/ ~  S3 F
obtain testicular and abdominal sonograms; how-
. {  X$ P* T2 [- ?( O) {ever, the family did not return for 4 months.
  j4 `2 i  {" D+ I7 m& kPhysical examination at this time revealed that the
! t4 G  B. w+ Dchild had grown 2.5 cm in 4 months and had gained
0 `- m$ n1 Q4 f0 q2 k2 kg of weight. Physical examination remained0 E' H; q/ \  |& a- \2 H# @9 u
unchanged. Surprisingly, the pubic hair almost com-
; c% L; @* a) x, m8 L% ^8 Zpletely disappeared except for a few vellous hairs at6 z* p+ Z) R% e/ w& F0 E
the base of the phallus. Testicular volume was still 2
' b* `% [5 k, E4 KmL, and the size of the penis remained unchanged.0 R- |; v+ t6 j. D3 b) F
The mother also said that the boy was no longer hav-( X& ?& a! I. @* E$ k" ~# ?
ing frequent erections.. W6 Z; k4 q# X5 p- g7 F
Both parents were again questioned about use of
" {: P3 m* s8 eany ointment/creams that they may have applied to/ Q* Y* [7 \! L$ [& Z
the child’s skin. This time the father admitted the/ n4 |( n7 I9 C: t* r% t0 b6 }
Topical Testosterone Exposure / Bhowmick et al 541! M7 ?( I  H4 v" _, H) n' W
use of testosterone gel twice daily that he was apply-
1 ^$ }' w& o. a$ @1 d2 S/ ping over his own shoulders, chest, and back area for
, d  ?! {* x' p1 L8 p+ }a year. The father also revealed he was embarrassed
/ v- `- D, |% a' w+ K# lto disclose that he was using a testosterone gel pre-! g/ p% w$ t, T' V1 q( `
scribed by his family physician for decreased libido& I3 [$ ~/ l$ O9 ~5 \- j* t! {; r
secondary to depression.
  n+ s( H+ N2 F, T$ u% ^. C2 C+ j7 ZThe child slept in the same bed with parents.
+ w8 }! e" _' `: p4 {The father would hug the baby and hold him on his  h" a0 e1 B$ \0 ^7 @" n4 @
chest for a considerable period of time, causing sig-! K% Z" N* S7 s1 z, \4 b9 [" W
nificant bare skin contact between baby and father.
& G" t: ~* D3 Q0 KThe father also admitted that after the phone call,( X: p4 E& }- N: ~( ]* _7 N6 Q: d
when he learned the testosterone level in the baby
) Y& A! M; _( p0 m) h- [was high, he then read the product information9 K3 F8 p) b% g1 i- K. N$ B6 k( g
packet and concluded that it was most likely the rea-, n0 t$ a. Y- E
son for the child’s virilization. At that time, they  y: D! u* b/ ^" r3 h
decided to put the baby in a separate bed, and the! m! Y% r  N0 z" O1 U5 T- h
father was not hugging him with bare skin and had1 N" G. l9 _7 ^/ I& t2 R8 `
been using protective clothing. A repeat testosterone- p" U/ H( E3 l0 A
test was ordered, but the family did not go to the1 [# k2 {+ I: y" {+ r1 C' A+ K
laboratory to obtain the test.
4 O1 M$ ]) v5 t: B6 y, WDiscussion
/ j8 r/ T# s+ X8 s" l6 R/ x7 WPrecocious puberty in boys is defined as secondary* W2 n$ U2 }: M" i
sexual development before 9 years of age.1,4) c  ]# }5 S( C
Precocious puberty is termed as central (true) when5 u# B- Z; l* R+ E, X) P& @8 M# R
it is caused by the premature activation of hypo-
0 f$ O; m1 S7 S+ W5 H; Bthalamic pituitary gonadal axis. CPP is more com-) y1 M" p! ^% x' ?' S
mon in girls than in boys.1,3 Most boys with CPP- `6 ?' t! x' u1 Q; S
may have a central nervous system lesion that is
" `. N2 Q6 U: \& |- wresponsible for the early activation of the hypothal-
9 U* ~) w* T$ ?/ }5 F3 Zamic pituitary gonadal axis.1-3 Thus, greater empha-
& P2 \) G& j! m  @1 n$ N7 k) G) ksis has been given to neuroradiologic imaging in
& j; x& t  ]+ R; c, _9 U/ L( ]# mboys with precocious puberty. In addition to viril-
8 P" }; g5 N, ^" vization, the clinical hallmark of CPP is the symmet-0 ~7 A" o8 @, d# J3 Q
rical testicular growth secondary to stimulation by) b+ j* V& H: m  F! O/ O
gonadotropins.1,3
+ j0 @% f* x/ L# L( @5 P, o, u6 e, mGonadotropin-independent peripheral preco-
* w/ n3 p; b5 L* L: {0 ncious puberty in boys also results from inappropriate
- E# c1 x  C/ e# l( Kandrogenic stimulation from either endogenous or
% K: j/ q8 b. [& g- w: g3 Nexogenous sources, nonpituitary gonadotropin stim-* p" M' @+ p# n8 u: j5 j: }
ulation, and rare activating mutations.3 Virilizing
( k; p8 {5 t' d+ t9 R" [* z6 qcongenital adrenal hyperplasia producing excessive
& z$ m( r1 l' e" J: w5 |, Qadrenal androgens is a common cause of precocious3 \; W2 z9 y6 z% F- |5 V
puberty in boys.3,4
0 }9 V' z! s0 D( P2 L7 U0 TThe most common form of congenital adrenal
7 X+ C& D! ]$ Lhyperplasia is the 21-hydroxylase enzyme deficiency.
2 u: i; L- G  I- _! IThe 11-β hydroxylase deficiency may also result in
9 b4 G/ F' Y+ \' R  M# r* eexcessive adrenal androgen production, and rarely,
1 o2 d8 z) F# R. _$ Xan adrenal tumor may also cause adrenal androgen0 T! t: E1 f+ I6 [" N! K: E' V: i
excess.1,3( Y' }! B* M' v' ]
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
: g" K* L) @2 g% b, C542 Clinical Pediatrics / Vol. 46, No. 6, July 2007" c6 x% F: ~0 d( [, E+ c/ T
A unique entity of male-limited gonadotropin-
3 D& E% f2 I4 v: B: r5 q: u+ O: windependent precocious puberty, which is also known$ Z& U/ }5 w* r2 }- s7 p9 M9 t
as testotoxicosis, may cause precocious puberty at a) I; G( g( A. P# ]3 W- E4 u) C9 q
very young age. The physical findings in these boys( ~5 b  A& P1 I- G/ ~. d
with this disorder are full pubertal development,
" N2 _, C1 {& a) N; b- Mincluding bilateral testicular growth, similar to boys
2 e/ J  Q7 T8 p+ _! ^' ~with CPP. The gonadotropin levels in this disorder
+ h2 {! D5 _  i5 O9 Rare suppressed to prepubertal levels and do not show
: P  p. j& [) {$ S. upubertal response of gonadotropin after gonadotropin-
8 M$ T9 D) r$ E' j6 Ereleasing hormone stimulation. This is a sex-linked2 o$ d5 h# _( i$ D0 Q1 N
autosomal dominant disorder that affects only% e$ K& s) t% N: C
males; therefore, other male members of the family9 _  R+ q/ N0 @; {; a- Q3 `; y" H
may have similar precocious puberty.3, [0 A" m5 f4 H/ S9 b* U# m5 g
In our patient, physical examination was incon-
9 e; T- g$ l9 Ysistent with true precocious puberty since his testi-: D. a2 ^+ G8 {7 d7 f0 }
cles were prepubertal in size. However, testotoxicosis! D" ^; m' r9 {7 O# M( t3 x' t$ ?" V
was in the differential diagnosis because his father
, i% \! g7 H- w: F4 G; L* N' g. _' x% jstarted puberty somewhat early, and occasionally,
- A5 R. Y1 Z, A4 {testicular enlargement is not that evident in the
1 n3 d# t5 p# L' Mbeginning of this process.1 In the absence of a neg-2 e! v1 G5 j0 W7 S7 c
ative initial history of androgen exposure, our5 T3 K! G9 P% d5 x" f* v
biggest concern was virilizing adrenal hyperplasia,- B+ P% M3 |' N4 a  G
either 21-hydroxylase deficiency or 11-β hydroxylase+ S5 N' c$ a1 h2 g
deficiency. Those diagnoses were excluded by find-
6 H0 Z0 u# T" m; g4 N% Oing the normal level of adrenal steroids.) {. j* }, D" W' p
The diagnosis of exogenous androgens was strongly
# g0 C7 m. L9 _" n9 J) Ksuspected in a follow-up visit after 4 months because$ \4 ^7 M) L& Z2 ]9 R$ _. J
the physical examination revealed the complete disap-, s# G3 F1 y' G# z4 K
pearance of pubic hair, normal growth velocity, and
+ V% {; t5 S9 H9 u$ G1 t. [. Adecreased erections. The father admitted using a testos-7 @" B: ^% T8 P8 k1 B0 P
terone gel, which he concealed at first visit. He was
' z1 d: b  }& k: ^7 ~) q" f# Ousing it rather frequently, twice a day. The Physicians’
4 F- F- y+ ~: N9 GDesk Reference, or package insert of this product, gel or
) l- [3 E" {  o4 S$ acream, cautions about dermal testosterone transfer to
8 M9 h) s, o% t, w- nunprotected females through direct skin exposure.
( S+ j1 V$ Y2 L4 U8 B' y: OSerum testosterone level was found to be 2 times the1 `! a% q) r+ [
baseline value in those females who were exposed to. R. S4 [0 a# {6 p
even 15 minutes of direct skin contact with their male
* [$ v9 G7 Z, t2 C0 Q4 Qpartners.6 However, when a shirt covered the applica-
& R4 m' i* y3 g' m# |. S  g' b% [tion site, this testosterone transfer was prevented.% u( ^1 |7 K* |3 B5 S
Our patient’s testosterone level was 60 ng/mL,* }5 |3 t. k( M* Y/ J
which was clearly high. Some studies suggest that7 O8 l( `7 |$ g1 u
dermal conversion of testosterone to dihydrotestos-5 M' n% e9 i7 p5 ?* F5 V, Y: J
terone, which is a more potent metabolite, is more
5 j& b9 N% S( m* Tactive in young children exposed to testosterone5 J0 V* l! f) s" E4 B4 R% w8 ~
exogenously7; however, we did not measure a dihy-
1 K$ u! S; a& M+ J' x2 |2 ldrotestosterone level in our patient. In addition to, S! k, |5 n8 g" v
virilization, exposure to exogenous testosterone in  t5 e4 a; r. d5 z/ W# V# j$ X
children results in an increase in growth velocity and
: t) s0 a/ b( h- _advanced bone age, as seen in our patient.
5 z1 \" U7 T: K: g5 rThe long-term effect of androgen exposure during: ?8 S0 y( z1 R8 @$ W
early childhood on pubertal development and final- ^8 c3 p& g8 O
adult height are not fully known and always remain4 g0 ]- }  S4 \* U2 P2 t4 V: y
a concern. Children treated with short-term testos-. s$ i* g9 i8 c! H; m$ M+ s
terone injection or topical androgen may exhibit some. V! g( t) P2 R+ e0 }& N
acceleration of the skeletal maturation; however, after
- @# H" k! p2 \3 u4 x$ `cessation of treatment, the rate of bone maturation
, C% \4 m+ `2 {decelerates and gradually returns to normal.8,9
. M$ C  S6 c" h" ~% ~There are conflicting reports and controversy* j! F" S8 Y# p3 U5 Q
over the effect of early androgen exposure on adult
" y  P6 T6 ]& V; B2 \- Bpenile length.10,11 Some reports suggest subnormal! J5 _; ~, V" p& m: M! d
adult penile length, apparently because of downreg-
2 R2 D# ~: ^0 \' D  a4 f( Oulation of androgen receptor number.10,12 However,
( T3 |5 r: I9 U6 H) iSutherland et al13 did not find a correlation between
7 S- A* c& G) ~! _! S( k- Zchildhood testosterone exposure and reduced adult; X4 D; e; k! b$ F& x
penile length in clinical studies.( P3 S0 `" k( H6 N
Nonetheless, we do not believe our patient is
5 ~  A  _3 ~: f5 Y/ Egoing to experience any of the untoward effects from2 y) i) k+ J9 Y+ h" A$ V
testosterone exposure as mentioned earlier because
" M) R' L( i; gthe exposure was not for a prolonged period of time.0 Q! k$ `- ^5 \. `' W; t
Although the bone age was advanced at the time of. K# g* u1 A2 o  r. c
diagnosis, the child had a normal growth velocity at" Y6 l/ L9 w, d
the follow-up visit. It is hoped that his final adult
* ~1 P0 @, n( L( Rheight will not be affected.
4 v' Q2 r# ~& m$ ~7 m7 B1 r/ [$ ]Although rarely reported, the widespread avail-' r% N- ~9 Z; K1 b) B; Z7 h
ability of androgen products in our society may8 w/ |' C# x7 q3 u6 I  U& S* L1 V
indeed cause more virilization in male or female
( t% e" g2 H1 h( hchildren than one would realize. Exposure to andro-
9 U; v3 I3 o+ t4 ^3 G' ?3 [* Ngen products must be considered and specific ques-
$ e( b8 M* Y% L" \$ Ptioning about the use of a testosterone product or+ G- v7 B! e- @  r* n/ e4 h
gel should be asked of the family members during' Q! Q. I/ t/ g0 z% _+ w/ v" s- d
the evaluation of any children who present with vir-
6 H* a; m" }0 f4 pilization or peripheral precocious puberty. The diag-
; Y8 X5 ^! V  o1 A1 U8 C2 i* w: snosis can be established by just a few tests and by! A: r& G$ O5 g* u  E7 r6 ?
appropriate history. The inability to obtain such a
" t! K5 H$ h  g6 z, [! L( l* O4 Vhistory, or failure to ask the specific questions, may& {& ~7 n& o8 g2 x0 K
result in extensive, unnecessary, and expensive
' N* q3 O3 \2 e7 ]6 B+ w2 |% `: finvestigation. The primary care physician should be4 o; E* k' r* w
aware of this fact, because most of these children/ _5 y4 J2 M5 o9 i
may initially present in their practice. The Physicians’% f# r! @7 d( Z2 ~5 o! r
Desk Reference and package insert should also put a
0 W! k( U8 F1 Pwarning about the virilizing effect on a male or
/ U) t6 F( L% W1 }( f1 X* ^! ~female child who might come in contact with some-. K4 Q2 F& W/ L# @: \
one using any of these products.
. A' d0 v/ B3 ]8 JReferences: D" T5 d/ K5 X( S- U
1. Styne DM. The testes: disorder of sexual differentiation, U7 f$ U3 m/ b& u' u: G0 [: Q
and puberty in the male. In: Sperling MA, ed. Pediatric2 h6 \- A$ O9 v; W3 F) b$ w
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;5 [" Y. S3 c' ?8 I! S9 {; g, p3 C
2002: 565-628.7 e3 {# h3 v& y4 k+ n
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
8 ~  X/ t* E6 `& `. B$ Gpuberty 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
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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

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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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