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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-Old5 G' H5 p/ i: n
Boy Induced by Indirect Topical
) Y0 P0 e$ q, NExposure to Testosterone9 b' _' V1 |" L; n1 l) q! R5 K8 r
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
, w0 P% G7 _1 [! _and Kenneth R. Rettig, MD13 J% B- T# {! d3 U$ e# T
Clinical Pediatrics
, G7 [% I# g/ f1 P& SVolume 46 Number 67 M* W9 e) _0 q+ G" @- m" ^
July 2007 540-543
& G$ L0 M$ r' t' Y) k! a© 2007 Sage Publications
( u5 e4 E1 t4 z. d10.1177/0009922806296651
4 y- o) l, @6 T, M; u8 Whttp://clp.sagepub.com! K7 d6 P; N/ F6 ]2 h6 L- F6 P
hosted at# j7 k8 P, ^2 E7 R" X2 w( f
http://online.sagepub.com
7 V2 }' s( `( p( [! YPrecocious puberty in boys, central or peripheral,
0 \( j2 H$ ^& y2 l8 h9 ]% V- gis a significant concern for physicians. Central- T: B9 t, ?2 [+ }( V: a! s
precocious puberty (CPP), which is mediated+ R* e  h1 |2 Z; c9 @# b$ U* k, Q
through the hypothalamic pituitary gonadal axis, has* n+ C0 E3 j( ~& G- h
a higher incidence of organic central nervous system5 s: b, }: b! F* I5 h$ n+ ?
lesions in boys.1,2 Virilization in boys, as manifested- V3 {* P7 S( f% M7 T
by enlargement of the penis, development of pubic" u9 j1 I' O  d( d
hair, and facial acne without enlargement of testi-
3 K6 B  d8 R  F4 ycles, suggests peripheral or pseudopuberty.1-3 We
& N1 W4 ?" Q9 V2 |1 yreport a 16-month-old boy who presented with the
2 v' X: ]! J: Z, v: T8 Penlargement of the phallus and pubic hair develop-7 T/ S' \# g1 m8 z8 l& T
ment without testicular enlargement, which was due
- ^; z* ^# R0 e" Hto the unintentional exposure to androgen gel used by# v/ Z! ^5 j* N% G$ Q3 n& g' ^
the father. The family initially concealed this infor-
  y% I, B. v' B# d" A, |7 {- jmation, resulting in an extensive work-up for this
5 j( O0 Z: w' S& Echild. Given the widespread and easy availability of
" M7 n+ B) f) e  f  L5 @testosterone gel and cream, we believe this is proba-# x, q; `" w& m2 j7 ~
bly more common than the rare case report in the3 v8 I3 r4 f' h; \: _' I( Z
literature.4* y3 x7 ~. W- s( E- W
Patient Report
+ W; P* P( \' ~0 F' w; UA 16-month-old white child was referred to the4 c* u) D) n+ E$ ^6 u
endocrine clinic by his pediatrician with the concern( a7 y+ R0 [  f4 q# a
of early sexual development. His mother noticed! C# d. O% Y. }5 w
light colored pubic hair development when he was! N3 F( Y8 L/ P7 ~6 i' y  y. j
From the 1Division of Pediatric Endocrinology, 2University of
: Y0 O, q& J$ B7 f8 a- O" BSouth Alabama Medical Center, Mobile, Alabama.
9 E" Q6 \5 G) K+ C3 qAddress correspondence to: Samar K. Bhowmick, MD, FACE,& U# R. x% T* W+ W; m$ W0 R. F+ K
Professor of Pediatrics, University of South Alabama, College of+ Q" ?' M: w; o# F
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
  c; \% u. ~% z3 ~e-mail: [email protected].
( f" U! s4 A) N2 i' k  dabout 6 to 7 months old, which progressively became0 _  y. Y9 Z' c( C! `
darker. She was also concerned about the enlarge-# p4 A( m. s8 b5 N; {+ v8 I
ment of his penis and frequent erections. The child& g3 R  u+ D" x% H
was the product of a full-term normal delivery, with3 ?/ F6 ^6 e" ?4 N: W. i
a birth weight of 7 lb 14 oz, and birth length of0 R, d( n. j8 [- ]2 l
20 inches. He was breast-fed throughout the first year
. a/ V8 ]) G( l  Q7 @of life and was still receiving breast milk along with% f5 _, f2 v9 J' m
solid food. He had no hospitalizations or surgery,2 \' B( u9 L( F8 ^, @
and his psychosocial and psychomotor development: A- h# t. M, C
was age appropriate.
' b3 U2 R( o2 R) YThe family history was remarkable for the father,
) W3 o$ l7 ~7 N0 Bwho was diagnosed with hypothyroidism at age 16,
# [& d! p0 Z# gwhich was treated with thyroxine. The father’s9 d8 e/ w; s, ]8 r
height was 6 feet, and he went through a somewhat4 Y1 S! `- C  S: C" w+ i
early puberty and had stopped growing by age 14.
& @& F! H$ V6 f$ z$ `1 QThe father denied taking any other medication. The3 v* g. D3 E: |8 L
child’s mother was in good health. Her menarche' l9 n) o2 p1 t. ]  i5 L
was at 11 years of age, and her height was at 5 feet
; `) H* g& {1 h( v, w4 @5 inches. There was no other family history of pre-
' C$ o; ^' @# hcocious sexual development in the first-degree rela-
/ q9 g/ s) }! E+ f8 itives. There were no siblings." `& x3 m* V* K2 @
Physical Examination
" Z/ u# i7 ~8 G0 m" S7 _, I) \/ EThe physical examination revealed a very active,9 P5 T0 m  ]9 N7 t- h) z
playful, and healthy boy. The vital signs documented! L8 a/ J& U. Z% l) S- _- W7 F
a blood pressure of 85/50 mm Hg, his length was- s7 t/ b2 A; Q4 U
90 cm (>97th percentile), and his weight was 14.4 kg+ k) B  e3 W) B# N6 J
(also >97th percentile). The observed yearly growth
) m% P; O. ~+ J5 ^velocity was 30 cm (12 inches). The examination of3 u8 W2 N! t+ \9 }% V8 z
the neck revealed no thyroid enlargement.
5 X: S/ F) G* B& \9 ~. N+ G) f% DThe genitourinary examination was remarkable for' v1 c2 p' i4 j( q
enlargement of the penis, with a stretched length of! J/ f3 ]* N! g
8 cm and a width of 2 cm. The glans penis was very well' L) U; r# i" l
developed. The pubic hair was Tanner II, mostly around
3 d9 b% R* B% N- t: W- v% D5406 x+ t; z. n* t8 e0 w
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from7 p: n, p7 d3 A: ?
the base of the phallus and was dark and curled. The
7 f9 q! f$ C2 m6 o( A9 C1 L- X3 M! M$ Otesticular volume was prepubertal at 2 mL each.
& y$ O3 k# f) E3 i" |The skin was moist and smooth and somewhat
. S8 @, C* O! u, @oily. No axillary hair was noted. There were no
' Q5 L1 Z" e+ l0 dabnormal skin pigmentations or café-au-lait spots.# @6 [, M1 A5 p+ }2 ]- H/ {
Neurologic evaluation showed deep tendon reflex 2+! w, X! y/ N8 Q1 E- i+ g0 F# t
bilateral and symmetrical. There was no suggestion
+ J* S& R* w# D6 i. U1 c% ~0 Y6 Xof papilledema.
% z- X- V  d1 f* {7 a1 qLaboratory Evaluation3 Q% c/ f: M  h
The bone age was consistent with 28 months by
. c7 L% Y9 I$ B/ k+ ?; p9 ^6 eusing the standard of Greulich and Pyle at a chrono-8 N$ G9 P" E  J7 B, q+ U
logic age of 16 months (advanced).5 Chromosomal0 F0 a4 K+ z: k( F
karyotype was 46XY. The thyroid function test
3 g) v$ c/ S9 C7 b# Tshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
1 n! m2 Y& }8 m, _9 e, ~0 s# llating hormone level was 1.3 µIU/mL (both normal).$ E" E+ i, K6 \0 o- y7 p1 X4 X# M8 T
The concentrations of serum electrolytes, blood
/ E; ?5 W' P: P3 Xurea nitrogen, creatinine, and calcium all were" F" W* |& g9 a* q3 [5 f
within normal range for his age. The concentration# n6 |5 I' o2 k" l
of serum 17-hydroxyprogesterone was 16 ng/dL
! U1 @0 _5 h1 A. R" }(normal, 3 to 90 ng/dL), androstenedione was 20
# a( a0 R# B) v. Eng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
) w8 X0 f, C! ^! \  ?1 o/ m& oterone was 38 ng/dL (normal, 50 to 760 ng/dL),! ~8 `1 E5 J) z$ A, z( ~' m
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
6 Y  t( v' [: B& g+ Y- V4 A" K1 A49ng/dL), 11-desoxycortisol (specific compound S)2 @% _! D- B) ~' m
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
3 y* R# [$ T7 y1 O! C- ntisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
2 p$ o  L8 x7 I5 F3 }testosterone was 60 ng/dL (normal <3 to 10 ng/dL),$ N8 B0 y- g" n
and β-human chorionic gonadotropin was less than
2 H/ ~3 u5 i. s! P& P9 L5 mIU/mL (normal <5 mIU/mL). Serum follicular
& t3 F; W9 B; a% Fstimulating hormone and leuteinizing hormone
# A( H$ }( r2 [/ N, n, C! J$ a7 econcentrations were less than 0.05 mIU/mL
* T6 `0 a0 {4 o$ T(prepubertal).  [: Y* l$ B, L% V
The parents were notified about the laboratory
% h8 G+ s$ e& ]0 x: _( Rresults and were informed that all of the tests were/ I# e& ]! M4 |
normal except the testosterone level was high. The
) S" G' f  a. d4 ^& b8 @follow-up visit was arranged within a few weeks to
/ s7 N+ ^3 {4 {  R8 V) N4 Nobtain testicular and abdominal sonograms; how-
5 s$ s" h. d, r: K/ bever, the family did not return for 4 months.
+ i0 j- C1 T& o, O9 OPhysical examination at this time revealed that the* Q0 P# W( b" A# e4 o! i" e/ V3 y
child had grown 2.5 cm in 4 months and had gained- G( V6 p7 z! T& g8 L* L: Y: ~& G
2 kg of weight. Physical examination remained8 s6 B8 O0 L1 A
unchanged. Surprisingly, the pubic hair almost com-
' r' y; p8 n) l8 f  ^$ D( opletely disappeared except for a few vellous hairs at, X3 L( `# S9 Q- p' x9 w1 R
the base of the phallus. Testicular volume was still 2
: ~' Q" S- `$ Z) `mL, and the size of the penis remained unchanged.) {* t0 S5 D# C8 \' L$ x/ k! B! {
The mother also said that the boy was no longer hav-
1 ?4 j) d9 g1 Sing frequent erections.* V: a! T) ?* {( d+ q) c7 A
Both parents were again questioned about use of
- T2 B5 z. ?6 pany ointment/creams that they may have applied to5 d$ V" u" x; i/ U1 S! q" q
the child’s skin. This time the father admitted the( |+ C; {1 d! [7 q' @2 B  C
Topical Testosterone Exposure / Bhowmick et al 541
5 |' A8 o9 Q4 a% i( euse of testosterone gel twice daily that he was apply-
* W4 n, K% k2 X* c% sing over his own shoulders, chest, and back area for6 j" E4 Q8 ]0 ]* q2 E0 l# d
a year. The father also revealed he was embarrassed
/ q4 J, L' E0 p/ uto disclose that he was using a testosterone gel pre-
# K! B8 g/ }. m0 v. E) j4 @2 T* {scribed by his family physician for decreased libido
  G' a9 F* Q2 F7 q4 z$ R  {7 @  usecondary to depression.
! B4 v: ^" ^/ L6 h, ]4 D* A6 S( V: mThe child slept in the same bed with parents.
5 ~0 }6 W! |5 CThe father would hug the baby and hold him on his
6 ~" J2 j% o4 s8 B' i: T3 Schest for a considerable period of time, causing sig-/ J, h) v0 x' k  x) {3 t" S! S* ~
nificant bare skin contact between baby and father.
: h5 D7 C+ y2 S/ @The father also admitted that after the phone call,  S0 ^* k7 x6 e# {) k
when he learned the testosterone level in the baby
8 x, A! D7 K# s' w) Ywas high, he then read the product information
' l/ r* [3 ?3 P# ]! _$ a& F6 l  p9 T" jpacket and concluded that it was most likely the rea-
$ k+ Q% t% B1 H  d' u' l6 Q$ Kson for the child’s virilization. At that time, they
/ i; P/ G2 ~7 k$ N/ fdecided to put the baby in a separate bed, and the
: r/ _# d% Z6 t% Y& s6 Bfather was not hugging him with bare skin and had% ~9 [2 G6 U0 Y0 b% v
been using protective clothing. A repeat testosterone
+ x3 M, g% M7 D) r* c# Ctest was ordered, but the family did not go to the+ K4 P4 s0 L; a& v% g$ k7 v0 B
laboratory to obtain the test., `; V! \) Z/ T! V% x
Discussion: s) D1 Y. z7 N/ z/ H
Precocious puberty in boys is defined as secondary; J% Q( \: q" G& Z& O# y; w
sexual development before 9 years of age.1,4+ s6 {- P* q& m
Precocious puberty is termed as central (true) when+ v9 U& c+ [- A; i  p
it is caused by the premature activation of hypo-6 {, k: G0 v1 b9 M8 S; Q
thalamic pituitary gonadal axis. CPP is more com-, Q5 V- f5 e9 ^
mon in girls than in boys.1,3 Most boys with CPP6 g  X* e8 i7 |# Z
may have a central nervous system lesion that is
& ^5 F  H* H% P" F9 Vresponsible for the early activation of the hypothal-, M2 C3 X) p9 ?) ^3 u" u
amic pituitary gonadal axis.1-3 Thus, greater empha-9 J9 n: E9 d- Z, e5 p/ o& D8 N5 u
sis has been given to neuroradiologic imaging in
5 S% L" m* I$ Fboys with precocious puberty. In addition to viril-1 _# Q' u: G& z3 G/ W; F
ization, the clinical hallmark of CPP is the symmet-0 c/ L1 N' J' _: v* A8 {, {4 N
rical testicular growth secondary to stimulation by# ?; q! W) ?7 ^; j& G) t4 x
gonadotropins.1,31 j" _* e; G/ I# e: ]1 I
Gonadotropin-independent peripheral preco-
5 q6 ~0 `+ I8 V  |" F5 e9 {" Ecious puberty in boys also results from inappropriate
  T3 o4 ^; J. l! c% @( Aandrogenic stimulation from either endogenous or
( m. v& I8 `( J. texogenous sources, nonpituitary gonadotropin stim-  J7 V( ]( Z% R; [4 f
ulation, and rare activating mutations.3 Virilizing8 v9 L4 A5 n+ F; j  |3 S
congenital adrenal hyperplasia producing excessive
( C2 }9 \* C6 tadrenal androgens is a common cause of precocious) o- X( P0 j* d7 b
puberty in boys.3,4
) c" r& n7 J9 w+ ~9 b% C9 K0 KThe most common form of congenital adrenal4 \! J; w6 {; S; M. z: G' o: I
hyperplasia is the 21-hydroxylase enzyme deficiency.3 e4 [& |3 X; A0 j& \
The 11-β hydroxylase deficiency may also result in9 A% m5 F( x/ n; _6 s
excessive adrenal androgen production, and rarely,
( h0 t7 E- W3 c5 L# ?; E  Ean adrenal tumor may also cause adrenal androgen
8 W- x8 h% _: Z% {; a5 K( |excess.1,35 \. Q0 E8 ~( ^/ V/ ^( k3 R" n
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
* f* x0 {& U  V1 S  V542 Clinical Pediatrics / Vol. 46, No. 6, July 20070 m( ~2 O' H# D' Z
A unique entity of male-limited gonadotropin-- e0 O& G: h! F" Q  b
independent precocious puberty, which is also known
5 A" ]. m2 {4 I; uas testotoxicosis, may cause precocious puberty at a
+ S& c% }1 f( overy young age. The physical findings in these boys9 y# K( }" S3 w: i) p  v. o
with this disorder are full pubertal development,, v( m3 W- i% T- v8 b7 b9 A
including bilateral testicular growth, similar to boys
+ T: }8 W: ?2 t) l+ M8 Kwith CPP. The gonadotropin levels in this disorder
& ]  ^) w$ `" L  f0 S3 M/ Y) Aare suppressed to prepubertal levels and do not show* o5 U6 g; N$ T
pubertal response of gonadotropin after gonadotropin-
/ C( s% N' b8 treleasing hormone stimulation. This is a sex-linked3 e- F5 b. [3 K9 Z2 s& q
autosomal dominant disorder that affects only" R" Y" I8 l: B0 g4 O4 M
males; therefore, other male members of the family
- e. N7 ~& o- ~/ K% Zmay have similar precocious puberty.32 M5 M" _* x/ a: R2 X# \
In our patient, physical examination was incon-9 s. J) J3 x& q2 x& k; I8 F  y8 ]
sistent with true precocious puberty since his testi-! R4 O' f% [$ p' F, o! _* ?
cles were prepubertal in size. However, testotoxicosis* F; v+ W  D" K  _8 p8 o
was in the differential diagnosis because his father0 r: u: j! }# _) F
started puberty somewhat early, and occasionally,- `7 C. a4 n  T" z8 U. D
testicular enlargement is not that evident in the
8 T; s3 o( ?$ F$ cbeginning of this process.1 In the absence of a neg-2 ~! E% A( D0 m- e
ative initial history of androgen exposure, our
6 B1 B' b  x2 q3 bbiggest concern was virilizing adrenal hyperplasia,  |6 h, i8 z0 R
either 21-hydroxylase deficiency or 11-β hydroxylase% O4 f. C7 B3 c5 Y5 {% M  B( H, I
deficiency. Those diagnoses were excluded by find-6 Z5 t# e1 s/ t/ s* A
ing the normal level of adrenal steroids.
% A) A9 z9 b5 I! Q5 ?The diagnosis of exogenous androgens was strongly
: |4 S! e1 e+ \! M( ^suspected in a follow-up visit after 4 months because8 C9 S, D: g3 Q: n, C& }+ \
the physical examination revealed the complete disap-
; f  e. X3 @, Bpearance of pubic hair, normal growth velocity, and
) J5 j, o; m! idecreased erections. The father admitted using a testos-2 Y9 |  F( A; v% b/ c
terone gel, which he concealed at first visit. He was
, v$ A/ z  \/ y3 B$ Dusing it rather frequently, twice a day. The Physicians’; u+ A7 z- h2 p9 o: q* L
Desk Reference, or package insert of this product, gel or
; ^6 S) e4 p8 h+ `6 d1 _: Hcream, cautions about dermal testosterone transfer to2 _, T) W5 z1 ?: h
unprotected females through direct skin exposure.
4 u" }; {  b# ^9 p" KSerum testosterone level was found to be 2 times the
& m2 u. z6 h' s. _' jbaseline value in those females who were exposed to) W: t7 o4 B6 U5 q: j
even 15 minutes of direct skin contact with their male! X0 V& B; [! k
partners.6 However, when a shirt covered the applica-2 r! e0 T2 e6 {. G
tion site, this testosterone transfer was prevented.
4 m) h" S; p0 O6 TOur patient’s testosterone level was 60 ng/mL,
2 g+ E+ f+ G, ?  A- {% W' dwhich was clearly high. Some studies suggest that
$ @! G$ E5 c6 p& ?# a7 {- ]: G) hdermal conversion of testosterone to dihydrotestos-
1 o. A( Q5 D- ]. A# K  vterone, which is a more potent metabolite, is more
! v% }$ A# R* \# ?$ N9 Vactive in young children exposed to testosterone
5 u( h- ~( C: x: ~" sexogenously7; however, we did not measure a dihy-$ q: n% p0 V. B' V9 `
drotestosterone level in our patient. In addition to4 e* |. U0 {" t/ |0 @
virilization, exposure to exogenous testosterone in
/ w! R4 \8 P/ x  k; Nchildren results in an increase in growth velocity and
* M* a( q6 R/ b; Uadvanced bone age, as seen in our patient./ R- {  x7 i$ ~* g2 P
The long-term effect of androgen exposure during/ u  W! `5 ^% R3 D4 G0 Z4 [" i0 f8 H
early childhood on pubertal development and final
1 z" E# b# l. R& M. h9 S7 k1 @9 Oadult height are not fully known and always remain
( L7 d: T; Y0 f7 Y1 N* Z/ h, [a concern. Children treated with short-term testos-
7 g$ E% ~5 M' n6 j2 p5 B9 iterone injection or topical androgen may exhibit some) |( X2 G( V9 z7 h8 C2 I" ^
acceleration of the skeletal maturation; however, after7 f4 T2 P0 l2 A* d/ p3 {
cessation of treatment, the rate of bone maturation  [. l' U6 w- q; q
decelerates and gradually returns to normal.8,9. ?& N& l. |! C% y
There are conflicting reports and controversy+ P+ A0 g. Z7 Q: r' K
over the effect of early androgen exposure on adult$ L, {3 w4 A2 X9 {6 F9 I
penile length.10,11 Some reports suggest subnormal' t  K, l6 A: E9 Z9 `. Q/ \/ n5 K
adult penile length, apparently because of downreg-
/ \2 {) y* l- x% |# `, |: e( M4 Culation of androgen receptor number.10,12 However,
( z& @3 m) |5 `+ S4 a- s/ bSutherland et al13 did not find a correlation between/ D0 C1 B' f  N8 r+ {9 @7 }5 E
childhood testosterone exposure and reduced adult; R6 Y  |7 K; r( o  ^. ?( T0 p
penile length in clinical studies.
* k6 t% e; K+ }  u+ y$ tNonetheless, we do not believe our patient is
' y- l$ |" y4 g8 Wgoing to experience any of the untoward effects from
5 o% N% x' q* v  J6 G! Gtestosterone exposure as mentioned earlier because, O: F/ W- W8 L0 s1 p9 V! v/ ^1 @* q0 k
the exposure was not for a prolonged period of time.) f. C7 Z3 x4 y' O& [3 s3 n- _
Although the bone age was advanced at the time of: {6 r9 W" u5 B  W% Y
diagnosis, the child had a normal growth velocity at
6 l8 C. x- c  L, v% C, Lthe follow-up visit. It is hoped that his final adult
1 Z  u1 B0 [7 q; {! C& V6 L/ y  Vheight will not be affected.9 S( y- i' g2 M/ Q+ @+ s) a# s; D/ \
Although rarely reported, the widespread avail-
# `$ X! J) {- x8 dability of androgen products in our society may8 n- ]/ s1 A# H" U+ h) ?1 i+ r
indeed cause more virilization in male or female
+ q& Y1 `+ P! \% I( h/ L8 `$ Echildren than one would realize. Exposure to andro-
$ Q* s. l9 ]* _6 L/ Cgen products must be considered and specific ques-4 O: r0 K, l6 I7 L! C; }
tioning about the use of a testosterone product or
# V1 H& M! J$ I/ }0 egel should be asked of the family members during' [9 {  N- q. u/ H& p1 u) }9 K
the evaluation of any children who present with vir-) N- h8 y2 F9 k, i, V
ilization or peripheral precocious puberty. The diag-
  \1 w! y+ O$ ^( F& g8 A/ S$ o4 gnosis can be established by just a few tests and by
$ Z4 B. ^  [  D$ r" `appropriate history. The inability to obtain such a/ i, l; L" E+ u. P% n
history, or failure to ask the specific questions, may
# X- i! V4 ^& b" t$ l! V) vresult in extensive, unnecessary, and expensive
0 X* ]" m# A* ^4 \" ]investigation. The primary care physician should be5 a5 V: a1 n/ [
aware of this fact, because most of these children+ M; o+ K2 V6 h4 @7 v
may initially present in their practice. The Physicians’
8 _$ x0 `! k% xDesk Reference and package insert should also put a
3 m5 \/ D+ ?. e1 K9 I$ Iwarning about the virilizing effect on a male or( I# t6 O3 x6 p7 s( \
female child who might come in contact with some-! p" ]- [+ I  O1 f
one using any of these products.8 g$ t% h) x+ }
References2 r1 ~) N, o4 P+ }2 t" m, w
1. Styne DM. The testes: disorder of sexual differentiation+ j+ |# x0 \4 w
and puberty in the male. In: Sperling MA, ed. Pediatric
. X" P: y; \2 Y/ s2 [3 mEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;# U( z( v) l0 F2 ~6 w
2002: 565-628.6 c0 `  e+ w3 b$ J: w/ A9 E, V
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious- J" A0 ]$ ~) j9 |% U
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
' |5 D' S6 [9 f- j; ^Boy Induced by Indirect Topical2 z% H- F; }1 v( O1 _( O! Q) Z
Exposure to Testosterone4 K0 r1 v, P5 ?# r) N
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
  I4 b2 ^$ j. R. y1 a8 Oand Kenneth R. Rettig, MD14 v" O; k* b! D* A1 P6 _# Q
Clinical Pediatrics$ ?) }8 e8 x' ^' k6 @
Volume 46 Number 66 n4 v; L/ o5 i1 _) H6 q
July 2007 540-5437 A% T" n4 H/ l2 q
© 2007 Sage Publications
% D  ]' _; T: s: T# d10.1177/0009922806296651
6 `5 Y/ v: w- S4 ~8 H. `http://clp.sagepub.com
6 R* U  g4 Z- h" P' \hosted at
; B! C& j$ N) w+ u0 Thttp://online.sagepub.com
$ u' S2 l  a0 C4 Z, R' }, W9 H/ {Precocious puberty in boys, central or peripheral,
7 h2 z$ l) B; F0 r% y& g$ uis a significant concern for physicians. Central. n5 l! |$ F7 M* B3 |1 A! s3 O, X
precocious puberty (CPP), which is mediated; j$ ~2 c  o3 U6 t  j; o# u
through the hypothalamic pituitary gonadal axis, has1 [  z- e& K$ Z% a
a higher incidence of organic central nervous system
/ }+ r9 G& C; o7 Plesions in boys.1,2 Virilization in boys, as manifested
" S3 j0 `) \9 h- \. }by enlargement of the penis, development of pubic
% p( E) j  i9 V& ehair, and facial acne without enlargement of testi-
6 y2 W0 }8 e7 P# |8 V3 `* Pcles, suggests peripheral or pseudopuberty.1-3 We. y+ E1 o6 S. L0 L% H
report a 16-month-old boy who presented with the
. X1 X/ r  u8 g  u# d/ u) Denlargement of the phallus and pubic hair develop-
$ o, y8 g2 F  a  s+ y: G( Vment without testicular enlargement, which was due
, ^  G9 S9 o; D% x) p3 fto the unintentional exposure to androgen gel used by. e; N8 ?8 O0 V4 z
the father. The family initially concealed this infor-
6 d+ F6 \& h# s& I" |mation, resulting in an extensive work-up for this: y* X! O* e4 _, G; z+ Z" @
child. Given the widespread and easy availability of: B! m9 o  T$ C. m2 D
testosterone gel and cream, we believe this is proba-$ \1 P+ {' L  U9 ?- X2 ^  o( L
bly more common than the rare case report in the
1 S5 u. x$ r. S) m6 Q3 Dliterature.4" L/ Q0 @& f3 Q. [4 o- u0 E+ u7 P
Patient Report
; I2 X) f1 ]. ?4 A3 FA 16-month-old white child was referred to the8 u3 o6 @$ F; v
endocrine clinic by his pediatrician with the concern
! n- U1 \) M+ ?/ R; g2 y1 hof early sexual development. His mother noticed
4 p& g& ?! E& Xlight colored pubic hair development when he was
) n0 e5 R* [  n- V: @9 _From the 1Division of Pediatric Endocrinology, 2University of0 B) w  z0 Z. V" L5 |8 A
South Alabama Medical Center, Mobile, Alabama.
' o9 M7 F" c5 x& O9 VAddress correspondence to: Samar K. Bhowmick, MD, FACE,: v* l- D2 \  C' f$ p# e
Professor of Pediatrics, University of South Alabama, College of
/ j: l# A! |  L2 L+ uMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
  c& V" K; A5 ~: \e-mail: [email protected].
+ {7 J) c$ q2 |2 T! \& m( X, ]about 6 to 7 months old, which progressively became
3 v3 d8 c3 k4 Odarker. She was also concerned about the enlarge-
" s  u6 P) Y% F$ Q  K: w+ J1 {ment of his penis and frequent erections. The child& d) R) x2 j1 H5 `5 Z! u. {
was the product of a full-term normal delivery, with
3 p9 y* ]1 U* t. `* oa birth weight of 7 lb 14 oz, and birth length of8 l: w3 P0 O5 |# K3 I7 J
20 inches. He was breast-fed throughout the first year
7 Z) L3 P, B) r) u1 Dof life and was still receiving breast milk along with
+ v: X8 ]5 p0 A5 i8 ^solid food. He had no hospitalizations or surgery,/ F0 \  G, `, u$ B* B6 W# [: V
and his psychosocial and psychomotor development0 c% J4 P, u& X7 s6 V7 O9 J: h
was age appropriate.
, l6 ]! N2 ~# A/ ]8 e' x. d; d% YThe family history was remarkable for the father,
6 t9 x2 W  \. xwho was diagnosed with hypothyroidism at age 16,
3 R  p8 s8 ^, ~' z. awhich was treated with thyroxine. The father’s
9 F6 u! _# J3 o7 ~3 qheight was 6 feet, and he went through a somewhat
- l/ C, {8 b/ S% |8 p# T  x! E  L* Searly puberty and had stopped growing by age 14.
  g3 _8 ]9 z) z% F. M; XThe father denied taking any other medication. The
9 ~4 N1 C, j/ Schild’s mother was in good health. Her menarche9 D  g; X! L" I" L
was at 11 years of age, and her height was at 5 feet
; g% k, a. S, b/ E6 f5 inches. There was no other family history of pre-, X7 E" J# C6 N1 Y; n
cocious sexual development in the first-degree rela-
, c- m% E5 T% A2 R0 Ptives. There were no siblings.
6 l2 \8 O$ S: S2 m9 j3 m' EPhysical Examination, @$ F6 a/ p5 M
The physical examination revealed a very active,
, u" `6 A* G8 f/ _5 @) uplayful, and healthy boy. The vital signs documented
8 A. C  e  P$ C5 z4 na blood pressure of 85/50 mm Hg, his length was1 s& ?% Z9 Q0 d" L1 _5 R
90 cm (>97th percentile), and his weight was 14.4 kg0 O2 T8 o+ g" C, Z/ B% _1 g" _3 k8 O
(also >97th percentile). The observed yearly growth1 ?2 [; h9 w7 ^7 u8 I3 j1 P
velocity was 30 cm (12 inches). The examination of
0 b; @8 x- a  Uthe neck revealed no thyroid enlargement.
* e- d# a1 q8 x2 CThe genitourinary examination was remarkable for
% X: Y3 }- L, |* Q1 _% Uenlargement of the penis, with a stretched length of
$ H/ z/ j" x* Q" t- h6 h8 cm and a width of 2 cm. The glans penis was very well
- @# d# G& ~+ ^  tdeveloped. The pubic hair was Tanner II, mostly around/ G, H- u7 B% E  ^
540  C4 a0 x( i* q7 p* J8 P/ E5 ?
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from: ^0 F6 Z4 R1 B4 W( {1 n9 }
the base of the phallus and was dark and curled. The
+ B, D) c! u( K. e7 H9 V' otesticular volume was prepubertal at 2 mL each." ~/ J2 [9 v2 C  ^3 R$ ^
The skin was moist and smooth and somewhat4 c7 ]; Q( }8 ~+ ]& W
oily. No axillary hair was noted. There were no+ M* m" ~; h: ^1 v+ W; H2 c, j9 k
abnormal skin pigmentations or café-au-lait spots.
& @: B. m$ M" }# Q$ l% |- F" INeurologic evaluation showed deep tendon reflex 2+1 P  H9 ?* {5 j9 {7 g7 T, V
bilateral and symmetrical. There was no suggestion" b" g2 B3 o! G3 b' ?  ^2 W5 q9 L
of papilledema.
& o! {9 p3 ^( `$ d% S0 Q- qLaboratory Evaluation9 C/ s* c( |% M' H/ z( U$ q2 n6 n
The bone age was consistent with 28 months by
# Q- U3 p; I# |, e) s  o/ a0 Yusing the standard of Greulich and Pyle at a chrono-
, i+ L2 y4 U% G' T' \logic age of 16 months (advanced).5 Chromosomal( k. k/ W2 `# j! _' [
karyotype was 46XY. The thyroid function test! T- G+ Y1 E$ G- }) s$ M
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
2 \: A9 i  \# n) v9 alating hormone level was 1.3 µIU/mL (both normal).
, R, y2 ^( b$ i$ d3 i: `3 {The concentrations of serum electrolytes, blood
" L5 t, l. E% E; m# m, }urea nitrogen, creatinine, and calcium all were
, x, n8 `# i3 xwithin normal range for his age. The concentration4 K1 C3 D/ k" A3 e& v
of serum 17-hydroxyprogesterone was 16 ng/dL
& h  Y4 J5 u6 ?(normal, 3 to 90 ng/dL), androstenedione was 20
- C* _8 P) X+ N- m8 H! z, F) Cng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-# t7 R; K1 R3 H, q" c  G) Q
terone was 38 ng/dL (normal, 50 to 760 ng/dL),/ O" \: j+ [: @
desoxycorticosterone was 4.3 ng/dL (normal, 7 to, s8 ]8 m) z& F% ~/ g
49ng/dL), 11-desoxycortisol (specific compound S)
( L" i* y' Z0 Awas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-- W  g4 ^. e0 z) H
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
& ?% ^! \6 H9 D; l! A, z; {testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
9 V1 u5 s8 k% x  j# f- `  N% Dand β-human chorionic gonadotropin was less than
5 n- }" V3 U' W5 mIU/mL (normal <5 mIU/mL). Serum follicular
! w: V" ]# a$ F1 W8 u4 @6 cstimulating hormone and leuteinizing hormone; {( o2 b4 w& x: M6 |8 \) f
concentrations were less than 0.05 mIU/mL
  |6 z9 b3 n# t$ y( ~(prepubertal).7 P' z6 ?. \3 j- f  R
The parents were notified about the laboratory
) D- R1 U' k) [9 E% w. ]9 ?4 L2 I( Iresults and were informed that all of the tests were5 ]- F5 p& ~3 e) _8 Y
normal except the testosterone level was high. The8 ~! {4 B+ d' @6 ~3 |' P+ G
follow-up visit was arranged within a few weeks to9 [+ [0 I2 ?7 R; }
obtain testicular and abdominal sonograms; how-
, f/ n5 k) |8 |, T! u! Iever, the family did not return for 4 months.4 U/ Y$ m7 @$ S/ d
Physical examination at this time revealed that the6 ^+ n0 N  R  D, R
child had grown 2.5 cm in 4 months and had gained6 N" d* o) d6 |* L2 Y* ]
2 kg of weight. Physical examination remained
& B, Z1 _2 c5 r+ w3 h3 O/ Eunchanged. Surprisingly, the pubic hair almost com-
9 h3 `' r$ v1 W0 s* r# Xpletely disappeared except for a few vellous hairs at
, ~( ^( b% x! w3 s& vthe base of the phallus. Testicular volume was still 2, D. f) I& ]1 V% \" u' t  W
mL, and the size of the penis remained unchanged.
: Q2 v  y# \* {9 I  c4 \0 _1 t/ @The mother also said that the boy was no longer hav-
$ V2 \$ R1 l3 A! N+ x4 f! ~ing frequent erections.1 d' R+ |! P9 l' Y* X  c& w8 L
Both parents were again questioned about use of
, J. t/ k  {  C8 e0 ~% t' ~' L0 p0 qany ointment/creams that they may have applied to5 v/ l$ _6 y. h* @! \
the child’s skin. This time the father admitted the) P& U3 M5 i' q
Topical Testosterone Exposure / Bhowmick et al 541
+ W$ i, q! Y' W* }: Q9 g9 Cuse of testosterone gel twice daily that he was apply-/ Y) `) o. c9 I4 o/ I% n" Z2 d
ing over his own shoulders, chest, and back area for1 K6 h& z" t& f4 {3 M6 q8 q( W
a year. The father also revealed he was embarrassed
4 R$ ~' m$ |% d% b9 ^  ito disclose that he was using a testosterone gel pre-3 D* {, J! @- m1 ~7 g
scribed by his family physician for decreased libido
* P  @3 u) p! D/ e2 O- N# msecondary to depression.8 }& Q4 I+ ?7 @+ E1 W
The child slept in the same bed with parents.( }" p  l+ u1 Y7 J# \7 ~+ J! N5 P
The father would hug the baby and hold him on his8 c& O1 Y% T, |; d6 i" W- _. C
chest for a considerable period of time, causing sig-( D$ t' ^9 ?& `8 }' j
nificant bare skin contact between baby and father.
# P- U7 {0 a6 }) l3 n. u  i, ^The father also admitted that after the phone call,9 B3 l, B. M+ c0 M+ w9 O" n
when he learned the testosterone level in the baby
7 x% t7 Q7 s; T" T" U4 Bwas high, he then read the product information
& {$ P: ]  G0 V5 t2 fpacket and concluded that it was most likely the rea-
5 }% T  j( p8 B$ ~$ m: Yson for the child’s virilization. At that time, they
0 `! ^; p* u. y8 G, V# ~* ~3 Gdecided to put the baby in a separate bed, and the
- a% }9 b/ k. f3 Z1 kfather was not hugging him with bare skin and had$ l: d5 d$ {4 Z! b
been using protective clothing. A repeat testosterone
. X, f) B+ Z  ^) ]2 Z. q# e1 C: ktest was ordered, but the family did not go to the
+ k/ o0 ]2 a' @- v! `9 b) Claboratory to obtain the test.
  i8 c3 O* P% D$ B1 K! T' ^0 @Discussion
8 m" i) M( H9 o+ h4 ~Precocious puberty in boys is defined as secondary
; o5 x6 j  @0 k; I9 p1 dsexual development before 9 years of age.1,4
" J+ }4 n# F& c; fPrecocious puberty is termed as central (true) when, ?; v8 k0 h  L+ \5 s
it is caused by the premature activation of hypo-
% a# k# ?( x: M; ?+ Z$ [1 jthalamic pituitary gonadal axis. CPP is more com-# d. v/ ^: F: d' k$ e
mon in girls than in boys.1,3 Most boys with CPP
. v* L3 k% s+ ?5 |may have a central nervous system lesion that is
! X8 H% [) E# D+ q$ }3 }responsible for the early activation of the hypothal-
# B4 b1 r  d, ?( uamic pituitary gonadal axis.1-3 Thus, greater empha-
* B7 Q) m1 \0 v* o- Csis has been given to neuroradiologic imaging in8 d3 d8 x& c1 P* H/ a; `
boys with precocious puberty. In addition to viril-
. [- ]; f0 `% v4 t/ e3 Eization, the clinical hallmark of CPP is the symmet-
. l+ V4 m1 n. D& |rical testicular growth secondary to stimulation by# U! E8 j- b8 s' [  z
gonadotropins.1,3  [& o8 F' q# E1 |, ~; L6 V
Gonadotropin-independent peripheral preco-
3 b% I% w; u; h+ }  m- tcious puberty in boys also results from inappropriate9 E+ c3 e8 G0 t8 [- h
androgenic stimulation from either endogenous or8 \3 h2 b4 Q* h! w2 a: Y* h
exogenous sources, nonpituitary gonadotropin stim-
4 F4 J" w( q$ }9 h! g6 O, lulation, and rare activating mutations.3 Virilizing
  ^/ E" N5 F& b: g+ `0 ncongenital adrenal hyperplasia producing excessive+ H: }! U  v1 m" X, \, {& c
adrenal androgens is a common cause of precocious# U: f6 _. i! ?" u; R  b
puberty in boys.3,4
7 V2 V8 u7 b4 j6 jThe most common form of congenital adrenal
1 V1 T* i- k$ Q7 jhyperplasia is the 21-hydroxylase enzyme deficiency.
% `8 m$ U# r+ {& E/ Z6 wThe 11-β hydroxylase deficiency may also result in+ C* d* Y& K8 P( `3 F
excessive adrenal androgen production, and rarely,
& x; v" ^8 x0 b  S+ x0 Uan adrenal tumor may also cause adrenal androgen
/ }7 |) V) g3 [6 cexcess.1,3
4 M2 J0 K  q4 K; hat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from8 W7 q# f+ Y7 s5 ?8 r
542 Clinical Pediatrics / Vol. 46, No. 6, July 20077 e9 B( R! Y" G% C7 [
A unique entity of male-limited gonadotropin-! N/ _2 i+ r; I$ n5 ^; ?9 _6 P6 k
independent precocious puberty, which is also known4 ^+ t: X& C5 v2 M1 E
as testotoxicosis, may cause precocious puberty at a/ R* K, e- n( w/ s: \& Q- i9 {
very young age. The physical findings in these boys
6 ]# s4 p# Z9 P0 t! w: Lwith this disorder are full pubertal development,, N, e! [. Y' `& p  b2 V6 f" \7 X* \
including bilateral testicular growth, similar to boys7 M% d/ u5 X, _/ b4 b( ^
with CPP. The gonadotropin levels in this disorder9 F2 F( Z5 h/ K/ C2 u9 l4 p/ y7 ?
are suppressed to prepubertal levels and do not show6 Z( z$ o& ^5 a% N; D5 S
pubertal response of gonadotropin after gonadotropin-; e& I; f0 @& f# u5 ]# b- h5 f
releasing hormone stimulation. This is a sex-linked
; e& {+ G3 v4 \  ^autosomal dominant disorder that affects only% U: {+ D0 G' J2 S0 t
males; therefore, other male members of the family5 ~! @+ ^6 T2 X3 \% d1 |9 l/ J
may have similar precocious puberty.3
% S1 c2 L; Y% ^7 WIn our patient, physical examination was incon-  ]( l, z4 S; ~7 j
sistent with true precocious puberty since his testi-
, C4 S; M1 W# D- Ycles were prepubertal in size. However, testotoxicosis  f1 I7 ^% K* p1 e
was in the differential diagnosis because his father* r; N. @, S# ]" ^% T
started puberty somewhat early, and occasionally,+ A+ m8 ?1 x* B" H: C/ N( J
testicular enlargement is not that evident in the
" z8 u) C  g2 K: A: p8 N: g* M3 |! g" Ubeginning of this process.1 In the absence of a neg-
+ b; U; u: J9 l6 d+ I( kative initial history of androgen exposure, our
4 d) ]9 a) h! kbiggest concern was virilizing adrenal hyperplasia,
: M$ B- W  g2 S4 F$ O. Seither 21-hydroxylase deficiency or 11-β hydroxylase( @- |/ t! U8 V- x
deficiency. Those diagnoses were excluded by find-
- Y* @! y$ F9 i* Ring the normal level of adrenal steroids.
' \! z5 E; n6 F3 zThe diagnosis of exogenous androgens was strongly) _9 T4 H2 F+ t  U; ~& Q
suspected in a follow-up visit after 4 months because
3 j+ ]) M7 t0 j6 D  k+ F8 q$ ^the physical examination revealed the complete disap-7 |8 T( R/ m' [# ~, S; c/ j
pearance of pubic hair, normal growth velocity, and! }$ U3 W+ O9 x4 f& \' H
decreased erections. The father admitted using a testos-
* u7 `# O3 D7 o- g( lterone gel, which he concealed at first visit. He was( R5 d! B) F3 a; t
using it rather frequently, twice a day. The Physicians’
, P9 ?" [+ m( Y) ADesk Reference, or package insert of this product, gel or5 ~3 S( L5 W, k, I
cream, cautions about dermal testosterone transfer to0 H9 d( E% ?3 G" A  `
unprotected females through direct skin exposure.9 S( y: t6 F/ O5 V7 K
Serum testosterone level was found to be 2 times the) s: F1 o* u# R- k
baseline value in those females who were exposed to
5 l0 o" |7 R: d! @& F. n; {! L0 Meven 15 minutes of direct skin contact with their male
/ D3 G9 E2 r. c# spartners.6 However, when a shirt covered the applica-
$ {1 q  F+ g7 U# M5 L# ktion site, this testosterone transfer was prevented.
: U$ o$ S1 B0 O! [4 COur patient’s testosterone level was 60 ng/mL,5 h' m3 U' C  d: }
which was clearly high. Some studies suggest that5 D4 H* f+ Z& q7 d( i: X
dermal conversion of testosterone to dihydrotestos-
) _6 e) m) W) b. T* hterone, which is a more potent metabolite, is more: w5 ~" ?1 ~# }9 E) {) C
active in young children exposed to testosterone5 {: p+ `+ [0 F7 J
exogenously7; however, we did not measure a dihy-
- z8 g- U! ?% ?  T" C& fdrotestosterone level in our patient. In addition to
- G* M/ R8 w. \! z; w! @% xvirilization, exposure to exogenous testosterone in
' \: }9 E$ q- l$ ]8 o* C$ Echildren results in an increase in growth velocity and
( z% e) F* p% R9 V7 F4 w) ~0 Sadvanced bone age, as seen in our patient.
3 T2 k, Z* j3 |' F2 S9 HThe long-term effect of androgen exposure during
( P! `& Q2 B2 G; U3 z$ Hearly childhood on pubertal development and final! U* l3 O  q7 O/ U/ \5 ]
adult height are not fully known and always remain
. _! ^1 ^) F% k  A# E8 q, e/ g* B; Ba concern. Children treated with short-term testos-
6 y0 T3 b8 _8 w: Lterone injection or topical androgen may exhibit some3 I% g  V4 \- _3 t4 m* J
acceleration of the skeletal maturation; however, after$ ~$ N( ?+ C/ m+ R. l) d
cessation of treatment, the rate of bone maturation2 C2 A. F3 d+ G! C# t; y+ ]! V
decelerates and gradually returns to normal.8,9
1 T3 z' }* ?6 N3 i- ^" kThere are conflicting reports and controversy
; Y8 {5 ?3 d1 L, b3 `4 iover the effect of early androgen exposure on adult, C. R2 v( I8 v1 Z/ w
penile length.10,11 Some reports suggest subnormal! h  n( H& O1 }0 z7 n. V# t
adult penile length, apparently because of downreg-7 B, N8 ]1 f7 N4 b, N+ {
ulation of androgen receptor number.10,12 However,* s" x) D7 C7 Q% e8 U
Sutherland et al13 did not find a correlation between! j7 N. R4 ^# v) W1 D- j
childhood testosterone exposure and reduced adult
4 {7 T" Q8 s* \2 o8 h0 q5 ~penile length in clinical studies.
* G4 F( N, A, u, O. cNonetheless, we do not believe our patient is
6 C) c  f7 Q- ~" W# W8 ugoing to experience any of the untoward effects from5 b( ?; M8 r- J
testosterone exposure as mentioned earlier because
# C( D* h( P7 [2 h1 y! |the exposure was not for a prolonged period of time.
. K% G( N4 r- h7 V2 F1 ]Although the bone age was advanced at the time of# B6 G: j0 d1 p* Q1 @% w
diagnosis, the child had a normal growth velocity at
2 |( }* y. f, Tthe follow-up visit. It is hoped that his final adult
) k; r" E1 @6 q( }: C% jheight will not be affected.
+ S) G* c+ h( U  AAlthough rarely reported, the widespread avail-
! I2 l( }" k3 t# x( L4 Z  l$ o  @ability of androgen products in our society may
$ t! }6 W% k8 Q, N0 X0 g6 J; }6 Dindeed cause more virilization in male or female
  {5 [1 _2 X; ^6 K9 `* ~children than one would realize. Exposure to andro-
' ?. h; q& i# X: T, ugen products must be considered and specific ques-+ V4 C8 m8 S/ x* F% q) D4 |4 b
tioning about the use of a testosterone product or
! y/ Z4 u. U$ N- _" @gel should be asked of the family members during: O6 k# ], U! `  P2 @7 P
the evaluation of any children who present with vir-
2 U# b4 \& M4 {% r* s% Tilization or peripheral precocious puberty. The diag-
# w8 _& N: {1 y3 \7 ]* Z' \nosis can be established by just a few tests and by
3 z) R2 g$ Q* v( C& t# l9 eappropriate history. The inability to obtain such a
% S- x' x9 F' C, q7 yhistory, or failure to ask the specific questions, may. [8 j: d% O$ ~1 R: \: h6 U  X' H: p. K
result in extensive, unnecessary, and expensive
/ w( {# q1 f0 e0 xinvestigation. The primary care physician should be
( j/ G! z+ r6 s: I8 oaware of this fact, because most of these children
" ~6 ^5 x' C  p; R9 h; q  C( wmay initially present in their practice. The Physicians’
5 v" E: m& }% _5 M% v* t- _. Y" vDesk Reference and package insert should also put a
6 B: q3 N( |* b  O/ ^. ?warning about the virilizing effect on a male or: M7 G5 Q) D# j+ E
female child who might come in contact with some-4 p7 X; p, z) d% |- ~, ]2 T
one using any of these products.2 c* N5 Q* P* K& |
References: Z3 q  V2 \: D( K
1. Styne DM. The testes: disorder of sexual differentiation
' M# T" e( V0 H- |7 K; Gand puberty in the male. In: Sperling MA, ed. Pediatric# J6 B, |8 H8 |& H) B
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
  [  @! H( v0 _- \! B  e2002: 565-628.' U+ F' A  T" H1 B! @% x1 I) A* [
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious" G7 h0 d& `9 B5 }% w, t
puberty in children with tumours of the suprasellar pineal
發表於 2025-1-7 21:59:43 | 顯示全部樓層
這個我收藏了!謝謝分享!WK的資源越來越豐富,這少不了大大的辛勞!
發表於 2025-1-10 10:43:39 | 顯示全部樓層
VIP精品區,資源無限好賺金任務區,輕松賺金幣
加入VIP,享受高級特權宣傳賺金又升級,超級棒
感謝大大的辛勞分享!我會繼續在WK關注大大的文章!
發表於 2025-1-11 22:18:01 | 顯示全部樓層
女厕偷拍辅导班主任尿尿老师的逼很嫩还有一点
發表於 2025-1-17 16:31:39 | 顯示全部樓層
VIP精品區,資源無限好賺金任務區,輕松賺金幣
加入VIP,享受高級特權宣傳賺金又升級,超級棒
4个什么样的?
發表於 2025-1-19 02:41:05 | 顯示全部樓層
! O  ~- \' K; P7 U
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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