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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
2 e- M" Q: q3 g. G; `/ x# Y0 h+ E2 qBoy Induced by Indirect Topical- k: r! S: d6 S) e
Exposure to Testosterone
4 Z3 ^. o6 J2 cSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,26 t+ p" V6 }: T$ S4 T  B! N
and Kenneth R. Rettig, MD1; o. _! G) {4 F/ `$ @/ Q
Clinical Pediatrics5 a/ g! A) \$ @' x# W* t: k& A4 [
Volume 46 Number 6
$ C1 z2 M# {. [July 2007 540-5439 ^! X& l+ G+ i% ?% [& l
© 2007 Sage Publications
' |- K% Y% ~; T) d# v6 J3 q10.1177/0009922806296651
- l& b8 c- z/ e8 Z' {9 shttp://clp.sagepub.com
1 m  s' k  O/ p: W1 fhosted at
$ y. `7 `% r6 P# ?1 X, P! q1 @http://online.sagepub.com, _( @/ p  Z( K. G
Precocious puberty in boys, central or peripheral,% P& |1 T; t. _$ b1 o, b
is a significant concern for physicians. Central+ h; t- `; }2 [8 A, Z4 H
precocious puberty (CPP), which is mediated
2 P$ M1 e6 z! x  ?through the hypothalamic pituitary gonadal axis, has
) k: j! n& e8 P) i! ?a higher incidence of organic central nervous system
$ A: z2 `# x& `' ~  Vlesions in boys.1,2 Virilization in boys, as manifested
3 K  d6 w. N' c' n0 s7 ^3 S4 m4 tby enlargement of the penis, development of pubic- z$ Z/ H, m' Q( P9 N; H
hair, and facial acne without enlargement of testi-. k/ O+ T+ a; O; x
cles, suggests peripheral or pseudopuberty.1-3 We0 M0 ^- g- D1 q4 v+ @# m, w7 g
report a 16-month-old boy who presented with the2 P2 ~8 ^: j& x3 g
enlargement of the phallus and pubic hair develop-
8 I* [1 Z. ]; h6 nment without testicular enlargement, which was due) }  c- F9 L! u7 e5 s# Q3 ?0 Q
to the unintentional exposure to androgen gel used by
/ J2 @3 H) [4 C$ T) N2 C4 Xthe father. The family initially concealed this infor-
6 Q, q% n' v6 Y+ Q% u. U% j/ i5 @mation, resulting in an extensive work-up for this
& a6 Q  B* ~5 b. i& [, E: J) Dchild. Given the widespread and easy availability of
6 V) P9 f, q! K: r5 r3 Dtestosterone gel and cream, we believe this is proba-8 x4 [0 J( a- y+ {: D
bly more common than the rare case report in the1 `; g( B0 N5 ?2 x; G4 j6 P
literature.4
0 e( Z6 Q- v, i- @# o9 e# _Patient Report
2 B/ U1 ]$ v( [A 16-month-old white child was referred to the/ ^# s# o' e6 v  |5 m4 v
endocrine clinic by his pediatrician with the concern
- w- j' e0 L# ?: D. m) Y6 [4 q; Kof early sexual development. His mother noticed
/ X7 P+ O- H5 c) ~# v0 `2 plight colored pubic hair development when he was
% I3 S. C: x' CFrom the 1Division of Pediatric Endocrinology, 2University of
+ |/ r$ P& m+ u  WSouth Alabama Medical Center, Mobile, Alabama.
8 I% `- H4 q8 ]* X3 Y, oAddress correspondence to: Samar K. Bhowmick, MD, FACE,
; Z! C% g3 q1 |9 E$ dProfessor of Pediatrics, University of South Alabama, College of0 J9 T3 Z+ R) S: x: i) E) l
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;) E7 A0 @- Y/ r6 O3 `( C% [) w
e-mail: [email protected].
  e# d/ ?% r- z& P9 ], s1 x8 Uabout 6 to 7 months old, which progressively became
; I/ K( ~. T# ]4 @; jdarker. She was also concerned about the enlarge-
. E. J8 y# b6 r% ]ment of his penis and frequent erections. The child; n2 h3 y* y$ j, P- P
was the product of a full-term normal delivery, with
0 J" s" I" W  l! aa birth weight of 7 lb 14 oz, and birth length of0 H6 f, `  P! R- v' z" U
20 inches. He was breast-fed throughout the first year/ a  g  Q# v3 T: c4 r+ O$ h
of life and was still receiving breast milk along with- D' t8 w1 Z8 I0 d$ Z
solid food. He had no hospitalizations or surgery,
# S) h7 |1 Y$ [6 i# z3 Y% Rand his psychosocial and psychomotor development
% J  m4 {) X( k$ e  M' Pwas age appropriate.' z5 [: J1 u9 ]& Q# C/ C9 v, r
The family history was remarkable for the father,
. d' f. ^3 W/ p! c! rwho was diagnosed with hypothyroidism at age 16,* }1 m' o1 v1 Y7 H! v
which was treated with thyroxine. The father’s) Z& Q5 q% E: @5 f2 K7 W
height was 6 feet, and he went through a somewhat! ~& J: \* D! G, G* n9 T7 z1 w
early puberty and had stopped growing by age 14.5 u& C8 c/ B2 u1 P
The father denied taking any other medication. The& S: R7 `% W9 Z  \' t; E
child’s mother was in good health. Her menarche
" R9 o- @0 p/ E1 [( ^) [was at 11 years of age, and her height was at 5 feet
6 ]& z2 R0 H! h) b. o5 inches. There was no other family history of pre-
' B) d9 r$ f0 p% C9 Scocious sexual development in the first-degree rela-! A. B0 P  `" C
tives. There were no siblings.
5 l1 _; q: c" p; \Physical Examination
9 d, f, h! r3 BThe physical examination revealed a very active,  r- [8 g" A* E/ b  g5 E1 d' d
playful, and healthy boy. The vital signs documented
2 Q1 l8 P+ p9 \; M8 Ta blood pressure of 85/50 mm Hg, his length was
5 W# r+ n( E) p6 v5 R3 T90 cm (>97th percentile), and his weight was 14.4 kg2 x5 |. a- o/ r5 T: m4 m+ m
(also >97th percentile). The observed yearly growth+ P$ A- q- s2 m$ |" `5 E( O1 ?
velocity was 30 cm (12 inches). The examination of
! n3 w2 c8 C. l' Wthe neck revealed no thyroid enlargement.
1 y" t- T! P. J: k7 q% H7 jThe genitourinary examination was remarkable for
' c% M$ c+ L  K( k: b  wenlargement of the penis, with a stretched length of
4 S' C) T% Q* u7 H7 Z8 cm and a width of 2 cm. The glans penis was very well
9 D  E- W0 j/ \& i7 fdeveloped. The pubic hair was Tanner II, mostly around: \. i: X2 b. b+ W  `& y
540
: P, S  _( i: g4 v8 g2 Hat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
& {% y0 _  ]/ j! o8 Kthe base of the phallus and was dark and curled. The: G- z) T" i& U
testicular volume was prepubertal at 2 mL each.2 {: }' I# k/ y
The skin was moist and smooth and somewhat
- [  {6 e' L, z; |oily. No axillary hair was noted. There were no, r% T( v9 T( F& L/ j" A
abnormal skin pigmentations or café-au-lait spots.
' f& W- m+ G. c( sNeurologic evaluation showed deep tendon reflex 2+* V: o) s  g, b. X
bilateral and symmetrical. There was no suggestion% ?' @# l' T) s- o
of papilledema./ l% c  K3 C  z6 G1 E0 Q3 p4 K' [- P
Laboratory Evaluation' m( b, M  V: }+ S0 V! ~
The bone age was consistent with 28 months by
$ }1 N1 H5 L' N4 \1 E) G, f# }6 susing the standard of Greulich and Pyle at a chrono-4 b9 J/ p. g1 i" j+ H' z8 Y
logic age of 16 months (advanced).5 Chromosomal
. |9 C- ~5 j9 f3 qkaryotype was 46XY. The thyroid function test
7 U0 h9 M7 x2 b0 d$ @2 zshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
- v' u) e) L3 Y+ D0 Glating hormone level was 1.3 µIU/mL (both normal).
6 F* V) E+ Y  ?4 X7 [The concentrations of serum electrolytes, blood8 Q& h% j# @9 B) o8 U$ m0 \
urea nitrogen, creatinine, and calcium all were
' m, c7 N9 w0 vwithin normal range for his age. The concentration- w7 n: W: L( @
of serum 17-hydroxyprogesterone was 16 ng/dL  Q! W6 L& q) T) P4 O
(normal, 3 to 90 ng/dL), androstenedione was 20
1 A; q" W( I4 n& ^4 wng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
( i5 c. s; |7 D% O: ^) ^! Bterone was 38 ng/dL (normal, 50 to 760 ng/dL),. f/ l! n! E; I$ R& o
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
! X0 c$ I% m* m. P49ng/dL), 11-desoxycortisol (specific compound S)) A! s4 `) C; T' k: H: \( P$ m
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-) D1 Q" Z! T' Y" V6 |5 _1 s& u
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
0 ^, B/ q: m+ vtestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
9 C( ]. i1 J! N4 P: M' c5 \/ fand β-human chorionic gonadotropin was less than
- n+ u/ }/ w" O/ O, P. ~5 mIU/mL (normal <5 mIU/mL). Serum follicular
8 S7 c9 N# q4 q6 ^/ tstimulating hormone and leuteinizing hormone0 u# {& x$ N2 E- }1 c1 m
concentrations were less than 0.05 mIU/mL
$ L6 C4 o# J, k: C5 R1 r: H, l(prepubertal).0 y. \9 n; N1 P
The parents were notified about the laboratory) m6 ]! H3 i# Y! [* r% d
results and were informed that all of the tests were- v# q: Y# s/ X7 r* t3 g
normal except the testosterone level was high. The. K5 O3 [7 W) g' n2 @, k' ?
follow-up visit was arranged within a few weeks to$ }9 t+ }* p2 u6 _$ _
obtain testicular and abdominal sonograms; how-
; r* S, g; \* M1 m" never, the family did not return for 4 months.
0 h% ^; L1 p! gPhysical examination at this time revealed that the) y. y5 }( R4 d  k" b' v8 `# x
child had grown 2.5 cm in 4 months and had gained' @, E9 x, a0 o7 L2 ?+ e
2 kg of weight. Physical examination remained
8 ^5 D* ^) N( W1 `unchanged. Surprisingly, the pubic hair almost com-
$ Y0 A3 U: z- l  lpletely disappeared except for a few vellous hairs at
1 _% [4 k! R: b. u6 K, a& Kthe base of the phallus. Testicular volume was still 2' ^! E3 Y  v( E+ z, r! q
mL, and the size of the penis remained unchanged.9 F/ p) h; U, @" S' l( l
The mother also said that the boy was no longer hav-6 A; _; e# o* d
ing frequent erections.
/ A/ c% t$ I1 }% z) x  MBoth parents were again questioned about use of5 G7 _- f5 X& k4 U  T2 v/ a2 g8 b
any ointment/creams that they may have applied to
, l/ y& H- ?- U8 M8 D; W/ s+ C" sthe child’s skin. This time the father admitted the9 m% F# ~- O" p% V
Topical Testosterone Exposure / Bhowmick et al 5411 d* A8 W% e$ V
use of testosterone gel twice daily that he was apply-+ f4 z9 @! v- \- u2 v
ing over his own shoulders, chest, and back area for
* w, F/ y' s6 w+ y; L: ba year. The father also revealed he was embarrassed
5 z( d7 r3 @9 t+ f/ g6 Z1 Ato disclose that he was using a testosterone gel pre-
- L% U- F: d4 v3 L; Tscribed by his family physician for decreased libido: l& W- B8 E# ?3 Z8 i& X$ A
secondary to depression.
4 S1 k- Z  Y! S* H: l/ _+ `) ~: Q  }The child slept in the same bed with parents.$ s/ \1 V9 }7 U
The father would hug the baby and hold him on his" S% k3 y) _' I
chest for a considerable period of time, causing sig-2 D8 d. i$ k: w% h2 K9 F  K
nificant bare skin contact between baby and father.
& Q8 C0 A4 j8 b3 B2 j2 k) DThe father also admitted that after the phone call,
. w  O) P- Z, S! ]' p+ v! ~when he learned the testosterone level in the baby4 ?* [* K4 S# N% x; l
was high, he then read the product information
$ O% H% S) p3 j2 Ypacket and concluded that it was most likely the rea-% c" W8 h% x) j4 @% G8 T
son for the child’s virilization. At that time, they
7 ]' s. e  s% p2 B, j. ~decided to put the baby in a separate bed, and the1 s9 g! o1 d! x( x
father was not hugging him with bare skin and had$ l4 \8 A- ?7 {6 @) E
been using protective clothing. A repeat testosterone
* y  P% J7 ]8 R  a, m  H4 itest was ordered, but the family did not go to the
, I" @, @; {, {5 f, w8 T/ S9 Hlaboratory to obtain the test.
5 L6 p( J2 N  z. V% {Discussion9 @7 P( ]" J3 T2 z0 K+ C1 o5 F" Y
Precocious puberty in boys is defined as secondary5 w  |, Z% B# H3 ~+ p: T6 z
sexual development before 9 years of age.1,4, B- m7 x* H  m7 ]
Precocious puberty is termed as central (true) when: i- c8 i4 C6 t0 [
it is caused by the premature activation of hypo-8 q7 }; z6 l) ?( X- [" H3 }
thalamic pituitary gonadal axis. CPP is more com-
% J( B, R$ \+ \8 bmon in girls than in boys.1,3 Most boys with CPP
3 c4 N$ L6 Y! E' Jmay have a central nervous system lesion that is: _2 v9 T" H+ J. C
responsible for the early activation of the hypothal-
. O/ l; y: K+ i1 uamic pituitary gonadal axis.1-3 Thus, greater empha-* X. ^5 U: A+ L1 I( T+ _7 O
sis has been given to neuroradiologic imaging in
! M: B8 @0 n6 f3 c8 l( j9 mboys with precocious puberty. In addition to viril-
+ D2 D5 V# Q8 U3 e; u, s: Hization, the clinical hallmark of CPP is the symmet-- O$ ^' K$ E, H8 \7 _
rical testicular growth secondary to stimulation by* @8 Y) V; |9 b& b
gonadotropins.1,30 l4 G* ^" q1 d5 p7 \* j8 r8 I, b
Gonadotropin-independent peripheral preco-6 n  O/ c# K7 D8 c6 W
cious puberty in boys also results from inappropriate
1 C/ t  r* m  ^, nandrogenic stimulation from either endogenous or
4 M+ t! f4 ]6 w' ?# Oexogenous sources, nonpituitary gonadotropin stim-: t$ O; K4 o0 U: i. Z( K5 C* n* }
ulation, and rare activating mutations.3 Virilizing
& F  Y  l5 o, x& r% ~congenital adrenal hyperplasia producing excessive
8 _! K2 G/ V- `; Y9 H: }adrenal androgens is a common cause of precocious: D  L* v  n/ U# p; ^" _4 t2 l
puberty in boys.3,4
4 ]3 T* e, p3 z0 wThe most common form of congenital adrenal5 p8 G8 e* |2 q0 S5 k
hyperplasia is the 21-hydroxylase enzyme deficiency.
9 O* C% J9 R! [9 o* xThe 11-β hydroxylase deficiency may also result in
7 u, i3 w* G3 F7 H5 A( A& lexcessive adrenal androgen production, and rarely,
* Y' q# e0 K/ Y4 C( f% a+ Fan adrenal tumor may also cause adrenal androgen
1 [# |8 f5 ]6 Z" X5 Hexcess.1,3: K- C9 b) Z: q  U
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
# O( B# x. l( Y+ u, d& s1 t542 Clinical Pediatrics / Vol. 46, No. 6, July 20071 O& _  j' w4 X; w2 @# O) p: H- a3 a
A unique entity of male-limited gonadotropin-
( m/ J! ^- A/ d' m- Jindependent precocious puberty, which is also known9 @0 r2 g; q0 f- ?; v
as testotoxicosis, may cause precocious puberty at a
2 z$ Q# P) U- gvery young age. The physical findings in these boys# M  g# U* M' i$ l% n) ~
with this disorder are full pubertal development,
9 N, X6 k- ?5 ~; c) j# A$ H/ Kincluding bilateral testicular growth, similar to boys( I1 |5 m6 P; A
with CPP. The gonadotropin levels in this disorder
# v- [$ `6 O! u, `! [are suppressed to prepubertal levels and do not show
' s% M: a# T* a8 W( y6 z: k$ Rpubertal response of gonadotropin after gonadotropin-3 G& L( j+ m* M9 x" p  ]
releasing hormone stimulation. This is a sex-linked" @9 b2 W5 ~8 A  c. z
autosomal dominant disorder that affects only) u+ {# Z# `5 X; g. {( F5 B
males; therefore, other male members of the family
) b4 v! A) w6 }3 amay have similar precocious puberty.3
  h% T. |, o- K$ zIn our patient, physical examination was incon-, ]! L% m* ?3 N4 y8 U$ C) T( t
sistent with true precocious puberty since his testi-" w) {/ s) J* x' J6 n, ~
cles were prepubertal in size. However, testotoxicosis
" M  |1 N. N7 \. B8 mwas in the differential diagnosis because his father: K& ~6 l+ ]( K  I* w
started puberty somewhat early, and occasionally,
" U8 V1 g) Y, s! H/ ftesticular enlargement is not that evident in the
" e! h; t2 K3 e0 T" |+ fbeginning of this process.1 In the absence of a neg-' ]& D, z4 `, g  D7 h6 q
ative initial history of androgen exposure, our0 q/ y$ ~9 ~. u
biggest concern was virilizing adrenal hyperplasia,
' d4 [2 k  K/ _% u7 ~1 heither 21-hydroxylase deficiency or 11-β hydroxylase
9 j5 k, ^8 [$ H  w5 C+ ndeficiency. Those diagnoses were excluded by find-
6 t5 K1 C4 P; _$ j" aing the normal level of adrenal steroids.* Z, w1 y2 T! n5 w7 |7 d  H
The diagnosis of exogenous androgens was strongly
1 I1 k8 H7 F7 v  ^3 \( o* ~1 B& W, esuspected in a follow-up visit after 4 months because
4 [, G$ H0 L0 P) i) M! N8 Lthe physical examination revealed the complete disap-4 y. j/ V8 d' m) m0 x' R5 Y
pearance of pubic hair, normal growth velocity, and
( Z% k$ g6 o2 Ddecreased erections. The father admitted using a testos-
3 A, o, _8 j9 c8 F( W3 \) iterone gel, which he concealed at first visit. He was
. Z9 O: P  E& w2 F! d7 i' b" Pusing it rather frequently, twice a day. The Physicians’
5 o. R4 z. c; |Desk Reference, or package insert of this product, gel or/ O# {) ~- s* m) c, L8 A  z
cream, cautions about dermal testosterone transfer to
' x8 c3 j7 A8 o2 z: L7 O- |  Eunprotected females through direct skin exposure.
/ e( j% {( g4 r8 `8 c* R+ b& tSerum testosterone level was found to be 2 times the
, c  \/ l& f- v/ X+ h7 @( jbaseline value in those females who were exposed to
! g6 p3 U: c  |& \. Geven 15 minutes of direct skin contact with their male& j( n" M" b0 ?' O7 c. s9 b7 c5 b
partners.6 However, when a shirt covered the applica-  n& H8 D: m/ [! T' z0 ~2 w4 f% i
tion site, this testosterone transfer was prevented.- O" d; L8 o, z8 r8 }0 v
Our patient’s testosterone level was 60 ng/mL,$ [; q8 y* l' x, o1 N% {" T
which was clearly high. Some studies suggest that  X5 m, z) D7 H0 s8 F* X
dermal conversion of testosterone to dihydrotestos-
: t3 I* g9 e7 ~- t/ }terone, which is a more potent metabolite, is more
4 X7 l1 \7 ^" tactive in young children exposed to testosterone% B- x0 B: O+ |0 ]8 ~, K
exogenously7; however, we did not measure a dihy-9 P6 Y9 }2 P. Y& r  h
drotestosterone level in our patient. In addition to
3 s1 n* b7 A+ |* O5 ?7 {# jvirilization, exposure to exogenous testosterone in6 M0 k( f% p; [! ~2 z! C$ B
children results in an increase in growth velocity and3 q' Y1 g- e/ ?9 k+ Q
advanced bone age, as seen in our patient.
$ v: _- F4 N: VThe long-term effect of androgen exposure during
# `& H/ t. b! {% [early childhood on pubertal development and final: v! Y& x! r0 Z9 X- z8 x8 M& T" n
adult height are not fully known and always remain) e4 g6 o% Z, G+ B) E
a concern. Children treated with short-term testos-2 E4 y  A! D) r8 c! e
terone injection or topical androgen may exhibit some
/ q% [* P2 G8 ?+ y* s: B6 nacceleration of the skeletal maturation; however, after
4 S% V3 r+ Y5 O! J/ Rcessation of treatment, the rate of bone maturation8 O7 v4 a- e3 T3 b' E& q
decelerates and gradually returns to normal.8,94 C+ n9 b2 @. A' W. u' V
There are conflicting reports and controversy
" K  w$ ~- C9 ^over the effect of early androgen exposure on adult
* K& E) ~2 [0 U% M. G4 P6 A4 g4 Gpenile length.10,11 Some reports suggest subnormal
0 }2 y1 Y) z3 J: ?5 Gadult penile length, apparently because of downreg-+ ~, q" N# @  h2 x! L
ulation of androgen receptor number.10,12 However,
2 z# R! a" e; |1 F; E( o0 y4 ISutherland et al13 did not find a correlation between) F- `3 y0 V# q' r
childhood testosterone exposure and reduced adult
' B# j) V+ v% {- Spenile length in clinical studies.% ?7 z0 a1 d8 `8 b( K& J" P& l* @
Nonetheless, we do not believe our patient is
: @# w: ^: t+ G' B/ m: zgoing to experience any of the untoward effects from
& N, B! g+ @9 S  y5 \/ |1 Rtestosterone exposure as mentioned earlier because7 z' ^  C( z6 S  f$ L9 C
the exposure was not for a prolonged period of time.1 k0 {. z/ {5 T) @
Although the bone age was advanced at the time of8 P1 i$ O: t8 J+ c% F
diagnosis, the child had a normal growth velocity at4 P( B: }4 O0 a* Z8 B1 v
the follow-up visit. It is hoped that his final adult
+ F/ ?; w1 P' r, Theight will not be affected.' ~. H5 j3 Q5 Z. E1 @
Although rarely reported, the widespread avail-4 q" S! n9 @9 ?
ability of androgen products in our society may0 d4 }  i) H+ |8 j; O
indeed cause more virilization in male or female% |9 I; b- [  O4 q6 {- f7 {0 m6 Q
children than one would realize. Exposure to andro-3 K: F+ X9 X9 p: H# Q1 O. b
gen products must be considered and specific ques-: T! _7 R3 p8 i1 M8 i( {
tioning about the use of a testosterone product or: i+ P0 c- p2 s4 N- s4 s
gel should be asked of the family members during
# H/ x9 D" V5 [the evaluation of any children who present with vir-
6 N& t5 l( ^! T3 I* u1 yilization or peripheral precocious puberty. The diag-
( g# n% ~6 G& R& S& Lnosis can be established by just a few tests and by6 E8 Y. @1 \# V) j
appropriate history. The inability to obtain such a7 r' @& D9 [3 H
history, or failure to ask the specific questions, may* x  N; X; P1 k. t) M% j5 p* T
result in extensive, unnecessary, and expensive5 V% k" x! B3 b
investigation. The primary care physician should be& T) S1 o. W& l* j
aware of this fact, because most of these children: r. L" b  ^+ a+ g
may initially present in their practice. The Physicians’
' F2 r  z, B- Q: V9 w; bDesk Reference and package insert should also put a
) \, I6 R2 v2 v' q4 P' s) v$ pwarning about the virilizing effect on a male or4 m% O9 v! M, q* V
female child who might come in contact with some-* `6 g& u9 t# \% p' T
one using any of these products.
: E5 v8 Z. ^, v2 jReferences
, q; z0 f" d5 S, ~1. Styne DM. The testes: disorder of sexual differentiation
# j8 j/ ^. U( \  F" E  Q; ]and puberty in the male. In: Sperling MA, ed. Pediatric2 k6 X" E7 K- x& n
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
5 j" R4 j- J6 V2 Q% ]+ k3 }+ e2002: 565-628.- S; }: X- m! h0 c& h1 M1 h$ h
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious4 ~; W% C: E  `8 @9 i( l; j8 |
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
7 m6 [  I$ a9 g2 o# N5 O& y+ rBoy Induced by Indirect Topical
; S% u6 _5 o- _/ t6 Y$ o% ~Exposure to Testosterone& s. s' U% F. Y# d6 j0 W* j2 D
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2' N/ C2 W9 v) k2 X) U
and Kenneth R. Rettig, MD1! Q4 p1 d4 M9 f' J" I8 f
Clinical Pediatrics
7 P. a+ U! s& u9 Q6 j3 Y/ fVolume 46 Number 6( j/ R5 B7 [+ k; Q+ p* p
July 2007 540-543' y2 F, e; v4 J  j0 X( S4 W
© 2007 Sage Publications
+ J9 v' W) E6 c+ {# r% x10.1177/0009922806296651  i. s& H% @4 r' C, V
http://clp.sagepub.com
: b2 ]7 x' V6 N# mhosted at
# w& q( M! e0 I9 K* b( Bhttp://online.sagepub.com
, W( L8 O. E+ }( Q9 G0 fPrecocious puberty in boys, central or peripheral,
/ ]! Q: o3 s- Vis a significant concern for physicians. Central
0 {+ E8 }5 P2 u7 f0 lprecocious puberty (CPP), which is mediated
( d4 X  E& K  pthrough the hypothalamic pituitary gonadal axis, has
7 `2 l" f2 [. ^# Ra higher incidence of organic central nervous system
& @' n! L  h9 D  m; K6 a& {# Llesions in boys.1,2 Virilization in boys, as manifested# x& Q$ k; d1 \$ ^8 X
by enlargement of the penis, development of pubic) e( O& K$ l3 X7 Y/ U
hair, and facial acne without enlargement of testi-
, Z- @+ q+ h9 x8 F; [cles, suggests peripheral or pseudopuberty.1-3 We6 D/ Y3 w2 ~/ L5 p9 |
report a 16-month-old boy who presented with the1 C3 B9 w$ F# K
enlargement of the phallus and pubic hair develop-: N$ q$ [4 \; E" {" p
ment without testicular enlargement, which was due: y. z4 a' h  t* O
to the unintentional exposure to androgen gel used by
3 V, `5 S* Z( K$ J7 ]# C3 j4 sthe father. The family initially concealed this infor-+ U& e7 Z% x6 S" E+ K, g
mation, resulting in an extensive work-up for this: t* o$ V; b0 u3 k  E! {5 N& r
child. Given the widespread and easy availability of% R, p; [/ _$ V& a" D& J
testosterone gel and cream, we believe this is proba-
: J8 F" [! ^4 C" Vbly more common than the rare case report in the
0 d) T$ c5 Z0 V, J  ]- X" m' Xliterature.4# R& ^7 J6 U" D( _0 f7 E0 m
Patient Report0 ~1 R! F$ T- t3 a- D
A 16-month-old white child was referred to the
$ V: i$ k7 s7 @( m$ y$ oendocrine clinic by his pediatrician with the concern
9 a* D. R" y% [) d4 |. O; l# l( ]3 Gof early sexual development. His mother noticed
" l+ G) j% O' K9 k  Ulight colored pubic hair development when he was/ }6 R; t( O/ }
From the 1Division of Pediatric Endocrinology, 2University of
# z! @9 T% I, e! SSouth Alabama Medical Center, Mobile, Alabama.
) Q& m& y. X9 n1 h: C( ~+ EAddress correspondence to: Samar K. Bhowmick, MD, FACE,
' m$ e7 J) p" uProfessor of Pediatrics, University of South Alabama, College of. Z$ S) m( o' D4 _  K( E. M' t3 x
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
# x) v0 \5 P- O9 }( j( I6 ~7 we-mail: [email protected].! X7 d* r/ a$ C7 D4 u# o
about 6 to 7 months old, which progressively became
9 }6 x5 l0 ?: h# @* _# C7 Bdarker. She was also concerned about the enlarge-
+ K2 }' X" M) N/ _* D: ?ment of his penis and frequent erections. The child
2 v- q; ?. B. }9 A" ^3 a' Twas the product of a full-term normal delivery, with4 @) G6 a  _( r7 g( k5 A7 f
a birth weight of 7 lb 14 oz, and birth length of, f9 J4 v" V5 I! K+ ?  @# ]9 [
20 inches. He was breast-fed throughout the first year
( x/ r/ ]- \3 ]. cof life and was still receiving breast milk along with
6 n: @  R" U4 z+ t9 h0 {solid food. He had no hospitalizations or surgery,
8 Q0 b# d! L6 V- v( mand his psychosocial and psychomotor development
' y  Q. j' X$ c1 \was age appropriate.
2 ?2 ^. p/ V1 ~; e) SThe family history was remarkable for the father,
8 Q& t2 v6 b6 Z- }who was diagnosed with hypothyroidism at age 16,
6 S" J; R/ Z$ `. b, ywhich was treated with thyroxine. The father’s0 {, t% F6 t- V/ _1 ?4 l% K- |
height was 6 feet, and he went through a somewhat: R' k0 n% {2 F" d4 g' q6 V
early puberty and had stopped growing by age 14.
5 o# G# w# g) I& n: b0 j; D- dThe father denied taking any other medication. The; [1 `: ?! h& S& N7 \$ ~. r
child’s mother was in good health. Her menarche! }. A4 A+ g0 h5 b# v: _& ^
was at 11 years of age, and her height was at 5 feet
, }# X8 @0 W: A) x  ^. r5 inches. There was no other family history of pre-
, g. D. `+ x* E$ Z* Ncocious sexual development in the first-degree rela-
; m4 o* h; k3 Q7 \8 c  K7 etives. There were no siblings.
8 `9 X- n) ^: G" aPhysical Examination
# B, A1 _: M' I3 gThe physical examination revealed a very active,
* C$ _- \: O  F3 k8 o9 bplayful, and healthy boy. The vital signs documented% z% _4 L* X2 v, Y* D0 q2 Z
a blood pressure of 85/50 mm Hg, his length was
% c- ?' `5 Y2 _% B90 cm (>97th percentile), and his weight was 14.4 kg
: K" `* i  g" C, o' n1 x(also >97th percentile). The observed yearly growth
6 D: p3 y- [+ R' q0 Z& D. f' `; I# {velocity was 30 cm (12 inches). The examination of/ G. O6 V2 B- L) |4 y, r
the neck revealed no thyroid enlargement.
7 Q8 a* e) {* z$ Z8 ~The genitourinary examination was remarkable for  ~1 i& c1 {! Z& D1 z; V! o
enlargement of the penis, with a stretched length of, t8 N! n' N! n
8 cm and a width of 2 cm. The glans penis was very well8 d- h1 V9 k/ V- @
developed. The pubic hair was Tanner II, mostly around( a, |9 Y. d4 A: u  p9 S0 y  x
540
5 P2 I( g2 B6 T, C+ l+ m1 Wat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
# d$ S1 n* E- ~+ {* j5 E7 Dthe base of the phallus and was dark and curled. The
9 k! O# u; L  M, O5 R/ Jtesticular volume was prepubertal at 2 mL each.9 I4 p0 u& b; W- {0 Y6 B5 U: J0 ~
The skin was moist and smooth and somewhat& o, _4 x- G8 }4 m. y- R- t
oily. No axillary hair was noted. There were no& ~3 J5 y4 s) _: e
abnormal skin pigmentations or café-au-lait spots.% w/ ^: _) Z$ ^0 N* F
Neurologic evaluation showed deep tendon reflex 2+" `8 L# S( ?+ {$ J/ U
bilateral and symmetrical. There was no suggestion0 c: g! c1 d2 J" D" w% S# `! a
of papilledema.
3 _* o4 c, a( A4 R" ]; ILaboratory Evaluation$ s6 i& \1 l  b$ p  g
The bone age was consistent with 28 months by4 M; I6 G( {$ x$ }: E* B2 l
using the standard of Greulich and Pyle at a chrono-
; Q2 _$ r( u6 C! Zlogic age of 16 months (advanced).5 Chromosomal5 n0 G% ~& ?) C4 R. y- C% \" ~
karyotype was 46XY. The thyroid function test6 _; G+ H. ~: X5 H5 E+ r( [
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
) F- k+ g6 r) ~: a( ]; O$ Rlating hormone level was 1.3 µIU/mL (both normal).
! R0 e; z0 U8 C6 JThe concentrations of serum electrolytes, blood! E4 j" Q- T9 p1 b9 c. I  n) y! ~/ w
urea nitrogen, creatinine, and calcium all were
* S- x. f$ A7 W# e5 Pwithin normal range for his age. The concentration$ ^; {' s3 S4 u
of serum 17-hydroxyprogesterone was 16 ng/dL
( J6 b4 J5 V' p2 T- |(normal, 3 to 90 ng/dL), androstenedione was 20
" |- f: l0 D3 e/ {6 ?8 `ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-1 O8 g' G9 I& t$ {, T, D* G
terone was 38 ng/dL (normal, 50 to 760 ng/dL),5 n9 o) _' z2 ?8 e6 |
desoxycorticosterone was 4.3 ng/dL (normal, 7 to8 d  _# r2 S; b3 R0 G
49ng/dL), 11-desoxycortisol (specific compound S)$ N$ h: z4 k. N. j' D# Y# c* a
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
* N- J% a# P& c; s. s2 Ntisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total/ l' h: x) |5 R) Z! J5 r3 Z
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),% l" a5 d! `8 h' D# p$ U1 k7 ?  l
and β-human chorionic gonadotropin was less than
, ~4 G8 `2 o6 O) }1 [. p3 S- m' o5 ~5 mIU/mL (normal <5 mIU/mL). Serum follicular
8 L! w( v0 Q4 ostimulating hormone and leuteinizing hormone
2 m" P* w0 @3 f  h" p9 u+ Xconcentrations were less than 0.05 mIU/mL! \3 F* _: T+ L6 T. @
(prepubertal).; n0 @; i! P8 h% W: @/ z
The parents were notified about the laboratory
4 J. K4 A+ j/ p# @" b3 Jresults and were informed that all of the tests were
; u& R8 p5 w* q  anormal except the testosterone level was high. The( d7 T7 [% Z+ q* I# m: r( x$ l
follow-up visit was arranged within a few weeks to
% A, f9 B+ h  f) b3 W3 @. V! {obtain testicular and abdominal sonograms; how-
4 a2 u, \  w. F# ?ever, the family did not return for 4 months.
" Y4 r2 B5 Y1 iPhysical examination at this time revealed that the
9 r% B4 P9 b( D' l" k- V& o5 lchild had grown 2.5 cm in 4 months and had gained7 V" U( Y$ N0 j2 F) |
2 kg of weight. Physical examination remained( q+ }; B7 b  p6 ?
unchanged. Surprisingly, the pubic hair almost com-7 Y% m( ]1 L+ ?1 F0 ]$ n; B5 T5 Q
pletely disappeared except for a few vellous hairs at
. e* X2 y. L9 z) A' bthe base of the phallus. Testicular volume was still 2
$ R2 {8 ^% _( Y$ LmL, and the size of the penis remained unchanged.' ~- l0 T% b# j% {: f' M
The mother also said that the boy was no longer hav-
) T( O6 }( `/ T$ c: u% Oing frequent erections.
4 j! U" Z  l8 f, e8 r- ?2 GBoth parents were again questioned about use of
- B8 q5 b% K2 r  x! ^any ointment/creams that they may have applied to0 B( F3 ~) J1 [  m9 ]  `8 n
the child’s skin. This time the father admitted the" M% w: t8 o' \/ m  F5 L
Topical Testosterone Exposure / Bhowmick et al 541* O" N! Y+ R- _1 \1 s
use of testosterone gel twice daily that he was apply-
7 r) S/ k% W& Y% Uing over his own shoulders, chest, and back area for- R! P) D: n2 t1 X8 D
a year. The father also revealed he was embarrassed" U2 B: \# G: O8 l4 i: y: M# @0 P6 p
to disclose that he was using a testosterone gel pre-
, H7 S5 L* m6 E2 v& I7 s0 V5 |scribed by his family physician for decreased libido) P6 u! ~$ X+ y" e9 T; Z; d
secondary to depression.6 c- }/ P. A. S, K! |2 L# n
The child slept in the same bed with parents.
# y4 ]: @# P- N# L, s5 Q! hThe father would hug the baby and hold him on his6 N3 d' k; X9 v/ e0 C1 u1 C; K! n
chest for a considerable period of time, causing sig-
) X4 j2 i% ^7 _' m# Cnificant bare skin contact between baby and father.( q0 X, M. b* H3 d" Y
The father also admitted that after the phone call,& |1 u3 S5 ^) |
when he learned the testosterone level in the baby
" k. {% W9 }1 N  x! K" ~was high, he then read the product information
( T& N' `  Z8 g: {" f5 {6 f" Gpacket and concluded that it was most likely the rea-0 W. h% L, @: ?# X3 H
son for the child’s virilization. At that time, they
) c- Q/ F, \1 X. m% ?0 G8 sdecided to put the baby in a separate bed, and the  ~2 A2 r( Z1 o- ^* p1 [$ V+ @
father was not hugging him with bare skin and had. _9 B3 s3 ]1 [  c' T- }
been using protective clothing. A repeat testosterone$ U; V" Y: ?( t: F
test was ordered, but the family did not go to the. D9 B" {, P) |$ Y. N# O
laboratory to obtain the test.! K) `+ i2 _9 M4 v) T' w
Discussion
2 J8 M, i% A+ K! m  s5 f  r8 p  sPrecocious puberty in boys is defined as secondary1 g4 K8 c; @, j5 a4 R6 n9 E
sexual development before 9 years of age.1,4
: G& j5 ~3 D4 Q; JPrecocious puberty is termed as central (true) when
7 a1 ?, e; @2 s0 Lit is caused by the premature activation of hypo-
$ T1 z, t' }* s/ g8 t0 \3 ?! ?+ ithalamic pituitary gonadal axis. CPP is more com-$ a  ]  J/ _* Y
mon in girls than in boys.1,3 Most boys with CPP. ~# ?$ @% T1 F1 u: E
may have a central nervous system lesion that is* Q6 |0 R% A: R
responsible for the early activation of the hypothal-+ ~& P/ q; B1 Y# _0 Z% i
amic pituitary gonadal axis.1-3 Thus, greater empha-9 E. a' d' E4 ?! A1 b+ m
sis has been given to neuroradiologic imaging in, Q8 V7 P) Z2 w; l4 t/ y# F: o7 ]
boys with precocious puberty. In addition to viril-  g, {% U6 G+ i0 m$ F
ization, the clinical hallmark of CPP is the symmet-
1 I& x( o" [& C5 `rical testicular growth secondary to stimulation by
( j* M$ |0 y% Mgonadotropins.1,30 q% q) W# r8 v8 R6 ?- S
Gonadotropin-independent peripheral preco-
2 |; ]2 m+ X7 @+ \0 s0 ~cious puberty in boys also results from inappropriate
8 P$ z* v2 K" E( J5 q# E" p5 handrogenic stimulation from either endogenous or
7 J' H* R/ |% ~" Sexogenous sources, nonpituitary gonadotropin stim-
4 ^. P* s+ e* uulation, and rare activating mutations.3 Virilizing3 N% u+ K. s' }( @6 F2 X4 P( r
congenital adrenal hyperplasia producing excessive# I# v  F- h% f( b2 r8 _
adrenal androgens is a common cause of precocious
+ `; b% p' E1 J1 d: fpuberty in boys.3,4
9 ~  T+ @" j8 Y2 yThe most common form of congenital adrenal
! I3 I9 u7 L- }8 G$ ]- fhyperplasia is the 21-hydroxylase enzyme deficiency.( |3 B  r' j+ m1 ^  F
The 11-β hydroxylase deficiency may also result in
# B1 |5 F$ @1 Qexcessive adrenal androgen production, and rarely,
0 ]- H7 f) v5 j* C7 Wan adrenal tumor may also cause adrenal androgen
# h! {( v" ^# l  y& O- E% Uexcess.1,3
! k3 o2 z: C( J7 m  Qat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
* M* ]. Q( Z1 N7 {, X0 U$ K542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
! i4 m7 y$ K: LA unique entity of male-limited gonadotropin-9 g- \% u! G; ?
independent precocious puberty, which is also known
# B5 M  K4 Q) E! K5 ]as testotoxicosis, may cause precocious puberty at a# G/ T6 Y! S$ l. m
very young age. The physical findings in these boys
/ i# Q0 p* U/ W5 bwith this disorder are full pubertal development,! R5 U. n, i, `6 }/ `2 d
including bilateral testicular growth, similar to boys
) o% x5 x. ]' b- W" O. }with CPP. The gonadotropin levels in this disorder8 H: U1 E6 o4 \& R/ ]4 v
are suppressed to prepubertal levels and do not show5 Q# F" I& a. e  H' e, N2 t( p# k
pubertal response of gonadotropin after gonadotropin-8 g3 H" g$ ]& k5 ~. E
releasing hormone stimulation. This is a sex-linked" L) O3 b% ]0 D- K. _# I& e
autosomal dominant disorder that affects only0 c  n1 H1 n  L
males; therefore, other male members of the family
+ G: U9 d9 h2 S+ V9 t: S2 Z% pmay have similar precocious puberty.3) R7 p& m: |. f9 Q5 [9 [( W& u6 b& o
In our patient, physical examination was incon-& R$ w% n" I. Q4 P% b
sistent with true precocious puberty since his testi-
5 }! l1 ]. S6 V, Ycles were prepubertal in size. However, testotoxicosis
3 s4 Q( S' H! G+ l; V: y3 nwas in the differential diagnosis because his father
- {) }& N& @4 [- z: [( Istarted puberty somewhat early, and occasionally,: }. u; Z5 o! U
testicular enlargement is not that evident in the
5 I' D$ w/ u$ T. V& [" ^( M0 k! Vbeginning of this process.1 In the absence of a neg-+ [8 N) `/ q' k* ^3 j9 ]
ative initial history of androgen exposure, our
1 `% R* [, b6 c' B  z% _2 Obiggest concern was virilizing adrenal hyperplasia,
0 p/ D# ~) C$ C' n; Eeither 21-hydroxylase deficiency or 11-β hydroxylase9 h, U# v( D1 I
deficiency. Those diagnoses were excluded by find-
! [; T7 T7 @! c& W1 k) ~* l5 Oing the normal level of adrenal steroids.
8 s+ |; Z' S" {7 L2 [+ y$ @' j" LThe diagnosis of exogenous androgens was strongly
, E' D9 f+ i7 i2 x( T% csuspected in a follow-up visit after 4 months because) C6 a' z$ Y- h
the physical examination revealed the complete disap-) }, K/ f% f. }- ^7 F8 ?( E  P$ V
pearance of pubic hair, normal growth velocity, and
4 r' @5 M; s$ k" F) R8 [% v+ n* hdecreased erections. The father admitted using a testos-
) C) J8 s, ~' X" A4 jterone gel, which he concealed at first visit. He was
% j8 G) f" z9 I1 Ausing it rather frequently, twice a day. The Physicians’
" o  J$ U9 L+ n1 C  mDesk Reference, or package insert of this product, gel or8 v9 Q. u# z% B& w: a
cream, cautions about dermal testosterone transfer to! Z5 G) S+ m0 D
unprotected females through direct skin exposure.$ a: U' H& G4 b" F9 K
Serum testosterone level was found to be 2 times the4 K! h* |: w( u, P- `0 H2 O
baseline value in those females who were exposed to3 X; U8 l, L: O9 |
even 15 minutes of direct skin contact with their male+ N/ q- r( R, r6 m% z; r' ]
partners.6 However, when a shirt covered the applica-- n2 u& C2 e$ n! a( s& t& a/ s3 g
tion site, this testosterone transfer was prevented.) {) f7 x& A+ p" p5 G5 S; _' j
Our patient’s testosterone level was 60 ng/mL," t% y7 ?+ v$ j" S
which was clearly high. Some studies suggest that+ w" W. y; r! N" |# p
dermal conversion of testosterone to dihydrotestos-% p1 D9 r' a  X2 }  o
terone, which is a more potent metabolite, is more
) v: e. @' q; l* D: ^, X$ c, Hactive in young children exposed to testosterone! G6 g' w( o( V* e; W- ^
exogenously7; however, we did not measure a dihy-
! A, Z) e+ l2 _, n$ ^. @drotestosterone level in our patient. In addition to
7 l  D) _. [, Z4 N6 H& Q% e: Pvirilization, exposure to exogenous testosterone in) R6 M. F% t& k# K6 x9 \$ N' k
children results in an increase in growth velocity and5 n9 z* N) X* [# b% X9 f
advanced bone age, as seen in our patient.
3 k) N" y( }3 L+ X7 a8 wThe long-term effect of androgen exposure during
5 Z1 \0 V6 }/ Hearly childhood on pubertal development and final
6 r. `, B* C8 H7 j7 O! zadult height are not fully known and always remain5 M3 w2 n$ @5 v7 n1 _/ M
a concern. Children treated with short-term testos-
8 m" P  ~5 k' k% D  P7 dterone injection or topical androgen may exhibit some
5 T- Z1 E# @$ D+ Z- U9 A; B5 p5 Sacceleration of the skeletal maturation; however, after) ?! k/ y; W% q# @% r- v6 s
cessation of treatment, the rate of bone maturation
6 k, ~3 t0 [# ^, B# hdecelerates and gradually returns to normal.8,9$ Z; p" E; n5 S0 _0 [  X* A
There are conflicting reports and controversy0 f$ Z+ _1 G+ T" B4 D
over the effect of early androgen exposure on adult
/ ^( t  g0 g0 R$ H3 |, S/ tpenile length.10,11 Some reports suggest subnormal0 @+ W' T! Z8 M9 ]* u
adult penile length, apparently because of downreg-
" a- f( \6 f/ N+ h4 sulation of androgen receptor number.10,12 However,
, j7 {! y: {/ j/ P4 J, X; j- B- }Sutherland et al13 did not find a correlation between
' H; ~0 f0 k: ]1 Tchildhood testosterone exposure and reduced adult. ~# o4 l! S' J" E* H4 ?0 G
penile length in clinical studies.$ Y0 [( e6 H/ }, `' E$ ]
Nonetheless, we do not believe our patient is
, V7 x3 n  [  A( e, u" A4 wgoing to experience any of the untoward effects from
! C+ U- P- ^0 `testosterone exposure as mentioned earlier because/ V' X0 f7 L0 ]* M$ @6 n
the exposure was not for a prolonged period of time.
) H' t0 N4 x$ P  L( o  ZAlthough the bone age was advanced at the time of
9 B- y+ H# k: ^& W3 X' [diagnosis, the child had a normal growth velocity at: |6 B& A- [9 j1 |6 J
the follow-up visit. It is hoped that his final adult
  B$ V0 y; v7 q" ?: b% qheight will not be affected.
0 w1 u0 G# i+ @( p" n5 a9 FAlthough rarely reported, the widespread avail-
" b1 C. T6 Y- |4 Qability of androgen products in our society may& z5 l7 Q* \  x$ C0 f- Q3 P
indeed cause more virilization in male or female
' V' {9 R6 j5 J, H) {8 N; Ochildren than one would realize. Exposure to andro-
+ A2 ^, ]/ L$ S) {: A! p% vgen products must be considered and specific ques-
; q6 C; c, m1 [: d# [tioning about the use of a testosterone product or# e/ G% O) s, k; f# K% q5 M( Q
gel should be asked of the family members during
) M: O5 h8 A" z1 f0 Jthe evaluation of any children who present with vir-
! B  ]4 e: P0 o- `6 z* rilization or peripheral precocious puberty. The diag-! @" l/ \/ }  X) [) j
nosis can be established by just a few tests and by
- ]) v+ s/ a. l- e- h& Tappropriate history. The inability to obtain such a
* R8 z3 y# n; |: V, n3 whistory, or failure to ask the specific questions, may
9 z6 @" g2 y, \4 ^+ T4 Presult in extensive, unnecessary, and expensive5 j+ A# ^: }$ ~
investigation. The primary care physician should be
% y" i, W" l2 x/ K1 raware of this fact, because most of these children
; B$ X$ z$ |4 d4 L. e8 `may initially present in their practice. The Physicians’
7 s8 v: {1 G, HDesk Reference and package insert should also put a
5 {7 p7 Y( o- {4 `- V9 s# kwarning about the virilizing effect on a male or8 c# @( A' j# ]9 }% n' L% [
female child who might come in contact with some-
2 L! i0 E' n$ U. Y6 C* lone using any of these products.. d8 e. n) ^# ~) @
References
1 H  b) P2 D* ]  v6 O. B2 f3 V  \1. Styne DM. The testes: disorder of sexual differentiation' _0 J/ A$ c( Q: ?8 n$ r
and puberty in the male. In: Sperling MA, ed. Pediatric+ P) I. O/ X& D+ V% h6 I
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
. u  g- l1 ]. l: |2 u2002: 565-628.8 }* A0 r/ b4 K8 C- V: e3 \
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
1 V1 B' T4 D! mpuberty 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
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感謝大大的辛勞分享!我會繼續在WK關注大大的文章!
發表於 2025-1-11 22:18:01 | 顯示全部樓層
女厕偷拍辅导班主任尿尿老师的逼很嫩还有一点
發表於 2025-1-17 16:31:39 | 顯示全部樓層
VIP精品區,資源無限好賺金任務區,輕松賺金幣
加入VIP,享受高級特權宣傳賺金又升級,超級棒
4个什么样的?
發表於 2025-1-19 02:41:05 | 顯示全部樓層

6 q  S& r5 s' t: f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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