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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-Old1 I( f% F+ z( e' c; n  _8 O
Boy Induced by Indirect Topical  N* ]$ [0 S9 R2 H6 W4 g
Exposure to Testosterone
  N8 P- J6 y6 z7 h0 j! B) MSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
+ y& \5 Z. ^( Eand Kenneth R. Rettig, MD18 ?- k" @5 M2 D6 i, R6 O: q
Clinical Pediatrics4 E4 X0 H# M' ~5 e' V
Volume 46 Number 6
" @) {: G3 }( o( d3 A; jJuly 2007 540-5439 X" Y& u( p7 o/ t- B, R
© 2007 Sage Publications
8 I% }4 p% N1 y( u10.1177/0009922806296651
+ J$ s% R, `4 e( Jhttp://clp.sagepub.com' N1 r% K9 N) b( n) U
hosted at
1 U9 z: O) ^5 Dhttp://online.sagepub.com* [5 g2 w4 {0 g4 H; i
Precocious puberty in boys, central or peripheral,
/ J( d- G' [- j1 G2 K) [is a significant concern for physicians. Central
2 H5 f1 ~- b) C. ~# Fprecocious puberty (CPP), which is mediated( g+ Z; ?$ a0 k" ?  q
through the hypothalamic pituitary gonadal axis, has
# ]* @8 y8 P  f, S  Ta higher incidence of organic central nervous system
8 `5 M  i9 Y) y3 B/ Wlesions in boys.1,2 Virilization in boys, as manifested
2 d/ j, N5 J0 [( Qby enlargement of the penis, development of pubic% B) p2 P4 q4 h3 k  s
hair, and facial acne without enlargement of testi-
5 n& h4 i, j5 Q, t% @' d* K) I8 b+ bcles, suggests peripheral or pseudopuberty.1-3 We9 q0 Q  c+ G3 c8 c/ {, j
report a 16-month-old boy who presented with the
! e% u5 S. T7 _" C# C5 Xenlargement of the phallus and pubic hair develop-6 Y% e7 n5 m! b
ment without testicular enlargement, which was due
) i# H+ O4 K' M6 lto the unintentional exposure to androgen gel used by3 \$ z* j& }* t: l& f/ R- M: s# t
the father. The family initially concealed this infor-
. Z) _# K; G% Z. zmation, resulting in an extensive work-up for this
/ z$ c$ o* N; g* M4 E: a' |5 Lchild. Given the widespread and easy availability of) v1 }- E& d/ F1 O% P1 e
testosterone gel and cream, we believe this is proba-! @% i; E0 i! w# G# l* [' p6 i
bly more common than the rare case report in the
. F  ~( W/ y# ]: d$ R) ?! P' p5 xliterature.4, o8 `6 B2 q% p2 w$ Z
Patient Report
# h9 M  D" r3 Q: A# SA 16-month-old white child was referred to the  k( H* g* G9 r
endocrine clinic by his pediatrician with the concern
' a' F3 h0 j9 L. p  K" @of early sexual development. His mother noticed
/ N. U- R1 W; f) B, ]light colored pubic hair development when he was
4 D9 c9 h! N6 M. I3 B( X; `! g) oFrom the 1Division of Pediatric Endocrinology, 2University of
: G* k/ E4 f; U) E  mSouth Alabama Medical Center, Mobile, Alabama.6 o8 t: O% o, c
Address correspondence to: Samar K. Bhowmick, MD, FACE,
$ }- o3 ?& K" X8 e8 L7 bProfessor of Pediatrics, University of South Alabama, College of
& M+ ?; U9 ]( HMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
2 v- r9 v& w6 v( b- [: we-mail: [email protected].
. o0 M' }) ]# p0 _, ^* Fabout 6 to 7 months old, which progressively became
# m8 y1 [1 C! Ddarker. She was also concerned about the enlarge-
% {! D2 j0 i) H, _8 t. vment of his penis and frequent erections. The child
( e; Z% t1 Z! U! D6 t. kwas the product of a full-term normal delivery, with" \+ t( [% G. h% N8 |$ d
a birth weight of 7 lb 14 oz, and birth length of! R" m* X) ^% f9 F) w* @
20 inches. He was breast-fed throughout the first year0 m# n, v0 G1 L7 j
of life and was still receiving breast milk along with, V% |" m$ u2 y3 p: T4 @2 @
solid food. He had no hospitalizations or surgery,! C) ?% X- V6 G# b
and his psychosocial and psychomotor development
  |& j  o. E" f! w: v( A9 ]1 L7 Twas age appropriate.
# y3 I: }( Y% H) m3 z9 B" OThe family history was remarkable for the father,
4 l) W: O1 d3 [6 A3 Xwho was diagnosed with hypothyroidism at age 16,
+ U. \$ S8 k$ P; T9 ~* ^which was treated with thyroxine. The father’s8 D& S$ M$ x7 F
height was 6 feet, and he went through a somewhat
, Y  U7 I; A, }early puberty and had stopped growing by age 14.
' D9 [8 v) b+ p/ GThe father denied taking any other medication. The/ d) O; c5 w3 y8 ~8 S* E
child’s mother was in good health. Her menarche
5 d/ ~; u6 \% N) gwas at 11 years of age, and her height was at 5 feet
+ K8 d/ `. `- J- P! {) @5 inches. There was no other family history of pre-, H; A) e6 ?. z7 y  ~) l, o1 D
cocious sexual development in the first-degree rela-
% j8 a/ k0 P) d: r- P% G0 t6 r& \; R/ }tives. There were no siblings.
" l( ]7 l! ]1 t# f/ _7 CPhysical Examination5 [2 m) U0 X, h* [9 \+ h
The physical examination revealed a very active,6 a7 \( o$ s" |9 g- K$ l+ F2 l( V
playful, and healthy boy. The vital signs documented) ~% o- F* M3 ]2 Q$ r6 [
a blood pressure of 85/50 mm Hg, his length was/ Y$ p0 @6 Q- R
90 cm (>97th percentile), and his weight was 14.4 kg
! a' B! C$ `! H) R. n4 p(also >97th percentile). The observed yearly growth
! A- [* m8 z3 o+ l5 V" t: pvelocity was 30 cm (12 inches). The examination of# P& i* V9 ^! U2 i  }; s3 ]% B
the neck revealed no thyroid enlargement.
  \6 L3 f4 J+ ?3 b& KThe genitourinary examination was remarkable for
' u/ k: F5 [* Denlargement of the penis, with a stretched length of
1 V' _" y# b' x* U  w8 B+ M0 K8 cm and a width of 2 cm. The glans penis was very well# S' O0 F1 x) o0 B; e
developed. The pubic hair was Tanner II, mostly around
8 `$ A1 {# I# M% `540- L- S- a8 U' L1 y
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
$ ?# V1 C9 R2 b! N! T& x+ fthe base of the phallus and was dark and curled. The' m2 P! z" O) y, J1 c( W
testicular volume was prepubertal at 2 mL each.! w4 j7 N7 P6 c/ j
The skin was moist and smooth and somewhat
5 n/ a. [9 j+ [& l. N# q$ P9 ^8 h/ ~6 Uoily. No axillary hair was noted. There were no
  e9 W3 t" h3 M( Habnormal skin pigmentations or café-au-lait spots.
6 K4 }( p. |: B4 W2 TNeurologic evaluation showed deep tendon reflex 2+0 w2 ?: r# z  C5 M
bilateral and symmetrical. There was no suggestion3 A: ^! ?# l7 W
of papilledema.
3 @" `* V2 t; d* i7 j' {, jLaboratory Evaluation
: Q2 p) q4 p! m: [. u$ S6 Z$ nThe bone age was consistent with 28 months by: A; o# }! i1 k
using the standard of Greulich and Pyle at a chrono-
) l3 [5 ^5 v* Z7 i7 [) ~logic age of 16 months (advanced).5 Chromosomal
  \8 {2 A- `; K' |- i! y( Okaryotype was 46XY. The thyroid function test
7 j  i. b, o( ^1 mshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
# \- V$ i6 z  n) K% S, m$ A$ y: s- Tlating hormone level was 1.3 µIU/mL (both normal).: K+ c/ N: G3 I; x2 ]% t5 u
The concentrations of serum electrolytes, blood
1 [3 L" a$ l( }  a# ^& e; A, turea nitrogen, creatinine, and calcium all were' E1 l# E4 O7 |2 P
within normal range for his age. The concentration
; H3 ]  S6 G# k2 y6 eof serum 17-hydroxyprogesterone was 16 ng/dL3 k# f1 I+ @3 ?) L8 l
(normal, 3 to 90 ng/dL), androstenedione was 20) j5 d$ c3 c* ]9 i; t4 _+ [
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
8 L0 I" e$ t2 M/ d! |+ uterone was 38 ng/dL (normal, 50 to 760 ng/dL),
0 a' i5 x! J' F1 A9 [# k6 Vdesoxycorticosterone was 4.3 ng/dL (normal, 7 to$ e) U6 d0 E8 P9 K
49ng/dL), 11-desoxycortisol (specific compound S)
: \/ T) d6 i! {# m; ^! z% X; Gwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
4 V  D) ?9 j( b+ ?tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total" W$ J6 \7 G+ i
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),# @% S) P% x" {7 x6 n7 m) |
and β-human chorionic gonadotropin was less than
8 a+ R$ ~( A% R7 q  F# k5 mIU/mL (normal <5 mIU/mL). Serum follicular: ^( t( P1 P' N8 F2 i9 S0 d# q
stimulating hormone and leuteinizing hormone
# E6 L: u$ i- i: A- V3 t) g. _concentrations were less than 0.05 mIU/mL
6 z' j2 A4 e/ A) D(prepubertal).& x0 M: g3 K9 w0 i; U) D3 F% |" A: t
The parents were notified about the laboratory' ]* G) P$ X5 a6 m4 B, y# R$ _
results and were informed that all of the tests were# e  \0 f( y; a+ U3 H6 H
normal except the testosterone level was high. The
+ v' i/ @- m8 K. y* ^: ifollow-up visit was arranged within a few weeks to6 J8 D5 l. w2 A
obtain testicular and abdominal sonograms; how-' P# P" ?7 c8 l, u9 L
ever, the family did not return for 4 months.
+ K. F, ~3 k! D4 _) Q/ r; b: IPhysical examination at this time revealed that the
* G2 g) P* ]( d+ `7 |9 T, _child had grown 2.5 cm in 4 months and had gained, u) c. y# [7 C% ^) V0 ?8 @% m
2 kg of weight. Physical examination remained0 M& r5 d3 J, x3 O9 h7 J
unchanged. Surprisingly, the pubic hair almost com-+ E3 K7 Q) S7 d- B9 q1 `
pletely disappeared except for a few vellous hairs at2 z8 u6 }# N4 X
the base of the phallus. Testicular volume was still 2: T* z( j3 B. t) Q8 Q8 `& A5 ?
mL, and the size of the penis remained unchanged.: g0 m0 J$ {) I* U  R
The mother also said that the boy was no longer hav-
, X6 v% r' A% `1 _( x+ ying frequent erections.* \" {: e" O% _
Both parents were again questioned about use of/ \' e9 W4 V# L3 l' Y
any ointment/creams that they may have applied to
& h) x. U8 v) {' d& L9 \. F1 e- kthe child’s skin. This time the father admitted the
6 ^+ x4 y3 ~" R; PTopical Testosterone Exposure / Bhowmick et al 541% D' U! L: s  s
use of testosterone gel twice daily that he was apply-7 k0 H4 O0 v, J) a2 c# y( c3 E
ing over his own shoulders, chest, and back area for
. v/ F1 u$ H" c' ?- Ta year. The father also revealed he was embarrassed
4 U9 K: t6 }) c# p' k, ato disclose that he was using a testosterone gel pre-
% {. e. t- Z7 O9 X7 |scribed by his family physician for decreased libido
/ z' i; @: l0 O/ H& i* o8 xsecondary to depression.
& e" p4 H& C5 l5 t, X0 _0 iThe child slept in the same bed with parents.
/ k* b5 _2 @% QThe father would hug the baby and hold him on his3 o* v: L3 Q5 X
chest for a considerable period of time, causing sig-1 z! D8 t- M0 D
nificant bare skin contact between baby and father." U5 h! `8 L* r* B) a
The father also admitted that after the phone call,
: J7 _( v  ^1 D% z( y0 K* \7 ywhen he learned the testosterone level in the baby4 h4 d6 @7 ~# \
was high, he then read the product information- X7 k) y' q5 C+ _
packet and concluded that it was most likely the rea-$ ]7 R; D; ?" B+ ~
son for the child’s virilization. At that time, they
0 m% T& y# X' rdecided to put the baby in a separate bed, and the. z7 p/ a: f; v5 O
father was not hugging him with bare skin and had, ]2 ^9 `  I' K# [7 t  Z
been using protective clothing. A repeat testosterone
; J2 s3 b# `! `4 E) y) T0 b9 ^test was ordered, but the family did not go to the, p* B! t+ k1 S, j$ l0 F
laboratory to obtain the test.9 @0 a+ a0 ^0 [5 U4 P
Discussion3 D3 a2 ^$ H3 J6 }% _! M0 A
Precocious puberty in boys is defined as secondary( z7 M% C. i/ }7 R
sexual development before 9 years of age.1,4
. R/ x) w9 I1 X' u3 K8 zPrecocious puberty is termed as central (true) when
+ H8 }1 }! s0 f. }0 xit is caused by the premature activation of hypo-: F' P& P& K5 C% z  ]9 ]
thalamic pituitary gonadal axis. CPP is more com-
( D. W; ]% \( U6 Y1 `1 F0 Emon in girls than in boys.1,3 Most boys with CPP! i) {# W( n0 W4 U3 x; H3 T
may have a central nervous system lesion that is
8 B; t/ I# ~/ N, Jresponsible for the early activation of the hypothal-6 Q/ x& s3 A! w0 b- W, D
amic pituitary gonadal axis.1-3 Thus, greater empha-/ D9 i! q( J: M  }0 r) }
sis has been given to neuroradiologic imaging in6 X1 J5 U- u; \, S. G: I* d
boys with precocious puberty. In addition to viril-
* o! G2 h. g# Zization, the clinical hallmark of CPP is the symmet-
* y. b* @, g) K. j+ o1 v1 U9 M, urical testicular growth secondary to stimulation by
" i& A. e5 d! v" bgonadotropins.1,3$ N& Q/ l' W0 v6 ?0 i7 n
Gonadotropin-independent peripheral preco-) Y7 k! m5 Z5 h! s: d$ l) L5 D
cious puberty in boys also results from inappropriate7 V( R, ^0 u5 ~1 Z
androgenic stimulation from either endogenous or
3 w2 o. o. q: t# rexogenous sources, nonpituitary gonadotropin stim-
9 a/ [( l# O6 L: }" a& Fulation, and rare activating mutations.3 Virilizing# M& D( r. v# y( D. F: G: e. n
congenital adrenal hyperplasia producing excessive1 E  e: S$ u! g
adrenal androgens is a common cause of precocious
4 r* D, `& J. [$ U' `puberty in boys.3,4
; d  K2 z- s2 E9 |$ ~8 i$ cThe most common form of congenital adrenal4 o/ G1 c/ ^1 Q9 O
hyperplasia is the 21-hydroxylase enzyme deficiency." f0 p( a8 b: j8 g+ v
The 11-β hydroxylase deficiency may also result in0 W6 ?( U( T/ ]8 ?/ A$ j9 _2 `: _
excessive adrenal androgen production, and rarely,
0 Q) _( ]* {3 i( Kan adrenal tumor may also cause adrenal androgen
) z, e2 p' j/ A) I4 pexcess.1,3, r4 W1 _5 a. P3 J
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
) j& |; q4 k0 B' p542 Clinical Pediatrics / Vol. 46, No. 6, July 20079 M3 n0 o, h" ?6 G0 U+ r
A unique entity of male-limited gonadotropin-9 j' c( O) ~+ R# a7 Y) J3 C
independent precocious puberty, which is also known3 H9 o4 j( u7 h% N# S- f' B
as testotoxicosis, may cause precocious puberty at a
# u+ V% \6 k- w9 kvery young age. The physical findings in these boys  Y0 F* ]4 q: x1 o. N% A2 y
with this disorder are full pubertal development,% p' j2 Z4 I, A6 H; S2 A$ {0 T2 C) B
including bilateral testicular growth, similar to boys
: p& T; t% Z8 V9 c$ F- Xwith CPP. The gonadotropin levels in this disorder
% h/ K0 I& l6 m  Q9 kare suppressed to prepubertal levels and do not show
$ L& G1 n; a& _0 Q$ l8 Epubertal response of gonadotropin after gonadotropin-0 I; O0 l5 v+ \& @  I/ _" m8 X6 k- d
releasing hormone stimulation. This is a sex-linked" H- o( B0 \- \+ y; f  ]
autosomal dominant disorder that affects only
* y0 j# j; ~6 V. g* F* I' omales; therefore, other male members of the family
! P2 a$ L8 k* B" B( @may have similar precocious puberty.3
: A- w7 J% n& r' V: AIn our patient, physical examination was incon-
8 m' e% ?7 o4 w0 k$ s9 S8 dsistent with true precocious puberty since his testi-1 [' X! L1 Z; [) f9 _
cles were prepubertal in size. However, testotoxicosis$ [, Z: w8 t" B- c" y6 t
was in the differential diagnosis because his father
6 u# s" G2 c( M2 ^6 Z" U6 W4 Gstarted puberty somewhat early, and occasionally,
! I) w% L3 W. i0 etesticular enlargement is not that evident in the
4 D- e8 Q+ [! i2 E8 Bbeginning of this process.1 In the absence of a neg-! b7 S. P. A, h
ative initial history of androgen exposure, our
3 b9 L1 c- |8 f7 Nbiggest concern was virilizing adrenal hyperplasia,/ n0 B% F; d1 V( C0 p$ \
either 21-hydroxylase deficiency or 11-β hydroxylase
9 E( l  F) `6 \7 |- [deficiency. Those diagnoses were excluded by find-% p! I4 j% N- ?3 `+ s
ing the normal level of adrenal steroids., d; X4 i. O: J5 `2 A
The diagnosis of exogenous androgens was strongly
6 {, Y6 l8 {" p" b# t8 I, b. Csuspected in a follow-up visit after 4 months because2 r) V8 k1 @5 }/ O& U0 u3 q
the physical examination revealed the complete disap-
' d1 G' H" c8 L( mpearance of pubic hair, normal growth velocity, and
3 ~( c7 f/ o; Z3 F. i5 Zdecreased erections. The father admitted using a testos-
, Q4 A+ Q6 n' v' D2 Gterone gel, which he concealed at first visit. He was8 K+ e. ]* s9 C1 K6 R, C2 T
using it rather frequently, twice a day. The Physicians’
1 |' v% `. g5 v2 g) x5 X' k) {Desk Reference, or package insert of this product, gel or
& _0 g# R- t* Z& r/ {7 Ccream, cautions about dermal testosterone transfer to0 i& m: A& J" Q/ m
unprotected females through direct skin exposure.; s- f7 `$ g! m! M
Serum testosterone level was found to be 2 times the9 Z0 D2 Y" n: c" _3 ^- y3 o
baseline value in those females who were exposed to
3 a% u9 b; }$ b. o3 k) A( Neven 15 minutes of direct skin contact with their male% F* x$ V9 E% F5 X9 H
partners.6 However, when a shirt covered the applica-
$ B! ]* X0 i3 V3 [tion site, this testosterone transfer was prevented.% X# @' R! M" s5 j3 i
Our patient’s testosterone level was 60 ng/mL,  j) U+ p4 C% W( M) h# i( e' Z
which was clearly high. Some studies suggest that
4 y! R% @/ u1 V. ]dermal conversion of testosterone to dihydrotestos-4 a( q8 {' x8 b# |
terone, which is a more potent metabolite, is more
& j2 K7 X/ P1 L# f& |active in young children exposed to testosterone  v* J+ a% b3 M& Y
exogenously7; however, we did not measure a dihy-
3 G2 O2 t) p! {6 D9 m0 x* xdrotestosterone level in our patient. In addition to
( M) ?$ b- ]8 i3 O# [virilization, exposure to exogenous testosterone in
+ \( U! I2 u4 g/ g( v: dchildren results in an increase in growth velocity and) ^- a* N6 A2 D' x: p% V
advanced bone age, as seen in our patient.
; [* ]$ k0 O: m9 T- bThe long-term effect of androgen exposure during. m' P3 E) [- [8 `
early childhood on pubertal development and final9 R5 p4 H2 t& i+ ], @2 o; J7 s7 d" q
adult height are not fully known and always remain6 j: H: H: c& [
a concern. Children treated with short-term testos-
. i2 K/ Z3 D9 W* Eterone injection or topical androgen may exhibit some
. E" l. I% l6 d& ~0 Zacceleration of the skeletal maturation; however, after9 b7 b+ H) o" _- N2 C
cessation of treatment, the rate of bone maturation: Z4 o. b) J' t
decelerates and gradually returns to normal.8,9
3 ~" H' Z- ?2 ~* F5 ?, ^# s5 I2 C4 ZThere are conflicting reports and controversy) J; D9 i7 v" T
over the effect of early androgen exposure on adult- p, R2 a/ q6 Q0 e# N6 p: g
penile length.10,11 Some reports suggest subnormal
2 g$ z- o3 ]: kadult penile length, apparently because of downreg-
' C) ~) d$ P2 Mulation of androgen receptor number.10,12 However,, O& {3 k8 {) j% f0 x& k3 I/ I. U
Sutherland et al13 did not find a correlation between  \2 y: O5 B; S
childhood testosterone exposure and reduced adult
" R; t$ d. z1 o* `8 {penile length in clinical studies.* a- F* T% C  _/ k. T$ h( l% u5 o+ Y
Nonetheless, we do not believe our patient is
1 i5 G: F; O( e, ~7 s0 Y# i' ^going to experience any of the untoward effects from, `: Z+ J8 D: l% {
testosterone exposure as mentioned earlier because
+ M4 b, ]# m$ {2 ethe exposure was not for a prolonged period of time.- R. I0 h( [7 k0 ?5 H# @
Although the bone age was advanced at the time of/ |0 l% H, W! N9 J6 s( Z
diagnosis, the child had a normal growth velocity at) `* |5 `. v/ r% t9 d
the follow-up visit. It is hoped that his final adult
; a' p4 \7 h- ?* xheight will not be affected.1 l4 X* B8 _" D. `
Although rarely reported, the widespread avail-
7 U, [6 G, s6 dability of androgen products in our society may
6 ?- g& W: l! z3 S6 Dindeed cause more virilization in male or female" X4 {2 q9 D0 A1 ]
children than one would realize. Exposure to andro-; I. W( A  S% M' q4 }1 y
gen products must be considered and specific ques-
; `. R( \9 T" k, u, x5 r* Z; b( itioning about the use of a testosterone product or
+ ?& p, N: ?" P. a9 Ggel should be asked of the family members during1 l/ s9 M8 l9 ]0 N' [
the evaluation of any children who present with vir-
: F, v4 j6 S' m" s, y( N0 Uilization or peripheral precocious puberty. The diag-# Z% n- a8 K8 C2 l
nosis can be established by just a few tests and by. R0 r2 j$ E6 R, R; X$ @
appropriate history. The inability to obtain such a8 o$ I% y3 N2 t# `. ^/ g: ^% }
history, or failure to ask the specific questions, may
- @0 J' s2 d; e1 Cresult in extensive, unnecessary, and expensive, S, H, L4 @& f1 D/ D2 _2 t
investigation. The primary care physician should be
& p% j& N2 V$ X0 A3 yaware of this fact, because most of these children; I5 [% e2 b1 P
may initially present in their practice. The Physicians’
* B5 l5 }! K  x% m$ h2 \Desk Reference and package insert should also put a0 B% m1 T% x& I  s5 k9 g; K1 [
warning about the virilizing effect on a male or( w& W1 H6 D8 r2 X6 M/ P
female child who might come in contact with some-
( X2 H/ O1 I3 Gone using any of these products.% i1 N/ x$ R$ r; J5 u) H8 ?# j
References+ |" P7 ^8 R  T, \5 b" u+ t
1. Styne DM. The testes: disorder of sexual differentiation
0 N( J% E" }1 Q/ q/ Rand puberty in the male. In: Sperling MA, ed. Pediatric
) x+ Y! E  h" g" n% BEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;% X$ r/ D$ A$ ^% i. M
2002: 565-628.
2 b' v7 z0 |% b2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious/ Z' P& M! V; k6 ?' t9 G) d
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
% w2 {" a9 C# _. B$ ]  ^2 [Boy Induced by Indirect Topical$ I" `+ i2 h! T. x0 \8 h: i+ Q
Exposure to Testosterone- [; t  E- h2 @3 y8 ^( V% ]5 ]
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
4 r) }1 j0 ]  C5 s- [3 land Kenneth R. Rettig, MD16 N8 I# I( j* N! x
Clinical Pediatrics% H7 }  ]8 R; d% y1 D4 g+ f
Volume 46 Number 6
/ Q% ?7 `& R4 o% }1 IJuly 2007 540-543
. x: j5 N: s9 D. b© 2007 Sage Publications) S8 [4 {% r0 }5 d0 C5 y& q
10.1177/0009922806296651
9 }9 x+ A! z( d" u% @) Xhttp://clp.sagepub.com8 r+ S/ L8 n6 \* D6 {' R: ?3 `
hosted at
$ _8 T( U% J% o! y7 e  H1 `0 N! T7 jhttp://online.sagepub.com
" r0 |: D+ b( R* T4 o: M+ f9 JPrecocious puberty in boys, central or peripheral,
' m% F7 H) X4 c* r2 J) Sis a significant concern for physicians. Central- n4 {  z; R" \
precocious puberty (CPP), which is mediated
' D4 j" d9 x" I6 h3 q' |; ]through the hypothalamic pituitary gonadal axis, has
. y9 t. \* a; z6 n( G0 ga higher incidence of organic central nervous system6 _) S1 i+ f# t8 Y
lesions in boys.1,2 Virilization in boys, as manifested
+ H+ o9 I: o+ h! Wby enlargement of the penis, development of pubic( `, K- Y  R; T! p7 I
hair, and facial acne without enlargement of testi-. \; p5 j5 s  O1 S$ m" Z- n
cles, suggests peripheral or pseudopuberty.1-3 We6 l4 O" ~7 R2 ^, `
report a 16-month-old boy who presented with the& k% ?6 \0 z. L# r" g4 }1 y/ J
enlargement of the phallus and pubic hair develop-# k5 l& r: U( Z. C
ment without testicular enlargement, which was due+ F1 f- O3 T  G' J
to the unintentional exposure to androgen gel used by
% e% k8 }) A7 Rthe father. The family initially concealed this infor-; Q3 M9 N( p& w
mation, resulting in an extensive work-up for this
0 q8 _7 k: N9 p) E# _% ~: Kchild. Given the widespread and easy availability of
+ K1 @, M' q& K# d# Mtestosterone gel and cream, we believe this is proba-' R% J* k0 Z/ x; r# F: z
bly more common than the rare case report in the
0 |7 B+ f6 w, Y% f8 B" a& Tliterature.43 x1 u. x0 `& U9 x3 U' U* I8 m
Patient Report
5 X$ k! g1 u0 [; A; \! q, w* m4 HA 16-month-old white child was referred to the" i" d$ J1 V; M3 [
endocrine clinic by his pediatrician with the concern4 e. j/ u5 c+ A7 ]' P7 j; @4 ~1 c5 f
of early sexual development. His mother noticed
: }8 H- @! b& Wlight colored pubic hair development when he was
2 \6 ?8 W: v3 q% U7 E$ xFrom the 1Division of Pediatric Endocrinology, 2University of
! s# T2 Y: T1 N$ N* p/ c6 jSouth Alabama Medical Center, Mobile, Alabama.: o4 A  T0 Y7 l  ~
Address correspondence to: Samar K. Bhowmick, MD, FACE,
; k3 ?+ v8 U! c4 ~Professor of Pediatrics, University of South Alabama, College of% a% M8 l' O; p) W5 {7 L) `
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;/ U$ D! w  S# K8 |2 j0 O: h- `; v
e-mail: [email protected].
$ D/ u' X$ s4 p, oabout 6 to 7 months old, which progressively became
: h( t% O/ A& p+ u1 k, f+ |8 bdarker. She was also concerned about the enlarge-
! A) c- j3 W( {* c" D! o. vment of his penis and frequent erections. The child
/ a, V  }& ]" b0 z0 uwas the product of a full-term normal delivery, with
* K( O5 E# o, A4 G1 Q# j) A7 ra birth weight of 7 lb 14 oz, and birth length of
" O& k2 ^, N) j, J. I: C20 inches. He was breast-fed throughout the first year
6 m7 k3 R5 M  y. \* Iof life and was still receiving breast milk along with$ W0 ^9 V; D/ R5 ?
solid food. He had no hospitalizations or surgery,8 m7 I4 C. p0 I5 W- Y2 H, _
and his psychosocial and psychomotor development% s. Q+ i( h% l5 F
was age appropriate.
& A; l1 a8 D* s! ~9 `- WThe family history was remarkable for the father,
5 h& S& j. A- N' bwho was diagnosed with hypothyroidism at age 16,# N% H; g5 {$ P
which was treated with thyroxine. The father’s: \5 v/ e' }' a$ `) x2 M8 V
height was 6 feet, and he went through a somewhat+ Z: l( p, x- m
early puberty and had stopped growing by age 14.
) D& {' K& c+ e1 E2 B+ B7 L% OThe father denied taking any other medication. The0 B3 X% q8 `1 B$ O9 h0 x
child’s mother was in good health. Her menarche( [. g4 s8 E- G# [9 a0 C1 _/ x
was at 11 years of age, and her height was at 5 feet
' U8 O  x8 p% _& f- z" A+ k5 inches. There was no other family history of pre-" k  `) J- U5 t; P, k8 l$ h/ [
cocious sexual development in the first-degree rela-# T% `( R8 a& a" d
tives. There were no siblings.
8 Y. o, X2 t$ oPhysical Examination
$ l9 E  T1 T% y& D7 @* W- e  rThe physical examination revealed a very active,
7 L5 {) V- D8 S3 F2 Xplayful, and healthy boy. The vital signs documented
& K1 g! M6 d$ n5 i5 g4 k6 G6 t6 za blood pressure of 85/50 mm Hg, his length was- z6 Q* M0 z! `8 G; a3 h+ e; U: W# k% N. q
90 cm (>97th percentile), and his weight was 14.4 kg
- v# J1 n* A6 E3 {4 I) n! i(also >97th percentile). The observed yearly growth0 R$ C# [! [/ v9 v/ F; p! ^
velocity was 30 cm (12 inches). The examination of
5 V9 _* O; F3 C& n5 O# d4 D9 A! kthe neck revealed no thyroid enlargement.9 ~! q4 A& q$ t7 j4 V; O
The genitourinary examination was remarkable for5 B. c" o" e, n, q- X
enlargement of the penis, with a stretched length of
2 h  ]' |, ?( s- I! J' ^8 cm and a width of 2 cm. The glans penis was very well
0 Y9 D8 n. |/ kdeveloped. The pubic hair was Tanner II, mostly around
4 t& j# X) O2 G4 j540) o# X% H! F0 d% k
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from- r4 Z# Z6 V& G6 V4 Y: q$ Y% \, G
the base of the phallus and was dark and curled. The! }1 d' }8 H- @. x: h8 R- W' F: w
testicular volume was prepubertal at 2 mL each.
! y( u8 h: w& q/ v. vThe skin was moist and smooth and somewhat
# h+ y  W7 p2 x' t  x: }2 _oily. No axillary hair was noted. There were no& d( }2 |3 Q+ m  ?* A
abnormal skin pigmentations or café-au-lait spots.! W- O( B+ {# {& Q0 K/ a% U$ i
Neurologic evaluation showed deep tendon reflex 2+
6 _+ ~7 T: h; _0 w+ P9 Rbilateral and symmetrical. There was no suggestion
" R5 }  t9 c- `5 ~1 hof papilledema.
1 J4 o! M+ g8 g: h2 h5 u5 OLaboratory Evaluation
5 Z0 z$ {/ y% J/ A4 S4 J3 ?' P. JThe bone age was consistent with 28 months by/ @. ]6 o! ~0 F2 j% f( `( X
using the standard of Greulich and Pyle at a chrono-
  ^: g2 `0 E+ D' l3 C# Vlogic age of 16 months (advanced).5 Chromosomal
) K6 x  L* O6 a* nkaryotype was 46XY. The thyroid function test
3 F% m2 K2 O6 L9 b! t7 \6 E6 rshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
4 ^" \+ _. S: A% B6 {1 u* jlating hormone level was 1.3 µIU/mL (both normal)., l& R5 s6 w* w# T) H% d
The concentrations of serum electrolytes, blood
; O& l; {: D, o. xurea nitrogen, creatinine, and calcium all were2 s$ q+ O/ Z$ A# G- k
within normal range for his age. The concentration
5 a. }3 A: `' ?; n, V' f9 A! k) E) Fof serum 17-hydroxyprogesterone was 16 ng/dL
+ G0 i5 o1 h2 r1 N; I% Z(normal, 3 to 90 ng/dL), androstenedione was 205 j& w% t/ }5 ~! ?
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-: P6 M6 b( g! O% r
terone was 38 ng/dL (normal, 50 to 760 ng/dL),- K5 M1 ^* S  e  N4 P
desoxycorticosterone was 4.3 ng/dL (normal, 7 to, d  L# b; C- D3 R2 k/ J
49ng/dL), 11-desoxycortisol (specific compound S)6 _2 L, w# s! b: ^4 G2 F" P* ^
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
+ h' {( `  B: G; I6 Q  P( [- |" ]3 Wtisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total' `) D) u6 l& y
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),% S+ d1 {' H3 n2 x9 L: B2 H
and β-human chorionic gonadotropin was less than
# p0 n7 ~& z: k4 t3 {0 ~! s! g5 mIU/mL (normal <5 mIU/mL). Serum follicular
& _5 }/ r7 p! |/ w5 ostimulating hormone and leuteinizing hormone
  `9 I1 l) b* U$ ]concentrations were less than 0.05 mIU/mL( l/ r* _) c2 p2 |
(prepubertal).
1 v  W  \7 R# z0 \& {7 lThe parents were notified about the laboratory- v2 u% u) l3 _8 N! `
results and were informed that all of the tests were$ ~' x+ I# ~+ G1 f# Y" a; t3 i7 N
normal except the testosterone level was high. The
! M" X' u6 |( e) Zfollow-up visit was arranged within a few weeks to
$ r) T, L+ ?& t1 q3 pobtain testicular and abdominal sonograms; how-
+ ]& L4 x% `, V' qever, the family did not return for 4 months.
8 z% B9 b  R; J+ XPhysical examination at this time revealed that the
! k1 L3 x! g# hchild had grown 2.5 cm in 4 months and had gained
) w' ~0 q% ]  v+ M: k3 c6 L2 kg of weight. Physical examination remained! |; ~. J- v8 w9 Y5 x
unchanged. Surprisingly, the pubic hair almost com-" r) @' ?# a) o
pletely disappeared except for a few vellous hairs at
% |! a+ T1 q. V, _$ tthe base of the phallus. Testicular volume was still 2
+ d2 S$ H3 i/ XmL, and the size of the penis remained unchanged.
4 ?: R5 J7 h# P2 GThe mother also said that the boy was no longer hav-7 V1 o+ ?  w/ I" C: @9 G0 e7 u
ing frequent erections.
6 F' [. Y8 i- ~6 ^( ABoth parents were again questioned about use of" ]2 e  J: d1 y3 {5 o$ a9 z  \% F+ Z
any ointment/creams that they may have applied to
" M3 B3 g/ X8 P# v+ A9 Y/ Cthe child’s skin. This time the father admitted the6 |. d9 B2 k; J0 ]- T
Topical Testosterone Exposure / Bhowmick et al 541
4 C7 R+ p3 S) Suse of testosterone gel twice daily that he was apply-
) k' t+ T, U. {1 q& h9 P0 C0 ]ing over his own shoulders, chest, and back area for' P, H' w# N9 P( G& n
a year. The father also revealed he was embarrassed
$ i- N; T0 O# A0 e% b0 Q8 pto disclose that he was using a testosterone gel pre-, Z& S' x7 h: r% k
scribed by his family physician for decreased libido
: e* ]4 Y, H( Z& W! ]secondary to depression.
; @  r# T, S' H  p! u# b+ }3 w# tThe child slept in the same bed with parents.
/ ^" b7 K! ~4 @$ ]2 r5 a& K9 |The father would hug the baby and hold him on his
: \6 A( r7 ]  M5 j/ B/ qchest for a considerable period of time, causing sig-
' ^' \- I9 d% h' c% _nificant bare skin contact between baby and father.1 w# Y. \2 V& R3 m, W
The father also admitted that after the phone call,
6 j! o6 Q+ T2 q# K8 J9 gwhen he learned the testosterone level in the baby
- N3 l5 Y" \' @0 W3 ~: |4 Zwas high, he then read the product information6 ]- s4 Y- ~# d; C8 e1 B9 j
packet and concluded that it was most likely the rea-+ ^0 u# P) V8 N2 l  t; n7 i3 x
son for the child’s virilization. At that time, they
* [& P) i# }5 ~decided to put the baby in a separate bed, and the* t* ~& j! j) n2 c: m" M. o9 b
father was not hugging him with bare skin and had. U4 a% j3 v/ x8 U# W
been using protective clothing. A repeat testosterone
, C" L, E- D- S; Ltest was ordered, but the family did not go to the
- B3 l5 b6 ~7 l: G6 l: L- E3 blaboratory to obtain the test.
1 Y! D$ I& A/ J' LDiscussion
  q' V3 Q+ [3 L  L$ o6 MPrecocious puberty in boys is defined as secondary
) K0 f7 z$ l: k, U- o# Msexual development before 9 years of age.1,4
8 f6 o+ B- M5 B& q- P# ], k8 }Precocious puberty is termed as central (true) when! K$ Q# M/ X5 T
it is caused by the premature activation of hypo-
9 R$ N, `8 R# w% mthalamic pituitary gonadal axis. CPP is more com-
  w- x1 K2 W( Y9 A1 P" Pmon in girls than in boys.1,3 Most boys with CPP' j# e7 |- e( l
may have a central nervous system lesion that is
1 u) J% N, }! v" d+ w7 c* B( Vresponsible for the early activation of the hypothal-& R; w1 I* L9 g3 b
amic pituitary gonadal axis.1-3 Thus, greater empha-
6 B0 l' i+ G* b* Rsis has been given to neuroradiologic imaging in# k2 V; ~3 r+ R2 R; ?+ ~3 D* c
boys with precocious puberty. In addition to viril-. V2 T' g- v3 ^  ^3 Z6 U
ization, the clinical hallmark of CPP is the symmet-
3 I! s; H9 i! s% `rical testicular growth secondary to stimulation by+ f- v& ?( o6 ~, Q3 i- C7 y/ d
gonadotropins.1,31 z* Q- F& X: ^9 x+ g) E( a! h
Gonadotropin-independent peripheral preco-
5 |4 J/ q1 Y* x* e+ B  d# o7 Mcious puberty in boys also results from inappropriate
1 m: u: W' L- y5 D8 I3 Kandrogenic stimulation from either endogenous or, `* L( y9 V# P5 V: |( F
exogenous sources, nonpituitary gonadotropin stim-2 `; M$ k( N/ V
ulation, and rare activating mutations.3 Virilizing. x  V: _9 T) H. W* T& J
congenital adrenal hyperplasia producing excessive
" o! A5 q) a0 c1 dadrenal androgens is a common cause of precocious; G$ I+ t9 e& S  p
puberty in boys.3,4  V- L5 {1 u3 m5 k9 U0 r" w& M, I
The most common form of congenital adrenal
5 e* W/ u9 i5 l: ?  T* _hyperplasia is the 21-hydroxylase enzyme deficiency.
1 m4 {4 c4 {3 x! A: ]* n9 n' }The 11-β hydroxylase deficiency may also result in3 r- P( G5 n5 B9 t2 O+ C6 q2 i& b
excessive adrenal androgen production, and rarely,
" `! i/ w# E9 S+ U  q. oan adrenal tumor may also cause adrenal androgen% l, p; h  @3 ]" ^7 Y# Y. J5 o
excess.1,3% j8 u/ x3 k1 b$ k7 K7 j
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
1 d7 l) i- s% G2 K* ?% b542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
& N0 `5 e: v1 D; e4 QA unique entity of male-limited gonadotropin-. S. F8 v% I5 V2 P. R$ s. ?
independent precocious puberty, which is also known1 u6 p2 ~+ y. A( j' E4 M
as testotoxicosis, may cause precocious puberty at a
6 ]9 U- V# H) jvery young age. The physical findings in these boys+ R  s2 t0 r" T; O( m
with this disorder are full pubertal development,7 \6 t' I" K0 Q7 O3 p! a) M- ^' e
including bilateral testicular growth, similar to boys- a1 m* V& o. z! M* N
with CPP. The gonadotropin levels in this disorder% I$ }8 R6 y* Y0 u3 Y
are suppressed to prepubertal levels and do not show
4 m- h# P9 l9 \- Fpubertal response of gonadotropin after gonadotropin-+ y1 @9 E7 S3 n! y  L; _8 w6 Q
releasing hormone stimulation. This is a sex-linked4 Y8 X/ H! M/ _6 e& I7 C
autosomal dominant disorder that affects only
$ m. {' y) O8 R# c  Z3 Z& Emales; therefore, other male members of the family
) i! S) `) b: }may have similar precocious puberty.3
" `. h+ a, O1 k- H4 J% OIn our patient, physical examination was incon-
% k; h3 `! m" \% gsistent with true precocious puberty since his testi-5 b( E( `; S) m
cles were prepubertal in size. However, testotoxicosis5 P; J' S9 E6 K2 g
was in the differential diagnosis because his father. Q* O" K% C1 O6 C. O1 E
started puberty somewhat early, and occasionally,
5 F6 ]0 N* R/ y+ S% h$ ftesticular enlargement is not that evident in the7 J% t) z) S7 A; C6 r" X
beginning of this process.1 In the absence of a neg-
+ f% s6 d* t( O) ^6 p/ L: q4 Uative initial history of androgen exposure, our
# R" k4 ?6 H& vbiggest concern was virilizing adrenal hyperplasia," e/ {) h" S$ s, B0 |
either 21-hydroxylase deficiency or 11-β hydroxylase
6 C8 H. C. r6 a3 V3 c) f$ t  _7 Q, Gdeficiency. Those diagnoses were excluded by find-
( n, f. Z) J9 h2 g1 m/ qing the normal level of adrenal steroids.
) ^$ G9 w% I: }The diagnosis of exogenous androgens was strongly) x& q: K+ ^9 Q0 }! G' M
suspected in a follow-up visit after 4 months because$ Y3 h; k! J  q3 [: M1 g
the physical examination revealed the complete disap-5 f* l( j  G/ @6 _- G
pearance of pubic hair, normal growth velocity, and
$ s$ u1 n) x5 L0 }: o6 b, F- q' bdecreased erections. The father admitted using a testos-7 P3 a# o9 u! W  `: r" L* W
terone gel, which he concealed at first visit. He was
) B0 \& @# d( m) @7 {  J( K: _using it rather frequently, twice a day. The Physicians’
* W% L4 Z9 F; M6 L: L7 @Desk Reference, or package insert of this product, gel or" x+ z, @' y1 u; |
cream, cautions about dermal testosterone transfer to8 Y! c+ ~9 b; W8 u% I' C* ~
unprotected females through direct skin exposure.
8 F3 H" b, ?& z* C0 D+ USerum testosterone level was found to be 2 times the  N' @  Q6 ?0 D4 h
baseline value in those females who were exposed to; S/ D* W2 P' z3 _
even 15 minutes of direct skin contact with their male
' v: |# `, v5 J% dpartners.6 However, when a shirt covered the applica-
; n( B) R; K2 m9 v. ]! Btion site, this testosterone transfer was prevented.; }9 A- K) h6 D! c
Our patient’s testosterone level was 60 ng/mL,( F  k. d. O. n! [7 q1 ^
which was clearly high. Some studies suggest that) Q3 O1 m; Z% J: W
dermal conversion of testosterone to dihydrotestos-
: I) l/ @: P7 p: T$ kterone, which is a more potent metabolite, is more2 c5 c& R7 ?1 F' b
active in young children exposed to testosterone( L: W1 G# F1 R* L! A
exogenously7; however, we did not measure a dihy-) M& h. V$ @5 g3 M* f
drotestosterone level in our patient. In addition to  ]) F1 |) H& I- w5 N  N/ {  w
virilization, exposure to exogenous testosterone in
3 `( S, g3 Y# D9 r+ |+ `" [$ M% h" Mchildren results in an increase in growth velocity and
/ l6 d6 v9 z6 j( a) l" ]3 aadvanced bone age, as seen in our patient.; _- D, ~' E0 o% U
The long-term effect of androgen exposure during2 D2 Q4 h- ]3 g2 ], C! K
early childhood on pubertal development and final. j& T: O4 [( D" F) ~: |
adult height are not fully known and always remain! }( I5 s; R2 L' |3 I
a concern. Children treated with short-term testos-0 t0 k" ^9 y! G* z+ X$ [7 u
terone injection or topical androgen may exhibit some
* [" v; G7 r* B/ Tacceleration of the skeletal maturation; however, after$ v* i" i% ^- s: |# b- P$ r
cessation of treatment, the rate of bone maturation
/ P0 ?& c" n* e0 E7 tdecelerates and gradually returns to normal.8,9/ D1 r/ |+ w7 G+ L
There are conflicting reports and controversy3 l4 q% P) k5 D# O* U
over the effect of early androgen exposure on adult  J0 q8 o. U) F# F
penile length.10,11 Some reports suggest subnormal4 C+ [2 S% |/ P! n; Y
adult penile length, apparently because of downreg-
: {$ Y) W9 p, I4 `! Kulation of androgen receptor number.10,12 However,: ?# t2 B$ L$ f" D5 t' U5 }/ a0 M
Sutherland et al13 did not find a correlation between
2 A1 O0 @% y! x) g* w1 u& T# i. Achildhood testosterone exposure and reduced adult# n! [1 I" P/ l8 L1 F, S7 [7 f
penile length in clinical studies.' M/ i8 T& |2 Q' w" r! ]
Nonetheless, we do not believe our patient is
. D1 T/ T; Y8 @  }( Dgoing to experience any of the untoward effects from
2 s$ P; l: w- ^) btestosterone exposure as mentioned earlier because5 j& G* ^+ M3 k* }  _& e
the exposure was not for a prolonged period of time., v; Z3 x& S8 k# s# K: f! w: _
Although the bone age was advanced at the time of
; g* f4 Z( Z6 H' Tdiagnosis, the child had a normal growth velocity at
; t1 I; |- l+ a- r, A& Mthe follow-up visit. It is hoped that his final adult
+ z0 X" h/ A) _) R4 T8 jheight will not be affected.
3 z0 j4 l, x5 w8 s% T6 `( x( MAlthough rarely reported, the widespread avail-: S( J% v& c" k5 }2 X' I
ability of androgen products in our society may
9 i2 C* g6 V) C7 H0 v4 O% b: Sindeed cause more virilization in male or female
# T$ E- f6 h5 n* U) U( U1 r7 Gchildren than one would realize. Exposure to andro-  D: Y  T% U5 h0 |+ o; h/ F# q
gen products must be considered and specific ques-
1 M5 y  |+ q) s0 s7 d; _$ {' _tioning about the use of a testosterone product or
( s# s/ E' s* N# O$ d% r) a3 o# xgel should be asked of the family members during0 C' o3 Q) y: K1 W8 j- X; Q4 c, o
the evaluation of any children who present with vir-
1 a. Y7 K8 _, S0 zilization or peripheral precocious puberty. The diag-% F: e- m0 j/ ~$ n4 r3 W5 E
nosis can be established by just a few tests and by
2 F9 m  s8 R6 {9 I' Xappropriate history. The inability to obtain such a
6 f4 z8 ?/ L# O& e& X' rhistory, or failure to ask the specific questions, may
7 @# A& F8 u5 X7 c. x- W7 Y) eresult in extensive, unnecessary, and expensive+ O" ~6 ]" R& S7 E/ e
investigation. The primary care physician should be
+ U1 x' r! l* f' j; e- J) r7 {aware of this fact, because most of these children8 I" P, T: V, `3 }- y3 v2 t1 R
may initially present in their practice. The Physicians’
1 d0 @- j6 w8 l! Z" ~Desk Reference and package insert should also put a
- q$ Z% u5 J; V  kwarning about the virilizing effect on a male or
) p" X- I5 }7 U. V3 w4 }female child who might come in contact with some-6 W0 m& U7 M* p( @4 e
one using any of these products.
8 K: o. z& ^1 g7 |) [; b# LReferences5 u6 I9 k# q! B, `3 I
1. Styne DM. The testes: disorder of sexual differentiation& S0 x2 }$ A( e2 b$ M% ?7 O' R
and puberty in the male. In: Sperling MA, ed. Pediatric
" j( P: T/ A5 |) j" J- J$ `3 ?0 xEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;, f( O& n9 v- z% m
2002: 565-628.
) b; t7 w% b* u+ Z2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious$ }: n* b) w' h. k6 z4 x
puberty 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
VIP精品區,資源無限好賺金任務區,輕松賺金幣
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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
! `8 b  t6 ~" h$ K3 n0 d. a. {
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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