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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) Q7 x& X) d7 ?8 V1 y$ L' D& F. y; L
Boy Induced by Indirect Topical+ @# a4 u' a2 M( @4 u
Exposure to Testosterone
. j& A3 Z1 U/ F& d7 u& [Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2! O& F  M( t8 C0 W, t2 m5 N9 O
and Kenneth R. Rettig, MD1
9 K, P& j9 l1 D6 H" d2 F  uClinical Pediatrics) {9 F" j# V# l6 Y
Volume 46 Number 6, U% Z; z6 J% a: t, p/ P* _4 F
July 2007 540-543
5 E0 l/ r+ j$ ?© 2007 Sage Publications
) t& ]5 X4 v* ]10.1177/0009922806296651$ I; D, S  y$ A1 u" g/ f7 q
http://clp.sagepub.com3 s2 ~4 v+ R( c7 c2 m1 m
hosted at
. j. T. M$ p1 g5 g: l) c8 Ohttp://online.sagepub.com
; R+ m( L' W, |: DPrecocious puberty in boys, central or peripheral,! R# A; h! J0 K4 T
is a significant concern for physicians. Central: M, p" W& Z4 S* K
precocious puberty (CPP), which is mediated
0 m% z) Q! v+ V! \3 m3 rthrough the hypothalamic pituitary gonadal axis, has5 K- {& D) D1 M6 I4 f" `% H
a higher incidence of organic central nervous system7 U( I1 I3 ~$ N) S
lesions in boys.1,2 Virilization in boys, as manifested
1 l4 x; Q+ x6 v$ M) @  l1 y. T- Hby enlargement of the penis, development of pubic* u: v) b1 S, P( P1 n
hair, and facial acne without enlargement of testi-% N, \, c" Q1 k& n8 ]
cles, suggests peripheral or pseudopuberty.1-3 We- O+ H- v) E' F  A$ p' q) _
report a 16-month-old boy who presented with the# z) P% P' S; O2 \
enlargement of the phallus and pubic hair develop-
; r6 h3 b+ o7 F: d+ m, T. lment without testicular enlargement, which was due5 D1 ^! i2 f, `
to the unintentional exposure to androgen gel used by
5 D1 R! E1 q2 T8 r, j. o+ j0 X# Ithe father. The family initially concealed this infor-4 ^- W/ g' O6 T
mation, resulting in an extensive work-up for this+ t# y' F7 d8 Z1 U6 s) p0 @
child. Given the widespread and easy availability of
3 o, d: D; x+ Etestosterone gel and cream, we believe this is proba-
8 d5 t9 j- I+ n9 V' w) Rbly more common than the rare case report in the: o  }6 v6 G3 l" y2 A9 `- L
literature.48 W) M6 U  Z, u0 M& o  t
Patient Report
9 Z- j# k" t9 N1 k. WA 16-month-old white child was referred to the# N( y* V# [4 f/ f4 @: A
endocrine clinic by his pediatrician with the concern4 F& I$ p( U( \* \/ U: z( J+ m
of early sexual development. His mother noticed# H$ R# M' U5 ]" \* c" w
light colored pubic hair development when he was
- M' W; P+ D0 x7 V4 [From the 1Division of Pediatric Endocrinology, 2University of1 N$ A/ V) P" J+ H' Y& w
South Alabama Medical Center, Mobile, Alabama.
$ t4 ^8 A% L& u# e- H: MAddress correspondence to: Samar K. Bhowmick, MD, FACE,
( E+ |/ @8 [9 B( z+ bProfessor of Pediatrics, University of South Alabama, College of6 A5 D$ f" E5 @" B$ \( L  L
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;: t. ]5 M5 A* O2 e
e-mail: [email protected].
0 H! k; i, [/ d) w0 T' `; wabout 6 to 7 months old, which progressively became
! O0 _4 B3 \3 p+ e& Q* Sdarker. She was also concerned about the enlarge-5 o* a, a1 o3 C! B
ment of his penis and frequent erections. The child
4 T8 L1 G( g$ P3 y/ Y* cwas the product of a full-term normal delivery, with" ~- z: [# M! R3 M$ O, u" a
a birth weight of 7 lb 14 oz, and birth length of; j2 h6 b! p; F  B9 Q
20 inches. He was breast-fed throughout the first year
' U3 P% W& T4 t+ qof life and was still receiving breast milk along with% V, n) d" ^- D6 |+ B
solid food. He had no hospitalizations or surgery,
3 Y8 n) o* \9 q+ L$ y* a9 zand his psychosocial and psychomotor development, A3 K, r* b% ?3 Q* k
was age appropriate./ u( w$ U% D  c; ^4 L, v
The family history was remarkable for the father,
" s3 M7 v  q1 l' uwho was diagnosed with hypothyroidism at age 16,
0 G5 Y2 X6 o* k' d/ pwhich was treated with thyroxine. The father’s
+ W# v  p* a& {# c  ^( Y) Nheight was 6 feet, and he went through a somewhat
# j4 y. G! w0 z+ }, a/ Z+ a! |% a7 P' eearly puberty and had stopped growing by age 14.
3 O3 m  m% f+ i, ]9 |% N/ r8 `The father denied taking any other medication. The
  u+ g% P. Y- Y" d0 b. h5 `3 w3 qchild’s mother was in good health. Her menarche  j7 U: D8 E, F7 S  z! y
was at 11 years of age, and her height was at 5 feet- H( B# Q' w/ |' j
5 inches. There was no other family history of pre-
: k4 ^. n. s0 i5 V4 zcocious sexual development in the first-degree rela-* T8 d. `; ]5 w6 ]  j% n2 l! a: n
tives. There were no siblings.
# O2 Y3 [2 a# ^% L/ ^Physical Examination
; e- z+ ?- o5 n* E: X  U, z- I& fThe physical examination revealed a very active,0 y, j0 w- e, @2 w, X& s5 \, o
playful, and healthy boy. The vital signs documented1 i. h' X& D/ |  [  A  U" _
a blood pressure of 85/50 mm Hg, his length was/ U8 C% p. o" p$ j
90 cm (>97th percentile), and his weight was 14.4 kg( d  K' C) m* M  e8 {
(also >97th percentile). The observed yearly growth
1 i5 g/ u& v8 u3 A% I4 ^5 Bvelocity was 30 cm (12 inches). The examination of
* l$ u0 _+ @  Athe neck revealed no thyroid enlargement.
6 z0 b5 ]' x4 _/ y, n; HThe genitourinary examination was remarkable for) X% d, F, U4 x
enlargement of the penis, with a stretched length of
  T- N* v$ F, m8 cm and a width of 2 cm. The glans penis was very well
/ q* Z5 Z, a7 |1 kdeveloped. The pubic hair was Tanner II, mostly around
7 H$ s6 u; P& a540  p! D# L( i+ b; ~9 k* S' n7 d% H
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
% s. D9 ^- D* k% l- f- `6 Qthe base of the phallus and was dark and curled. The
3 T/ A+ m' L2 N$ ntesticular volume was prepubertal at 2 mL each.+ e. g4 o* Y% Y) }
The skin was moist and smooth and somewhat
$ X) e( q6 ^  s( M. k$ Z: N1 ~oily. No axillary hair was noted. There were no* O, ?' M) v) X7 W
abnormal skin pigmentations or café-au-lait spots.( D- S/ i! q- K: P1 d- J
Neurologic evaluation showed deep tendon reflex 2+
9 u# z7 p( p3 d$ w# Y/ x: y7 Bbilateral and symmetrical. There was no suggestion) \* p: G' B+ v+ F3 N
of papilledema.& c, P. X1 |2 A' d  [* {
Laboratory Evaluation
9 Q7 g- q; Z; L  ?, K( B2 I1 OThe bone age was consistent with 28 months by
( N9 j* A! [1 q8 susing the standard of Greulich and Pyle at a chrono-& i( j- y; N( W4 F, r
logic age of 16 months (advanced).5 Chromosomal5 d8 h6 h. X" Q
karyotype was 46XY. The thyroid function test
, P/ C5 {: t9 F+ `5 O$ h5 Tshowed a free T4 of 1.69 ng/dL, and thyroid stimu-5 |. E( N3 T4 Y
lating hormone level was 1.3 µIU/mL (both normal).2 e) D" s! Z( B% Z# H8 o& c
The concentrations of serum electrolytes, blood# z- v$ b) `6 k3 \
urea nitrogen, creatinine, and calcium all were
! p9 q( j, A/ Cwithin normal range for his age. The concentration0 U* Z- q: |; k! l$ q/ ^# f3 b
of serum 17-hydroxyprogesterone was 16 ng/dL; D6 A! r9 s1 U3 [6 ?. B
(normal, 3 to 90 ng/dL), androstenedione was 20/ Q1 {: C" V. [+ g- w' C" t) \5 r
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
) O) d# c. ?; Nterone was 38 ng/dL (normal, 50 to 760 ng/dL),
! N( g! b& A0 G' {/ r; n3 tdesoxycorticosterone was 4.3 ng/dL (normal, 7 to
/ U4 w( p3 Y' P( x# I49ng/dL), 11-desoxycortisol (specific compound S)
7 v- R0 Z  X' }1 I3 W4 [& Cwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-- O* i& ~' Q( a0 N: q: p" K
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total# K: z* J* t  W9 s! M  Z0 h; N& |
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),0 G# z+ l! o, V. c
and β-human chorionic gonadotropin was less than
* j+ N- A: l! O3 y" Q5 mIU/mL (normal <5 mIU/mL). Serum follicular
) P0 H7 G7 U& w: mstimulating hormone and leuteinizing hormone
' _6 F2 w) b( ^/ |+ T! Pconcentrations were less than 0.05 mIU/mL
) _8 D- p' R- Q8 t% {(prepubertal).! z4 i4 f8 r. ^5 K2 ?8 y
The parents were notified about the laboratory0 o) A: y* E" f& F
results and were informed that all of the tests were0 g' v- F$ g1 Z' _; v. D8 K
normal except the testosterone level was high. The- P" ^- a8 f. R( y9 [; i7 w
follow-up visit was arranged within a few weeks to; K3 }% z; f* y, K3 E/ v9 c
obtain testicular and abdominal sonograms; how-
- e7 S& \' v6 tever, the family did not return for 4 months.
; v" @5 P# W  ]6 Y6 e2 s: Z. f( NPhysical examination at this time revealed that the
* g5 m3 }' |* T# p1 C" H8 Xchild had grown 2.5 cm in 4 months and had gained- J0 A( Z7 }% j/ K( {& p
2 kg of weight. Physical examination remained. }" i$ M+ Y) `* x
unchanged. Surprisingly, the pubic hair almost com-' [1 }2 e/ q) c
pletely disappeared except for a few vellous hairs at: f. @& F" j8 C) l" U
the base of the phallus. Testicular volume was still 2% F1 S3 H, Q$ U4 a# B7 ^$ I- @
mL, and the size of the penis remained unchanged.8 ~6 ~6 L$ A0 v6 d
The mother also said that the boy was no longer hav-
; `( ?) A$ t$ S) D  g: d, z* hing frequent erections.
4 w7 `% q$ _+ \7 \Both parents were again questioned about use of
) n# c2 _) a, A, ~1 a8 Many ointment/creams that they may have applied to6 n, N, j/ h6 V9 k
the child’s skin. This time the father admitted the
; `6 W! ~3 M- Z- q) Y8 M2 i* T# }Topical Testosterone Exposure / Bhowmick et al 541
* V2 b6 V2 x- `& X+ ^  E/ Yuse of testosterone gel twice daily that he was apply-$ I/ t7 G. I, h; A# m  _
ing over his own shoulders, chest, and back area for. L4 F; y$ U0 |* I; W1 I7 Z
a year. The father also revealed he was embarrassed! I& d$ f: F! U6 I
to disclose that he was using a testosterone gel pre-; j% E1 ?2 d  y
scribed by his family physician for decreased libido/ i& u7 Q: K7 f8 B
secondary to depression.
; T3 Q5 ?! m* {3 \+ t3 VThe child slept in the same bed with parents.
6 g/ P4 c% x# V5 j0 bThe father would hug the baby and hold him on his
3 F) r& [" L% kchest for a considerable period of time, causing sig-: d" b# v& s; f  C* S' L8 k. i
nificant bare skin contact between baby and father.# m+ R( L9 l2 d2 ]# n. `% O
The father also admitted that after the phone call,5 V# V9 ?; u. q  O2 C. _( x) R
when he learned the testosterone level in the baby
& h4 r' i( o  }was high, he then read the product information
7 j' x: X8 {3 V# z6 opacket and concluded that it was most likely the rea-
; M1 N6 b" @) L2 J3 C) ]son for the child’s virilization. At that time, they# [4 R4 D$ Z& v9 e( n
decided to put the baby in a separate bed, and the3 G& O& ^! `1 M) y9 c& w: r
father was not hugging him with bare skin and had
, x2 [  @  c3 d8 n" u& _) a6 }0 sbeen using protective clothing. A repeat testosterone
+ E* z7 h- o9 S$ v* Dtest was ordered, but the family did not go to the$ Y! U; i$ R7 l! t" E
laboratory to obtain the test.4 o, m6 ?( v( k, h% _7 s  Z2 R* k
Discussion
& y# \  L1 A' T$ l& XPrecocious puberty in boys is defined as secondary! r2 i; o4 @/ o2 Z* M& y2 Z1 X9 x
sexual development before 9 years of age.1,47 W  u% A$ Z9 d, Y
Precocious puberty is termed as central (true) when
' @0 v7 C! T2 ]; c! }# uit is caused by the premature activation of hypo-
: v" ~; Z5 Q; ~; P6 w7 ]; D% @thalamic pituitary gonadal axis. CPP is more com-
- @3 w) P: Z7 T- H, ~8 ]3 |mon in girls than in boys.1,3 Most boys with CPP) N6 |% j. V% f, K0 V% L/ i
may have a central nervous system lesion that is+ @0 N+ `2 k9 \- c7 ]; }( n9 A
responsible for the early activation of the hypothal-
7 x% a; d$ J) U- ?amic pituitary gonadal axis.1-3 Thus, greater empha-
; I  H+ }4 W2 w6 G' Csis has been given to neuroradiologic imaging in$ p2 p1 m% [7 Q# n
boys with precocious puberty. In addition to viril-  ^& o. J7 F% K" N% J
ization, the clinical hallmark of CPP is the symmet-7 v; _$ Q' q7 J$ f. o0 G8 g
rical testicular growth secondary to stimulation by- `" G* K- u5 N' b/ Q
gonadotropins.1,3! R: s/ S! O1 w3 g: ]% z$ c5 W5 f
Gonadotropin-independent peripheral preco-+ N+ Y0 A$ M  O' v( z. c
cious puberty in boys also results from inappropriate
$ x+ A3 @  S) b4 ~, |  c* S" n- ]androgenic stimulation from either endogenous or0 ~+ r1 e/ T( ^- y/ \
exogenous sources, nonpituitary gonadotropin stim-7 L/ m- f( q+ E* ]
ulation, and rare activating mutations.3 Virilizing: Z( {& b. Z& ~0 C4 e6 t4 e
congenital adrenal hyperplasia producing excessive3 v8 `7 u& a$ E: l
adrenal androgens is a common cause of precocious
3 W! Y; v* j8 fpuberty in boys.3,4) s& V, S' k$ E# B7 B- [
The most common form of congenital adrenal
+ ~9 |6 ^  b" b( L4 l$ Nhyperplasia is the 21-hydroxylase enzyme deficiency.+ g# Z3 f* i9 l4 V) l  l. E. I: @
The 11-β hydroxylase deficiency may also result in7 C: x  v" e. U" Y. `
excessive adrenal androgen production, and rarely,: N# f) j+ G) [  {$ k
an adrenal tumor may also cause adrenal androgen, X! P2 v) k( _% e. N
excess.1,3; V: H! z* K! y) B& |
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
) X% l$ I$ {; w/ K" _3 a/ w542 Clinical Pediatrics / Vol. 46, No. 6, July 2007+ Y# J0 e; P* Z. a* ]( l8 d
A unique entity of male-limited gonadotropin-
4 p7 L! Z& `+ @  D) O# b% F7 Tindependent precocious puberty, which is also known; ^& j6 H0 c* ?0 W9 h; |
as testotoxicosis, may cause precocious puberty at a1 N/ B$ G' l) G9 C' I- Z& A
very young age. The physical findings in these boys
. e$ l# D6 d  o9 ~with this disorder are full pubertal development,. ^6 i- W9 D4 U) ~
including bilateral testicular growth, similar to boys
, e0 L7 s& _+ F. k4 ^$ nwith CPP. The gonadotropin levels in this disorder
; k. D) ^5 z7 n; Sare suppressed to prepubertal levels and do not show( z& Q, y. h* O8 c  {: Y
pubertal response of gonadotropin after gonadotropin-! D4 A  e; k5 U* i, O1 i. P; C
releasing hormone stimulation. This is a sex-linked7 {# `2 ?  [+ K
autosomal dominant disorder that affects only+ V9 S* {3 Y1 C" b
males; therefore, other male members of the family2 E& l7 s3 s+ Q  Q9 l( l
may have similar precocious puberty.3
3 t' b) O* x; i4 LIn our patient, physical examination was incon-
9 y& i; }2 C) U0 Bsistent with true precocious puberty since his testi-* _9 H$ g: @6 o' c) C  ^  x3 |
cles were prepubertal in size. However, testotoxicosis
" C; W: _: H! _  F# q6 f" ^0 awas in the differential diagnosis because his father5 P2 a* F" I" ?) R! U
started puberty somewhat early, and occasionally,
1 O  g( a* F) k, ]5 t; H  [* ttesticular enlargement is not that evident in the9 Q' a6 }. c' Y$ G
beginning of this process.1 In the absence of a neg-2 n0 {' ~1 ~9 w# g
ative initial history of androgen exposure, our
4 A( c, {6 B: V# h: lbiggest concern was virilizing adrenal hyperplasia,. L6 o( \% P. U. T
either 21-hydroxylase deficiency or 11-β hydroxylase
) \' ^' [+ E- E) C8 Vdeficiency. Those diagnoses were excluded by find-& o) M& c; O, S3 Y5 \' E# I, y/ r% v
ing the normal level of adrenal steroids." C) D: z, n; ?
The diagnosis of exogenous androgens was strongly/ U$ ]( z2 g! b2 W& K
suspected in a follow-up visit after 4 months because
9 A" C8 ]. U' \the physical examination revealed the complete disap-
1 `# @# K: d" l) x  Dpearance of pubic hair, normal growth velocity, and
3 ~6 n, G; {3 d9 |" ldecreased erections. The father admitted using a testos-2 _! B0 C# n, j) B. q. \
terone gel, which he concealed at first visit. He was. Q: ?% y& H: p- s
using it rather frequently, twice a day. The Physicians’# Y9 W9 E3 |4 c* g9 `3 y6 f9 a
Desk Reference, or package insert of this product, gel or- f* g# X" w% H
cream, cautions about dermal testosterone transfer to
$ L. L4 k3 Z; ^. N; sunprotected females through direct skin exposure.
- U. G1 s% K1 b' v) ^Serum testosterone level was found to be 2 times the
- V6 @% d1 x7 _8 n; L; Nbaseline value in those females who were exposed to
" v8 I/ h. n2 v- Weven 15 minutes of direct skin contact with their male
6 N7 J0 e  `  |& d& Epartners.6 However, when a shirt covered the applica-
( o  S$ n5 o. c8 Stion site, this testosterone transfer was prevented.
- }3 N+ E' D4 B9 a3 nOur patient’s testosterone level was 60 ng/mL,
4 n: K. g7 A# Y0 }9 Nwhich was clearly high. Some studies suggest that+ G" j6 X& E% k* M) c4 b- d4 t
dermal conversion of testosterone to dihydrotestos-
8 E  q' g+ S( Q* b7 W9 Qterone, which is a more potent metabolite, is more; F' d% B3 m6 ~+ ?0 n1 L; Y5 P
active in young children exposed to testosterone
+ L3 a& p' U, Z$ ~( i5 xexogenously7; however, we did not measure a dihy-
* R$ p( y. @/ n- ?% w/ V7 mdrotestosterone level in our patient. In addition to  n2 V/ B" p# s5 {; P
virilization, exposure to exogenous testosterone in
# u4 k3 n# i5 r7 Z' {children results in an increase in growth velocity and1 T! \. X5 j/ X+ z
advanced bone age, as seen in our patient.
& Y; l3 e" g: i4 ]  ^5 ^The long-term effect of androgen exposure during
2 I. I1 e! H: K5 f* r( Oearly childhood on pubertal development and final+ l6 `: M( H6 G- p4 r; a
adult height are not fully known and always remain
8 H. z4 M) y' d3 P/ ?7 [( |" Ja concern. Children treated with short-term testos-, {! @% Z% c; Z4 `9 T
terone injection or topical androgen may exhibit some
7 u5 Z8 F" A5 F# facceleration of the skeletal maturation; however, after
/ d9 ~+ @5 V: V' m0 M5 H7 @cessation of treatment, the rate of bone maturation& r6 l# l; o% i
decelerates and gradually returns to normal.8,9
5 D9 K% B+ c6 ?/ e! O; SThere are conflicting reports and controversy  e# R' J7 m0 k0 R) [/ ^
over the effect of early androgen exposure on adult
; E8 w( V# A$ h3 @penile length.10,11 Some reports suggest subnormal! z, B: h  Q! @8 l# E. D2 U
adult penile length, apparently because of downreg-. ?, o0 Y9 h! ~3 @8 S5 G6 [0 ^
ulation of androgen receptor number.10,12 However,
. Z* K7 H9 q0 x- V0 QSutherland et al13 did not find a correlation between/ s, o5 w+ l2 `  q$ U; J( v
childhood testosterone exposure and reduced adult3 n* S0 a/ ?3 l4 g6 a( {
penile length in clinical studies., r4 f, G% c3 _$ s- x
Nonetheless, we do not believe our patient is
' i! w# G( X$ i6 P; G' sgoing to experience any of the untoward effects from% v( s0 b( Q; B- b7 [9 G1 R
testosterone exposure as mentioned earlier because! X# v5 ^6 y4 t2 s' i  X$ \
the exposure was not for a prolonged period of time.) o! Q! J5 P9 P3 E7 u. |
Although the bone age was advanced at the time of7 s$ @- g& m$ k' u; k! n+ D6 F5 D
diagnosis, the child had a normal growth velocity at4 o& W) V  h8 }, I  y, H  G
the follow-up visit. It is hoped that his final adult( o0 s7 M/ `& P. U  j  _, O
height will not be affected.. t9 ]0 L  b' j
Although rarely reported, the widespread avail-7 g3 B+ r8 B3 g, l6 H+ \
ability of androgen products in our society may
0 F4 q& _) x/ P% r. y: Hindeed cause more virilization in male or female% T% c' G1 {3 {# }/ M: E. {. I% ]9 ^
children than one would realize. Exposure to andro-' t8 p$ c0 `, Y; s. }
gen products must be considered and specific ques-; |) ]4 r+ v# p5 u
tioning about the use of a testosterone product or
( M" o) S2 ?/ Agel should be asked of the family members during
7 ?* Y+ S* }9 X8 t7 i2 O: Qthe evaluation of any children who present with vir-5 L' X. _" `# U7 F6 d$ z
ilization or peripheral precocious puberty. The diag-
  a2 z( Z) r+ |% Z% A' i  E6 T" znosis can be established by just a few tests and by* M* A4 I1 b6 z7 E  H# _) B
appropriate history. The inability to obtain such a
7 [& B% x( a* Shistory, or failure to ask the specific questions, may
3 s* @2 W  U- Z2 a6 X' M5 oresult in extensive, unnecessary, and expensive4 g* \3 W6 u8 D
investigation. The primary care physician should be# f$ y" {$ U" X( J7 u
aware of this fact, because most of these children
6 n6 k# r/ D, a; A4 G- _may initially present in their practice. The Physicians’
4 n7 J- c, [: U- [( W  xDesk Reference and package insert should also put a
7 F: ?1 h! H8 r( f) K+ fwarning about the virilizing effect on a male or' ^7 D3 d* p6 `& j$ Y
female child who might come in contact with some-
4 m, \: v" r: B) Q$ u1 oone using any of these products.5 z; e! E' ]: O3 I0 }8 e+ z0 l; {
References
1 h% e$ |0 f6 U! W' Q, P% S1. Styne DM. The testes: disorder of sexual differentiation
% H2 @! G4 X! g4 H. Mand puberty in the male. In: Sperling MA, ed. Pediatric, V5 ]! Y9 h% i4 y$ |, b
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;. f; O" {" w/ ^# ]! |$ W0 J
2002: 565-628.
' a- K" z" q$ h% d, s% P, P2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
3 @: M. B5 b  |: ]" o3 |6 S: jpuberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
4 V& |+ }' h" z, R7 sBoy Induced by Indirect Topical$ C* w" d! B8 u6 T( E! D% Z) T8 Q- y4 e
Exposure to Testosterone
0 P4 N5 T$ `! O7 ISamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
, j1 `. M9 k9 W% M# v9 _1 Rand Kenneth R. Rettig, MD1
$ @4 f2 ~/ _7 B5 t3 [& m, KClinical Pediatrics+ l# D5 R% W3 O# a. _% K2 |
Volume 46 Number 6
! u3 C+ T- G7 O- d' h$ F1 h$ iJuly 2007 540-543
1 O3 j# @5 c% F1 ~8 i© 2007 Sage Publications" ~; X8 |0 W9 T8 D$ [% O
10.1177/0009922806296651
* \/ @4 A$ T  O( l  Phttp://clp.sagepub.com+ K: d' Z2 P6 q0 m5 Q( Y/ X
hosted at
: u0 I: B# {: ~: ~" U! g" I1 yhttp://online.sagepub.com- W; \, p3 B; ?1 ~& X
Precocious puberty in boys, central or peripheral,/ z1 K# h3 y9 Q  @
is a significant concern for physicians. Central6 Q- T9 d. {. h
precocious puberty (CPP), which is mediated% Y- E3 ?/ `# Q% I# ?* a$ }
through the hypothalamic pituitary gonadal axis, has% m/ b% z: w. \: U& _
a higher incidence of organic central nervous system
( e8 q4 ^2 T. Nlesions in boys.1,2 Virilization in boys, as manifested8 M, _- @  u7 p: [- I
by enlargement of the penis, development of pubic
0 T2 c' f: m( L. ~0 a% v1 W& rhair, and facial acne without enlargement of testi-8 ]' P# @1 Q3 ?. q# i" \
cles, suggests peripheral or pseudopuberty.1-3 We
! ?) D6 m4 o, i" p+ `. z  J, I! Qreport a 16-month-old boy who presented with the( X2 y$ K7 n4 }% r
enlargement of the phallus and pubic hair develop-
" ~1 k/ v% G, J) W' qment without testicular enlargement, which was due
8 |3 R, c* u( Kto the unintentional exposure to androgen gel used by
8 Z) i  |* i; x; s0 E3 g8 z% Z7 fthe father. The family initially concealed this infor-
/ \+ F. q* a& V9 a5 q4 r( f# Wmation, resulting in an extensive work-up for this% ], A# [4 k; h( Y; _
child. Given the widespread and easy availability of$ c8 O+ |# z2 e! U. N
testosterone gel and cream, we believe this is proba-$ D0 r3 x; c# e, t& Y
bly more common than the rare case report in the
/ K9 k; R( f4 T0 q+ C2 ^: ?literature.4
/ V/ D" d2 g. e: x( PPatient Report
7 R3 u9 _3 ^6 V% ?$ k; DA 16-month-old white child was referred to the& B; \+ V% Z$ `- J
endocrine clinic by his pediatrician with the concern2 r6 M' R+ j/ E' C  [" s6 s
of early sexual development. His mother noticed
  r, _0 r* f9 o; F' Z; Tlight colored pubic hair development when he was" ~. p0 U( x+ Y  D2 ~
From the 1Division of Pediatric Endocrinology, 2University of2 P4 y6 }' ~5 y8 A
South Alabama Medical Center, Mobile, Alabama.: @9 X4 J$ G# G& z
Address correspondence to: Samar K. Bhowmick, MD, FACE," L; ]- y' a$ L& y! _4 b& B
Professor of Pediatrics, University of South Alabama, College of
5 t$ r* Z( n) oMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
7 M8 z0 h* I- `/ ?2 B0 Je-mail: [email protected].
" |6 O* y  O5 ?& babout 6 to 7 months old, which progressively became
, U1 ~2 A' a) |$ q. Ldarker. She was also concerned about the enlarge-8 O% [  n% B) W; [! x5 x
ment of his penis and frequent erections. The child
* l* G  ]# Q$ B" jwas the product of a full-term normal delivery, with
+ c! P9 }* K- O* c0 j4 r, Ja birth weight of 7 lb 14 oz, and birth length of
  J; `8 t9 C4 N/ H) H20 inches. He was breast-fed throughout the first year2 X2 f2 ~- {* [, u# L; F3 U6 N4 X( F4 Z5 y
of life and was still receiving breast milk along with
5 ], G* _3 y% y+ Y8 hsolid food. He had no hospitalizations or surgery,- V2 D- w1 I5 ^) \2 e0 t. q
and his psychosocial and psychomotor development
; \9 g9 V  h# t4 P% D4 ~% ?was age appropriate.3 C& ?2 a2 P" }$ I
The family history was remarkable for the father,
( l$ g! e; ^' d& ?, y1 I3 A6 @who was diagnosed with hypothyroidism at age 16,
3 u( ~* {/ [6 a8 N3 W6 M5 [which was treated with thyroxine. The father’s0 u! K7 V* L, l1 @0 H
height was 6 feet, and he went through a somewhat: y' v2 c0 ^) u  c) J/ B
early puberty and had stopped growing by age 14.
9 `$ \3 {9 G( JThe father denied taking any other medication. The
1 k$ ^* ~# N( Z* q3 hchild’s mother was in good health. Her menarche/ ?. J/ _+ G9 p! C/ X
was at 11 years of age, and her height was at 5 feet* B/ c) [9 F5 N. s7 y/ s! K# f9 u( E
5 inches. There was no other family history of pre-
, f( h) K6 F+ L7 z( C  Bcocious sexual development in the first-degree rela-3 h8 u+ s# n0 z; W& ^) A
tives. There were no siblings.
" x! S' A, q6 j+ iPhysical Examination2 u; T6 m! d$ U+ k( P, V- L
The physical examination revealed a very active,* g& M# O6 J5 G) v/ Y' v  ?
playful, and healthy boy. The vital signs documented  P5 C) w$ S+ ]8 i/ m& [3 T- @
a blood pressure of 85/50 mm Hg, his length was( g/ Z- L# o* g# h, e8 m
90 cm (>97th percentile), and his weight was 14.4 kg) R9 L' ?8 x5 U* n
(also >97th percentile). The observed yearly growth2 z' V; y& D8 |7 P* }  u# S0 d3 R4 x
velocity was 30 cm (12 inches). The examination of. h; r3 w' u, C) n1 ^0 {
the neck revealed no thyroid enlargement.( j; H$ V4 B: r. K4 J/ W! m# t
The genitourinary examination was remarkable for0 V: q3 E! z( m6 n8 X/ {( @
enlargement of the penis, with a stretched length of
3 w4 {$ T8 G# U4 t8 cm and a width of 2 cm. The glans penis was very well9 ]( d! }: g! L" d8 n, Q1 ]
developed. The pubic hair was Tanner II, mostly around" A8 n, O; H- T( `2 b* j
540
9 C' p: M* R& |& \; _9 Sat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
1 _3 w+ o! t0 V0 ^9 p7 Y4 Ythe base of the phallus and was dark and curled. The
. w* E4 l* m7 E& Ptesticular volume was prepubertal at 2 mL each.1 s7 h9 H, h9 [0 Q6 @5 _
The skin was moist and smooth and somewhat
1 [" c6 j4 t( W& zoily. No axillary hair was noted. There were no
9 t1 T, c5 Y: h( v7 X2 k' F! ~abnormal skin pigmentations or café-au-lait spots.
) G  t/ u" R3 @: e" i5 [Neurologic evaluation showed deep tendon reflex 2+( Q0 w1 i2 u" ]3 |
bilateral and symmetrical. There was no suggestion  u/ H0 c7 p+ m0 |
of papilledema.# F9 L* N* H' V& G5 a5 ?; [/ z+ Q
Laboratory Evaluation# k$ g5 V+ g/ w2 r) B  t! i
The bone age was consistent with 28 months by& T2 I  l1 c( B( c6 v9 D7 Z& o0 ~
using the standard of Greulich and Pyle at a chrono-
# t# A0 \) t/ A4 P7 P1 Blogic age of 16 months (advanced).5 Chromosomal: z$ O5 y' [& V1 j; v4 N, i; I
karyotype was 46XY. The thyroid function test
6 w* k6 a4 x* h, v- p  _, pshowed a free T4 of 1.69 ng/dL, and thyroid stimu-/ v& g+ {# N* T
lating hormone level was 1.3 µIU/mL (both normal).% B* [! T, A' L
The concentrations of serum electrolytes, blood3 \& }7 }8 B/ W. `& Z( {0 O
urea nitrogen, creatinine, and calcium all were' \- E# l6 e! g+ a5 s9 T
within normal range for his age. The concentration% d8 L: R3 q8 @* n3 r
of serum 17-hydroxyprogesterone was 16 ng/dL
  j/ n2 X7 A3 Q1 c6 \(normal, 3 to 90 ng/dL), androstenedione was 20
' z# x6 `+ E, wng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
; a/ p6 m: h; U# U# h. n& X1 wterone was 38 ng/dL (normal, 50 to 760 ng/dL),! _9 a; y3 U6 S' ~% g: |
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
" Y5 Z6 r/ O& b. n+ R' W' Q1 f49ng/dL), 11-desoxycortisol (specific compound S)1 l8 x3 f: t$ g3 a3 y' [- Q  A
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-( f* H( ~/ O- J6 p
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
4 g- c! g% [+ j/ |testosterone was 60 ng/dL (normal <3 to 10 ng/dL),' D5 Q6 C, V) w) m" @4 [
and β-human chorionic gonadotropin was less than
0 v$ Q$ \3 b8 m0 o) w7 `5 mIU/mL (normal <5 mIU/mL). Serum follicular
: v% S5 R4 l/ j- O: Astimulating hormone and leuteinizing hormone
" ?. M6 S4 [* b& i: J& y- J/ W. O) rconcentrations were less than 0.05 mIU/mL9 i0 X& t5 e. ~/ t) ^2 o, J
(prepubertal)./ ?4 n( O! m4 u4 i  M* A
The parents were notified about the laboratory
# \) k9 I" G" Xresults and were informed that all of the tests were" A/ P7 r2 Z& J
normal except the testosterone level was high. The
: g' C- r7 K$ E; g! |follow-up visit was arranged within a few weeks to
3 o" E( o3 R2 ~) Y8 gobtain testicular and abdominal sonograms; how-: w3 b+ ?: \4 ^- z
ever, the family did not return for 4 months.0 R7 i7 H% B8 `, K
Physical examination at this time revealed that the
( {$ z6 a! J9 B- y% Gchild had grown 2.5 cm in 4 months and had gained
. S( Z/ V: E: s: h: M2 kg of weight. Physical examination remained5 c* J' ^# M/ V5 B4 b
unchanged. Surprisingly, the pubic hair almost com-3 a+ F" X8 \. l; g. D% X
pletely disappeared except for a few vellous hairs at- A4 z7 A6 D7 ?/ v! [: x: \
the base of the phallus. Testicular volume was still 2
( u3 `# b$ }3 p& d9 p3 X" hmL, and the size of the penis remained unchanged.# G0 n; X! n! k1 C
The mother also said that the boy was no longer hav-
/ u8 U) {6 l5 Z8 i2 ?3 ~, Cing frequent erections.
, V! S# m/ ]6 M/ VBoth parents were again questioned about use of1 b5 n* J2 X' v' y% P# {
any ointment/creams that they may have applied to, c* g! h9 P3 ~5 R
the child’s skin. This time the father admitted the% ^8 S8 g0 p. f' j& r
Topical Testosterone Exposure / Bhowmick et al 541
( H% u0 @+ E% C) }6 nuse of testosterone gel twice daily that he was apply-
8 T( {+ I* B& }6 e6 s0 C7 _! King over his own shoulders, chest, and back area for' o) Q  Q2 v9 A1 L+ b* S3 F2 B+ F+ D
a year. The father also revealed he was embarrassed* a0 i3 g( M' F* I/ h* i6 a. u
to disclose that he was using a testosterone gel pre-
: J  P) Z% \0 |5 Y; X  n) oscribed by his family physician for decreased libido
- ^, {6 t3 s" \2 q9 e4 qsecondary to depression.
/ o7 h& }0 R, x0 I& S0 pThe child slept in the same bed with parents.
4 s! V( r  N$ GThe father would hug the baby and hold him on his
+ R3 [- ^/ d4 |chest for a considerable period of time, causing sig-
9 c' i; @# }, P/ {* B+ I' W2 o" M( ], Anificant bare skin contact between baby and father.) Z( t8 F7 B: u  l+ y
The father also admitted that after the phone call,
3 ^% p# z. y2 T: n7 Gwhen he learned the testosterone level in the baby
5 g0 x, w  c2 F! M/ T8 ?2 E+ A+ }was high, he then read the product information
* n$ v: D$ G# J% J5 npacket and concluded that it was most likely the rea-
! t5 D6 M4 L6 B  |4 J% Z' T7 Ason for the child’s virilization. At that time, they
* L7 t2 s3 i: [( u( d# G' _- A: xdecided to put the baby in a separate bed, and the5 \' m. `( s' E5 e, Q/ {2 s
father was not hugging him with bare skin and had
5 c- I5 T0 o' f* i0 S- pbeen using protective clothing. A repeat testosterone
8 l$ _, K. Q4 h* _: Btest was ordered, but the family did not go to the  h" q- t+ q& z, h5 t: ]" E
laboratory to obtain the test.
0 w  r4 f. G7 u7 s9 S) GDiscussion  P# m* l3 r" B' M: D* b  k
Precocious puberty in boys is defined as secondary
+ D* s' G- E1 @' }" J* }sexual development before 9 years of age.1,4
" `& u& @0 m/ N$ Y- W# XPrecocious puberty is termed as central (true) when
) T' q% ?9 R7 U6 S1 A& x" W5 Sit is caused by the premature activation of hypo-+ b6 T% q' E5 I( a0 A; D5 l  w
thalamic pituitary gonadal axis. CPP is more com-
' w  B; c& d4 H! @mon in girls than in boys.1,3 Most boys with CPP
0 K6 S. D9 J; A" Z) lmay have a central nervous system lesion that is
) S/ X: W- I' s: q2 N) Z3 I; zresponsible for the early activation of the hypothal-3 e* N% Q2 E4 [/ ]) V! o
amic pituitary gonadal axis.1-3 Thus, greater empha-
% b$ u& ^' j% ]) e) a8 D8 csis has been given to neuroradiologic imaging in1 \' G" M+ v2 h# d* r
boys with precocious puberty. In addition to viril-2 X9 J4 |  R0 J/ z$ s- V
ization, the clinical hallmark of CPP is the symmet-
6 L# m! O( o6 n! ~, h, E! Yrical testicular growth secondary to stimulation by
/ }/ P7 r$ C7 ?! h  I6 d* G: _/ z9 L) lgonadotropins.1,32 [- T7 C( P% L0 x  n, ^  Q
Gonadotropin-independent peripheral preco-
: h5 G9 Q* N1 W7 Q9 `cious puberty in boys also results from inappropriate
1 I' m9 R" h( A8 v6 h7 w$ Tandrogenic stimulation from either endogenous or
+ w& }8 q( G& N7 G6 u2 p3 Iexogenous sources, nonpituitary gonadotropin stim-. `7 r' g' a' x# W: f# m
ulation, and rare activating mutations.3 Virilizing3 W( z3 _: R& g& k) \5 u; f- i
congenital adrenal hyperplasia producing excessive1 E! p! V% `! I7 [( q
adrenal androgens is a common cause of precocious& ]) t2 q3 q. U2 |- D+ `
puberty in boys.3,4# G: [7 Z+ i1 i8 m, v, v
The most common form of congenital adrenal( [1 l' y5 f2 h9 Z4 B( r. g% K
hyperplasia is the 21-hydroxylase enzyme deficiency.9 p& F' I+ n6 v/ e
The 11-β hydroxylase deficiency may also result in
! q4 F: V6 Z8 X; H3 aexcessive adrenal androgen production, and rarely,
! w. m, u: }/ E8 H8 J0 Han adrenal tumor may also cause adrenal androgen
4 b0 Z" b& A: j) D7 Wexcess.1,3
% d% M% F4 O% [; b/ k: D% K2 K& Uat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from. X/ ^8 R/ ?" d' o* N4 |
542 Clinical Pediatrics / Vol. 46, No. 6, July 20072 {; a, h3 w. y0 V7 s
A unique entity of male-limited gonadotropin-
* |- ]! ?+ a" T* q- {independent precocious puberty, which is also known9 g7 t& `4 {. w; {( _
as testotoxicosis, may cause precocious puberty at a
: ^- a6 p( }$ p/ O# a- p* ]" Every young age. The physical findings in these boys
1 \1 l! f( |% r! o8 m: z% s3 `5 ~with this disorder are full pubertal development,
2 A7 _/ K( ^1 X- hincluding bilateral testicular growth, similar to boys
, Z7 |" E% ~3 }( h/ lwith CPP. The gonadotropin levels in this disorder0 u1 h4 c- h7 c( e
are suppressed to prepubertal levels and do not show- f  i2 O' W1 }  M+ e
pubertal response of gonadotropin after gonadotropin-2 k+ w2 p# o5 f  _6 r" \0 a
releasing hormone stimulation. This is a sex-linked8 O1 l5 Z; ~/ K# q1 X, }7 P7 p! g
autosomal dominant disorder that affects only4 ]0 X6 _$ E2 U" e
males; therefore, other male members of the family
/ m* u) s7 r4 B5 s( ?may have similar precocious puberty.3
0 J0 O6 Y$ x- o, i& ?In our patient, physical examination was incon-& \1 u* o' t1 X! W( j: ~
sistent with true precocious puberty since his testi-
) i4 ~' K  Z/ z. Acles were prepubertal in size. However, testotoxicosis
+ K" v1 S4 ]+ }8 Qwas in the differential diagnosis because his father- S& Z, H4 x& R0 w: K
started puberty somewhat early, and occasionally,
" Z7 N: C! L% P2 b' s7 r1 Vtesticular enlargement is not that evident in the: p! I: \( T; O' g% k
beginning of this process.1 In the absence of a neg-6 X: j) k/ }! h8 o
ative initial history of androgen exposure, our5 k; c/ \4 Q6 C+ p- P
biggest concern was virilizing adrenal hyperplasia,' t% L& p' k# m$ P$ @
either 21-hydroxylase deficiency or 11-β hydroxylase4 _7 q& O! b, T( L
deficiency. Those diagnoses were excluded by find-
: Y. O% t2 K4 V' _! }9 r& K9 Qing the normal level of adrenal steroids.3 |; E4 S3 t' H" T3 K  \
The diagnosis of exogenous androgens was strongly
+ s$ |* T& i0 }: Msuspected in a follow-up visit after 4 months because
- F: m7 `* R7 J" A2 `the physical examination revealed the complete disap-
3 J  ?$ l+ i5 d6 P3 K+ g7 Ypearance of pubic hair, normal growth velocity, and% X- ~5 B# _4 d. L+ Z  D% t
decreased erections. The father admitted using a testos-( v( h1 X, R3 q2 ]. ^
terone gel, which he concealed at first visit. He was' L% a+ @5 r- v( F( D
using it rather frequently, twice a day. The Physicians’
# m% E8 g: D% x6 U" wDesk Reference, or package insert of this product, gel or
- |$ a' X2 }! S& O6 \/ b; ccream, cautions about dermal testosterone transfer to9 t  X" f/ ?* o7 a( p  f
unprotected females through direct skin exposure.
0 _9 `" l$ i' |Serum testosterone level was found to be 2 times the0 E  j% v8 ]2 {# S' A' H' _
baseline value in those females who were exposed to- ?7 N2 [9 F, _! l7 ?5 F2 v
even 15 minutes of direct skin contact with their male: J3 Z0 s- `3 M
partners.6 However, when a shirt covered the applica-
4 O- |6 j6 h0 Q4 }; s6 Rtion site, this testosterone transfer was prevented.2 P5 e- j9 x9 Y
Our patient’s testosterone level was 60 ng/mL,0 A3 E8 z2 D, x) `2 C
which was clearly high. Some studies suggest that9 s7 i* \* L- e. x" d, w; a# ?. |7 d
dermal conversion of testosterone to dihydrotestos-$ n4 g) X# N7 s7 W
terone, which is a more potent metabolite, is more
# V3 l' G& J" Ractive in young children exposed to testosterone$ G% p( U: T8 {
exogenously7; however, we did not measure a dihy-
+ [& z: s) I! jdrotestosterone level in our patient. In addition to
& l0 V4 G  J7 n7 V: ?! ?virilization, exposure to exogenous testosterone in
! X* o7 U  C# l0 m2 W! k9 cchildren results in an increase in growth velocity and  ?+ t/ Z, p7 }1 e  Q+ ^7 I9 _
advanced bone age, as seen in our patient.* D& y: Z( {0 T% M
The long-term effect of androgen exposure during2 j0 {0 f8 k( A1 h
early childhood on pubertal development and final
& t- a$ y) z  w3 eadult height are not fully known and always remain
6 t% ~5 d; e% t  |a concern. Children treated with short-term testos-: z9 J! p4 Y* m8 p9 q2 s( M/ Z
terone injection or topical androgen may exhibit some- i; ]2 H0 `' p9 L- I2 G  a2 H
acceleration of the skeletal maturation; however, after! _0 j2 T/ Q, s; g# N" Z
cessation of treatment, the rate of bone maturation, W) B3 \$ E7 M' Y: B
decelerates and gradually returns to normal.8,9) ]5 s6 @7 r8 Y
There are conflicting reports and controversy
' v+ o4 _" P8 {% y$ r* ?over the effect of early androgen exposure on adult, ]' i3 X3 i6 T2 X
penile length.10,11 Some reports suggest subnormal2 Z% d, J; a: l5 h: d! \
adult penile length, apparently because of downreg-
  B& ?# M4 E5 ?" ~ulation of androgen receptor number.10,12 However,7 t" ~: Z0 q. C# V6 ~$ p8 a
Sutherland et al13 did not find a correlation between4 c8 c' O: y% C
childhood testosterone exposure and reduced adult
5 b7 m! w! Q  C7 y' u6 p. |penile length in clinical studies.
6 g  P3 y0 T& G( f$ bNonetheless, we do not believe our patient is
# W( {! @. v7 Wgoing to experience any of the untoward effects from
5 J' h  l9 Q( n: qtestosterone exposure as mentioned earlier because5 G6 ]8 T! z3 t' `" |
the exposure was not for a prolonged period of time.
5 r4 f# b7 K, WAlthough the bone age was advanced at the time of' |* z, U1 G4 i8 ~
diagnosis, the child had a normal growth velocity at" ]8 {( ~2 e' O7 V/ D) w- P* t0 p
the follow-up visit. It is hoped that his final adult
! q$ [+ d2 H  x2 R- P5 x2 eheight will not be affected.
+ w; B- _  E  A& A" L8 {Although rarely reported, the widespread avail-
6 v0 A# O. ]  P/ V" _* aability of androgen products in our society may3 ~9 u0 {. S3 N1 S% D2 v
indeed cause more virilization in male or female
/ F6 J- Q3 i: p4 q; }' {2 [9 Gchildren than one would realize. Exposure to andro-
: D7 O6 J0 l5 W+ C7 v& igen products must be considered and specific ques-1 C1 b8 p6 p% q, `7 T* d9 P( U3 y
tioning about the use of a testosterone product or
7 k: G+ M$ b; W) A* Egel should be asked of the family members during
4 ?& \7 j! [. c' |, dthe evaluation of any children who present with vir-
& f" ^+ x! \8 Q  @" s0 E. x% ailization or peripheral precocious puberty. The diag-
1 S' {0 s3 n) U8 enosis can be established by just a few tests and by: S+ J2 J8 x7 [. }& Y0 [/ I" T
appropriate history. The inability to obtain such a9 N9 z! [+ X: L/ f5 j* a! S5 D
history, or failure to ask the specific questions, may' Q& j* b% t5 j" @+ @
result in extensive, unnecessary, and expensive
1 G4 X& f/ V+ `7 Yinvestigation. The primary care physician should be* I: y- `& @  c. P% ^
aware of this fact, because most of these children
# C3 _3 i6 g0 u- S2 d7 u0 umay initially present in their practice. The Physicians’- U4 m9 t! u' o3 X) _; e
Desk Reference and package insert should also put a
) H' @! F" |. j  [2 ?6 |9 N4 Gwarning about the virilizing effect on a male or& s; S5 C: w1 R% K4 \& `
female child who might come in contact with some-
  o4 k( o' O/ d; o6 xone using any of these products.
' \7 f" P* {  Z8 W' W2 PReferences* y5 o4 B' }6 X0 C0 D
1. Styne DM. The testes: disorder of sexual differentiation
( @5 O; D1 ^4 p, O' D7 g; I9 }  qand puberty in the male. In: Sperling MA, ed. Pediatric
. C7 U& n) Z! E; A# w4 LEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
+ E# T2 M0 j% x5 z7 V2002: 565-628.' G2 ~9 j0 F' Z+ q0 l
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
/ K1 ]1 }) X8 m6 Npuberty in children with tumours of the suprasellar pineal
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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

% E: B1 L. P' P3 U  L2 M) i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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