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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
% L  m  M* S1 HBoy Induced by Indirect Topical% P& l3 A* n* q. f
Exposure to Testosterone; X9 C' k5 \0 i
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
. }0 E6 ^7 _; M$ Qand Kenneth R. Rettig, MD1: F! M* q/ r# a7 A: y5 X2 y* W
Clinical Pediatrics
! a# r/ E! R7 B% z  Y9 _$ i5 I2 JVolume 46 Number 6
$ i# }* L" M  D9 [July 2007 540-543" b0 R( F2 g1 M- S$ p6 s3 @
© 2007 Sage Publications
0 ?& q: g+ _" C2 `( e10.1177/0009922806296651
- U* _) \$ |! Y9 ]http://clp.sagepub.com* v5 e/ G& _& d3 b
hosted at' y4 k- v& }/ G% c$ a/ \
http://online.sagepub.com: R5 p6 S4 h% D5 f& Z
Precocious puberty in boys, central or peripheral,$ f% J2 H/ M$ r2 t" G
is a significant concern for physicians. Central0 C' h6 q7 r- E7 m
precocious puberty (CPP), which is mediated
% O! j/ q! J: U5 }7 Othrough the hypothalamic pituitary gonadal axis, has
, H, @: i, M- C2 ?- }+ Da higher incidence of organic central nervous system/ \) k2 N9 E" Y/ g
lesions in boys.1,2 Virilization in boys, as manifested
. W0 d7 E6 w$ Rby enlargement of the penis, development of pubic  s1 u* x: A) X3 F& K
hair, and facial acne without enlargement of testi-# w2 B; u9 [4 u8 t  ~
cles, suggests peripheral or pseudopuberty.1-3 We* t2 K6 X8 Y/ Z
report a 16-month-old boy who presented with the
, k" |+ R: k6 tenlargement of the phallus and pubic hair develop-% {/ N, i: [7 e; l$ @' ~& _
ment without testicular enlargement, which was due
7 W" P5 z1 e0 R$ uto the unintentional exposure to androgen gel used by
- o% y- j! r/ l& ~: K# tthe father. The family initially concealed this infor-  M' ~& J. N4 W6 \% e
mation, resulting in an extensive work-up for this
$ n9 R0 |! b7 f+ Schild. Given the widespread and easy availability of" R: T% r4 i9 P" r. @
testosterone gel and cream, we believe this is proba-* c1 @2 ~6 y8 ?( }
bly more common than the rare case report in the: ~2 a6 [) C, q$ p7 {
literature.44 n. o# p# d# Z1 {' F  h& U4 y
Patient Report  y8 |0 {/ Z6 g3 g( K$ l
A 16-month-old white child was referred to the
9 B& `2 \7 ?, S( p0 Iendocrine clinic by his pediatrician with the concern) i) }9 o7 e) C: g0 `9 [7 B0 Q
of early sexual development. His mother noticed% t& `( {  R/ V$ A  |( f% S
light colored pubic hair development when he was
; l' s0 L7 Z* k/ h: S* G! i! x' @$ yFrom the 1Division of Pediatric Endocrinology, 2University of0 E. c6 z  I9 S2 Y1 l( q: d
South Alabama Medical Center, Mobile, Alabama.
$ s) h5 ~( ^; ~- I" F3 vAddress correspondence to: Samar K. Bhowmick, MD, FACE,
; H; |: y3 q6 y: fProfessor of Pediatrics, University of South Alabama, College of, i0 k6 m) J1 x/ |1 {
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
4 D  ?# \. r% |7 me-mail: [email protected].
' z" y  p/ V% V5 zabout 6 to 7 months old, which progressively became
6 ?  i0 P$ k. |- v# A* a5 W$ H0 F" Qdarker. She was also concerned about the enlarge-- m7 P) B, S8 H7 _2 w
ment of his penis and frequent erections. The child; @$ ]6 V0 C1 b0 y  p& i
was the product of a full-term normal delivery, with
, _! k: R* O' \a birth weight of 7 lb 14 oz, and birth length of% {7 Y' c5 t/ _5 X
20 inches. He was breast-fed throughout the first year
: {5 W( F% _) k& U5 p! v5 Nof life and was still receiving breast milk along with
8 m9 z) P* P5 y1 s- tsolid food. He had no hospitalizations or surgery,
  h9 h" i* `3 ]4 oand his psychosocial and psychomotor development" O; @. F6 w0 W6 d5 m6 _" m; U
was age appropriate.
/ c- i7 I: h9 Z5 S; u) F. o% Y6 N: cThe family history was remarkable for the father,. x0 W/ o* v. C' N5 Z+ h
who was diagnosed with hypothyroidism at age 16,
# {+ a) F6 |& Z- g3 U: Qwhich was treated with thyroxine. The father’s5 r3 h. R6 F3 r0 {3 ^
height was 6 feet, and he went through a somewhat
* p: w5 b) R9 uearly puberty and had stopped growing by age 14.
6 ?. @9 ?/ c6 m# E. K6 M/ N( _The father denied taking any other medication. The
* v( J: a* W; g, p! dchild’s mother was in good health. Her menarche
2 a2 ]) |& G" m, Fwas at 11 years of age, and her height was at 5 feet1 l' I$ Y4 r$ ]
5 inches. There was no other family history of pre-2 q6 Y  n/ X! [  W
cocious sexual development in the first-degree rela-5 H7 \8 F0 C6 o0 p- \( G2 V
tives. There were no siblings.
# \: C9 x7 J3 S, UPhysical Examination0 p/ J9 S4 r3 I$ Y) M, J5 D) p
The physical examination revealed a very active,
' U2 J+ t' r: o4 X( Nplayful, and healthy boy. The vital signs documented
) X9 s( ]% Y, j( \: w: Ja blood pressure of 85/50 mm Hg, his length was
- t$ t' S; j3 N5 Q90 cm (>97th percentile), and his weight was 14.4 kg" v1 T/ }6 B: Y7 {" I& C! N& d. i  ^
(also >97th percentile). The observed yearly growth% k. B& I" L' Q$ w" W" `" r
velocity was 30 cm (12 inches). The examination of
# t- T! r( H- D# L/ a" G' k# Bthe neck revealed no thyroid enlargement.
- Q' {3 Y0 r8 Z- Q3 f2 v2 VThe genitourinary examination was remarkable for
1 }- L. D2 H, z: L+ _enlargement of the penis, with a stretched length of
5 |6 Q1 Q' L% [4 r, f( U8 cm and a width of 2 cm. The glans penis was very well- B' G% _7 u2 h" U- ?3 X
developed. The pubic hair was Tanner II, mostly around
  W* k8 E" F, `* F540
0 p+ _  M- K5 B! Pat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
% U/ N4 m7 p7 @8 v6 Dthe base of the phallus and was dark and curled. The
4 y& G3 e' n. U; Xtesticular volume was prepubertal at 2 mL each.% b7 q( t; j. E! w  P
The skin was moist and smooth and somewhat
# ?$ E1 p5 p' H/ k, x% yoily. No axillary hair was noted. There were no3 g, u  e% k' q4 g) t& @- p' c6 a
abnormal skin pigmentations or café-au-lait spots.; b. m# |" G8 H# u2 C
Neurologic evaluation showed deep tendon reflex 2+
  q3 T! q/ A1 q& R- Z$ s. cbilateral and symmetrical. There was no suggestion
9 n& y0 P" @8 |4 Y' L4 Aof papilledema.
) y5 J) x+ u- o# u6 wLaboratory Evaluation
( f; i) |4 K# ZThe bone age was consistent with 28 months by) x) t/ M" g* S( H) I+ |7 ^
using the standard of Greulich and Pyle at a chrono-7 O$ h1 W0 l, W
logic age of 16 months (advanced).5 Chromosomal
+ o* @+ o! @& }! l& r7 jkaryotype was 46XY. The thyroid function test9 j4 W; E4 `, o4 q$ [1 L
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
( v- ^- V7 L8 ~; r  D& X4 U1 w6 Nlating hormone level was 1.3 µIU/mL (both normal).! p# H& Y% ^1 Z: I
The concentrations of serum electrolytes, blood
% j- G$ i4 S' surea nitrogen, creatinine, and calcium all were
, j, p7 s0 i8 F% G$ ywithin normal range for his age. The concentration, e$ i) `5 R$ ^; e
of serum 17-hydroxyprogesterone was 16 ng/dL/ r' T" d/ d/ A% v" n6 A4 t
(normal, 3 to 90 ng/dL), androstenedione was 20" I( b% M, M0 B
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-8 `3 K# Y0 m3 }9 p
terone was 38 ng/dL (normal, 50 to 760 ng/dL),3 @$ b0 z$ n. c8 \, ]8 ~9 l
desoxycorticosterone was 4.3 ng/dL (normal, 7 to- r  s. x- H! z. u- w
49ng/dL), 11-desoxycortisol (specific compound S)# ^' H2 c- m# Q: Y. b
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-! t7 y, X" j: W  {
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total" ]" e& j6 j1 T0 K/ X
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),2 X1 n9 I! N8 k9 c3 Y% u% a1 d$ B
and β-human chorionic gonadotropin was less than) d) ]6 w& [( r
5 mIU/mL (normal <5 mIU/mL). Serum follicular$ Z* w6 G; m; g$ g
stimulating hormone and leuteinizing hormone
# f4 r, G$ ^& `/ f* ]concentrations were less than 0.05 mIU/mL
3 O' S9 \# T' _+ m3 [+ M0 }+ H5 r9 v(prepubertal)." {- P* t# |5 l8 y% }9 N0 Z8 Q
The parents were notified about the laboratory
7 n& g. t7 T% f2 X* zresults and were informed that all of the tests were6 z3 a1 z: l4 Z4 g6 k
normal except the testosterone level was high. The
7 `4 t$ V: H7 B( N. yfollow-up visit was arranged within a few weeks to# x& P& r# v6 e  m
obtain testicular and abdominal sonograms; how-0 @) P* d0 b" i1 u
ever, the family did not return for 4 months.
' d. o3 u6 h3 aPhysical examination at this time revealed that the2 `/ M# @' N! Z. o: l# S
child had grown 2.5 cm in 4 months and had gained
8 H& V5 C" L9 l! l, e2 kg of weight. Physical examination remained/ M, X' n  f* X
unchanged. Surprisingly, the pubic hair almost com-7 q. p7 G. @. l' D
pletely disappeared except for a few vellous hairs at
) O6 o6 u% G6 r# q, X* z, D+ C( ?the base of the phallus. Testicular volume was still 2) ^6 ]' I, g0 ~) x
mL, and the size of the penis remained unchanged.
  e7 `! `# [, N0 Z! j, rThe mother also said that the boy was no longer hav-) @/ L9 O9 @7 m- b
ing frequent erections.
$ `: g/ u6 R* s0 i. O1 @9 IBoth parents were again questioned about use of
& P' A. x7 G5 @. ^any ointment/creams that they may have applied to
0 [/ X# K# t: H( Bthe child’s skin. This time the father admitted the1 D0 c. m2 [0 f+ ~
Topical Testosterone Exposure / Bhowmick et al 541! s$ ?" r- R& c0 ]8 }1 t
use of testosterone gel twice daily that he was apply-
/ |4 g! g6 z9 V! d3 s* B& s, Fing over his own shoulders, chest, and back area for; I2 l6 a* ~6 J# c
a year. The father also revealed he was embarrassed
; f+ S# B* H0 w2 }to disclose that he was using a testosterone gel pre-/ I5 H/ B/ r; w8 D# i
scribed by his family physician for decreased libido8 H* ?6 H7 ~! L8 B
secondary to depression.
& v& |" u9 S0 e: {8 aThe child slept in the same bed with parents.* e9 b$ x/ m! x. I% w$ P" c
The father would hug the baby and hold him on his
; ]1 ]5 C' [8 p' t4 m& r, fchest for a considerable period of time, causing sig-
! l! \5 I6 E1 Rnificant bare skin contact between baby and father.
6 q' p8 Y& y9 D' H6 f9 oThe father also admitted that after the phone call,
9 m7 {% k; S  z7 f; owhen he learned the testosterone level in the baby
2 F( c# F* w2 \6 ?9 {was high, he then read the product information
3 A+ V: o0 C: epacket and concluded that it was most likely the rea-) n& z% Z( ]/ k) `# y+ x, X
son for the child’s virilization. At that time, they
- h$ n" Q# H. ^- n" W  sdecided to put the baby in a separate bed, and the
+ p. d9 m- A1 m' A- Qfather was not hugging him with bare skin and had
! ?% v" _5 {; Dbeen using protective clothing. A repeat testosterone6 L1 [5 @; Y. n  T
test was ordered, but the family did not go to the8 u$ f1 o0 S. m5 a  j/ _3 x
laboratory to obtain the test.5 w4 a( i1 S3 q, r1 `: T% N/ g
Discussion. |6 P4 v  P! Q1 M
Precocious puberty in boys is defined as secondary( ?, B# m: Q; S6 W0 q  l. ^
sexual development before 9 years of age.1,4/ @% \+ i- h8 j% J" x, F- U5 ?- J3 E
Precocious puberty is termed as central (true) when
- k, [/ I3 q. m& O8 }! M. H9 dit is caused by the premature activation of hypo-/ e2 O( m! ^8 C, e$ N& X6 `
thalamic pituitary gonadal axis. CPP is more com-
9 z9 Q' o; u8 n3 hmon in girls than in boys.1,3 Most boys with CPP
6 b8 J* }# r5 ]3 W. q  V* ~may have a central nervous system lesion that is
! e4 F+ U" G3 I0 K5 e! R( \5 Wresponsible for the early activation of the hypothal-5 J, m0 G( n4 w9 H
amic pituitary gonadal axis.1-3 Thus, greater empha-
, o. F5 y% d1 k5 x5 a1 O7 dsis has been given to neuroradiologic imaging in* |* M/ M* H6 J* ~. y. }
boys with precocious puberty. In addition to viril-: ?7 j3 ^9 Q3 x8 W; Q
ization, the clinical hallmark of CPP is the symmet-4 o, n) ~  [1 I
rical testicular growth secondary to stimulation by5 s2 P- W; q& O1 S% {% {5 \/ l
gonadotropins.1,3$ ~3 ~0 [( ?* k
Gonadotropin-independent peripheral preco-5 @) b* ?5 M% t; e& ?5 g. E9 \2 X
cious puberty in boys also results from inappropriate
9 f6 k9 @+ ^4 R0 Y9 candrogenic stimulation from either endogenous or
/ n- A  z5 c  B5 j2 C4 w4 d' lexogenous sources, nonpituitary gonadotropin stim-1 ^/ E$ q( R( h
ulation, and rare activating mutations.3 Virilizing
6 U3 ]) g# g" u% |( Xcongenital adrenal hyperplasia producing excessive
5 E9 c; P/ k; W- g7 |" ]adrenal androgens is a common cause of precocious
3 ^! S$ Y& |$ q5 W& ?  V, ppuberty in boys.3,4- ~$ u4 Q, I: R* {& Q9 d
The most common form of congenital adrenal! `% M0 Y% `$ w. C. v
hyperplasia is the 21-hydroxylase enzyme deficiency.
: u- N4 B2 D! r% ^# v$ y# @The 11-β hydroxylase deficiency may also result in% B& b2 U8 G3 D" W
excessive adrenal androgen production, and rarely,/ c4 S$ v3 t7 Y/ n! f+ b3 T0 ^, s
an adrenal tumor may also cause adrenal androgen, |7 j  T, t, n$ K/ M9 ?- f0 o) x
excess.1,3$ A' W" A8 T2 }6 c: _
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from! C5 l. w  K) N# y
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007( g5 O; G& S" {% C
A unique entity of male-limited gonadotropin-  i1 E, T7 L  A) e- c
independent precocious puberty, which is also known6 Y- e3 ~" _+ _0 Q
as testotoxicosis, may cause precocious puberty at a
. y. }3 j6 X, X( p! A" S; Dvery young age. The physical findings in these boys0 c/ z8 \! }6 K4 m
with this disorder are full pubertal development,
2 p% g$ N; a" i4 ~including bilateral testicular growth, similar to boys6 H, p7 g' O7 V3 u2 U& I
with CPP. The gonadotropin levels in this disorder2 q) F8 k1 t" e; |+ F/ y( A" o
are suppressed to prepubertal levels and do not show5 B$ C- r- }2 A3 X7 a' e: m( v+ s
pubertal response of gonadotropin after gonadotropin-$ L- Q1 V" F* W- A' w4 s& @4 ~# |
releasing hormone stimulation. This is a sex-linked/ j. \' Z/ S* J5 N8 H" n5 b6 e) l
autosomal dominant disorder that affects only) `! e4 r+ ]9 s) z
males; therefore, other male members of the family
3 h2 j: D+ S, o/ {- z- i9 i. Wmay have similar precocious puberty.3+ ^- G" o6 y3 x
In our patient, physical examination was incon-1 i+ f1 m- ], r
sistent with true precocious puberty since his testi-/ H/ \8 Z) R# p* I5 z
cles were prepubertal in size. However, testotoxicosis
( h9 V5 q( m$ i; Nwas in the differential diagnosis because his father7 [- ]6 o5 T& s: W6 R* ^6 F; P
started puberty somewhat early, and occasionally,
8 Z- T9 Q0 Q# s5 f% x9 A  K  ctesticular enlargement is not that evident in the
7 A& m" y; H' B* j5 d- Nbeginning of this process.1 In the absence of a neg-8 l9 u, Z7 I5 f9 L- R% d  Z
ative initial history of androgen exposure, our
+ a7 O$ h: n1 s3 w7 {, a; zbiggest concern was virilizing adrenal hyperplasia,6 }; C8 E% K( W4 ?4 p
either 21-hydroxylase deficiency or 11-β hydroxylase
, e5 p6 P3 R& i. H  r9 xdeficiency. Those diagnoses were excluded by find-
( q% m+ H! f2 F0 y% E" O; q* King the normal level of adrenal steroids.3 l8 Q1 {2 I6 }$ {- m$ `0 s
The diagnosis of exogenous androgens was strongly
1 l% H* U1 z- |% e4 S/ Ksuspected in a follow-up visit after 4 months because
* Z+ {6 _9 q  Nthe physical examination revealed the complete disap-
6 z5 j5 ]( [9 F: Kpearance of pubic hair, normal growth velocity, and
7 V/ C# m7 ~- Adecreased erections. The father admitted using a testos-) X  Z8 i# n2 `
terone gel, which he concealed at first visit. He was9 L, u5 `; j  Y1 U/ E( h
using it rather frequently, twice a day. The Physicians’7 [" a5 U+ y( Y6 K+ S7 L
Desk Reference, or package insert of this product, gel or
* V0 r' H8 `: [0 c% Ncream, cautions about dermal testosterone transfer to0 g( f9 Y; W5 j# D
unprotected females through direct skin exposure.0 |7 w$ C7 A& ?9 [% P* P8 ]$ ^) L
Serum testosterone level was found to be 2 times the0 r7 \; W# `6 j
baseline value in those females who were exposed to/ U. P' ]0 P' R6 \$ ?
even 15 minutes of direct skin contact with their male& M( m: j) Z4 G" N
partners.6 However, when a shirt covered the applica-
8 F5 [  e  z% v$ M" Gtion site, this testosterone transfer was prevented.
9 }3 g" B/ ]" j# jOur patient’s testosterone level was 60 ng/mL,
& b6 Y' d9 ~9 U5 wwhich was clearly high. Some studies suggest that
' L6 W" m: J; N6 k& gdermal conversion of testosterone to dihydrotestos-) V6 l" L+ K! b( c% R/ L9 n5 M
terone, which is a more potent metabolite, is more: C* B# G" ~! Y8 j! j3 m- n' c9 }
active in young children exposed to testosterone
! }0 ]7 P0 m) k6 P% Wexogenously7; however, we did not measure a dihy-& t4 r) l' _9 ]0 n0 R  Z
drotestosterone level in our patient. In addition to
+ T4 I# H) ?+ V( M% f( z: Q5 ^% K# cvirilization, exposure to exogenous testosterone in
/ q1 {5 H# y2 ]5 P1 t1 @6 ]. tchildren results in an increase in growth velocity and
8 i4 J3 B' ^& ?! Y( b$ @& o9 _advanced bone age, as seen in our patient.
6 O  |  h6 J+ s- T! |The long-term effect of androgen exposure during
" A$ q* X- ~8 c3 I  D. W& Kearly childhood on pubertal development and final; n* H6 f% S- j) ^1 _, m) N
adult height are not fully known and always remain
* J. J$ D5 q' o3 E- c) P' s7 La concern. Children treated with short-term testos-3 r* O( O: k4 i5 g
terone injection or topical androgen may exhibit some
7 j0 m5 y/ j9 ?( }5 L) K0 _2 ^* Z; Pacceleration of the skeletal maturation; however, after
- p  w# S, D$ Y  \( P% Pcessation of treatment, the rate of bone maturation
2 |1 r8 Z( i% A) F' m$ K/ q% [9 odecelerates and gradually returns to normal.8,9
+ B3 c: u1 M2 r$ o/ p" z6 f. }There are conflicting reports and controversy
) o0 R2 D* B+ \+ K! w* ~2 ]0 xover the effect of early androgen exposure on adult8 D/ a5 w/ ]- t: u3 a: x, P! ]( G
penile length.10,11 Some reports suggest subnormal
1 m) p) \' o2 B1 L9 O8 Vadult penile length, apparently because of downreg-
* y& I% B7 c7 F& i5 Tulation of androgen receptor number.10,12 However,
$ x+ _; L2 Q, R/ \% oSutherland et al13 did not find a correlation between
+ E3 k; D' K3 v9 o" achildhood testosterone exposure and reduced adult
! m2 C- m. v# D6 L7 h: n1 Mpenile length in clinical studies.
8 j% k9 a6 H) y: R( e  |2 ?Nonetheless, we do not believe our patient is3 Z( L( o( w/ u1 J: `! P. j
going to experience any of the untoward effects from9 w' \1 M3 D# Q0 \! i* i9 Q
testosterone exposure as mentioned earlier because8 v) Q, n' w" c4 n3 V  R9 y: O
the exposure was not for a prolonged period of time.  s! w7 K' ?. p
Although the bone age was advanced at the time of- I( s& r) N/ W3 C3 x
diagnosis, the child had a normal growth velocity at
, t/ j( k$ {1 s& `the follow-up visit. It is hoped that his final adult
, F( \/ V; O8 p) q3 n0 `* Wheight will not be affected.* U1 K9 x% H& Q$ E+ `2 D
Although rarely reported, the widespread avail-
+ S' S. q& B4 x3 u& Gability of androgen products in our society may
, }1 ~5 Z2 k4 P- s; S6 vindeed cause more virilization in male or female
& V+ ?  E8 K3 z0 q1 @) r# O+ g2 bchildren than one would realize. Exposure to andro-3 a9 X4 h, p; b
gen products must be considered and specific ques-
- m8 Z$ D% V. l" utioning about the use of a testosterone product or- _) N  b! u6 L# ^$ m+ R
gel should be asked of the family members during
4 F+ v. ]# v; {/ O  @the evaluation of any children who present with vir-
' z# D3 U+ Y- Q0 filization or peripheral precocious puberty. The diag-
* C& z6 l, E6 U! E* G+ B9 U- mnosis can be established by just a few tests and by& r  Q+ f0 O3 Q4 F( Z) P# _9 _
appropriate history. The inability to obtain such a' m% o- M# k8 o5 O2 `% \5 f4 \
history, or failure to ask the specific questions, may
' d  K$ {3 n/ }$ Y) v& ~8 F* oresult in extensive, unnecessary, and expensive5 F) Z/ X( r! k! M$ w& m: V9 t
investigation. The primary care physician should be
" ?& O" V+ {, oaware of this fact, because most of these children
  p+ h, K( T$ Q+ C' W- V& Kmay initially present in their practice. The Physicians’7 c- m% U6 A1 \) S7 J- D- Q' B! q
Desk Reference and package insert should also put a/ j! y; O3 |& Y' I! C9 H
warning about the virilizing effect on a male or
# j( B- }0 j$ Mfemale child who might come in contact with some-4 v$ T7 F) ^/ l) l
one using any of these products.% {( T, K! ]4 E5 t
References' @8 }6 U+ W4 {0 e1 Y( G) k  M
1. Styne DM. The testes: disorder of sexual differentiation
( w* F5 ~" P2 J2 x0 G3 fand puberty in the male. In: Sperling MA, ed. Pediatric% U/ H  d% S* ?7 c! L- ]
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
- k/ O! t8 i; H/ Y$ t2002: 565-628.3 c5 V0 @) m: a6 g
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious2 w# D% a* F0 {# l% [9 t
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old; {) u2 g- t, s- A( A  I, B& `$ c% z" ^
Boy Induced by Indirect Topical
8 P) ]0 C- k' @4 f5 Q$ vExposure to Testosterone
' b6 f$ b: Z0 S% q6 H0 f+ xSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
9 H4 G8 i9 `% A3 t% c+ `and Kenneth R. Rettig, MD1
5 U  `. m# I% kClinical Pediatrics
& c, }# Q! N% q2 y& R+ U4 W0 dVolume 46 Number 6
6 a9 Q' e8 T2 X+ r/ R0 x3 oJuly 2007 540-5432 r6 f/ G/ v" S3 |
© 2007 Sage Publications
  \9 p7 O" o: e( j' z10.1177/0009922806296651
& d7 v0 f0 J* |8 Z% _; dhttp://clp.sagepub.com
! z: w% z' @3 {( D9 a( [1 ehosted at
2 c0 [8 h4 c# f; {- e3 p/ ihttp://online.sagepub.com
. O2 o7 V) c. Y5 RPrecocious puberty in boys, central or peripheral,
2 b" ~- _6 a9 ais a significant concern for physicians. Central
# r- c, h3 y; V; D( f4 g( qprecocious puberty (CPP), which is mediated
. F2 O% b( Z" D9 {2 Q" W3 Bthrough the hypothalamic pituitary gonadal axis, has# ^! N0 L/ o: I
a higher incidence of organic central nervous system8 s/ b! Q* w5 z! ^
lesions in boys.1,2 Virilization in boys, as manifested
* B& R) L' D# ~9 \. P+ m, ]+ Fby enlargement of the penis, development of pubic" |3 U; O" O* p6 P: I% N6 `8 l  B3 c
hair, and facial acne without enlargement of testi-+ ^7 o: j+ l" H( C  y# H
cles, suggests peripheral or pseudopuberty.1-3 We
0 H$ S  s& h+ m! I; v2 [# `9 vreport a 16-month-old boy who presented with the
) S! m1 ~& S0 t& _enlargement of the phallus and pubic hair develop-: U% A2 i1 d' i8 l
ment without testicular enlargement, which was due7 B1 W& {0 G$ e3 M4 p/ o! C% D- e
to the unintentional exposure to androgen gel used by
# K" d0 ^; B9 A/ v  C0 v! Jthe father. The family initially concealed this infor-# E- P; _4 Z8 S6 f+ L* l: A" ?
mation, resulting in an extensive work-up for this; P# D2 a6 m9 y4 {% E; I4 ~8 u
child. Given the widespread and easy availability of
- x9 W5 n: ~3 u! U  \$ O# Ttestosterone gel and cream, we believe this is proba-
' F( P# o$ C) O% Y- r3 G9 e& v1 fbly more common than the rare case report in the
9 u& I/ b& h/ Fliterature.4- L5 s  a8 `/ v4 A7 _
Patient Report+ C. B7 P+ h) m# f! E) I+ b4 L
A 16-month-old white child was referred to the7 i0 R( P0 L' z
endocrine clinic by his pediatrician with the concern
; A( k' g1 P- v. |4 T; f2 Dof early sexual development. His mother noticed
0 j3 s* x; M3 t: F7 a- Jlight colored pubic hair development when he was
0 a: c' j% k! |5 E9 \' v: sFrom the 1Division of Pediatric Endocrinology, 2University of
( U9 Q9 D' Y, f, k0 WSouth Alabama Medical Center, Mobile, Alabama.7 I) \; t3 e" I, U5 r  o* O/ ]8 S* I( ~
Address correspondence to: Samar K. Bhowmick, MD, FACE,
6 ~- Z& E. E' h9 L- z3 \Professor of Pediatrics, University of South Alabama, College of
& Y: M! ?3 S7 U. ]$ D+ R: a2 F( ~) ?  @Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;3 Z# ~. W0 o2 q: B
e-mail: [email protected].
" h" ^6 J) u7 l, @2 q1 ~about 6 to 7 months old, which progressively became. B$ g: W+ I. E+ d4 ?; Y
darker. She was also concerned about the enlarge-
+ x2 v5 c# f/ l. n; }+ x' y6 ?ment of his penis and frequent erections. The child9 \/ U0 u  Y6 J5 d: M8 h
was the product of a full-term normal delivery, with
& G% O  V" B6 A% ?. u( ca birth weight of 7 lb 14 oz, and birth length of
! P% ]8 H# @# b- B20 inches. He was breast-fed throughout the first year
. ]8 u& D$ K+ n, `of life and was still receiving breast milk along with
% P* T: b" J' f0 o% qsolid food. He had no hospitalizations or surgery,1 g+ {: i% a2 h9 P$ k' E
and his psychosocial and psychomotor development! e6 w8 X6 F$ s$ {) ?5 C) U
was age appropriate.
+ H8 a% L* Q/ SThe family history was remarkable for the father,
0 V! A2 P  P3 W* Y* s6 Dwho was diagnosed with hypothyroidism at age 16,# O& g# @8 O1 J: t# y
which was treated with thyroxine. The father’s
+ ]# @8 z9 V: p, ?. s% j, Theight was 6 feet, and he went through a somewhat
" [7 J/ N: ^" u* O2 j: m( Gearly puberty and had stopped growing by age 14.
3 Z: c, u; I' Z. G& CThe father denied taking any other medication. The
1 g& t; C$ E6 {. x0 Achild’s mother was in good health. Her menarche. m  F3 l5 A/ y8 w
was at 11 years of age, and her height was at 5 feet" S* B4 R, n+ h$ P  s: L- l( Z
5 inches. There was no other family history of pre-
' N/ P, W. Z7 |! Q/ z0 V, Mcocious sexual development in the first-degree rela-# z, |$ Y' V6 \0 \) X
tives. There were no siblings.. K% }! [) t' e" j5 R$ B
Physical Examination
6 W0 S2 A9 k- {  xThe physical examination revealed a very active,/ i- }( H" D( q. w
playful, and healthy boy. The vital signs documented
, o! |2 b; C* k0 a; H) \a blood pressure of 85/50 mm Hg, his length was" ], Y  x5 O3 W$ m% c' _
90 cm (>97th percentile), and his weight was 14.4 kg
3 k9 \: Y3 k; v6 U! l( |; b(also >97th percentile). The observed yearly growth
& d& L, _6 I' p+ Y/ d) ~8 |velocity was 30 cm (12 inches). The examination of! o3 L8 d( [: c$ o4 J
the neck revealed no thyroid enlargement.
0 K+ |5 M3 o% x+ f5 XThe genitourinary examination was remarkable for
4 o% a& N1 q" A5 r) ?enlargement of the penis, with a stretched length of5 {* ^. Y" L' a; i8 P6 C" j2 f
8 cm and a width of 2 cm. The glans penis was very well; B4 Q) f/ O: Y# m  h" o) w
developed. The pubic hair was Tanner II, mostly around
, g% V: E6 B+ [0 B540
! {. m' `. o1 v# r. V; hat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
2 F1 [+ e9 V) `) o! ^! Bthe base of the phallus and was dark and curled. The% s! z/ O* O( l0 i) p6 C. U
testicular volume was prepubertal at 2 mL each.
9 {$ W  d3 O* B" M6 I7 FThe skin was moist and smooth and somewhat
. a+ M  h( {9 Q& v7 roily. No axillary hair was noted. There were no
' u7 |& V8 J4 b8 L9 p7 V  q: b# q" Y8 tabnormal skin pigmentations or café-au-lait spots.
& s0 w" E0 h3 e( x( _& xNeurologic evaluation showed deep tendon reflex 2++ O, F: g! l% b# ^
bilateral and symmetrical. There was no suggestion
1 J( J2 U8 c$ a. z0 S- r: Yof papilledema.
* R% J5 s! j9 s- d6 \  g: nLaboratory Evaluation$ v" \; _8 A0 k/ Q1 j
The bone age was consistent with 28 months by8 ]. t* ]- g* O% Z
using the standard of Greulich and Pyle at a chrono-# Q  q, V, l8 e9 Q. J6 G4 C
logic age of 16 months (advanced).5 Chromosomal
- F3 j2 x9 D" q. ]: pkaryotype was 46XY. The thyroid function test# h5 n! T( C7 D0 f4 ~) c
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
3 q+ V) d+ j+ _2 R0 J: Llating hormone level was 1.3 µIU/mL (both normal).  [% p6 z$ @' E7 J2 b( E3 @
The concentrations of serum electrolytes, blood
& W  s6 A- p# H7 P4 h' ^  L# ^urea nitrogen, creatinine, and calcium all were
' _0 m3 x9 Z8 m. {within normal range for his age. The concentration
5 t& p; ~- n: d6 Eof serum 17-hydroxyprogesterone was 16 ng/dL- D! F8 T+ {6 K
(normal, 3 to 90 ng/dL), androstenedione was 20
  w( C, B/ M) m1 a5 kng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
' X' W3 l  N2 n% x; H/ z" Vterone was 38 ng/dL (normal, 50 to 760 ng/dL),
: m9 F- c- I# n. Q7 ]desoxycorticosterone was 4.3 ng/dL (normal, 7 to. F* ]7 H) r  \! P8 m
49ng/dL), 11-desoxycortisol (specific compound S)
# Q8 Y3 r; K5 D( G2 ]% Hwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
, u! J" i! w2 c" D7 u/ `; Ytisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total3 f4 K# `% S7 }
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
8 Q# N2 ~/ ?5 V" o' [' r, b7 Hand β-human chorionic gonadotropin was less than1 i" M7 A* r# h3 L
5 mIU/mL (normal <5 mIU/mL). Serum follicular+ _; C3 N( B4 d
stimulating hormone and leuteinizing hormone3 [& T6 h& v5 y  r' y% u
concentrations were less than 0.05 mIU/mL
0 {! w+ }9 Q/ I2 ?(prepubertal).
  J) J# m% k/ ]+ i9 U2 xThe parents were notified about the laboratory
( m0 G0 }) q/ g: ]" {' j% N# Yresults and were informed that all of the tests were: ]! _# c4 m% {9 C  [5 E
normal except the testosterone level was high. The
2 a" h1 r/ i$ x$ O( Rfollow-up visit was arranged within a few weeks to
# |0 D) n3 S9 L2 H$ D* E7 r2 N+ kobtain testicular and abdominal sonograms; how-" d# ?8 v6 b' R; G. m" |' B5 b
ever, the family did not return for 4 months.6 q: i  @8 w+ [: U
Physical examination at this time revealed that the8 Z$ k$ ^5 H& }9 d; q0 {
child had grown 2.5 cm in 4 months and had gained7 A* l3 V+ y6 c' P1 x6 N
2 kg of weight. Physical examination remained
3 g/ T8 T3 Q' c/ s- h5 punchanged. Surprisingly, the pubic hair almost com-
5 c, f: J' V0 [0 b* |' N6 |pletely disappeared except for a few vellous hairs at1 `2 t) F: {; ~3 A0 z# r
the base of the phallus. Testicular volume was still 2
% @- B( E3 H9 F$ r- DmL, and the size of the penis remained unchanged.
7 n7 A( Q9 Z% WThe mother also said that the boy was no longer hav-+ C# }  W& r, M9 H! n
ing frequent erections.* G( Y  G% Z3 [2 k% ^2 Y) T% ?$ v
Both parents were again questioned about use of8 Z7 O& b% |1 W/ B
any ointment/creams that they may have applied to) h+ r5 N+ _5 @' E5 @. P" h
the child’s skin. This time the father admitted the
+ o6 e0 a5 ]* F; O0 k( s0 XTopical Testosterone Exposure / Bhowmick et al 541
0 R( Y+ N' f# c$ s2 |) q7 [; puse of testosterone gel twice daily that he was apply-
5 G; ]. e7 Z! F' C' W+ L  Ning over his own shoulders, chest, and back area for; {) ^3 J1 Z8 t; ?& A2 x9 w0 P, m
a year. The father also revealed he was embarrassed
( O, o( `: ]( Rto disclose that he was using a testosterone gel pre-
+ ^: l9 h4 b! w6 ~$ U! x9 y/ D* |scribed by his family physician for decreased libido: d  O( p0 P; \% \
secondary to depression.
5 P, ?& w3 E5 M9 Y# J) j, k; @$ V8 FThe child slept in the same bed with parents.
1 S' R9 H: {) h. g8 PThe father would hug the baby and hold him on his
8 f% e0 N, v, ~* H# i4 O; r8 Uchest for a considerable period of time, causing sig-, g3 r; u" l/ B* V
nificant bare skin contact between baby and father.
* ~7 X" k( m8 d8 V* p$ I- KThe father also admitted that after the phone call,
$ n' f) N6 c% q/ F2 f# i6 iwhen he learned the testosterone level in the baby
3 S" p! L" `3 \( n, z" mwas high, he then read the product information7 y, V) s7 D5 p* e
packet and concluded that it was most likely the rea-
* c! d$ S% a% m: D' b- Vson for the child’s virilization. At that time, they, \, d) J" d4 p" Z5 K6 \
decided to put the baby in a separate bed, and the2 V0 F) A5 U/ i  y" o9 [& i+ L0 F% b! I
father was not hugging him with bare skin and had# c+ c7 k$ K) h. L% e+ F% O+ D( D
been using protective clothing. A repeat testosterone
' m' D7 N9 m" `/ X8 Ltest was ordered, but the family did not go to the5 D6 [, Z4 u5 }# T: C) @
laboratory to obtain the test.  X7 X" j  a. Z
Discussion2 a. s2 E5 W, ]2 |( v
Precocious puberty in boys is defined as secondary
& R, x0 w# Z; [sexual development before 9 years of age.1,4" p1 P9 n) `3 i, n
Precocious puberty is termed as central (true) when
7 X9 D: S/ F, _# M. X+ ^2 fit is caused by the premature activation of hypo-% z+ I+ F: _0 z9 Z9 `. C
thalamic pituitary gonadal axis. CPP is more com-4 m2 r& J: J( @) {! G8 `, @
mon in girls than in boys.1,3 Most boys with CPP
7 u7 Y+ Q0 x2 F& L9 Mmay have a central nervous system lesion that is% m2 s# H$ D0 |- H2 _5 F0 x
responsible for the early activation of the hypothal-
9 T. b5 H7 t1 t; camic pituitary gonadal axis.1-3 Thus, greater empha-9 X! f+ ~. L1 M* n9 M+ M
sis has been given to neuroradiologic imaging in6 n7 T2 _2 F7 r# I5 r3 q8 @( N
boys with precocious puberty. In addition to viril-4 n, A) N% b6 Z5 P. [
ization, the clinical hallmark of CPP is the symmet-+ {! T- y) c; A1 `
rical testicular growth secondary to stimulation by
/ y# K; C6 S) c, r8 J% n7 Y% kgonadotropins.1,3' v6 E0 x* x1 Y8 t  S7 B2 W# h
Gonadotropin-independent peripheral preco-
5 ~& W+ G! |. T0 @& s8 I/ jcious puberty in boys also results from inappropriate
7 F$ s$ N6 a& t1 `androgenic stimulation from either endogenous or
" l( @* E3 @( L4 `  f- f  iexogenous sources, nonpituitary gonadotropin stim-  `; E" Z* o3 Y' s
ulation, and rare activating mutations.3 Virilizing
% R/ G" b# [+ Y, u. s4 N7 y; ocongenital adrenal hyperplasia producing excessive
, ~/ l) Q- A+ V$ d" H. K* E2 _  {adrenal androgens is a common cause of precocious
& l; \9 J- {" m: _9 @! apuberty in boys.3,4
% p9 `3 ~* w4 |; R7 WThe most common form of congenital adrenal) k3 C1 C$ Y/ p! Y1 ^0 _  W
hyperplasia is the 21-hydroxylase enzyme deficiency.2 G, H2 K" Y+ I4 e' E' k! z
The 11-β hydroxylase deficiency may also result in
! c  `$ ~$ d* z& a, T1 Nexcessive adrenal androgen production, and rarely,
5 m# X0 r. C8 l( K+ G, U) [an adrenal tumor may also cause adrenal androgen
7 Q! E) R: P8 {5 A( Sexcess.1,3
6 m1 O# E4 j9 P1 u4 d  a% s: w9 N+ Qat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
( f  j  `8 E% r' G- e8 ?542 Clinical Pediatrics / Vol. 46, No. 6, July 20072 \0 C( Q4 q/ _$ v9 r
A unique entity of male-limited gonadotropin-) _- J+ e/ l' h6 K/ K
independent precocious puberty, which is also known
. i5 D2 x3 b/ ^4 I& B* jas testotoxicosis, may cause precocious puberty at a7 L$ l3 o1 u) m8 x) {' i; Y
very young age. The physical findings in these boys+ e! @2 k0 h3 E5 F, `
with this disorder are full pubertal development,
% [. D; g8 [+ h. D6 B! nincluding bilateral testicular growth, similar to boys, n6 R5 _; r9 r6 I+ p' f+ s9 Q
with CPP. The gonadotropin levels in this disorder
/ r$ I2 Z$ ]: o: Z- Rare suppressed to prepubertal levels and do not show
: M# H1 H6 y5 U  Bpubertal response of gonadotropin after gonadotropin-6 d$ s& Y2 h: I. I- N4 r  O
releasing hormone stimulation. This is a sex-linked0 F& {# ?+ x7 G
autosomal dominant disorder that affects only9 m& y2 G. F7 I  n4 D
males; therefore, other male members of the family6 _3 X2 A$ B4 i/ ^0 v
may have similar precocious puberty.30 t  E  Z$ y$ C  B
In our patient, physical examination was incon-
4 a0 f/ o% o  S, S  p0 }# Usistent with true precocious puberty since his testi-% a$ G% X' j9 L  i& p( r
cles were prepubertal in size. However, testotoxicosis0 I& r9 g; F' H( g  \3 O
was in the differential diagnosis because his father
6 o# i, A0 c' ]( Kstarted puberty somewhat early, and occasionally,
( P" K7 ~  t+ Z' w. ~testicular enlargement is not that evident in the/ W( u0 D7 @. B2 {2 V  z. d9 U
beginning of this process.1 In the absence of a neg-
7 M( ?% h4 E; P; b* pative initial history of androgen exposure, our
. y  |+ w3 V- ybiggest concern was virilizing adrenal hyperplasia,# \+ p+ @& J7 P+ e8 T+ X5 s/ e
either 21-hydroxylase deficiency or 11-β hydroxylase
% n$ ?4 o( E; y: s  ]) edeficiency. Those diagnoses were excluded by find-
( O1 `! |0 }6 v2 K7 M9 F. ling the normal level of adrenal steroids.
0 u) C# B' U4 t% u' g9 t1 AThe diagnosis of exogenous androgens was strongly1 I8 q! M! k; a6 A+ o+ l/ ]
suspected in a follow-up visit after 4 months because
5 \/ L7 P) j9 J5 Bthe physical examination revealed the complete disap-
( Y' T' x5 r/ E! i( Kpearance of pubic hair, normal growth velocity, and- O/ J& b& y3 g0 S$ N0 ]4 L
decreased erections. The father admitted using a testos-& I; B1 F" p' S! Z) ~. s0 N
terone gel, which he concealed at first visit. He was
8 y' q3 n7 w+ ousing it rather frequently, twice a day. The Physicians’
9 n5 P; v3 K7 |" o9 S' o8 SDesk Reference, or package insert of this product, gel or  O& K+ w6 e. `0 e  F
cream, cautions about dermal testosterone transfer to. M1 t+ H% m8 q
unprotected females through direct skin exposure.. n' j; `) j- v1 J
Serum testosterone level was found to be 2 times the7 v3 {! b% N* m2 D# a3 u- p; F
baseline value in those females who were exposed to& U/ A/ i' u$ @& [/ \
even 15 minutes of direct skin contact with their male
8 H8 o' }9 ~2 v8 u( Upartners.6 However, when a shirt covered the applica-7 N' n' x( d' Q; }4 f, H
tion site, this testosterone transfer was prevented.  l# g7 r9 X. D1 B6 j; _
Our patient’s testosterone level was 60 ng/mL,6 e& N* j" S: w
which was clearly high. Some studies suggest that
( f1 ?, R, Z. Bdermal conversion of testosterone to dihydrotestos-
' l, R3 V" v$ `terone, which is a more potent metabolite, is more! w* [  _! O4 a8 R% D
active in young children exposed to testosterone( r1 I* h- d2 k8 H
exogenously7; however, we did not measure a dihy-4 K. V9 @5 C( T
drotestosterone level in our patient. In addition to/ a- p$ _; P; X
virilization, exposure to exogenous testosterone in! I9 G: I% q, q( `! J5 ~
children results in an increase in growth velocity and5 v' k3 T- P* V( ?
advanced bone age, as seen in our patient.
3 W) {* {6 H7 }) h- `% F+ @The long-term effect of androgen exposure during2 l6 t+ y0 i. L8 P" Q' i* G
early childhood on pubertal development and final
9 W$ C% b( ]8 `: [adult height are not fully known and always remain- R& s8 f5 n; @' K' ^1 R' b$ v
a concern. Children treated with short-term testos-
! o( y& u+ B6 {2 j5 ^terone injection or topical androgen may exhibit some
3 Q' @8 N  T+ A$ i. d, gacceleration of the skeletal maturation; however, after4 ~3 P6 N. t) ^& [! ]% j
cessation of treatment, the rate of bone maturation
3 b1 x5 _' D4 }/ q. C, Sdecelerates and gradually returns to normal.8,9: e+ f* D* o4 H( {
There are conflicting reports and controversy
& j0 Y5 i! I$ j2 Lover the effect of early androgen exposure on adult
5 ~9 V+ r- `: X& F/ apenile length.10,11 Some reports suggest subnormal
) Z& J$ \- ~; X9 _  \' uadult penile length, apparently because of downreg-
4 O, p8 I+ G5 x9 Z5 \6 ~+ eulation of androgen receptor number.10,12 However,
& j; L, Q9 }9 DSutherland et al13 did not find a correlation between8 ~7 v/ `/ \8 p4 Y( K
childhood testosterone exposure and reduced adult
% r5 N3 F8 k4 `8 G$ jpenile length in clinical studies.1 T3 ?; M5 _8 |; ^1 g9 m9 G' @4 k' z
Nonetheless, we do not believe our patient is
7 i# z# W4 t( l3 D& ~9 bgoing to experience any of the untoward effects from9 S+ T. D2 u: C3 G7 C; ~: S8 q7 L
testosterone exposure as mentioned earlier because
, w* _9 p# T' Kthe exposure was not for a prolonged period of time.
7 p; q; c8 ]9 Q2 K4 h6 xAlthough the bone age was advanced at the time of
8 v5 `3 q; u; B; w5 Rdiagnosis, the child had a normal growth velocity at3 m" q9 M9 M( F5 o
the follow-up visit. It is hoped that his final adult
! f" D- y, q2 R+ `  Y/ H+ |- t1 K; Hheight will not be affected.
9 ^- N( T  B& v6 I0 yAlthough rarely reported, the widespread avail-' f  ?* \8 o7 P. F
ability of androgen products in our society may
& P; A6 H9 P9 ]# {+ I3 pindeed cause more virilization in male or female
0 M# p+ [/ |" Ychildren than one would realize. Exposure to andro-
* z( _6 E% J, Q& L1 d# G7 ggen products must be considered and specific ques-* N4 H' |! C/ p. @8 L
tioning about the use of a testosterone product or" ~; p. R4 U4 M, A
gel should be asked of the family members during6 n1 P) U: r1 ?9 _- m
the evaluation of any children who present with vir-- R1 p, E$ w( u' W/ K/ k8 \
ilization or peripheral precocious puberty. The diag-
1 x+ O0 n. Q) S; C0 pnosis can be established by just a few tests and by1 f8 E' ]7 o) r0 m
appropriate history. The inability to obtain such a5 `' J! |2 w/ j% i% t2 c8 N9 V
history, or failure to ask the specific questions, may
# N7 j; k/ h! V  ^8 Q" {result in extensive, unnecessary, and expensive
; u  G, a9 O6 }, z/ q, N  Rinvestigation. The primary care physician should be7 S* ]1 X; A1 ], v
aware of this fact, because most of these children- `7 t# P4 D: z* d7 A+ ^/ y
may initially present in their practice. The Physicians’
& N" `+ r- b3 b7 \+ b: h$ P/ P! v  |Desk Reference and package insert should also put a
. U6 X/ b( ]# e+ t* u2 bwarning about the virilizing effect on a male or
/ r0 w. @/ G, w! ?6 Mfemale child who might come in contact with some-
7 r( t, s) Z* hone using any of these products.$ t# M+ Q4 I+ T$ W1 \- _4 H
References0 V* B9 f8 b. m  C/ H9 {  o# Y2 s
1. Styne DM. The testes: disorder of sexual differentiation
1 A( F8 b7 C! }0 U2 Fand puberty in the male. In: Sperling MA, ed. Pediatric
% o6 y  I  O7 p) N" O, Y1 h0 [Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;  \$ b& c* G' S. v
2002: 565-628.- b+ S4 m: I# L5 Y
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious' V; U$ r! ~+ |# C7 O
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
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4个什么样的?
發表於 2025-1-19 02:41:05 | 顯示全部樓層

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發表於 2025-3-8 22:04:50 | 顯示全部樓層
絕對的好貼!謝謝啊!逐字逐圖地看完這個帖子以後,我的心久久不能平靜,感恩啊!
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