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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
$ Z/ [' M& p. ^9 S& {Boy Induced by Indirect Topical
' [. a5 ^5 S6 tExposure to Testosterone# Q) Y0 j' j/ n7 t9 }
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
" V) D+ |% o7 B% [4 ~5 F6 fand Kenneth R. Rettig, MD1
9 Q. u: x( z0 \, W# Q: D2 |Clinical Pediatrics6 [) I2 [9 E4 m/ {  p( r4 @; o
Volume 46 Number 6$ u3 K$ U0 E, Y  I4 t" Z8 g3 L
July 2007 540-543
( D% g  [7 n- R© 2007 Sage Publications# _. f* e( ?* G
10.1177/0009922806296651; c) }( b; ~: n1 I
http://clp.sagepub.com  p3 y2 @4 i( R1 `
hosted at
& b* q4 g- ]9 `2 i7 S( R. ]http://online.sagepub.com
3 o$ _, v# g) w' S# F8 }2 l' g. uPrecocious puberty in boys, central or peripheral,
3 G9 x* A' L" {* Q9 R0 j5 u+ Ois a significant concern for physicians. Central
& J2 J6 V1 K% p+ y, Xprecocious puberty (CPP), which is mediated
. C) E* n  E4 z! r# v9 Vthrough the hypothalamic pituitary gonadal axis, has  P& `  R0 p2 q1 s3 E
a higher incidence of organic central nervous system# K8 Z3 F( R4 n9 T' ?2 C
lesions in boys.1,2 Virilization in boys, as manifested1 D% o* T* e, J6 @
by enlargement of the penis, development of pubic- \' p7 }& w( j1 a) r4 ~$ h# N4 k
hair, and facial acne without enlargement of testi-
: y6 e6 h) q* [; G7 U7 @, o/ {% pcles, suggests peripheral or pseudopuberty.1-3 We
5 m) Y% Y) I% f& I+ L' V: T* S% I" H, Y# oreport a 16-month-old boy who presented with the
6 f9 Y% k: f0 n& W# Uenlargement of the phallus and pubic hair develop-$ `4 Q& K) i' U: l  N8 _- A
ment without testicular enlargement, which was due; \8 z3 c& A* p' C; ]+ }# f
to the unintentional exposure to androgen gel used by; K+ e6 i: i5 x9 ]% r- x$ n
the father. The family initially concealed this infor-
$ X1 X9 P) o# S  S0 y5 ?! Gmation, resulting in an extensive work-up for this) N/ D/ U; }5 |7 I% _; d: u, n
child. Given the widespread and easy availability of+ }( L, U5 _, j9 K8 E1 W. q
testosterone gel and cream, we believe this is proba-
. k, X. N& J7 I" Dbly more common than the rare case report in the/ M# S$ O' N" s
literature.4
- Y8 S" ]% |7 K- RPatient Report7 _& H4 C* y( O: r8 E* y$ C
A 16-month-old white child was referred to the+ R9 j) X( T5 _. v
endocrine clinic by his pediatrician with the concern
% E6 ]6 @; x& d4 j7 x% P: K% Lof early sexual development. His mother noticed' s) m+ p- t; ?& ]) X- \  r
light colored pubic hair development when he was+ \$ P/ D" Z) a- |' x
From the 1Division of Pediatric Endocrinology, 2University of% J4 X1 S: k2 a" {) L
South Alabama Medical Center, Mobile, Alabama.- r8 a) |; N/ b
Address correspondence to: Samar K. Bhowmick, MD, FACE,
5 E9 v$ F# m; n: F2 RProfessor of Pediatrics, University of South Alabama, College of; F! C" H0 X; T# u
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
7 \' t8 y' W- de-mail: [email protected].& V6 R+ |( |% p( r2 {% t: M
about 6 to 7 months old, which progressively became, A' o# N( ?* Z2 T! ^
darker. She was also concerned about the enlarge-7 v' C5 b4 u* `0 W+ Y
ment of his penis and frequent erections. The child; X6 @$ I+ i8 |$ s9 ~2 Q% j
was the product of a full-term normal delivery, with
7 V# I& {' a" Y* E) N0 {" Ia birth weight of 7 lb 14 oz, and birth length of3 _! ^7 B& |! }
20 inches. He was breast-fed throughout the first year
1 A( e5 p2 Z4 j5 C) A) q# |" y9 y# cof life and was still receiving breast milk along with
& M9 j# ]. @, U$ G$ y" B3 r( D) ysolid food. He had no hospitalizations or surgery,
4 [4 r; e1 o& u3 t% O/ band his psychosocial and psychomotor development
7 a3 U+ l4 p3 T; Qwas age appropriate.
9 d) c5 z7 ?4 H5 p" fThe family history was remarkable for the father,
8 T0 z& D5 _' Hwho was diagnosed with hypothyroidism at age 16,, ]& V& w' W- a" ^, B6 u
which was treated with thyroxine. The father’s
8 y0 D8 C9 S  ]9 R1 S( G2 d; rheight was 6 feet, and he went through a somewhat6 @$ g# W5 b) P
early puberty and had stopped growing by age 14.
' q, w: G9 n2 ?3 r6 wThe father denied taking any other medication. The% _, k) H' z$ e0 r3 f+ P
child’s mother was in good health. Her menarche  S7 }" k- E8 h1 Z6 g
was at 11 years of age, and her height was at 5 feet
4 l; P2 k" |4 i' q5 inches. There was no other family history of pre-0 F+ X9 a; Q7 D7 L  `2 D1 ?
cocious sexual development in the first-degree rela-
" y# J5 E# Q8 @0 j$ Z' l* ]; ztives. There were no siblings.8 i$ |, |4 z+ W' o7 n' _
Physical Examination/ n2 ^- a' J4 l- F$ l
The physical examination revealed a very active,7 z+ P+ \6 D2 M- s# t2 ?
playful, and healthy boy. The vital signs documented
# U4 X  ^* A# I# ?a blood pressure of 85/50 mm Hg, his length was! g9 [- e8 @# W
90 cm (>97th percentile), and his weight was 14.4 kg" t4 R, u. ]6 E0 m& t5 A& k- ]& i
(also >97th percentile). The observed yearly growth" e( F. r+ t) S
velocity was 30 cm (12 inches). The examination of1 I( `. A% c( v7 j
the neck revealed no thyroid enlargement.
( X( |1 T3 ^' ~. yThe genitourinary examination was remarkable for
0 S5 H% b! F$ q6 ~enlargement of the penis, with a stretched length of
7 r$ z4 {* E: ]; x* e" b/ a2 w8 cm and a width of 2 cm. The glans penis was very well' ~! J3 B" W+ W
developed. The pubic hair was Tanner II, mostly around3 T) K" Q; B. ?- ~* [6 f- d- B; n
540
4 j9 \, q# [, i! W( y2 Z- |at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
3 N# B6 p  {, c5 _. lthe base of the phallus and was dark and curled. The
( E# ~( a, U5 m& w2 T( i" ctesticular volume was prepubertal at 2 mL each.
: l, ~, C2 b. L* U# _! VThe skin was moist and smooth and somewhat) e) ?! b( C5 P' e/ _' C4 }% g) t
oily. No axillary hair was noted. There were no
) g. d/ S7 p# h. o" `- Jabnormal skin pigmentations or café-au-lait spots.
' C% d, J# P/ s6 r2 TNeurologic evaluation showed deep tendon reflex 2+
- v$ c5 h8 R4 ~- M9 ybilateral and symmetrical. There was no suggestion
( |  H8 T- h" V9 V  C4 y* ~of papilledema.. c; {0 m; G. j2 A  j8 m
Laboratory Evaluation2 Y0 a" o  [$ ?0 X
The bone age was consistent with 28 months by+ H! W% z) o8 [3 M( K  Y" U
using the standard of Greulich and Pyle at a chrono-
3 ?# B3 }! G) R) ^7 o$ T2 flogic age of 16 months (advanced).5 Chromosomal
/ f( n! {7 ~4 k, O% O4 Fkaryotype was 46XY. The thyroid function test3 e! F9 r4 o0 k5 F3 {
showed a free T4 of 1.69 ng/dL, and thyroid stimu-" q0 F! s. u; L/ C. _$ J, R
lating hormone level was 1.3 µIU/mL (both normal).
. \8 b+ T9 O& ~& K& tThe concentrations of serum electrolytes, blood: w7 e: y) l$ d! s
urea nitrogen, creatinine, and calcium all were
" b$ f7 S9 O8 m2 `0 j. mwithin normal range for his age. The concentration$ F& p: Z, m# f+ E! Z
of serum 17-hydroxyprogesterone was 16 ng/dL8 s) i2 y; X) @8 `8 w+ p
(normal, 3 to 90 ng/dL), androstenedione was 20
1 z5 f/ _- g' S' Ing/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
% M9 r# ~2 h1 ?1 Z7 fterone was 38 ng/dL (normal, 50 to 760 ng/dL),
' k( k$ h! g* Y2 o; @desoxycorticosterone was 4.3 ng/dL (normal, 7 to
, x6 @1 A% U: Y* k: C49ng/dL), 11-desoxycortisol (specific compound S)) u. c. ^) {4 F
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-5 o  M( S: H0 {+ l  O9 R
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total) O& i1 R1 A+ U+ S5 C
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),3 l( O$ l2 M3 L/ J
and β-human chorionic gonadotropin was less than
) \7 ?* A! v% k+ X( t/ m. `5 mIU/mL (normal <5 mIU/mL). Serum follicular- [- f* [6 f$ X. p/ z% B  n; V
stimulating hormone and leuteinizing hormone* T/ t* \& G: y3 s4 w
concentrations were less than 0.05 mIU/mL! s9 C: q9 B' t$ l
(prepubertal).+ M2 @3 F: s+ t$ G! A9 Q7 G# G
The parents were notified about the laboratory! y. J/ G8 o0 `7 t, x% b
results and were informed that all of the tests were
1 p% G1 o( D* ~, S/ `# t4 `normal except the testosterone level was high. The
9 L! N8 ]8 G  P' Z0 I9 o  }follow-up visit was arranged within a few weeks to1 U/ v# T. x$ ~3 v3 J  C1 \$ c7 ]
obtain testicular and abdominal sonograms; how-
, x5 F- F* j# W# {3 Hever, the family did not return for 4 months.
* m! W7 J. k% R, P9 i7 lPhysical examination at this time revealed that the2 r% ]  ?2 v/ q+ J
child had grown 2.5 cm in 4 months and had gained7 y4 F2 V; i$ b5 ?- V
2 kg of weight. Physical examination remained
& A. [# R6 }9 H4 H, xunchanged. Surprisingly, the pubic hair almost com-
3 [4 h! w2 V( h: x( \pletely disappeared except for a few vellous hairs at6 t# V9 j* K% g- F
the base of the phallus. Testicular volume was still 2% v; p3 f) b2 w: h! W, O* ^. U
mL, and the size of the penis remained unchanged.
; L9 d+ V" S0 m5 u0 _" SThe mother also said that the boy was no longer hav-
! K# F, B. G/ R, g- B) u( Aing frequent erections.
5 |; q/ W1 }! [$ \6 d; LBoth parents were again questioned about use of
3 x  b! I6 B- Yany ointment/creams that they may have applied to- r4 U; i9 B5 J7 g- o$ i
the child’s skin. This time the father admitted the; A1 p+ |' y9 u8 G% y- y
Topical Testosterone Exposure / Bhowmick et al 541
- N  D& y8 o' Muse of testosterone gel twice daily that he was apply-4 V( d- U0 W: Y- j# h# @
ing over his own shoulders, chest, and back area for9 c8 f+ s6 E+ X6 f: |
a year. The father also revealed he was embarrassed/ _" c) W0 M5 W8 t
to disclose that he was using a testosterone gel pre-% `9 o9 t5 e* g
scribed by his family physician for decreased libido, a1 F% Y' V% |" Q: s5 k
secondary to depression.6 o2 R( b4 u+ `( \' {  l1 p
The child slept in the same bed with parents.
& {: ?* [1 F2 l' A# d2 a; e1 j5 yThe father would hug the baby and hold him on his
2 t2 z, l. q$ ^chest for a considerable period of time, causing sig-% C. @) r* t1 B6 v# t' G
nificant bare skin contact between baby and father.
: Q% w' q' ?! G. Z. B& ~- J# KThe father also admitted that after the phone call,* I* [# G$ |/ t. F
when he learned the testosterone level in the baby
1 X3 d# c8 d( ~+ [, y5 `. Jwas high, he then read the product information% P: W; S% A1 T
packet and concluded that it was most likely the rea-7 ]. z. E/ f( i6 U( f4 g
son for the child’s virilization. At that time, they
6 e6 o- T9 e' \' edecided to put the baby in a separate bed, and the
* b/ S: E7 j* U( D" P' N" ^6 Pfather was not hugging him with bare skin and had
5 v& ~  K! P/ D& G- O0 G" \) B5 rbeen using protective clothing. A repeat testosterone) c( t; u3 C1 c) x" j: T$ j+ |
test was ordered, but the family did not go to the# z) f7 V' e7 q: c
laboratory to obtain the test.
5 r4 T8 F% |) _0 F/ F) LDiscussion
5 {6 W) {; x! j  \& WPrecocious puberty in boys is defined as secondary
& D" \/ t) t9 W8 _* K8 x0 c0 s, {sexual development before 9 years of age.1,4
4 ~: l- t8 ?; S1 S5 OPrecocious puberty is termed as central (true) when* f! p' s. R5 B" C( ?" Z
it is caused by the premature activation of hypo-
# g& S$ S1 s/ F2 H( e: Uthalamic pituitary gonadal axis. CPP is more com-$ L9 U  |" L5 u# z7 R6 I
mon in girls than in boys.1,3 Most boys with CPP/ q) N( V9 d1 \5 i% Y
may have a central nervous system lesion that is# p6 Q0 A8 Z4 W/ A6 u
responsible for the early activation of the hypothal-
, S9 \% i# A: S6 O0 }* Namic pituitary gonadal axis.1-3 Thus, greater empha-7 g; ?# q0 A3 }* M/ h% Z6 j
sis has been given to neuroradiologic imaging in
7 ~  N- L0 }' f" }+ X$ xboys with precocious puberty. In addition to viril-, W" ^, Q+ S, W- i# \
ization, the clinical hallmark of CPP is the symmet-& o, S0 ]! K& r3 u
rical testicular growth secondary to stimulation by
  B, [0 ]. ?4 R( k' h4 sgonadotropins.1,31 k# t: |& H( b
Gonadotropin-independent peripheral preco-
3 Q. I3 F( z) [7 F9 Ucious puberty in boys also results from inappropriate# {; L! h% ?: J& X- T
androgenic stimulation from either endogenous or
$ j" g) p7 y- v2 a1 p7 pexogenous sources, nonpituitary gonadotropin stim-
/ l, A0 Z. D" o% k' b# Julation, and rare activating mutations.3 Virilizing6 Z: R6 B3 x5 h) \/ \
congenital adrenal hyperplasia producing excessive
0 r: a. y3 s: L6 V' m9 P; X! k" Jadrenal androgens is a common cause of precocious' C! S: G4 ~! a- u2 z
puberty in boys.3,4
7 d- ~7 R* N, c( YThe most common form of congenital adrenal
7 d0 {8 t, s3 `hyperplasia is the 21-hydroxylase enzyme deficiency.  l& \/ c0 e4 h9 @
The 11-β hydroxylase deficiency may also result in
1 W  L, B3 r& H3 Jexcessive adrenal androgen production, and rarely,/ {1 V4 Z6 N1 x$ X1 o0 \% m
an adrenal tumor may also cause adrenal androgen; h; i' w2 |4 Y& s8 v, R
excess.1,3
9 X# S# `3 P2 W+ n: i" ^at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from8 b& f: S+ J% r
542 Clinical Pediatrics / Vol. 46, No. 6, July 20079 G- E! {5 E3 c  l9 X" [
A unique entity of male-limited gonadotropin-$ N( a9 ?2 H5 B1 p
independent precocious puberty, which is also known+ i  e* [% _" M
as testotoxicosis, may cause precocious puberty at a
' S; N! o$ H# S0 f; I( rvery young age. The physical findings in these boys* _8 ^/ |! c6 @" y& X  E
with this disorder are full pubertal development,7 P3 t8 a; N) R& V8 |
including bilateral testicular growth, similar to boys3 P1 d  A" L, x1 n" _
with CPP. The gonadotropin levels in this disorder
8 P2 b' @) G+ {are suppressed to prepubertal levels and do not show% U( D' h) f! L" e% z
pubertal response of gonadotropin after gonadotropin-
, J1 w% g( V" b: j  Y- `releasing hormone stimulation. This is a sex-linked- N( A2 t0 x7 k$ U5 K8 `
autosomal dominant disorder that affects only2 j4 [4 |3 q, D% o7 E% Z
males; therefore, other male members of the family% G/ k+ R* g5 I3 o. Y& V9 ~4 S
may have similar precocious puberty.3
9 l$ o+ s1 o# y$ C- I9 gIn our patient, physical examination was incon-6 A( o- O' u+ p' g( r( i, L* Q- W
sistent with true precocious puberty since his testi-
6 x$ f, H% _+ ^( Z5 U  `! @+ Dcles were prepubertal in size. However, testotoxicosis! l! X) `# v6 ^" Y* O2 l
was in the differential diagnosis because his father4 P+ ]5 R! G6 a, ^8 w! ^
started puberty somewhat early, and occasionally,$ N1 [5 \0 i. p. W
testicular enlargement is not that evident in the& F2 ~  n7 }0 e, v. ^. s) T5 v9 f
beginning of this process.1 In the absence of a neg-% P1 ~- s/ L7 g; N/ H8 ^" t6 d
ative initial history of androgen exposure, our
% m& m% Z3 ]" rbiggest concern was virilizing adrenal hyperplasia,
- U) \& O" q3 Neither 21-hydroxylase deficiency or 11-β hydroxylase
8 p1 D& }- {2 G2 \: u1 ?deficiency. Those diagnoses were excluded by find-% K/ ?7 q% W" k& V! ]6 }
ing the normal level of adrenal steroids.; x$ W' N: H% o( W) A$ x
The diagnosis of exogenous androgens was strongly. Z  z7 |& P( l" N' \7 h3 g+ g5 d
suspected in a follow-up visit after 4 months because
- ^+ Y/ i8 C  {8 qthe physical examination revealed the complete disap-% e1 Q6 e* V- j6 T6 R4 o. S
pearance of pubic hair, normal growth velocity, and' x  N& H5 N% V& t
decreased erections. The father admitted using a testos-
5 j  D. U. C) E1 i' Y/ pterone gel, which he concealed at first visit. He was
" x0 w: \: ~5 a* F: {using it rather frequently, twice a day. The Physicians’
, X7 Y2 D' ~' TDesk Reference, or package insert of this product, gel or
, @* c& }- I$ A0 @/ Q9 [0 _" M( H7 ?cream, cautions about dermal testosterone transfer to
6 P4 Z0 m& t1 T2 M9 punprotected females through direct skin exposure.
3 _! x8 ?9 B5 Z6 b0 eSerum testosterone level was found to be 2 times the
# V8 ~; D: {3 V% ~" O7 u6 z6 l0 N3 gbaseline value in those females who were exposed to
/ R) k* b6 F& r9 X7 C  Z& zeven 15 minutes of direct skin contact with their male1 `) @9 i; z9 |
partners.6 However, when a shirt covered the applica-
( K# F& j) M. etion site, this testosterone transfer was prevented.
7 r, y7 W* @8 N  j+ n  cOur patient’s testosterone level was 60 ng/mL,8 p3 f2 J- |) b& b9 ]
which was clearly high. Some studies suggest that
1 H* `; z# v1 e6 S# }dermal conversion of testosterone to dihydrotestos-& T# j4 w. j8 N, j  Z9 D
terone, which is a more potent metabolite, is more$ d$ G7 X2 v. [! g
active in young children exposed to testosterone
7 K/ Q4 J  w$ V* L* uexogenously7; however, we did not measure a dihy-
- u( B3 A3 L- {0 @% l) tdrotestosterone level in our patient. In addition to
/ j' K1 t! Q$ j% Y+ E- Z$ Kvirilization, exposure to exogenous testosterone in. U* J) s( B. L9 K1 _4 V
children results in an increase in growth velocity and8 h7 N$ ]- b- a0 T9 Z; {
advanced bone age, as seen in our patient.
+ M  c; O2 z+ v# KThe long-term effect of androgen exposure during. y* g$ @* I* @8 j  S
early childhood on pubertal development and final3 w* W* e: f( y/ f! c' N4 Y
adult height are not fully known and always remain
7 i, k- t" N2 ?5 s' ga concern. Children treated with short-term testos-
& {! k- l; s1 s6 y7 K, Zterone injection or topical androgen may exhibit some
% t) }9 |# x3 u. n* p, j8 Racceleration of the skeletal maturation; however, after" V7 j* p; S% j
cessation of treatment, the rate of bone maturation
5 _& v% \4 z1 r8 Fdecelerates and gradually returns to normal.8,92 r6 W' z4 `: J4 H: ?7 t$ H
There are conflicting reports and controversy' J9 b) x* o/ Y4 u% ^9 \
over the effect of early androgen exposure on adult
" s" h3 q, e7 n0 upenile length.10,11 Some reports suggest subnormal% Q/ c5 C8 w1 y9 Z; }2 n
adult penile length, apparently because of downreg-
0 G2 L$ L' X2 P( J9 M/ Lulation of androgen receptor number.10,12 However,  E/ b, d6 F5 q+ l* O- h5 e
Sutherland et al13 did not find a correlation between
2 P* B  S( Z3 J  Xchildhood testosterone exposure and reduced adult7 k) I! Q7 G0 b( r' X, R: V7 D
penile length in clinical studies.
# q8 [8 C' o' jNonetheless, we do not believe our patient is
$ X) g0 H5 k& ~( v% \" lgoing to experience any of the untoward effects from
1 w1 u. U4 j6 i7 I1 ntestosterone exposure as mentioned earlier because
; K2 i0 n( [* v+ p) M  V. V7 y% kthe exposure was not for a prolonged period of time.
3 J" W9 m# U; h/ x6 hAlthough the bone age was advanced at the time of' E  }6 W6 R% z2 h
diagnosis, the child had a normal growth velocity at
& q0 O' \9 f: }& m) @$ Pthe follow-up visit. It is hoped that his final adult! E% S7 H3 h- l9 W8 E% z3 m
height will not be affected.1 W, A$ ?5 r' x5 H  o4 }
Although rarely reported, the widespread avail-
; [5 U- {" T3 gability of androgen products in our society may+ E4 w0 Y5 s' k  q. I
indeed cause more virilization in male or female( g6 ]* P+ ^/ p( m
children than one would realize. Exposure to andro-
9 x- R2 S7 ~. J. J' bgen products must be considered and specific ques-
# s3 @) N( I# }- n/ }' I  K# t+ ftioning about the use of a testosterone product or
4 K& y) N. ?: R+ lgel should be asked of the family members during9 s; V+ ~+ x: _7 P5 h2 O& e
the evaluation of any children who present with vir-
% r% X6 D& R7 ]# u% vilization or peripheral precocious puberty. The diag-9 b. g. S; E1 a( M0 q2 y
nosis can be established by just a few tests and by
9 I0 r. V2 V$ j  o$ d/ X8 S1 kappropriate history. The inability to obtain such a7 \2 t" U) H! t6 P" H
history, or failure to ask the specific questions, may" ^- _  ~3 U; p, J* R# ~% A
result in extensive, unnecessary, and expensive
. H7 I; ~1 u! h" o7 i/ H% @investigation. The primary care physician should be3 j4 K/ N' I0 l) W; j. K
aware of this fact, because most of these children
2 |( O: v5 G  F2 dmay initially present in their practice. The Physicians’
' s5 B3 g) L# p7 z# |' EDesk Reference and package insert should also put a1 n; J+ z% a: Z4 J
warning about the virilizing effect on a male or
7 ^7 @% V5 z/ Q' w1 K2 L: vfemale child who might come in contact with some-* r% J: k9 L( |' A# e6 Q
one using any of these products.
6 ~% K7 R$ X6 d; \* \1 z1 }References* L. j( n$ z9 R8 ?9 p" E
1. Styne DM. The testes: disorder of sexual differentiation" o/ s; }8 ?4 n; s" [
and puberty in the male. In: Sperling MA, ed. Pediatric
; i: M1 F. R4 J, [Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
7 T5 c, G/ r+ f) k2002: 565-628.
5 A1 ]5 Q" W0 T2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
1 }+ d  L6 L' S# ?puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old8 j/ k3 y, N) p5 X
Boy Induced by Indirect Topical# B7 B+ `5 R* B$ ^
Exposure to Testosterone
! u0 v- M. U& z8 M, ~: X% RSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2. ~* V2 G/ ^" E  @9 b/ h: J
and Kenneth R. Rettig, MD11 A0 F8 g( m; O/ N
Clinical Pediatrics' u2 O* d/ y$ U& h8 T
Volume 46 Number 6
% q3 y$ g% d; L6 l; r2 x! {July 2007 540-543& \( |  R- e+ R1 q, U0 m
© 2007 Sage Publications  [- f& C! `4 O7 f$ i
10.1177/0009922806296651
& e4 o2 f2 G9 a& s2 Q; x3 v( _http://clp.sagepub.com8 L" D0 g1 S  H! I
hosted at
- e: ~$ F2 E- d8 Y" Y, X; Uhttp://online.sagepub.com
, G* J' T; x* W; G. nPrecocious puberty in boys, central or peripheral,
) O" Y0 b" n$ ais a significant concern for physicians. Central
. P& O2 o9 O. u* qprecocious puberty (CPP), which is mediated4 l4 M- A' F4 ]
through the hypothalamic pituitary gonadal axis, has# W, x  [! s  b- c, V8 t
a higher incidence of organic central nervous system
+ W3 e$ y9 ?+ F/ o' v) vlesions in boys.1,2 Virilization in boys, as manifested- ]1 O, l( Q1 g' D% U5 V, b
by enlargement of the penis, development of pubic
: ]% e+ C' {/ J/ Whair, and facial acne without enlargement of testi-0 I! h6 v; Z0 y4 M6 ~) @; X
cles, suggests peripheral or pseudopuberty.1-3 We
0 A- q9 b2 C5 t6 i& O( r! Breport a 16-month-old boy who presented with the
* w0 a8 N. S' ?) {4 Denlargement of the phallus and pubic hair develop-
$ G* Y  s( |. i6 o& Mment without testicular enlargement, which was due1 j0 k( m5 E! U7 P2 g# T5 Q
to the unintentional exposure to androgen gel used by
2 a. ?& l9 T% b1 e! j3 S1 jthe father. The family initially concealed this infor-
& ]: Z) V9 ^% h9 Y; cmation, resulting in an extensive work-up for this
9 N* ~3 R( {- S1 `! v- D, Achild. Given the widespread and easy availability of
3 {! _+ @1 p0 f  \5 Y; ]testosterone gel and cream, we believe this is proba-$ W, p+ P+ G; n, T
bly more common than the rare case report in the
7 M& d7 ~4 r5 O/ W/ N+ |0 O: w/ }6 r" Wliterature.4
. c( Z4 n, e5 j6 }) h5 QPatient Report
" u! |2 t( e( V$ U* l9 p. ~A 16-month-old white child was referred to the! b0 v5 O, I/ L6 q/ j: N
endocrine clinic by his pediatrician with the concern) h0 s4 e8 h* U# R
of early sexual development. His mother noticed& H; c; n6 K; Y/ P1 |6 {  t
light colored pubic hair development when he was
) \4 u/ Q; n6 b. GFrom the 1Division of Pediatric Endocrinology, 2University of/ O8 Q( I7 a- i. O2 i; ^- T
South Alabama Medical Center, Mobile, Alabama.  d3 ~7 {1 o9 ~) Q
Address correspondence to: Samar K. Bhowmick, MD, FACE,9 B8 y' {  I! @# X: }3 {
Professor of Pediatrics, University of South Alabama, College of
% R- U5 K/ z; V& \0 o7 }2 I9 SMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
4 `' Q, i1 k. R. A& O& j9 L+ ]! `  fe-mail: [email protected].
! F! ]" n3 w, \$ K# {about 6 to 7 months old, which progressively became
& {$ W$ y5 f. L- [; x1 qdarker. She was also concerned about the enlarge-6 @: Q) u6 o" g, C6 e. p
ment of his penis and frequent erections. The child
" {  k  v, x2 y9 k: p3 I  Rwas the product of a full-term normal delivery, with
, J) C( Z: M. k: U$ x3 c: na birth weight of 7 lb 14 oz, and birth length of7 g1 R( n5 D: y( C1 [5 x1 x
20 inches. He was breast-fed throughout the first year
5 P+ Y; q$ j. d3 O5 [of life and was still receiving breast milk along with
7 ?: c3 P5 L6 b( [* X3 i9 o+ W9 gsolid food. He had no hospitalizations or surgery,
& B2 z( a" i* D6 i3 r6 land his psychosocial and psychomotor development
* K" g8 g, V; K  q; Y' q6 {was age appropriate.3 L( V! s- x' {1 M2 _6 h! f
The family history was remarkable for the father,
0 H4 b7 Q) E# O& }' J8 \1 w; ewho was diagnosed with hypothyroidism at age 16,
. e2 q* J: Q2 C3 w" R& Cwhich was treated with thyroxine. The father’s- s4 z6 @6 A$ t- o  t2 j9 I
height was 6 feet, and he went through a somewhat7 Q: U2 Z0 u$ m- @7 G8 Z
early puberty and had stopped growing by age 14.2 B+ E7 n. W7 ?9 w/ w
The father denied taking any other medication. The5 I0 N# U- x0 d
child’s mother was in good health. Her menarche0 {1 k( [/ w5 c/ ^" j2 b
was at 11 years of age, and her height was at 5 feet
" D8 u* `( B9 B' L' F% \5 inches. There was no other family history of pre-
. A0 L! l! \$ B( y: z$ ycocious sexual development in the first-degree rela-( _+ D0 k& a+ j# b. {) w
tives. There were no siblings.
$ u; P* _. ?; A' oPhysical Examination+ G4 P4 d  g7 x  b% X' {( Y
The physical examination revealed a very active,
2 ^7 Q9 `" H7 a' ^# Uplayful, and healthy boy. The vital signs documented, ~8 ]0 R% Y3 A% L8 S
a blood pressure of 85/50 mm Hg, his length was
7 {5 A/ [3 q, i7 C: b90 cm (>97th percentile), and his weight was 14.4 kg/ r0 ?6 v" R" Q2 b& f
(also >97th percentile). The observed yearly growth! w: ?" S" ]. r& Y& ~& R
velocity was 30 cm (12 inches). The examination of4 |2 |* ?2 p# M$ |0 g
the neck revealed no thyroid enlargement.
+ F+ a4 a) z. A% ^- R/ l. h3 }The genitourinary examination was remarkable for1 F6 N- A1 E( J: }+ T& _8 j8 c
enlargement of the penis, with a stretched length of
6 q% X- _9 r* Y( d# v4 x8 cm and a width of 2 cm. The glans penis was very well
. T8 z2 T- R) ~/ g2 B& U; odeveloped. The pubic hair was Tanner II, mostly around9 n9 h1 [8 a( \! R
540
' @8 f! T9 ^0 u! \8 x* vat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
* M% q/ G1 r3 X- c( N, I0 ?9 A# mthe base of the phallus and was dark and curled. The
6 A/ e  {' n- \! etesticular volume was prepubertal at 2 mL each.
& r  x% F7 t" g6 _) _The skin was moist and smooth and somewhat6 p9 r' Q! h0 a* l: D5 F) ]* A$ N
oily. No axillary hair was noted. There were no
$ f' |4 ]4 g2 S9 m% B7 {. pabnormal skin pigmentations or café-au-lait spots.5 @8 O. N! }5 \3 D' H, F
Neurologic evaluation showed deep tendon reflex 2+
3 Q0 x# C$ a# F- G# [bilateral and symmetrical. There was no suggestion9 }* i7 v5 }3 @2 w8 w- R
of papilledema.2 s% T! k* e, ~9 D1 p
Laboratory Evaluation
1 g  O$ x+ i& T. G; p% b2 V7 cThe bone age was consistent with 28 months by
! q& ]7 B! o1 ^& m8 {6 _; s8 Busing the standard of Greulich and Pyle at a chrono-: _# O1 u0 a) S' Q- V& m0 n
logic age of 16 months (advanced).5 Chromosomal
7 e% X7 T/ Y1 Y! q  n2 |karyotype was 46XY. The thyroid function test. P- O( U1 ?( W* F
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
) D3 N) ^2 L5 W7 p, E; Glating hormone level was 1.3 µIU/mL (both normal).
+ K! ^6 I, v' i1 e3 Z- OThe concentrations of serum electrolytes, blood: p& ]# c( Q1 c$ @* U& L
urea nitrogen, creatinine, and calcium all were
8 L) T2 m, X& F! _9 J8 h& C6 jwithin normal range for his age. The concentration$ `/ Z' h. g/ x2 E5 U; e
of serum 17-hydroxyprogesterone was 16 ng/dL
& s* z, B# C9 M, o6 M(normal, 3 to 90 ng/dL), androstenedione was 20
8 }. x0 q/ b& t' ?# B2 U- Cng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-6 d* N5 S& v! l+ @$ F4 [6 C
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
% S" J  m# N3 S" @6 \/ \/ Qdesoxycorticosterone was 4.3 ng/dL (normal, 7 to
$ K8 R4 r! L1 C! A* R49ng/dL), 11-desoxycortisol (specific compound S)
3 y0 {9 K0 c3 b8 e7 |- q4 \was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-4 P- H% b  @$ U0 t& [
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
1 Z% x! b# T* a- D$ X/ S5 I& I- Rtestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
* n9 d/ L  h# aand β-human chorionic gonadotropin was less than: O. Y9 H+ X2 N/ A
5 mIU/mL (normal <5 mIU/mL). Serum follicular# ?6 r6 ?5 J( U6 t& L. t8 t5 `3 S
stimulating hormone and leuteinizing hormone
7 Y0 F& S+ J2 k% u" p3 |concentrations were less than 0.05 mIU/mL$ j: u! K9 H+ I2 N) {& H  B
(prepubertal).5 _& q2 Z& G- P/ N
The parents were notified about the laboratory
. p8 F: g; X9 ^results and were informed that all of the tests were
7 [( a+ v' ^( \7 h4 Ynormal except the testosterone level was high. The
; J% F8 F) C% j% A4 w# ~9 Ifollow-up visit was arranged within a few weeks to) K+ u8 O# j8 f% I& ~
obtain testicular and abdominal sonograms; how-
4 x0 [. ]$ J5 h0 S% z8 Kever, the family did not return for 4 months.& |+ x: l" W" ~  w
Physical examination at this time revealed that the
7 T3 x* z6 J- v7 N) u" Wchild had grown 2.5 cm in 4 months and had gained
8 k) m8 g% h/ R! ?: x3 M8 z' ~2 kg of weight. Physical examination remained
6 z. w" u0 Q, L3 v. N# r% [+ Gunchanged. Surprisingly, the pubic hair almost com-
# w- a1 I) @) p* Qpletely disappeared except for a few vellous hairs at
. h" d+ x; x; i# a; ]- Wthe base of the phallus. Testicular volume was still 2
/ b$ G8 W* g# V8 k4 m8 _6 b; gmL, and the size of the penis remained unchanged.7 o2 a( M: @2 e+ f  Q4 {
The mother also said that the boy was no longer hav-$ r2 o- ^* \( X$ D" m7 l7 a
ing frequent erections.
0 G4 [# Z& n. b  |2 N+ |( ?$ UBoth parents were again questioned about use of1 Y4 O2 k! V! \( q; e5 ?
any ointment/creams that they may have applied to
3 N2 ~4 A- @! t/ e$ j1 [0 E4 qthe child’s skin. This time the father admitted the
9 [$ v2 B8 x; k# ]Topical Testosterone Exposure / Bhowmick et al 541
, P/ W; e$ s2 Q8 C' I+ w0 L2 [use of testosterone gel twice daily that he was apply-
3 a$ n+ N- K  J$ B6 A" Q. xing over his own shoulders, chest, and back area for
. L/ b; s- L: V8 ~a year. The father also revealed he was embarrassed
% M9 A1 k: {+ x8 Pto disclose that he was using a testosterone gel pre-0 L9 ]% E* M! l3 k1 K+ ?
scribed by his family physician for decreased libido5 y% z/ W  ^6 W, Q  }+ J: `9 |8 ]5 U
secondary to depression.
% R! l1 i' W7 m  X1 d, [8 wThe child slept in the same bed with parents.7 R9 y7 B# z0 e; O! O# Y( T9 U
The father would hug the baby and hold him on his1 }3 Y6 c% m/ K* ~! r$ w
chest for a considerable period of time, causing sig-
+ l8 U# I7 ?/ c. H  M7 E8 tnificant bare skin contact between baby and father.3 K% O& i4 h2 C
The father also admitted that after the phone call,
- H$ t) `: ]9 _& [- P( @; _& lwhen he learned the testosterone level in the baby) q3 z" x  Z/ O6 K2 P
was high, he then read the product information! r; x2 ~3 U2 i  y0 d
packet and concluded that it was most likely the rea-) r: A: ^; l8 D; h
son for the child’s virilization. At that time, they
- A6 |/ t5 ]3 J7 u3 f: Ydecided to put the baby in a separate bed, and the
* L7 _5 `% @  ]% }# ]father was not hugging him with bare skin and had4 \( a, t3 B9 v
been using protective clothing. A repeat testosterone
1 ]. x( S: W+ x/ L: ~test was ordered, but the family did not go to the
' v3 v; N4 }% Xlaboratory to obtain the test.
9 S! I3 S# f/ ~3 j2 }Discussion3 _' G; Y, X2 U& i1 J; {8 @! L6 }1 i7 R
Precocious puberty in boys is defined as secondary
- }2 d% G& [) s( Tsexual development before 9 years of age.1,4* w  O5 ?8 q; `* p% b! n
Precocious puberty is termed as central (true) when: c7 _4 B, k$ V' ]1 {! S" I
it is caused by the premature activation of hypo-' C! S+ M* X0 v8 W. P% \
thalamic pituitary gonadal axis. CPP is more com-
& f9 ]$ X* F( k4 ^( emon in girls than in boys.1,3 Most boys with CPP  Q8 S4 ^& I1 s/ ~: D$ R
may have a central nervous system lesion that is
  F; ^9 N9 i' a* U; Bresponsible for the early activation of the hypothal-
; E4 I% c$ ?! G6 L3 A; Vamic pituitary gonadal axis.1-3 Thus, greater empha-
- D( n3 n4 Z5 f8 [4 tsis has been given to neuroradiologic imaging in  J5 Z/ d* |% }# K5 }& q
boys with precocious puberty. In addition to viril-, k7 _0 a2 Z' l1 T9 A
ization, the clinical hallmark of CPP is the symmet-; j" `! A3 w1 x) L- B
rical testicular growth secondary to stimulation by
$ G1 ~/ G( d- q% c' [gonadotropins.1,3/ y; y  ~  x6 O1 Q* D" b
Gonadotropin-independent peripheral preco-) x' f# J' H7 U* N- _
cious puberty in boys also results from inappropriate% `4 l. O: z7 b: q& L
androgenic stimulation from either endogenous or! C! C7 O% ^5 V; g  M9 {
exogenous sources, nonpituitary gonadotropin stim-
4 k! i; |& V( x% v9 \" Aulation, and rare activating mutations.3 Virilizing
- t1 w3 n2 V: ]+ P4 R9 Q9 ocongenital adrenal hyperplasia producing excessive/ E6 X1 C/ i5 N8 [6 P( O
adrenal androgens is a common cause of precocious+ [/ l4 `8 @" Y4 K3 N6 ~
puberty in boys.3,4
  W( u4 b# g6 ^' m' eThe most common form of congenital adrenal: w# [$ n$ L6 {
hyperplasia is the 21-hydroxylase enzyme deficiency.
+ f, `, v+ j8 OThe 11-β hydroxylase deficiency may also result in
2 P$ u7 \/ h& @( n* kexcessive adrenal androgen production, and rarely,- \. S' f7 d9 _5 s' Q, Y
an adrenal tumor may also cause adrenal androgen
% p' l7 O0 S' r, o/ c- Z0 {  Bexcess.1,3
+ M$ Q( ?$ e& Q" I( w: e, ]at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from2 O' P5 T2 t0 O
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
' [' c% b' S: q) Z* ?" A6 c' TA unique entity of male-limited gonadotropin-
' i3 Q0 R, r( a/ ?2 cindependent precocious puberty, which is also known
: b) h- Z/ G& r4 A$ `as testotoxicosis, may cause precocious puberty at a' A% S. w$ B. |; _; L8 V
very young age. The physical findings in these boys, q) R- K& N1 D% I
with this disorder are full pubertal development,, f6 E' y3 W; {& {
including bilateral testicular growth, similar to boys# g  K6 u: I! j/ w$ ^# i4 @
with CPP. The gonadotropin levels in this disorder
! I' a+ ~, S4 K8 S, L# L& Iare suppressed to prepubertal levels and do not show/ S0 x% Z# i: j
pubertal response of gonadotropin after gonadotropin-( l' }1 Q/ {* R' m9 N  Y$ R* u2 N
releasing hormone stimulation. This is a sex-linked! @3 Q! _- |; a- O6 @
autosomal dominant disorder that affects only2 p& I# m6 T- z$ [+ k; r+ `6 k
males; therefore, other male members of the family* J1 k! z' I# V, o$ Z
may have similar precocious puberty.38 F" C" S8 D$ Z
In our patient, physical examination was incon-$ {8 p. H2 a! L: q5 D* H
sistent with true precocious puberty since his testi-3 M8 i% V! y- R& H" `% u
cles were prepubertal in size. However, testotoxicosis% c" m9 ]5 g$ @2 v2 i) u3 q6 D+ J6 Z
was in the differential diagnosis because his father! a2 [& ?. D  V) f
started puberty somewhat early, and occasionally,
* D+ W# |3 x8 t: {' Atesticular enlargement is not that evident in the
5 d$ ?' R- W6 V9 lbeginning of this process.1 In the absence of a neg-& p7 _! R( x8 R8 F1 s2 C
ative initial history of androgen exposure, our
4 D) d" ~. @+ w0 O5 m5 }3 abiggest concern was virilizing adrenal hyperplasia,3 y. y# a  O+ f$ ~. {, F$ }- D
either 21-hydroxylase deficiency or 11-β hydroxylase+ L0 w7 t/ L6 \( ^, d1 }- x
deficiency. Those diagnoses were excluded by find-: U# i+ }( f# `6 b) ?
ing the normal level of adrenal steroids.( R& c1 f4 y% y, @
The diagnosis of exogenous androgens was strongly9 r# `. n) B2 |- O4 ?- I1 v
suspected in a follow-up visit after 4 months because
% d1 v" l" Z* V2 I" jthe physical examination revealed the complete disap-
- i' k! \3 r5 A( R. P; w6 T2 H) G: ~pearance of pubic hair, normal growth velocity, and
/ X" @& S9 }/ r+ e$ R9 ]decreased erections. The father admitted using a testos-
0 f( H' _/ T- O+ s/ U/ eterone gel, which he concealed at first visit. He was2 g! W8 p4 ~* a& J* n5 U) b
using it rather frequently, twice a day. The Physicians’8 g# E2 C* c9 I, {) @' x' z( D
Desk Reference, or package insert of this product, gel or4 s- D$ Y  |0 K4 l$ ~- W
cream, cautions about dermal testosterone transfer to6 _" N1 |% t- q% l& R+ C9 ~! ]
unprotected females through direct skin exposure.8 m; B, d, H+ N
Serum testosterone level was found to be 2 times the
4 \7 w" q* u' A( l' U$ c$ @7 c( Ebaseline value in those females who were exposed to% o' g6 S2 x4 |5 d, c& G
even 15 minutes of direct skin contact with their male4 U" M- ^' E) b/ |
partners.6 However, when a shirt covered the applica-) H1 i4 m- m1 [8 |3 F
tion site, this testosterone transfer was prevented.
1 v$ k6 h+ I' k4 c* y5 cOur patient’s testosterone level was 60 ng/mL,
% m3 \0 H: P6 j0 f( R; w# ~: e" G! V: gwhich was clearly high. Some studies suggest that
1 w$ I6 \# N2 R+ ~- k" Zdermal conversion of testosterone to dihydrotestos-% X. |' c/ y0 {0 {+ R  W
terone, which is a more potent metabolite, is more
' a, ]6 e$ P: \/ U  Jactive in young children exposed to testosterone* w8 a  U: `3 N; w( q
exogenously7; however, we did not measure a dihy-
0 v4 k! ^( q; b# Adrotestosterone level in our patient. In addition to9 R+ m7 f1 s+ B' |( _
virilization, exposure to exogenous testosterone in
# o0 ?1 Q7 [+ Mchildren results in an increase in growth velocity and
% s/ O+ S; v- I% c! Cadvanced bone age, as seen in our patient.
1 W) o3 m4 V1 h9 mThe long-term effect of androgen exposure during
9 o- q: a; j7 [2 ]% }early childhood on pubertal development and final
. ~- S, Z9 T2 q: J1 c# O; zadult height are not fully known and always remain
" C2 r: Q; n$ Ba concern. Children treated with short-term testos-
( n  O2 F: P* s$ i& gterone injection or topical androgen may exhibit some
7 E/ l: H, X9 i1 w% Xacceleration of the skeletal maturation; however, after) U) x; L; c# d, n, v+ `) r
cessation of treatment, the rate of bone maturation
; A/ w: N) T" B! I7 R0 Tdecelerates and gradually returns to normal.8,9. T. y& d0 h& e* \5 |' z
There are conflicting reports and controversy* z9 H: M' |" m9 p, a
over the effect of early androgen exposure on adult2 @1 p" B; R. V# f
penile length.10,11 Some reports suggest subnormal
/ \9 g' l1 q/ k: Padult penile length, apparently because of downreg-
5 W9 X. j1 i, c. zulation of androgen receptor number.10,12 However,
' D6 Y: D4 N0 D4 |1 N& ESutherland et al13 did not find a correlation between
+ y# s5 M, {, W8 Q' Schildhood testosterone exposure and reduced adult& Q/ M4 n. N5 `9 _
penile length in clinical studies.
3 v5 `$ B9 e# R7 y  }! ?4 D3 `/ GNonetheless, we do not believe our patient is
5 V: x4 K/ y" Fgoing to experience any of the untoward effects from
/ ~& N2 [  @5 N6 ^: z5 b, H: r. rtestosterone exposure as mentioned earlier because
( @2 |3 U0 Z7 x% Ethe exposure was not for a prolonged period of time.  {" O( I& }5 N* n/ _
Although the bone age was advanced at the time of
- ]1 z, V. Z" r4 h$ ?diagnosis, the child had a normal growth velocity at7 X2 }3 D9 {0 r
the follow-up visit. It is hoped that his final adult% ?+ o0 M# u1 K5 ^& v
height will not be affected.; t) y# l4 W: Z
Although rarely reported, the widespread avail-
5 i' E( `+ I  O& G6 _ability of androgen products in our society may
8 s- W. s- P1 P2 m  I8 k! Hindeed cause more virilization in male or female6 a- j4 ^8 a7 J# m; z. W
children than one would realize. Exposure to andro-
' X/ m" O7 A( Z$ Xgen products must be considered and specific ques-
. Q& |# W: @3 K* a5 M2 qtioning about the use of a testosterone product or
# j; B4 I6 L6 c4 ]) c4 A" Jgel should be asked of the family members during
( m4 X' j+ U+ }% l( b; pthe evaluation of any children who present with vir-2 Y' ^& a: D# _$ |; o3 N
ilization or peripheral precocious puberty. The diag-% k8 D+ {* o# M1 c4 y; M
nosis can be established by just a few tests and by$ T: C9 D3 I3 G8 M* N( N3 s  E: d# q) c
appropriate history. The inability to obtain such a/ _8 Z8 n; J6 A9 f* }% z
history, or failure to ask the specific questions, may
/ Q8 h! _; l1 n- b$ j, iresult in extensive, unnecessary, and expensive
( B- h' L' t5 l0 F4 Einvestigation. The primary care physician should be
/ ?+ Y7 i" V0 Laware of this fact, because most of these children
% E) E* J$ y# I4 }3 V& @$ gmay initially present in their practice. The Physicians’7 d; J9 L  D# z! _, T
Desk Reference and package insert should also put a
0 T6 P% G  \. p) e+ d8 {warning about the virilizing effect on a male or* ]/ W8 s9 s6 Y4 p' m8 `" I$ x
female child who might come in contact with some-- _) _1 W, n. [9 b7 J( P0 r7 W
one using any of these products.4 Y2 X# \7 L+ F& B6 f- G0 \2 U
References
2 c* j5 M% [9 {" W4 C  o1. Styne DM. The testes: disorder of sexual differentiation1 _  ^2 ?% _" V% d
and puberty in the male. In: Sperling MA, ed. Pediatric
& l  s: R- h5 V- i+ ?Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
, T% W  T, D3 \6 T7 D# Z2002: 565-628.  Z+ f+ s  [* G. d
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
/ _. z" m; H0 Q, Gpuberty in children with tumours of the suprasellar pineal
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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
. ~3 _" b* r4 R& l! Z& K  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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