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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
  |+ f9 Q) `* b# v/ ~- UBoy Induced by Indirect Topical  D5 s8 p; A1 [
Exposure to Testosterone& ]8 t7 }* p% u9 R" Y( X# a+ ?
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,27 y0 s# P5 N- O5 ^2 B- D' G# q: ^
and Kenneth R. Rettig, MD13 g8 {! n+ s& m" M
Clinical Pediatrics8 [5 b: A$ Y3 x8 I. u& A- }
Volume 46 Number 6
& {1 Q% w  n! sJuly 2007 540-543
" q3 `7 Q& s  E4 X  _© 2007 Sage Publications
( d/ k+ @# N- {, l10.1177/0009922806296651) c. W$ L9 k5 \9 L8 G5 z0 ~3 ?
http://clp.sagepub.com' O, z4 f- w) c4 Q
hosted at
% \2 s" H) e$ Khttp://online.sagepub.com' ~" s% o: Z2 R+ `
Precocious puberty in boys, central or peripheral,1 `0 v/ Y9 w; i5 O
is a significant concern for physicians. Central8 o6 _/ x+ F. T
precocious puberty (CPP), which is mediated3 l! l" D8 M# Y) s" E
through the hypothalamic pituitary gonadal axis, has
7 s% m6 z( w7 d* L2 g) ia higher incidence of organic central nervous system5 h) x( P' ]7 K: T% }
lesions in boys.1,2 Virilization in boys, as manifested+ M4 ?; u' \) Z
by enlargement of the penis, development of pubic2 y8 z- ^1 D" q% V0 y8 U9 `$ t) g
hair, and facial acne without enlargement of testi-
: ?0 o8 @' V# N: _7 \cles, suggests peripheral or pseudopuberty.1-3 We
' R% ?; a( X: U$ Dreport a 16-month-old boy who presented with the
$ J0 X6 a: a, F) E9 Q2 ^enlargement of the phallus and pubic hair develop-
, n& k5 @. G8 J2 J( X! w6 ^ment without testicular enlargement, which was due; G. i. k* M. Q* Z" G
to the unintentional exposure to androgen gel used by
: Q2 x# B# l5 u3 a/ b9 `8 Cthe father. The family initially concealed this infor-
- A, T0 L, r7 e" K7 Zmation, resulting in an extensive work-up for this. S+ E$ W" a+ |* _# W, \+ M/ P0 n
child. Given the widespread and easy availability of
* s# x3 C/ w  U" W2 v( o/ k6 ktestosterone gel and cream, we believe this is proba-9 Z9 N5 q8 u- D- z( ^
bly more common than the rare case report in the& e. R, ^- j4 @  U
literature.46 T" b4 t; ^% y( T& G+ G3 u
Patient Report
4 f! {( C8 H1 R6 J4 N; W. }A 16-month-old white child was referred to the7 ~9 d+ |5 e5 N2 N5 d
endocrine clinic by his pediatrician with the concern$ e8 t. \/ A2 V. I. O' E) @! V
of early sexual development. His mother noticed. g5 H7 G( `7 h
light colored pubic hair development when he was
3 Z, D1 ^2 H2 d8 _9 a/ `From the 1Division of Pediatric Endocrinology, 2University of
- e: T" j. U) n; m( mSouth Alabama Medical Center, Mobile, Alabama.' _7 H+ Q  [. K! O" N$ B3 n% J
Address correspondence to: Samar K. Bhowmick, MD, FACE,
& S: I; o0 n8 n9 ?% d0 X8 WProfessor of Pediatrics, University of South Alabama, College of- Z4 U. }" H, m# w  G
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;8 n" t( a& Q* m9 \5 b  d# E. g' x
e-mail: [email protected].1 A% ~, a0 V3 n- b
about 6 to 7 months old, which progressively became$ T4 q8 v1 o4 b  T- I$ l
darker. She was also concerned about the enlarge-7 m. N% d7 U  J- a5 l9 A
ment of his penis and frequent erections. The child
8 i9 y' B* m2 A5 Vwas the product of a full-term normal delivery, with
, Q* }& a! ^3 D- L# ba birth weight of 7 lb 14 oz, and birth length of' z/ R& x! J* d2 p8 r% D
20 inches. He was breast-fed throughout the first year+ Q' ]6 q, w, B& S" n
of life and was still receiving breast milk along with
6 u4 H/ q7 \$ u* W, }solid food. He had no hospitalizations or surgery,& F; \3 W4 ~: N7 `; U. h
and his psychosocial and psychomotor development# ^/ A" q+ m. g, m
was age appropriate.
+ G# u% s# c  g) XThe family history was remarkable for the father,
$ M  Z' i# s6 W, \who was diagnosed with hypothyroidism at age 16,- u3 f7 y, R$ _
which was treated with thyroxine. The father’s" U  M, e9 \9 L7 h/ Y0 q
height was 6 feet, and he went through a somewhat
; G( E; l1 v) T. |) hearly puberty and had stopped growing by age 14.
) z$ i6 |: c; E& eThe father denied taking any other medication. The
; P1 p6 L; _# Z- d) uchild’s mother was in good health. Her menarche" W3 j  f( q+ S
was at 11 years of age, and her height was at 5 feet
; g5 J- \& l/ R/ n- ?1 z# q& [5 inches. There was no other family history of pre-
5 N- h) i3 s7 @cocious sexual development in the first-degree rela-- s1 _: a4 A0 B, o# S: Y0 @
tives. There were no siblings.
# M1 o! }4 t# z; jPhysical Examination3 h; O7 F1 j! N
The physical examination revealed a very active,6 H4 z+ a; D& I7 s3 V8 m$ S& j
playful, and healthy boy. The vital signs documented( }: b% R$ Y4 R5 |7 H
a blood pressure of 85/50 mm Hg, his length was
+ Y% G1 ?2 ~! w( V! a' y" ~) |8 A90 cm (>97th percentile), and his weight was 14.4 kg
  c( A4 d) \+ ~, j) g(also >97th percentile). The observed yearly growth
, o/ v% k3 a1 d+ H, T7 Jvelocity was 30 cm (12 inches). The examination of
. U; l7 x7 {, {! r+ kthe neck revealed no thyroid enlargement.
, f( A2 f& I5 F, U7 ~* cThe genitourinary examination was remarkable for
  W5 w- r  r/ Z, k: t9 G1 Z5 qenlargement of the penis, with a stretched length of
8 F" W; L! x- S" n0 J+ y8 cm and a width of 2 cm. The glans penis was very well# [- a1 [' G. s; H/ U5 S/ g
developed. The pubic hair was Tanner II, mostly around7 e1 ~1 }7 |' S
5409 k6 Y# G0 u6 F8 t# G
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from2 E! G! q5 ~- n% b
the base of the phallus and was dark and curled. The
# |( _4 `+ r& qtesticular volume was prepubertal at 2 mL each.
: U' G: W  |  m9 IThe skin was moist and smooth and somewhat
# ~, {  I  c& Koily. No axillary hair was noted. There were no
% s1 q5 a4 c' }0 u$ b$ o3 M7 B4 _# cabnormal skin pigmentations or café-au-lait spots.
, ^% I+ b+ v6 R/ H: z9 _7 |6 Q' @Neurologic evaluation showed deep tendon reflex 2+. q' x% ~/ m1 F/ {0 C- z
bilateral and symmetrical. There was no suggestion
2 d" a  a9 d9 z3 E7 Sof papilledema.
( {+ @# L, O( U" M1 qLaboratory Evaluation
) N' K' I4 _' cThe bone age was consistent with 28 months by
& i9 M* @9 A9 s6 cusing the standard of Greulich and Pyle at a chrono-  w" t: s- X+ |5 _0 k7 J2 }
logic age of 16 months (advanced).5 Chromosomal
' {7 \$ A( W1 W3 ]karyotype was 46XY. The thyroid function test
% L' F( b7 [7 i8 c- `1 Ushowed a free T4 of 1.69 ng/dL, and thyroid stimu-" k3 u3 P3 O# s. I. o
lating hormone level was 1.3 µIU/mL (both normal).
# ?/ D9 P0 o4 S: Z. gThe concentrations of serum electrolytes, blood' @- }% a: C5 v. p1 w& w  S, ~
urea nitrogen, creatinine, and calcium all were) o# m# k6 _7 k2 r
within normal range for his age. The concentration  j) V$ P  S" T; \: _& X9 P3 `
of serum 17-hydroxyprogesterone was 16 ng/dL& V* d9 ~' N/ X
(normal, 3 to 90 ng/dL), androstenedione was 20
; O1 m8 L# [7 z4 S8 mng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-$ }; Z0 \( A4 m- J6 s: m) T
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
% {; ]9 z& G9 udesoxycorticosterone was 4.3 ng/dL (normal, 7 to
7 V7 D0 d/ v, z  l, l' x5 H  X49ng/dL), 11-desoxycortisol (specific compound S)
4 x" ]* S7 m2 W. c- ~was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
" Y& G0 B) M9 `# Wtisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total8 ]4 I9 o& S  V& y8 e
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),0 p8 V' a7 H3 t( N
and β-human chorionic gonadotropin was less than2 R, l# M* o  O: o- W" W) k  i
5 mIU/mL (normal <5 mIU/mL). Serum follicular
9 N. r  _: y- }: X8 bstimulating hormone and leuteinizing hormone7 i( ~* x, {* ^, T$ U
concentrations were less than 0.05 mIU/mL
, X3 H3 T4 ]8 `9 k6 F) ]+ a(prepubertal).
) z+ o/ f- l9 i1 kThe parents were notified about the laboratory
6 F# `7 J6 y8 eresults and were informed that all of the tests were% \4 a# w/ S6 k# _
normal except the testosterone level was high. The6 Z9 ^7 m2 i2 c
follow-up visit was arranged within a few weeks to
) j& S) ]4 L$ a3 l/ `( S" }& i1 mobtain testicular and abdominal sonograms; how-
- c5 @! o) W5 \, x  a0 S& vever, the family did not return for 4 months.4 _0 O% d% j! o0 [
Physical examination at this time revealed that the) L: ]% t; W& c. a' v
child had grown 2.5 cm in 4 months and had gained
: c% T7 c7 p& L  \2 kg of weight. Physical examination remained
2 }2 A' ]0 I" Q& p3 t/ [unchanged. Surprisingly, the pubic hair almost com-
8 k) z- M: p: e) E. Q8 {! Spletely disappeared except for a few vellous hairs at
& C8 E# S! Z) G9 @, [& S7 Tthe base of the phallus. Testicular volume was still 2
+ X# l. _1 x  g' c. ZmL, and the size of the penis remained unchanged.* `; N! [& `* t9 j9 G* G
The mother also said that the boy was no longer hav-  r' Y1 x0 M: M; Y
ing frequent erections.
, ^- U* J0 Y. L( LBoth parents were again questioned about use of4 p% W3 J0 p  \3 Y) ~: p
any ointment/creams that they may have applied to
& n  l+ U7 {8 |- l+ Q; ?- ethe child’s skin. This time the father admitted the" Y/ r; p+ w# X' P
Topical Testosterone Exposure / Bhowmick et al 541
( `1 t) s: @- @- P7 k: Q) Q3 Wuse of testosterone gel twice daily that he was apply-
2 u+ ^( K6 l, F2 H  Y- oing over his own shoulders, chest, and back area for
- C+ b2 {- a+ y) z* A0 F6 v& }a year. The father also revealed he was embarrassed
  j) D' ?# z" Y# ], R+ D) H7 S' @# ito disclose that he was using a testosterone gel pre-, e9 C- g- ~7 i
scribed by his family physician for decreased libido
$ ~4 }# p" S" D( H. gsecondary to depression.
+ |& B8 l: V( f/ PThe child slept in the same bed with parents./ I4 y. _0 e7 o2 `7 K
The father would hug the baby and hold him on his% w1 r9 `4 ]5 b1 @. o/ O
chest for a considerable period of time, causing sig-& \( k- ^  r+ B
nificant bare skin contact between baby and father.
, d2 E# B2 r9 `- P7 o- SThe father also admitted that after the phone call,/ d) Q1 T5 {- B' K: m. K! ~( Y
when he learned the testosterone level in the baby/ D' Y5 d0 R1 b$ B( }; e5 P* x7 b
was high, he then read the product information
7 z5 r: C$ x9 B1 Z; z8 w% opacket and concluded that it was most likely the rea-
2 C! _  Y* F9 d3 a6 yson for the child’s virilization. At that time, they% Q6 @+ O  m) P
decided to put the baby in a separate bed, and the" ?1 ?8 n' l7 P2 w$ z! [" t
father was not hugging him with bare skin and had; W8 }3 M/ T( ?/ n: {" v) f
been using protective clothing. A repeat testosterone7 t& E8 G. G) d8 Q
test was ordered, but the family did not go to the
$ K; S0 \8 p( glaboratory to obtain the test.
+ ^& |8 P9 L! b- Y6 P2 _* F% d; EDiscussion+ I/ F, T5 R3 ^% i) J+ l- P) X
Precocious puberty in boys is defined as secondary# U, }# ^% T/ H
sexual development before 9 years of age.1,4- a: t4 o: v" }" M: X, r7 U5 C
Precocious puberty is termed as central (true) when) L, T5 a5 ~' s; F. J" z* \
it is caused by the premature activation of hypo-
( i0 X  s& A0 q. O0 Q+ P3 |' Xthalamic pituitary gonadal axis. CPP is more com-
1 _' S; S. e& p) Fmon in girls than in boys.1,3 Most boys with CPP+ t7 _- v# [6 T6 z/ }& B
may have a central nervous system lesion that is
- A) K% ?1 F) E3 Sresponsible for the early activation of the hypothal-  Y$ Q# a, Y* [6 ?+ c% f
amic pituitary gonadal axis.1-3 Thus, greater empha-) t' [+ R" ]0 ]3 `2 V5 g
sis has been given to neuroradiologic imaging in
* A2 {$ s6 O9 v7 Wboys with precocious puberty. In addition to viril-$ D/ ~$ O, M' ?
ization, the clinical hallmark of CPP is the symmet-
' D3 ?% i& b7 }2 Drical testicular growth secondary to stimulation by
1 O- d; w, P& o; I' w, j8 l  vgonadotropins.1,3
$ z% m5 l+ R7 l* C, VGonadotropin-independent peripheral preco-9 }$ a- D9 K' D: H/ |
cious puberty in boys also results from inappropriate
% U" p0 a# H1 f* z3 G4 X8 fandrogenic stimulation from either endogenous or
4 S5 L; r' t/ Q' dexogenous sources, nonpituitary gonadotropin stim-7 `; H$ [/ j  ?6 {* i( {/ P
ulation, and rare activating mutations.3 Virilizing
2 M( ]2 Q" I' S, hcongenital adrenal hyperplasia producing excessive! N8 }9 [8 i  x3 @3 h6 T2 J
adrenal androgens is a common cause of precocious1 W+ }6 @& k- M9 }* N- Y
puberty in boys.3,4. v! E. f, U+ X3 U; G
The most common form of congenital adrenal
) B# a$ z9 g) r3 ~0 G$ dhyperplasia is the 21-hydroxylase enzyme deficiency.4 _3 N# o3 Z& S9 J
The 11-β hydroxylase deficiency may also result in8 Z" h8 @9 N5 q. S5 ?% Q! L- _( r
excessive adrenal androgen production, and rarely,
9 g) ^- Q0 ^/ ~, Q) kan adrenal tumor may also cause adrenal androgen+ E( v9 X  n$ l0 p/ w; k
excess.1,3
% I0 M6 N  Q9 {& H& Z& {at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
' H/ t3 n; c3 x) S542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
7 }' ?  e8 A# S' d+ @% KA unique entity of male-limited gonadotropin-
4 @% y0 O$ N) oindependent precocious puberty, which is also known! B/ ]6 Y5 {0 {  N. U0 q
as testotoxicosis, may cause precocious puberty at a, t, b( @6 Z  K# N" L
very young age. The physical findings in these boys% o; F  Z5 Z& z' j
with this disorder are full pubertal development,2 o) z& s9 h2 C' S; R" R( ]9 l0 N: T
including bilateral testicular growth, similar to boys
7 W# |7 `: ^$ v9 @+ J+ Uwith CPP. The gonadotropin levels in this disorder
0 x2 O9 ^" |+ O) C6 j) f9 `are suppressed to prepubertal levels and do not show  i2 X5 [+ T9 B( c% X6 [% n
pubertal response of gonadotropin after gonadotropin-
+ z6 C! Z4 ~- W* s1 }: @# V+ V  B% \releasing hormone stimulation. This is a sex-linked% o+ J& M7 h, V7 e* Y- ?
autosomal dominant disorder that affects only) L3 M* W4 Z7 h% J& K* f+ @
males; therefore, other male members of the family
2 {& b. G: e6 Z  k! ?4 p$ b# Emay have similar precocious puberty.3$ ]( G; D+ f% p/ M' d) X
In our patient, physical examination was incon-+ W2 ~+ z2 K& q- t$ E, P$ n* P0 D
sistent with true precocious puberty since his testi-
- ^: p  u; d; m* l% Q0 x; icles were prepubertal in size. However, testotoxicosis6 I" v. I$ k2 Q+ P
was in the differential diagnosis because his father
+ B# P( z& _3 ~1 g, C# y: Gstarted puberty somewhat early, and occasionally,2 I4 W" K# i1 k/ Q5 K" |! ~+ G
testicular enlargement is not that evident in the3 n- c/ Z7 h+ ^# R" }  y# x
beginning of this process.1 In the absence of a neg-9 x8 ~, \- o3 |4 n& A1 R0 N2 r
ative initial history of androgen exposure, our; S& c  j6 N1 C* X$ u( N( B
biggest concern was virilizing adrenal hyperplasia,& W) E) L- G7 [& ~* c  T4 u: s3 H8 b1 h
either 21-hydroxylase deficiency or 11-β hydroxylase
. q/ ^0 j. i3 I% w- o2 c" h7 q1 {deficiency. Those diagnoses were excluded by find-1 ]: }; M. O9 H
ing the normal level of adrenal steroids.
0 `* ?& m# e1 _8 }$ r6 D; MThe diagnosis of exogenous androgens was strongly
0 ?" P2 M; g8 D$ P$ y6 U4 zsuspected in a follow-up visit after 4 months because
9 e. w2 B; L2 F, _the physical examination revealed the complete disap-
" L9 c3 M; J+ \5 T7 `: l) Jpearance of pubic hair, normal growth velocity, and$ E. ]6 K% Q" {$ n  A" z: o# v0 r
decreased erections. The father admitted using a testos-
. J$ _- a; @/ ?4 c) Eterone gel, which he concealed at first visit. He was+ j6 I, c, R1 F! e
using it rather frequently, twice a day. The Physicians’
9 A  x0 I, W& w& _Desk Reference, or package insert of this product, gel or5 i1 |7 S1 C$ v! s. b
cream, cautions about dermal testosterone transfer to
6 h; B4 p- {  V: G$ A$ Xunprotected females through direct skin exposure." y6 E/ r0 b8 x& K, B, g/ `% \
Serum testosterone level was found to be 2 times the
& u$ ~% e1 w! D. \, ?baseline value in those females who were exposed to
3 ^; S( p6 Q) D9 x0 s& a& qeven 15 minutes of direct skin contact with their male& }. ]5 m' z# ~
partners.6 However, when a shirt covered the applica-
1 ~" F) ]1 K; }% ttion site, this testosterone transfer was prevented.
9 @* A/ M* S8 T5 ]Our patient’s testosterone level was 60 ng/mL,$ x; C! I  K# p' e* _! T2 x
which was clearly high. Some studies suggest that, B4 Q! b9 I) S3 ~1 C
dermal conversion of testosterone to dihydrotestos-
; h* R- t6 o: f8 H  Z+ b) i9 lterone, which is a more potent metabolite, is more/ o2 e4 ?% J/ v- p8 ?" J6 |
active in young children exposed to testosterone
$ m3 r  p3 l3 s7 mexogenously7; however, we did not measure a dihy-) a* H3 V# b. j: |. j
drotestosterone level in our patient. In addition to2 t5 D4 N4 O: B
virilization, exposure to exogenous testosterone in( k7 [3 d/ R* y. l- s( o  o6 |
children results in an increase in growth velocity and
& t' O* B- [" b; F: H: T% `advanced bone age, as seen in our patient.
4 N% f2 X6 L9 e# n6 a$ V' N. w- QThe long-term effect of androgen exposure during- o, a9 v/ r* j1 Y  \7 C
early childhood on pubertal development and final
9 i7 L. x3 L4 radult height are not fully known and always remain
. A( @* W3 E& S, o5 X/ e' i1 ua concern. Children treated with short-term testos-
# O9 h3 O" h" P# L! w0 _  Iterone injection or topical androgen may exhibit some
4 l% k) q0 E' G8 k' g: Cacceleration of the skeletal maturation; however, after$ V4 _) M* l2 o& a
cessation of treatment, the rate of bone maturation
# c* |" C& w7 mdecelerates and gradually returns to normal.8,9/ V- k) ?3 p: |8 q
There are conflicting reports and controversy. c5 _3 H+ P) m
over the effect of early androgen exposure on adult* G1 A- K" e. U1 C
penile length.10,11 Some reports suggest subnormal
( M0 _- Q3 _" \* b5 H) s/ gadult penile length, apparently because of downreg-8 v, m" `; q' @% [: z. a- L
ulation of androgen receptor number.10,12 However,) c) v% h( V# d) H3 L" s, S) y
Sutherland et al13 did not find a correlation between& f! ~- X0 m3 g% n! `
childhood testosterone exposure and reduced adult+ n( h5 J0 N+ q& L
penile length in clinical studies.
+ `; F% O: G1 g! H$ NNonetheless, we do not believe our patient is
- k; \: m) ]! ]2 l2 b$ ggoing to experience any of the untoward effects from* o+ C6 ?$ q; M: r! h/ f( z
testosterone exposure as mentioned earlier because0 H7 }. ]* S6 ^- g/ o3 }
the exposure was not for a prolonged period of time.8 W! r/ P; Q  h0 u9 l
Although the bone age was advanced at the time of/ _. o2 W% A# M1 Y. S0 ?
diagnosis, the child had a normal growth velocity at2 ~: u8 x6 l$ S4 F
the follow-up visit. It is hoped that his final adult& r8 a; |; k* p
height will not be affected.
9 ?2 d* d2 B7 J7 mAlthough rarely reported, the widespread avail-
8 e( [& ]; w1 C5 F8 ^ability of androgen products in our society may
% [$ T4 C5 g8 E+ e! I( tindeed cause more virilization in male or female
/ y# T/ P3 k0 G, S5 W* rchildren than one would realize. Exposure to andro-" n8 Y% \3 K* y  F2 ~
gen products must be considered and specific ques-$ l9 c1 }" D1 X" b7 A) G3 y
tioning about the use of a testosterone product or
' O# s: H6 \" m2 @! j1 Y7 P! Y6 Zgel should be asked of the family members during
+ j+ n+ u) ?$ N5 O0 W" uthe evaluation of any children who present with vir-
; E. g# o7 k6 O7 Nilization or peripheral precocious puberty. The diag-
6 D8 e5 G  B3 E: o' f; e# qnosis can be established by just a few tests and by+ @8 V% G- T& W4 N3 Q
appropriate history. The inability to obtain such a
- l- N0 j& L/ t5 c- N$ S( @$ yhistory, or failure to ask the specific questions, may0 _- a! Y, s: {& A! k
result in extensive, unnecessary, and expensive+ b; j0 }# N% V" _3 P4 M
investigation. The primary care physician should be
# t/ b0 I1 Y* a1 x3 o) q( daware of this fact, because most of these children
$ q" n' u$ V1 smay initially present in their practice. The Physicians’  d0 N* Z; ]/ O
Desk Reference and package insert should also put a2 N: P  P8 V1 |. t
warning about the virilizing effect on a male or( q  D: m, G5 O9 D3 D# ]* ?
female child who might come in contact with some-
6 }9 c$ E8 r! H0 |7 M# ~4 Rone using any of these products.
8 j/ L6 r" O: ?) }+ YReferences
% k) U" A7 g" P1. Styne DM. The testes: disorder of sexual differentiation
# P0 s' X/ u* u5 `2 J' v$ wand puberty in the male. In: Sperling MA, ed. Pediatric
1 t2 ]; {* W& J8 P5 XEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
6 L" k) X1 x2 |+ r, g2002: 565-628.3 [5 v% s+ u" l6 r# r* ^
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious: h# l1 M/ [. [$ X) I1 x
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
7 S/ q1 X* \( v1 q3 ]8 w; E0 K$ sBoy Induced by Indirect Topical1 m* }5 C. j8 X  O  I7 U
Exposure to Testosterone
3 g' T8 f* u1 G) y1 X3 \7 |: OSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
& h7 J4 V( h. E( Z) dand Kenneth R. Rettig, MD1
" L7 U) I8 a$ x. ], L) lClinical Pediatrics( J' q$ |7 Z& ?& {( j3 A6 U
Volume 46 Number 6
: T* |" X* @2 I+ M3 t6 }3 CJuly 2007 540-543( X: `4 p/ b) N/ `2 g1 I
© 2007 Sage Publications
7 D+ @5 H- n3 Z$ g- F10.1177/0009922806296651: F" @2 X! T1 b: K# N" G
http://clp.sagepub.com( E5 _0 l2 E8 D4 z: _
hosted at1 e  y" i# d* u6 N. C, V! e
http://online.sagepub.com4 N. F3 U% z; F% L
Precocious puberty in boys, central or peripheral,
" D  M% A% y/ o( m, G7 v2 ^is a significant concern for physicians. Central
: [) g% e% ]: A+ H: vprecocious puberty (CPP), which is mediated# N  [- _3 z+ E" a8 A
through the hypothalamic pituitary gonadal axis, has
, {1 q8 D+ {; B* H1 w# u9 @. ^a higher incidence of organic central nervous system/ O5 ?$ `: H. l
lesions in boys.1,2 Virilization in boys, as manifested" H# ]; v8 s3 p. l
by enlargement of the penis, development of pubic
$ q7 Q8 V6 m( h5 ~hair, and facial acne without enlargement of testi-, G3 A* }$ D0 ]: j6 F! ^7 H
cles, suggests peripheral or pseudopuberty.1-3 We
- z2 Y: Q2 g' Z, f% v: M+ zreport a 16-month-old boy who presented with the
' K4 M6 A- k5 S: H6 M; ]enlargement of the phallus and pubic hair develop-% ?+ l1 M! v# f7 O6 I8 s8 S
ment without testicular enlargement, which was due
) L3 u) R. X% p* _# m1 ?9 qto the unintentional exposure to androgen gel used by
7 Z0 }; \0 C5 `# K. A$ qthe father. The family initially concealed this infor-
: c0 h5 w2 k2 |( C  omation, resulting in an extensive work-up for this
# N- \) C2 r8 o; v  J" E7 S  @child. Given the widespread and easy availability of
/ ?3 r8 s4 j/ i& g8 l# h" l3 Gtestosterone gel and cream, we believe this is proba-
" u, @5 D0 C! g8 G! C5 Vbly more common than the rare case report in the
3 q) ]5 t. @! E3 Aliterature.4
( F; ]; m+ a# QPatient Report# R' r' I7 \/ }7 c
A 16-month-old white child was referred to the" w! e  N9 C* r4 h4 Q2 I) s
endocrine clinic by his pediatrician with the concern
7 D1 p" g8 t3 Z& D: @2 C( O; o6 Bof early sexual development. His mother noticed
, i' f+ T0 U. F$ Olight colored pubic hair development when he was8 S$ B% {( y: W# f1 J% f
From the 1Division of Pediatric Endocrinology, 2University of6 F5 D2 t) ~1 [& j
South Alabama Medical Center, Mobile, Alabama./ h. J# D1 U9 q! E" t% ]6 F$ n$ T" Y. R
Address correspondence to: Samar K. Bhowmick, MD, FACE,
* O/ C  h* ~- k7 PProfessor of Pediatrics, University of South Alabama, College of
4 {' U! Y) b% k, |2 G& y8 X- n$ }Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;5 |9 D) n0 h( A8 i0 C& a5 d$ A
e-mail: [email protected]." T5 \  T; H/ O0 X
about 6 to 7 months old, which progressively became2 {- O( p  n6 y. d' g& d  ~7 [2 f5 k  Q
darker. She was also concerned about the enlarge-+ h4 Q% v$ {% a0 \  ]* @$ `
ment of his penis and frequent erections. The child& L. u" m" I3 y4 o  V- k
was the product of a full-term normal delivery, with/ y; r+ P6 J; ^$ P
a birth weight of 7 lb 14 oz, and birth length of1 N: q: H4 g% y% _
20 inches. He was breast-fed throughout the first year
) [1 F; q5 G- k6 p7 o8 {, iof life and was still receiving breast milk along with
* o, \, Q" b4 D& `9 Tsolid food. He had no hospitalizations or surgery,% `" ]+ J3 J" D8 F2 ?
and his psychosocial and psychomotor development6 X* m* k, a( R$ G/ H
was age appropriate.1 X/ S5 @. R* w5 e8 `) p& V
The family history was remarkable for the father,
2 E& D. F7 E9 H9 Z: V" U3 Lwho was diagnosed with hypothyroidism at age 16,# m. a3 W9 t# T+ b! G
which was treated with thyroxine. The father’s- k: O6 n, G% {+ {
height was 6 feet, and he went through a somewhat
8 \- _5 f; e8 k: G% @early puberty and had stopped growing by age 14.
% P! x4 j% Z0 {8 XThe father denied taking any other medication. The
9 G7 g1 Q5 ]5 Z& q- v% echild’s mother was in good health. Her menarche
9 z8 z% T# e, K& Xwas at 11 years of age, and her height was at 5 feet. Z. _' q- Y1 z' u* J
5 inches. There was no other family history of pre-3 B! z/ b7 K; V( f! j
cocious sexual development in the first-degree rela-
3 @. D6 O9 w5 x6 m, z6 stives. There were no siblings.
! r4 p2 V; y7 h7 aPhysical Examination+ `: P) P$ k( i) R1 ^7 a) D
The physical examination revealed a very active,- u8 B" M6 Y  @6 q0 T
playful, and healthy boy. The vital signs documented+ w. q% t% L0 }6 U: u. f
a blood pressure of 85/50 mm Hg, his length was4 Y% c- l6 O* }  B" E1 F7 t9 _
90 cm (>97th percentile), and his weight was 14.4 kg
; H( z% y# c% I* V% \(also >97th percentile). The observed yearly growth4 E6 \5 A( Z& ]+ `/ j6 |- P- n( j
velocity was 30 cm (12 inches). The examination of
' L4 @% Y0 j* ^9 W) }1 ~the neck revealed no thyroid enlargement.+ D  p/ i( i  H; Q2 J
The genitourinary examination was remarkable for& X/ k( @1 a, s6 v% i/ I; R
enlargement of the penis, with a stretched length of
4 o$ f) }# J( N  P, _8 cm and a width of 2 cm. The glans penis was very well
1 q& V8 O, z: O, a4 C) l9 Jdeveloped. The pubic hair was Tanner II, mostly around$ l3 a0 O% ]# I. d, h
540' J& @0 ^1 i+ i- \+ j4 w
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from- u1 V* F, |; m( t
the base of the phallus and was dark and curled. The: |. k) M( y; O* o  R$ G
testicular volume was prepubertal at 2 mL each.
+ y$ y! [, b  N% ?  Y7 XThe skin was moist and smooth and somewhat# C  {5 l* v5 d3 l' z$ E
oily. No axillary hair was noted. There were no
9 s! A; H% W- N6 b8 y6 u, rabnormal skin pigmentations or café-au-lait spots.9 Z4 [! f4 c  o/ ~! C9 Y+ z: P7 g
Neurologic evaluation showed deep tendon reflex 2+( [9 e/ G( M0 t0 ], J5 B( j
bilateral and symmetrical. There was no suggestion! M! Z3 N8 ]9 t9 z5 J) i) [9 a
of papilledema.
8 L0 D& `5 D$ v4 k: w# r0 M4 uLaboratory Evaluation
5 ^8 G4 g. J* `: f8 T+ \" sThe bone age was consistent with 28 months by
5 g$ s2 Q! E% F8 y* B) P* xusing the standard of Greulich and Pyle at a chrono-
1 Q1 f9 Q3 \- {( \: f; rlogic age of 16 months (advanced).5 Chromosomal
* i2 |5 y4 r# S; ^karyotype was 46XY. The thyroid function test
  p4 s# ^# e5 m& m, a' O6 ^showed a free T4 of 1.69 ng/dL, and thyroid stimu-  ^, P. I2 m0 g! D0 S' w
lating hormone level was 1.3 µIU/mL (both normal).
# E$ c2 m: }! m  V/ J6 D' cThe concentrations of serum electrolytes, blood
6 c+ v' t# V+ z$ @# ]- Curea nitrogen, creatinine, and calcium all were
9 ?! x2 o! w# ~1 k- I3 nwithin normal range for his age. The concentration
, G* R/ P: b$ r! z8 _! t5 H: Yof serum 17-hydroxyprogesterone was 16 ng/dL% w5 I6 N+ X1 d
(normal, 3 to 90 ng/dL), androstenedione was 20  m% L& S* q; R. W
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-( [+ F% M" q5 T/ z' Z9 F. v5 P
terone was 38 ng/dL (normal, 50 to 760 ng/dL),9 e* j2 |6 p% Y% N: i
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
, `* j8 j6 @' e7 }7 R' Y49ng/dL), 11-desoxycortisol (specific compound S)( Z2 |1 {0 I6 z
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-4 i. S+ R8 a( J% I! G* Z
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total* B8 n" M# _8 }3 ]! U9 g
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),) B) j- U- M; ]. }; V
and β-human chorionic gonadotropin was less than
# N* R0 v# l" \8 M% {5 mIU/mL (normal <5 mIU/mL). Serum follicular1 P% n4 ^9 m$ u" P0 B# c) N
stimulating hormone and leuteinizing hormone
- [. i) N, Q% T. b/ ~( b3 i- nconcentrations were less than 0.05 mIU/mL
, `9 l- X; Y1 [% r(prepubertal).
2 d* ~7 V6 Z2 j1 hThe parents were notified about the laboratory
, H1 s5 A$ _8 B  ^3 P! Tresults and were informed that all of the tests were# J+ i8 |% Y) E# R* q' D7 K
normal except the testosterone level was high. The$ ?3 K3 f$ w1 v8 ]. Y3 Y3 I/ u
follow-up visit was arranged within a few weeks to" v5 ?+ T0 H' i7 I& ?3 c
obtain testicular and abdominal sonograms; how-! X! F) u( {6 J& L
ever, the family did not return for 4 months.
( {$ v8 T% ]4 X& k3 p9 F3 D, QPhysical examination at this time revealed that the
: J6 b! O9 f- i5 N  G# z6 l# v$ a+ ?' y  vchild had grown 2.5 cm in 4 months and had gained
( S: t% v0 P( _+ ^$ t6 m( B  N) \$ b; l2 kg of weight. Physical examination remained: ^$ Z$ A( m3 o
unchanged. Surprisingly, the pubic hair almost com-; J7 L7 b4 F3 R
pletely disappeared except for a few vellous hairs at
+ T  r* Z( Z$ ethe base of the phallus. Testicular volume was still 2' ~8 e& U' J5 S0 H6 e
mL, and the size of the penis remained unchanged.
6 K; q; q8 ?: g, I% n2 H7 [The mother also said that the boy was no longer hav-6 C! N9 P  n$ F: `" h: w' J0 R
ing frequent erections.
9 b0 _# t" g( lBoth parents were again questioned about use of; F, f5 ?+ S5 F, @  s. C
any ointment/creams that they may have applied to
  Q- {) Y4 Y! r) p7 Dthe child’s skin. This time the father admitted the( k% j9 h) r# S5 r, |! ?/ F
Topical Testosterone Exposure / Bhowmick et al 5415 q7 u8 W" a6 e  o
use of testosterone gel twice daily that he was apply-1 ^5 K4 r" ?6 u* f& _% I. g  T9 {9 i
ing over his own shoulders, chest, and back area for8 X' p2 ^1 U8 _8 r3 ?  M
a year. The father also revealed he was embarrassed
) f6 N, E, S8 V$ Y. eto disclose that he was using a testosterone gel pre-% g3 \; g- e. [
scribed by his family physician for decreased libido
2 H( g5 p5 L5 }$ y$ p- Tsecondary to depression.- n$ F1 ~. B; E
The child slept in the same bed with parents.
* ^( y  u. Q# ^- a3 J' m) Z$ J( ZThe father would hug the baby and hold him on his
! F! G0 _/ B% I1 ]7 m. I# Tchest for a considerable period of time, causing sig-
+ R1 e/ l. ~- ynificant bare skin contact between baby and father.
, J& u7 @2 i: t2 w, oThe father also admitted that after the phone call,2 |+ }: i# _5 P$ w) P' ^- F' @& j9 h
when he learned the testosterone level in the baby
8 H3 |6 y* f- N1 x. s# Fwas high, he then read the product information2 @# q5 D% O& N: f3 j) }
packet and concluded that it was most likely the rea-$ C$ o0 {# E5 P. V, ?2 \/ [" g
son for the child’s virilization. At that time, they
% m7 o; S3 H- ~# s- B0 ?decided to put the baby in a separate bed, and the
- y/ ~4 |9 Y# h" O2 }father was not hugging him with bare skin and had7 |9 Z+ ]8 m: W4 Y) T8 K
been using protective clothing. A repeat testosterone
' W+ F0 _. [4 U; a+ Ntest was ordered, but the family did not go to the
$ M1 |* w' g2 A1 l) A1 Dlaboratory to obtain the test.3 z7 {3 L9 N5 |9 y6 d; Z
Discussion
( U2 c" e6 \' C( W3 B# cPrecocious puberty in boys is defined as secondary
' V3 k% g2 Z. m# @) Ksexual development before 9 years of age.1,4" m0 H) O7 D7 K& W
Precocious puberty is termed as central (true) when; E. g6 g" n4 r% _! D/ m! B. S
it is caused by the premature activation of hypo-
* i( l6 ]5 X/ ithalamic pituitary gonadal axis. CPP is more com-
/ Y' }7 \4 `1 X9 O& Cmon in girls than in boys.1,3 Most boys with CPP
: n( G8 s0 o" R* p4 u( rmay have a central nervous system lesion that is
1 v; Q, x+ x. n- ^' P" Y. Yresponsible for the early activation of the hypothal-
3 c$ T$ Z9 e' r# J% P& B# Namic pituitary gonadal axis.1-3 Thus, greater empha-
: U/ F( `" @% |8 w7 Asis has been given to neuroradiologic imaging in
# ?  ?0 C+ s5 w- W& n. l5 r( iboys with precocious puberty. In addition to viril-
0 C8 [6 D! a0 m# x! ^1 Mization, the clinical hallmark of CPP is the symmet-
3 Z8 l4 G# U9 u: h# _rical testicular growth secondary to stimulation by
/ c9 p% T% k5 F' D$ |gonadotropins.1,3( }" z) {3 b, A5 ]
Gonadotropin-independent peripheral preco-# T8 G  W' D8 Z0 J
cious puberty in boys also results from inappropriate
& K; V. t0 c& Pandrogenic stimulation from either endogenous or
; P4 L; {7 [+ S) [- h& o* `exogenous sources, nonpituitary gonadotropin stim-
1 e( w7 _9 R: E2 F/ Hulation, and rare activating mutations.3 Virilizing8 v2 ]4 Q7 _0 [# z$ a7 E
congenital adrenal hyperplasia producing excessive6 L. a& q) ?& V1 x+ J
adrenal androgens is a common cause of precocious
5 M+ `. E2 L1 b! S. ?4 Epuberty in boys.3,4; I& h" W1 j2 J
The most common form of congenital adrenal* o# S* e) _* w; O9 Y$ A, P
hyperplasia is the 21-hydroxylase enzyme deficiency.
" ?/ e& I: k- x2 {6 o. z8 mThe 11-β hydroxylase deficiency may also result in
1 x+ b8 F/ N6 v% ?, z0 yexcessive adrenal androgen production, and rarely,+ c) ~) Y3 J6 B8 f7 R5 h, `7 f
an adrenal tumor may also cause adrenal androgen% F0 d7 g7 E2 d2 P
excess.1,3
4 o, h# b+ Q; [3 r6 L, t# Z- Nat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from3 l# w5 m7 k2 l- u# }/ m$ R4 ]
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
) b# Q% q/ G! j5 iA unique entity of male-limited gonadotropin-
/ A" S" N  K" N2 i, U- e9 L+ cindependent precocious puberty, which is also known
) ~. M4 w( o  s) t4 a# |1 O0 p5 ^as testotoxicosis, may cause precocious puberty at a; v# V# [7 D  c, {: }# ?
very young age. The physical findings in these boys
4 B/ e: c# R! l( h) _( rwith this disorder are full pubertal development,1 }) Y( ^4 {; q# K8 \8 ~
including bilateral testicular growth, similar to boys
! ]: f0 K$ j# Hwith CPP. The gonadotropin levels in this disorder
+ O$ E( T- M& N! q& xare suppressed to prepubertal levels and do not show; h* f5 t& p3 X
pubertal response of gonadotropin after gonadotropin-# j# z5 Z4 Z" _4 @
releasing hormone stimulation. This is a sex-linked
- Y) g- i! g4 T4 t$ t" Rautosomal dominant disorder that affects only& g8 Y; M' C% f. |5 J" o
males; therefore, other male members of the family
$ M$ @; \- l5 O1 @, P( tmay have similar precocious puberty.3
) T- E. Z$ b  o. _2 uIn our patient, physical examination was incon-; x. v& i; Q7 j5 d
sistent with true precocious puberty since his testi-
! f1 M# R3 |) X' L, Jcles were prepubertal in size. However, testotoxicosis
. C8 f# e2 h% M+ K8 n9 Q7 gwas in the differential diagnosis because his father* Z2 p/ g& S- a8 L
started puberty somewhat early, and occasionally,0 e% F; \1 `! D7 p
testicular enlargement is not that evident in the# q6 _8 m" I1 q; `: d3 O3 Z
beginning of this process.1 In the absence of a neg-
+ Y3 ?, v( k" u; q1 V7 R' U$ Fative initial history of androgen exposure, our! {/ Z) a) O# N0 @4 @: Q, q# k0 w
biggest concern was virilizing adrenal hyperplasia,. c8 x% g' W* y+ P$ P, V
either 21-hydroxylase deficiency or 11-β hydroxylase0 _: B( e1 S2 P
deficiency. Those diagnoses were excluded by find-
) G( f7 u* l$ x" Hing the normal level of adrenal steroids.
$ ]/ V- q% i/ z) ~$ ZThe diagnosis of exogenous androgens was strongly9 T' T( \5 B( z0 g' \
suspected in a follow-up visit after 4 months because* @) e/ T$ Q) B5 [
the physical examination revealed the complete disap-
/ Q& x3 q% ~2 {8 I7 C/ d" @pearance of pubic hair, normal growth velocity, and/ ~; ~' H! x, k6 Y
decreased erections. The father admitted using a testos-
" @9 U! S+ Z/ T; ?( ?1 zterone gel, which he concealed at first visit. He was$ A. e; n5 x0 B  f/ G% e
using it rather frequently, twice a day. The Physicians’7 y/ o8 ^% O% v
Desk Reference, or package insert of this product, gel or  ?+ R$ }* \: J8 J  x
cream, cautions about dermal testosterone transfer to- `; U! e0 g; l" e2 y, o: Z
unprotected females through direct skin exposure.
; X# b. a1 X: U7 }% XSerum testosterone level was found to be 2 times the/ b1 F0 W; K% t. A8 i
baseline value in those females who were exposed to
+ t3 D- n/ H$ u. ieven 15 minutes of direct skin contact with their male+ x: ~4 I/ }# s9 |$ F0 s: y
partners.6 However, when a shirt covered the applica-& N* I4 W) b" x1 q6 _. G3 O
tion site, this testosterone transfer was prevented.
& ^$ G9 f* Q5 O6 XOur patient’s testosterone level was 60 ng/mL,
* c1 n4 x+ r; y- ~- Twhich was clearly high. Some studies suggest that
% E: u0 C) ^* \- H0 v* i, W. xdermal conversion of testosterone to dihydrotestos-' m4 d; o, w2 p/ W
terone, which is a more potent metabolite, is more
3 w8 O  r( C' E# K5 pactive in young children exposed to testosterone% L8 Q# q5 b6 r6 X/ t% k
exogenously7; however, we did not measure a dihy-- H3 S3 m7 L0 h. ^% V3 I# i$ v; l) p
drotestosterone level in our patient. In addition to
- X6 i& y- s$ lvirilization, exposure to exogenous testosterone in/ X7 t, p/ F1 G4 N3 |
children results in an increase in growth velocity and& o* E& e" ?: i8 G5 ?
advanced bone age, as seen in our patient.8 |' w6 }. R5 z: p
The long-term effect of androgen exposure during. O6 P  _: ^0 L7 j2 V/ S& p% R
early childhood on pubertal development and final
  [/ U- W* l$ X! K# n5 M, Tadult height are not fully known and always remain
* Q: j  J2 P( U% da concern. Children treated with short-term testos-9 x7 N+ X1 X! l& H
terone injection or topical androgen may exhibit some
' Z  j: p: m. H' R$ {. [' Wacceleration of the skeletal maturation; however, after
9 F* H% O- ]" c" R7 E! \& dcessation of treatment, the rate of bone maturation( v* f+ N9 t$ f& J0 z& B
decelerates and gradually returns to normal.8,9  i  P7 c; k: u) K, d; L8 a
There are conflicting reports and controversy$ u) P- y5 j0 g3 [( n: r
over the effect of early androgen exposure on adult
  K: y9 w& n) w2 y! r- [penile length.10,11 Some reports suggest subnormal
2 x6 W" W- a/ n7 g6 v- Qadult penile length, apparently because of downreg-3 Y$ r. ?3 w5 ?' x: r" z
ulation of androgen receptor number.10,12 However,
3 T3 v: e' P2 a3 ^4 i0 r/ tSutherland et al13 did not find a correlation between
1 Y0 ?" X) t  Ychildhood testosterone exposure and reduced adult7 C' ?0 N, @9 S  h& U
penile length in clinical studies.
, Q' Q/ E1 B; J' M8 n2 |Nonetheless, we do not believe our patient is
9 |" i/ Y5 j; z9 i5 T; h% Rgoing to experience any of the untoward effects from
) b) z1 q1 {" K% j4 B6 qtestosterone exposure as mentioned earlier because; V8 H" g) U% J. \0 x. t
the exposure was not for a prolonged period of time.
2 t& F7 O) u4 B2 j- \4 RAlthough the bone age was advanced at the time of- S, g5 l  L: q0 i
diagnosis, the child had a normal growth velocity at
, X4 K% c( l" I; |! Tthe follow-up visit. It is hoped that his final adult
- _: f/ y- @7 |+ Q" Q: ?2 Jheight will not be affected.
! u8 ?4 x- W& t! `+ a: @6 m% eAlthough rarely reported, the widespread avail-
; u' R5 i! C8 M+ fability of androgen products in our society may
( q. h) n  ^( Q1 ~0 Gindeed cause more virilization in male or female
: _0 R$ `. z" r; {: Y! l& wchildren than one would realize. Exposure to andro-: F' O0 T0 ~2 f! _
gen products must be considered and specific ques-
/ F4 H2 u4 i/ g( }0 R4 Ntioning about the use of a testosterone product or# `7 y, |6 r8 ?5 f
gel should be asked of the family members during
" w2 |3 ^. A$ h7 P$ q, E( Vthe evaluation of any children who present with vir-
9 Y6 j6 P# X9 b4 e2 v$ x" s% _ilization or peripheral precocious puberty. The diag-" |) v2 V& c: G7 p3 E8 T' ^7 _; N
nosis can be established by just a few tests and by1 O5 b' ]3 ~1 _
appropriate history. The inability to obtain such a
" W- y1 H4 n* S# Y2 e2 b3 f! shistory, or failure to ask the specific questions, may! a9 k' e! U: u, `
result in extensive, unnecessary, and expensive1 x  j- }$ h5 K: M; p$ o5 k
investigation. The primary care physician should be
- ^4 i+ ]' g$ ~/ q% J1 \aware of this fact, because most of these children
& x7 j  b+ r* I. V/ O, |$ umay initially present in their practice. The Physicians’
: U+ b( X, S$ ^" V2 B3 ?0 ]: i6 g& F) HDesk Reference and package insert should also put a
8 P* w0 W- S! u3 o+ n2 D: ?, b6 Cwarning about the virilizing effect on a male or7 K  W3 z' ]8 N+ \6 L
female child who might come in contact with some-; O' X0 ^- c3 {& o* B6 O
one using any of these products.
' R) j- \; ~4 c0 H' AReferences
4 G$ ^/ _2 F2 I1. Styne DM. The testes: disorder of sexual differentiation
1 H" n* S0 O7 _. O8 ~and puberty in the male. In: Sperling MA, ed. Pediatric
. I0 }3 Z6 ?7 L1 S1 X* W# mEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;! [- L/ Z) I7 j
2002: 565-628.: j; z4 M5 ]2 M; v. e3 _6 x
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
. Z& z0 {7 T, j5 U5 M0 mpuberty 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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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

, Y; h1 v' {- m5 U3 Z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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