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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
0 O2 l# w. L' N1 |- SBoy Induced by Indirect Topical
2 q! i1 i6 |# j$ NExposure to Testosterone
5 h# n& _! Q! ^8 _4 R7 OSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2' p1 }# v( H, k5 s3 o6 B
and Kenneth R. Rettig, MD1% K& G3 `+ \" i; [4 I6 P+ U) y
Clinical Pediatrics3 r9 b( C# e1 S7 H4 P% M) a% G7 C
Volume 46 Number 60 N2 _8 W2 V  B; b8 Z* L
July 2007 540-543  p) @0 a' a7 m  P" [. ~
© 2007 Sage Publications4 F% [+ E  E4 Q2 y3 b! A4 l7 v
10.1177/0009922806296651
/ P; g( b+ w, X- T5 Ohttp://clp.sagepub.com
9 T9 }/ W; k& y) |  U+ ]0 Q( ]5 Rhosted at
6 O- {, E  e  i7 Whttp://online.sagepub.com2 g; H: R" h- ]# }$ c8 t6 \
Precocious puberty in boys, central or peripheral,
) K; x9 G6 l% A& I2 m) mis a significant concern for physicians. Central2 l0 P8 {: I" j3 Z& O1 z
precocious puberty (CPP), which is mediated
1 S* I' ~* Q- S; A5 N" hthrough the hypothalamic pituitary gonadal axis, has
0 |% _3 _8 E5 a/ E8 ja higher incidence of organic central nervous system& Z( O( i' B# Z4 W
lesions in boys.1,2 Virilization in boys, as manifested
; T2 _! s! {$ K- E* ?by enlargement of the penis, development of pubic
5 _# q" `2 @' ~+ Z4 H2 e/ W, d4 Bhair, and facial acne without enlargement of testi-
' E1 l$ t# Z; h% e8 k# u8 ecles, suggests peripheral or pseudopuberty.1-3 We  Z# F3 t/ f" ]0 Z2 ]+ Z6 z0 @% E
report a 16-month-old boy who presented with the
7 E  V% k  i1 n" Denlargement of the phallus and pubic hair develop-
2 G. ^  ?) Y& Q1 F, qment without testicular enlargement, which was due4 Q& e" C# i( y7 Z* \! v
to the unintentional exposure to androgen gel used by( k6 M7 n2 D0 _$ z( q' b
the father. The family initially concealed this infor-0 y0 q6 s6 R6 ]7 _5 \2 s! b7 D
mation, resulting in an extensive work-up for this. R2 p( ~; ?/ R5 m7 t4 l" F' g4 f
child. Given the widespread and easy availability of
% i+ N+ K9 A* r! D+ i  ~2 Ctestosterone gel and cream, we believe this is proba-+ N- K5 y$ k# i6 m( P5 R: _* S
bly more common than the rare case report in the, L1 t* v* k1 [! X/ I7 @
literature.4
- A" o' h! U- B5 f9 V/ QPatient Report
, B& g7 H2 Q3 T- Y- q& cA 16-month-old white child was referred to the
5 o. x: p* d: a4 a( h/ p1 E. q* Lendocrine clinic by his pediatrician with the concern
! v3 q. }4 B: zof early sexual development. His mother noticed. J# j; R2 R( H# O
light colored pubic hair development when he was0 c% e, }1 Q8 [* _) {4 e
From the 1Division of Pediatric Endocrinology, 2University of! c$ b1 [! q3 Z6 t5 F7 f
South Alabama Medical Center, Mobile, Alabama.4 S& O3 L: s. R+ n/ s, O
Address correspondence to: Samar K. Bhowmick, MD, FACE,% H4 Z7 h- ~2 {6 N5 ~$ r. `
Professor of Pediatrics, University of South Alabama, College of
- }- y3 h9 b: PMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
6 `/ b5 N$ k1 h% Qe-mail: [email protected].
7 E" v! W1 L* D, {* D5 M" [( Tabout 6 to 7 months old, which progressively became
9 \+ m/ i+ \, a. c; Rdarker. She was also concerned about the enlarge-
7 k5 i+ Q: v$ h# P2 bment of his penis and frequent erections. The child
" ?" F# c4 J' j* ?( ]$ mwas the product of a full-term normal delivery, with5 n  I/ V* F# A& C
a birth weight of 7 lb 14 oz, and birth length of* [* h: b" @% |# E. [! R
20 inches. He was breast-fed throughout the first year
/ `  @, s8 P; ]) V: H' k5 x% dof life and was still receiving breast milk along with
  Y* U& N  j# K6 F9 Y7 k/ _solid food. He had no hospitalizations or surgery,& `& b. V4 w7 X. {/ `6 @* n2 }
and his psychosocial and psychomotor development
$ }/ E9 c' x' Q8 \" ^* A+ }) Jwas age appropriate.  e# D, d+ o, _
The family history was remarkable for the father,
6 ^" x! w3 v& T) |who was diagnosed with hypothyroidism at age 16,
8 u& I& c9 F7 f$ F% j/ Hwhich was treated with thyroxine. The father’s5 n* U  q. S4 f3 ~
height was 6 feet, and he went through a somewhat
7 U) g/ \4 t$ |; Q5 v# v4 kearly puberty and had stopped growing by age 14.9 V6 b3 ?- d1 M& H/ z$ L
The father denied taking any other medication. The
. N$ a& b5 W. {child’s mother was in good health. Her menarche. x; m6 _$ R+ N7 }. S' K
was at 11 years of age, and her height was at 5 feet+ v! b; A( j3 D7 U  i* _- m4 r
5 inches. There was no other family history of pre-7 `1 J+ U9 H4 j9 [' p' Y7 K
cocious sexual development in the first-degree rela-
. t: X" M+ M3 x) a$ F/ ^tives. There were no siblings.
' ], K7 N) x+ i5 I# BPhysical Examination
' M2 \4 T# q+ uThe physical examination revealed a very active,
' O3 A0 I# z: n9 tplayful, and healthy boy. The vital signs documented4 \5 r  j9 P9 O* j
a blood pressure of 85/50 mm Hg, his length was
: V5 [0 ~- g% L( I% N3 \90 cm (>97th percentile), and his weight was 14.4 kg5 [2 N6 o' c/ }' R, e  A/ c
(also >97th percentile). The observed yearly growth4 ?. e! g+ P- f
velocity was 30 cm (12 inches). The examination of# @9 Z# s* Z1 o- W- K3 t$ c
the neck revealed no thyroid enlargement.0 q4 h/ |% Q1 |/ e# p7 R
The genitourinary examination was remarkable for( O  L2 H8 q+ J- r# o
enlargement of the penis, with a stretched length of( g5 z/ Y: \4 d  B5 K- n, `% S
8 cm and a width of 2 cm. The glans penis was very well. g4 G9 Q! P% j7 `- P
developed. The pubic hair was Tanner II, mostly around- w/ c: y0 S4 D8 ~; x# ^
540
" o' C( w/ O  j8 W/ b2 Vat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
3 v) A* C! r3 dthe base of the phallus and was dark and curled. The
5 h& d- D# M* O' k$ i) Wtesticular volume was prepubertal at 2 mL each.8 j2 @6 E* a6 u. s
The skin was moist and smooth and somewhat7 \# i' A! U9 w5 C" x
oily. No axillary hair was noted. There were no
& o7 |/ d7 W2 v  ]abnormal skin pigmentations or café-au-lait spots.
- ]2 C/ Y7 @4 p: O- E3 c/ TNeurologic evaluation showed deep tendon reflex 2+
3 t+ Z/ v6 m( y+ {- O# x# Abilateral and symmetrical. There was no suggestion
+ M* n$ Q" f2 ^: S6 F) }- U1 uof papilledema.8 i+ L2 ]) w1 \  T3 s
Laboratory Evaluation
5 U: U  }/ o- y* |  ]* |4 bThe bone age was consistent with 28 months by1 g( _4 c) M# w' t; j+ R$ j- \
using the standard of Greulich and Pyle at a chrono-
  v$ t7 U' Z" A6 |6 H$ Jlogic age of 16 months (advanced).5 Chromosomal" ]0 ]2 L+ z( @# T' }; i
karyotype was 46XY. The thyroid function test
; i/ q, ^! ^& _# Q/ B( Rshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
2 M" M; d" N  B7 _lating hormone level was 1.3 µIU/mL (both normal).' ?/ r3 x2 `1 W$ m
The concentrations of serum electrolytes, blood' g$ X4 g2 _# a5 _6 X' o, o: `
urea nitrogen, creatinine, and calcium all were
: @* F$ p" x$ @5 L3 E5 T7 J5 t. iwithin normal range for his age. The concentration
3 ~; y  |& n8 O) A, B% R9 Wof serum 17-hydroxyprogesterone was 16 ng/dL9 u: W, Z4 ^% |/ F
(normal, 3 to 90 ng/dL), androstenedione was 20- A; p0 o7 d9 W
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-1 `& A1 |! f2 X5 D  m1 K1 I
terone was 38 ng/dL (normal, 50 to 760 ng/dL),! r0 @, F; _% _  g! y8 }
desoxycorticosterone was 4.3 ng/dL (normal, 7 to: k& e. I% [; V8 U: f- `( }
49ng/dL), 11-desoxycortisol (specific compound S)
" y4 m( f4 i2 i8 K1 swas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-; K) O2 W+ R' v9 Y# a" y! p
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total: p" _( ?* X& ?) R4 u
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
) Q$ Q, g7 W3 a! {0 _and β-human chorionic gonadotropin was less than+ Q1 Q; ?9 ^6 e0 F: H% R9 d4 E1 g
5 mIU/mL (normal <5 mIU/mL). Serum follicular
% u" H# M. q" I- K' lstimulating hormone and leuteinizing hormone
9 A# [7 [: {5 ^" [) m4 R. S& V' ~concentrations were less than 0.05 mIU/mL
! y- w$ Q+ a) w! p( y(prepubertal).* A" i. q9 e5 K9 O& D/ R8 v
The parents were notified about the laboratory. d- N5 j% M& P: t, m1 ?
results and were informed that all of the tests were7 g+ N( ?8 f0 ^2 [& T: }# q
normal except the testosterone level was high. The
5 y( R1 ?, A* k: xfollow-up visit was arranged within a few weeks to9 }8 {, x: E! \8 V7 g3 j
obtain testicular and abdominal sonograms; how-
2 U# L# x( g$ Rever, the family did not return for 4 months.
, e1 {& \5 {" ^: @Physical examination at this time revealed that the" B/ Y. T6 J. O3 s
child had grown 2.5 cm in 4 months and had gained
) w5 A/ c0 v2 r$ W2 kg of weight. Physical examination remained4 M& D) F, b) w
unchanged. Surprisingly, the pubic hair almost com-3 s: K; ]- f# y% P. y4 `% S
pletely disappeared except for a few vellous hairs at
% J2 L9 U7 s7 [9 _2 gthe base of the phallus. Testicular volume was still 25 y5 g7 g$ n: V4 O
mL, and the size of the penis remained unchanged.9 F" ]4 N8 s( E1 g3 \8 ^3 T. i1 a' G
The mother also said that the boy was no longer hav-
! x1 e0 b8 o. b# J0 ging frequent erections.
, m# S8 {; I6 y$ n( [" kBoth parents were again questioned about use of
* p0 x! }6 }  \, E& O! Uany ointment/creams that they may have applied to
. O3 w7 b# a" R9 J4 `* Sthe child’s skin. This time the father admitted the" w2 ~; V$ c# n- k# R1 c
Topical Testosterone Exposure / Bhowmick et al 541# N! [5 e  g* Z3 H( {% P
use of testosterone gel twice daily that he was apply-! f8 x2 ^( N" w
ing over his own shoulders, chest, and back area for
% s) s' i" |7 i1 }) G5 Ma year. The father also revealed he was embarrassed
: }- t3 p, h4 Z2 Gto disclose that he was using a testosterone gel pre-' D2 F/ k" _  o5 h
scribed by his family physician for decreased libido3 Q; N! H2 _' b6 n5 v* _5 Z
secondary to depression.+ B' N2 d- u+ X  {8 J+ |6 }4 ?
The child slept in the same bed with parents./ T$ ~+ l* f" y
The father would hug the baby and hold him on his, m9 ?9 i1 c: o; l5 r8 _+ c
chest for a considerable period of time, causing sig-9 \# Z6 v# V% C/ M
nificant bare skin contact between baby and father.
6 f0 Y) x$ z! j! V6 pThe father also admitted that after the phone call,
9 k) T! @% j- A9 e' _, F( mwhen he learned the testosterone level in the baby* I* U& l  e. g# B
was high, he then read the product information
" p) x; Z0 H, c  {" Hpacket and concluded that it was most likely the rea-
  m- V0 {3 J/ s& P5 t! yson for the child’s virilization. At that time, they
: X2 j5 v& O: A# qdecided to put the baby in a separate bed, and the  L! s4 M% v3 v* l  l
father was not hugging him with bare skin and had
0 y9 u. c; n# b- B0 p3 m  Xbeen using protective clothing. A repeat testosterone  U) U+ D3 w+ E2 o& k$ `4 m
test was ordered, but the family did not go to the
) v  ^4 ]. P! V# f/ ^- Ilaboratory to obtain the test.3 \. Q9 X6 k# p: j0 k4 ^
Discussion9 ?( u6 i$ \" N2 M
Precocious puberty in boys is defined as secondary/ s; ]3 R! e- e  ]6 a' ]6 _& B* Z
sexual development before 9 years of age.1,46 N( h4 J- s* l  q: {# i
Precocious puberty is termed as central (true) when
0 _4 B  ]& H; K) V/ q+ @- c9 |it is caused by the premature activation of hypo-+ t4 {. w$ t1 f5 V, V. G5 V) Z2 I
thalamic pituitary gonadal axis. CPP is more com-
3 Q) j, i! |: ~* w3 \mon in girls than in boys.1,3 Most boys with CPP- |0 S8 l" {9 R% T4 Z) ~
may have a central nervous system lesion that is* @1 p! o3 ?; N9 J
responsible for the early activation of the hypothal-
1 l! O5 `) K$ G8 F4 b* \amic pituitary gonadal axis.1-3 Thus, greater empha-: I9 V/ T, n* c& U
sis has been given to neuroradiologic imaging in
4 f2 A& L, a& {7 Y3 ^9 t0 aboys with precocious puberty. In addition to viril-
# i4 }+ e( Q2 c) L/ _0 Vization, the clinical hallmark of CPP is the symmet-
8 L( A1 `8 M( Hrical testicular growth secondary to stimulation by' o( h+ b$ `. w" C% n
gonadotropins.1,37 d4 \- x6 ]. A2 Q! a/ n/ V
Gonadotropin-independent peripheral preco-
/ Y: i1 t! \5 i0 f: V$ K( F1 Mcious puberty in boys also results from inappropriate
% a2 G6 X5 G0 Landrogenic stimulation from either endogenous or5 R0 w: k5 e5 d
exogenous sources, nonpituitary gonadotropin stim-3 T' r$ c% s# a$ I6 T$ D0 Q
ulation, and rare activating mutations.3 Virilizing
2 ~5 U5 f* C0 {2 D8 D5 jcongenital adrenal hyperplasia producing excessive
6 b, d) ?# Y: Fadrenal androgens is a common cause of precocious: Z( J( t/ J9 c1 i
puberty in boys.3,4* o: |/ s" U, A% L8 W
The most common form of congenital adrenal
  \4 t0 W  k4 N( [; b9 khyperplasia is the 21-hydroxylase enzyme deficiency.+ u  }; q( s- d$ ?$ c; C  z
The 11-β hydroxylase deficiency may also result in$ E2 V3 `  n2 K: T! j
excessive adrenal androgen production, and rarely,/ q8 j7 Q* D# |9 L
an adrenal tumor may also cause adrenal androgen
$ V- p, {% d8 P. K2 J3 G5 R, U3 cexcess.1,3% M6 a$ g7 O0 n0 H/ K% _8 P
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
$ B1 o. R4 C9 ]. o4 D0 ^542 Clinical Pediatrics / Vol. 46, No. 6, July 20077 L$ C- t# |& N0 J9 ^( X
A unique entity of male-limited gonadotropin-) p' {& c# e. F' U9 y5 X0 t
independent precocious puberty, which is also known8 {* Q2 }; T2 j- y1 f5 I2 a4 z
as testotoxicosis, may cause precocious puberty at a" }% T/ a6 E% G4 b$ |; `( s$ J: \9 i
very young age. The physical findings in these boys
2 I6 @# T2 s; F& E( dwith this disorder are full pubertal development,4 B7 {6 h6 k. X- ^8 M
including bilateral testicular growth, similar to boys5 I8 O2 ~( N  [; r& }% e
with CPP. The gonadotropin levels in this disorder7 w( v! @9 ^4 x) V) ~; S* H. e
are suppressed to prepubertal levels and do not show
/ a4 Q" q7 ]7 i! g% dpubertal response of gonadotropin after gonadotropin-
% i- `& u% ~0 ?releasing hormone stimulation. This is a sex-linked
4 G: b* o. |  [, F: O! H8 Y$ rautosomal dominant disorder that affects only
  m  k2 e5 V5 |6 S, Emales; therefore, other male members of the family
$ Q$ N; W2 ?5 r( ]may have similar precocious puberty.3
. E+ k# d5 x1 J4 t3 zIn our patient, physical examination was incon-
+ j) L9 H3 ?( s! z! G2 bsistent with true precocious puberty since his testi-
9 s, o5 }( i7 h4 x3 _: Dcles were prepubertal in size. However, testotoxicosis
5 Q" }# d' A- y3 x1 ^4 X2 lwas in the differential diagnosis because his father0 _7 ~% `/ v: u; C5 S! U
started puberty somewhat early, and occasionally,
+ Y3 j3 C  T5 ]7 z+ I; f# T3 Stesticular enlargement is not that evident in the1 u1 C6 Z- \8 [- S& [0 H( U# I
beginning of this process.1 In the absence of a neg-# Q; b: S6 o) K5 W$ Y
ative initial history of androgen exposure, our9 L$ O/ O1 J! ]3 H. k4 v
biggest concern was virilizing adrenal hyperplasia,( s! T$ b0 L; Q, o
either 21-hydroxylase deficiency or 11-β hydroxylase: x; g) E! T4 D3 v! o3 \
deficiency. Those diagnoses were excluded by find-
# p' L( a: y# v, E9 b1 cing the normal level of adrenal steroids.4 A" m0 @, n; j
The diagnosis of exogenous androgens was strongly* T0 S' w5 j" k) B0 P
suspected in a follow-up visit after 4 months because
5 ~8 J) E  P' u, |; _& `the physical examination revealed the complete disap-; R- E8 l4 [# O) c: e+ j
pearance of pubic hair, normal growth velocity, and3 c* x! G, e2 d; d2 h7 ~
decreased erections. The father admitted using a testos-
4 s6 y+ v$ p$ I1 rterone gel, which he concealed at first visit. He was) b: y6 d8 b( r2 W
using it rather frequently, twice a day. The Physicians’9 G  n$ f' [4 I/ T4 K% O- v4 y
Desk Reference, or package insert of this product, gel or% ?* p; `. [- J' ~# p9 S0 p
cream, cautions about dermal testosterone transfer to2 F$ H5 l: _2 i  d1 P/ y' F7 I! }
unprotected females through direct skin exposure.
, X* q, D; J4 O! ~& o) ~Serum testosterone level was found to be 2 times the8 _2 M: |; I* G7 h/ o3 e
baseline value in those females who were exposed to
  h, M3 v, @) m6 P( a& S6 o' }. meven 15 minutes of direct skin contact with their male; l1 B$ d# T% g& [
partners.6 However, when a shirt covered the applica-
6 Y% E. R* X- S* H% F, Ktion site, this testosterone transfer was prevented.
) \+ Z! B3 r- i0 ^* bOur patient’s testosterone level was 60 ng/mL,+ G, l9 j+ v! a4 l3 h" ~# U
which was clearly high. Some studies suggest that
9 g' p3 Z. h) z' N4 `+ jdermal conversion of testosterone to dihydrotestos-, J+ t! |( O# H4 Q
terone, which is a more potent metabolite, is more
/ K( p! D' [: Z8 o* Nactive in young children exposed to testosterone
% x0 U  ~) d0 ]exogenously7; however, we did not measure a dihy-
. b8 [) c6 G" h# _; i; B6 sdrotestosterone level in our patient. In addition to* _- b% ]$ N+ `8 A
virilization, exposure to exogenous testosterone in
6 l' m1 a* L% z) H; pchildren results in an increase in growth velocity and, Q4 R; k' Z: o9 X1 P# l
advanced bone age, as seen in our patient.
, J- q" q  i2 ^! cThe long-term effect of androgen exposure during0 h0 {. P3 o, {( K0 H* \
early childhood on pubertal development and final
" \9 G  N# V+ J3 [3 wadult height are not fully known and always remain
% U% b& ~+ ]( |8 la concern. Children treated with short-term testos-
8 Y; u% |% q$ b4 F) o7 |9 ?6 Mterone injection or topical androgen may exhibit some8 D4 U; z+ N8 p
acceleration of the skeletal maturation; however, after3 F2 ^. @, `2 i1 z  V
cessation of treatment, the rate of bone maturation
  u. a% r5 S. A- Y- O% mdecelerates and gradually returns to normal.8,9" \' v4 L  `( L, Z
There are conflicting reports and controversy
8 g. b& O9 m% H# O; s0 Gover the effect of early androgen exposure on adult: F; _; y7 q. ]) }
penile length.10,11 Some reports suggest subnormal
5 C8 Z" x" j- fadult penile length, apparently because of downreg-
4 _, z  k7 W# U# V! P# ^! d- v3 |ulation of androgen receptor number.10,12 However,) G* I3 a) S; @* Q* ]! _  Z& Z$ y
Sutherland et al13 did not find a correlation between
2 z2 o$ x7 V# [; t1 vchildhood testosterone exposure and reduced adult% d$ n8 f/ p/ P3 Q& k- E
penile length in clinical studies.7 b6 `$ C$ I; l/ l6 d
Nonetheless, we do not believe our patient is
6 m" l6 H8 {8 L+ O/ ]going to experience any of the untoward effects from
' F. s; ]+ t' H8 v5 L+ d$ ttestosterone exposure as mentioned earlier because
9 k( i% B4 w2 y5 kthe exposure was not for a prolonged period of time.0 z* @2 d; z2 j1 A& P7 z0 k
Although the bone age was advanced at the time of2 o. F5 @% d& P/ R2 C% ~' }9 ]
diagnosis, the child had a normal growth velocity at
( X- N* k  r  a: M0 V7 P2 E; Athe follow-up visit. It is hoped that his final adult
  E7 Y) o* K  x" x" @height will not be affected.+ }0 S& s8 H9 z( q. p0 O
Although rarely reported, the widespread avail-
" D" W& r) l* l! X' ~9 tability of androgen products in our society may
9 E/ f% N# n3 j) P3 d! G" Findeed cause more virilization in male or female
! o' ?' \% D. _- uchildren than one would realize. Exposure to andro-
+ _; d& X: }( Q( T" f8 ~gen products must be considered and specific ques-
0 @; O' m8 t+ G+ ktioning about the use of a testosterone product or4 h# G0 h. d# S0 \( _  _6 m$ u
gel should be asked of the family members during
2 n1 H4 i0 U& l6 _9 I9 _) a7 p4 g- }the evaluation of any children who present with vir-
! k& i2 z$ }9 Qilization or peripheral precocious puberty. The diag-
& s+ D! _; o# @! f5 ~0 R1 e# O/ _nosis can be established by just a few tests and by
3 G5 `. v. L! l3 i* T6 S& Z, U  Xappropriate history. The inability to obtain such a7 l# E" ?5 v" q4 E
history, or failure to ask the specific questions, may7 A- X/ P9 B/ S- f0 T2 F
result in extensive, unnecessary, and expensive
0 P/ q6 i6 t& t1 Pinvestigation. The primary care physician should be
! K. _- C1 E; O$ s0 x6 s& ?' Kaware of this fact, because most of these children
0 D8 Z+ Y9 p- Gmay initially present in their practice. The Physicians’3 q: C% V0 d" m
Desk Reference and package insert should also put a
5 Z5 C; X3 a& B3 |( x, P2 cwarning about the virilizing effect on a male or' _( Z& {! ^) ?% P4 c6 @3 s
female child who might come in contact with some-
! n6 u5 h9 \8 I" x( yone using any of these products.( Y3 `/ J. p; ?; u7 p7 B
References
" F+ V  E" s, O' u& T, @- V1. Styne DM. The testes: disorder of sexual differentiation
* w" z4 O: |; i6 t# fand puberty in the male. In: Sperling MA, ed. Pediatric
1 P9 Q0 X# [5 C# ^- C1 K% y6 ?Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;$ F" R- _5 |/ N
2002: 565-628.* m. T2 z0 K% Q
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious0 R3 f6 n# V! f7 \6 w% ^; A) _
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old$ g" s2 i! ~; c2 G
Boy Induced by Indirect Topical$ n! h% C* J8 p; C* k
Exposure to Testosterone  V& g8 F3 i& U6 h  \3 b
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2- O, C( Z8 `( S- {/ N
and Kenneth R. Rettig, MD1' M% ]7 P+ k( d; l
Clinical Pediatrics
; X8 @6 R  H2 T+ V* \% G8 `( T& rVolume 46 Number 6
  ~* N$ O+ {. Z* ZJuly 2007 540-543
4 h, P% t# W& F3 r4 s© 2007 Sage Publications
( O- S; w8 h* ]- h10.1177/0009922806296651
$ p( ?1 x8 ~* M, ]8 S/ u* ]* b( {$ ^& Zhttp://clp.sagepub.com0 T- X! X+ T. ^. h1 s
hosted at) x% ^6 Z( V+ c5 R/ u6 _2 _
http://online.sagepub.com/ H- X! s( _, F0 [
Precocious puberty in boys, central or peripheral,0 f- \% V& ]5 _- ]. h
is a significant concern for physicians. Central
5 {5 E# m3 ~8 A  n9 cprecocious puberty (CPP), which is mediated: K: @1 t: [& P3 n  _
through the hypothalamic pituitary gonadal axis, has3 ~! K+ L% Z, C4 v, Y
a higher incidence of organic central nervous system
4 s4 l4 c1 Q5 O/ z) ^lesions in boys.1,2 Virilization in boys, as manifested( G) j9 A( w) n7 P' |7 H
by enlargement of the penis, development of pubic
1 b% m% Z' D  E' s. P( M* h8 nhair, and facial acne without enlargement of testi-
4 D, ~* `: w! Z7 i, I% pcles, suggests peripheral or pseudopuberty.1-3 We& B, ]- G2 e5 F6 l" k# N5 b
report a 16-month-old boy who presented with the
  G  k6 q* _# s. [# Fenlargement of the phallus and pubic hair develop-: e: x/ w7 s: p  f
ment without testicular enlargement, which was due9 g' r' K+ {& O' a* T, y
to the unintentional exposure to androgen gel used by
# ?9 Y4 R. U- z4 Q/ @" T: pthe father. The family initially concealed this infor-
# z7 e$ S, Z4 F/ Y- emation, resulting in an extensive work-up for this+ k! G$ x0 F2 A' p- S
child. Given the widespread and easy availability of
3 ~2 K- ]8 U( V! u/ \; ?testosterone gel and cream, we believe this is proba-# Q6 Y1 w) K) e) p8 Y" L' H
bly more common than the rare case report in the
& G8 n9 W: V+ r: U: z+ Y1 r4 Tliterature.4
% w4 j+ D7 d8 m! x- ?+ u7 }, hPatient Report
/ g2 h- i, c! o7 G# FA 16-month-old white child was referred to the& F( y9 |  }: A' N
endocrine clinic by his pediatrician with the concern# r+ T$ \8 \3 B. C, t9 r: e
of early sexual development. His mother noticed
' X1 M0 W/ E# D) t) a& e, k3 Wlight colored pubic hair development when he was
6 J! ^" E3 u+ d& K3 I9 WFrom the 1Division of Pediatric Endocrinology, 2University of
" a' ^3 m5 y1 q6 pSouth Alabama Medical Center, Mobile, Alabama.$ S( D! d) G* p/ @0 v# d+ D
Address correspondence to: Samar K. Bhowmick, MD, FACE,
: q: ?. a% {9 [  F1 S( p: h4 S* cProfessor of Pediatrics, University of South Alabama, College of6 ~. d; h! E& M! \# K" S! w
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;( N% z: }% r6 U1 [
e-mail: [email protected].* e) {% H) h3 k* m
about 6 to 7 months old, which progressively became
% Q& k' ^2 \6 L+ U1 d. [/ v# Fdarker. She was also concerned about the enlarge-1 o& Y8 j7 d# j' t1 f) I8 y5 u/ o
ment of his penis and frequent erections. The child
0 T/ i* Y  g. T1 w. l3 Jwas the product of a full-term normal delivery, with
  \/ f: c+ e7 [3 sa birth weight of 7 lb 14 oz, and birth length of
& h" ]4 Q7 P. _9 U: ^3 ^20 inches. He was breast-fed throughout the first year
5 x3 [! y- \; Y1 j. fof life and was still receiving breast milk along with+ ^& F. n! R" _, e* B
solid food. He had no hospitalizations or surgery,
- q/ T4 b& x% K9 m0 W$ Nand his psychosocial and psychomotor development- z& f& v/ R, s' V- O! q# a/ [6 R
was age appropriate.
7 M% d! W$ A8 b  u& h/ a0 zThe family history was remarkable for the father,6 {5 o6 x7 P7 t. t3 Z( j: K# G
who was diagnosed with hypothyroidism at age 16,5 t3 l7 ^( E4 c' `' N
which was treated with thyroxine. The father’s. n; G9 p( q, y$ {3 _& z: i: ^& H
height was 6 feet, and he went through a somewhat
$ c) T* Y) y( R, C6 g: M: R) `early puberty and had stopped growing by age 14.( f8 y4 _9 T( `7 B2 b4 l+ U  J" _
The father denied taking any other medication. The
  O% J5 C7 u. K+ i9 F: Hchild’s mother was in good health. Her menarche
; U$ g' g+ m  t$ P1 X3 `: v. K+ zwas at 11 years of age, and her height was at 5 feet
, c2 P0 Z$ I8 h+ H3 y4 y# `5 inches. There was no other family history of pre-1 V; u5 r' v8 R. D
cocious sexual development in the first-degree rela-
# l9 C+ k  S; V, s# J  e/ F+ `% Ntives. There were no siblings.* |8 N4 F7 l$ C4 I( _  E* m8 f
Physical Examination
5 H& ]+ i: c7 j% k! }- r! C( kThe physical examination revealed a very active,- W  {0 s+ ]! D  C- B
playful, and healthy boy. The vital signs documented: c8 m* _$ {, o! q( c3 d
a blood pressure of 85/50 mm Hg, his length was/ k' W) ]8 W& Y0 E+ u3 t" s
90 cm (>97th percentile), and his weight was 14.4 kg
! `4 x, L) v( g, D+ A. O4 c& J2 n(also >97th percentile). The observed yearly growth  O3 _" t* b( E8 r2 T
velocity was 30 cm (12 inches). The examination of9 X. e$ y8 e( F3 J8 ?3 G) X
the neck revealed no thyroid enlargement.
$ T" L: T, c) cThe genitourinary examination was remarkable for3 t" y# W* s1 f
enlargement of the penis, with a stretched length of
1 {; C- H0 N7 A$ u, z) a8 cm and a width of 2 cm. The glans penis was very well
! Q3 }# |: O5 D2 Q$ M* A* J! g; Ydeveloped. The pubic hair was Tanner II, mostly around; o, B2 B! P: h) H% h" j
540  p0 i4 @( n1 j
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
$ d9 U3 h: a) v! F( D9 Qthe base of the phallus and was dark and curled. The
( x7 B3 U+ D! w( P. otesticular volume was prepubertal at 2 mL each.) M: g; f% m. m, L5 g* w+ Z
The skin was moist and smooth and somewhat
6 a  Q& m; E" @) U# ?+ Noily. No axillary hair was noted. There were no5 _- o$ d* N# Z& U) y" J3 @
abnormal skin pigmentations or café-au-lait spots.
! \9 |" |! Z! _" l/ R0 x* b: l: z" BNeurologic evaluation showed deep tendon reflex 2+) r$ t: u& U% [: N
bilateral and symmetrical. There was no suggestion; X, ~' ^, N* `2 m6 O
of papilledema.
2 }% u/ z( g7 @+ |  T5 o6 bLaboratory Evaluation- t  B* i6 W9 o' O1 x; [
The bone age was consistent with 28 months by
- O/ I. x% V& _0 i& t6 eusing the standard of Greulich and Pyle at a chrono-# F  g% A8 L$ @8 J
logic age of 16 months (advanced).5 Chromosomal& o  |* }& h& L+ @2 b
karyotype was 46XY. The thyroid function test, Z* v  l, Q/ W" [0 n# B
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
3 [3 S/ x. z) M4 I! nlating hormone level was 1.3 µIU/mL (both normal).7 o! N) M: C/ A# [. C! F
The concentrations of serum electrolytes, blood
- M' M5 }' e" x0 b1 {" V8 Zurea nitrogen, creatinine, and calcium all were, k1 N4 Y. H* X- \& S  r
within normal range for his age. The concentration
9 v  O, \3 }( Q" s2 \of serum 17-hydroxyprogesterone was 16 ng/dL7 F: W' D7 A& C/ z
(normal, 3 to 90 ng/dL), androstenedione was 20& Y' n$ ]8 ~8 I
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
' W% |. d8 L3 h. h8 s' @& |' Fterone was 38 ng/dL (normal, 50 to 760 ng/dL),' q$ K: w- a( w/ j$ H. |
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
1 X' l' G; g2 `49ng/dL), 11-desoxycortisol (specific compound S)2 v" t3 b2 R, K6 I# D
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-; K& b' f8 U3 d! y0 X
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total- e& C. R' Y$ B0 O# z( C+ O' }
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
) P1 a1 [& }; iand β-human chorionic gonadotropin was less than: _: F3 O. J/ t' a/ U
5 mIU/mL (normal <5 mIU/mL). Serum follicular
6 `3 \! p4 T  j; Pstimulating hormone and leuteinizing hormone
2 ~+ t$ H/ [+ m$ B9 H" B( ?concentrations were less than 0.05 mIU/mL) ~' r/ b# E, r0 r
(prepubertal).
" d' b. A0 J. W) C; m% P4 g: D! DThe parents were notified about the laboratory8 I  q7 w3 G6 w1 L2 L/ q6 l3 f1 h. D
results and were informed that all of the tests were0 M  M) X# X$ q0 P1 m$ @$ x
normal except the testosterone level was high. The
+ J' T# }3 z2 o# g! q! h" Nfollow-up visit was arranged within a few weeks to" |# v: v6 G4 H; X- b
obtain testicular and abdominal sonograms; how-
2 P. Y/ T! z# F/ Wever, the family did not return for 4 months.
9 k! l8 |" y5 ^6 z, i, s( P. LPhysical examination at this time revealed that the
5 _. B  I6 N8 N! f4 _child had grown 2.5 cm in 4 months and had gained
9 f3 n; a, U' p# N0 p2 kg of weight. Physical examination remained
5 t, j' Q; A8 V! j# F5 O- Funchanged. Surprisingly, the pubic hair almost com-
% W& w% N7 \& ]6 upletely disappeared except for a few vellous hairs at
! L$ q/ w/ \6 I" g% pthe base of the phallus. Testicular volume was still 2
" O3 {5 o. ?  c) B2 e' X2 D2 K1 }mL, and the size of the penis remained unchanged.
1 q2 E$ P  z# M. wThe mother also said that the boy was no longer hav-
  C# p# G" b) D, N% W( Ving frequent erections.+ N! }3 X4 A6 `2 T4 E; e
Both parents were again questioned about use of
, E9 }% W3 ?) Gany ointment/creams that they may have applied to! x* A( J7 G  z
the child’s skin. This time the father admitted the  K+ t$ ^4 @$ J0 x
Topical Testosterone Exposure / Bhowmick et al 541/ k* I6 S7 T5 y5 \6 `
use of testosterone gel twice daily that he was apply-- g; ^- `# Y( O8 I
ing over his own shoulders, chest, and back area for5 n8 G+ R9 [3 j% @# d! H& J
a year. The father also revealed he was embarrassed* y% Z/ `# t/ `6 r. `: q/ t/ h* H
to disclose that he was using a testosterone gel pre-4 s3 O" @( g0 [8 _! E. ^) R5 A
scribed by his family physician for decreased libido
! i% z; O* ~* Z9 y) S. f( m0 @secondary to depression.1 j4 v( R7 u7 q
The child slept in the same bed with parents.  y) b9 r- n2 |4 F: h
The father would hug the baby and hold him on his
  M; @/ e% {) v- [: Z8 Echest for a considerable period of time, causing sig-! L- y+ H) T6 p/ p4 J1 N( n  G
nificant bare skin contact between baby and father.( y* p& Z0 R2 I4 V* q' |( j
The father also admitted that after the phone call,% H7 L+ x0 G* T6 V
when he learned the testosterone level in the baby* i) s9 A1 c) W' {5 a6 T7 b! G% u( {
was high, he then read the product information
8 g* A. X2 w2 _- Ppacket and concluded that it was most likely the rea-
% N! ~  Y) t# ~son for the child’s virilization. At that time, they* u5 Y  v$ m& C+ h& t. Q- @
decided to put the baby in a separate bed, and the
& r5 P6 s" D- r9 Kfather was not hugging him with bare skin and had
, x% I- B1 b+ rbeen using protective clothing. A repeat testosterone. |5 u# J: A, U+ d0 T% W
test was ordered, but the family did not go to the  [& h1 X; |9 i  u1 i( g
laboratory to obtain the test.
) w  z' p- ~6 Q1 Z+ w8 U. lDiscussion
: d; F! }$ D2 c2 l8 v/ d" gPrecocious puberty in boys is defined as secondary: B' L) Y& w6 R' r
sexual development before 9 years of age.1,4. O9 ]% v0 k" V( C1 J  B5 Z
Precocious puberty is termed as central (true) when
  T. @2 S# t) p2 Q/ \( e, k" Pit is caused by the premature activation of hypo-
  M/ \& @, N5 }4 w1 c) u; E: Zthalamic pituitary gonadal axis. CPP is more com-
# u3 w) T  U9 _( Q8 kmon in girls than in boys.1,3 Most boys with CPP
! v) v" i* a  t# Emay have a central nervous system lesion that is
2 A7 }9 F5 W0 q/ _responsible for the early activation of the hypothal-
' d; M2 b- q* g( w4 B9 K) a8 t  oamic pituitary gonadal axis.1-3 Thus, greater empha-
& t/ K' S# u7 csis has been given to neuroradiologic imaging in. q! b+ k1 w6 z; N* s
boys with precocious puberty. In addition to viril-
- F- m0 l  f7 x" t3 Y6 |; xization, the clinical hallmark of CPP is the symmet-( l/ o1 t& p" h9 d. s- B
rical testicular growth secondary to stimulation by2 b# d0 v6 e7 l! b7 Q  S$ V
gonadotropins.1,3
' h9 S3 T% C& |5 @7 m, MGonadotropin-independent peripheral preco-6 L# w) p6 G# x# G! l
cious puberty in boys also results from inappropriate" x2 T& u, g9 z5 t7 a) h
androgenic stimulation from either endogenous or% y. \% v+ t+ X
exogenous sources, nonpituitary gonadotropin stim-- a2 e  O% E* K4 z6 [' o
ulation, and rare activating mutations.3 Virilizing
( I( Y9 ^$ u& Bcongenital adrenal hyperplasia producing excessive
4 w% v1 O7 m6 y5 W" c+ D; R# @adrenal androgens is a common cause of precocious
# @$ v$ b& n+ J0 L" ^puberty in boys.3,4
; a; i, k  @$ F; Y) c, ?* v/ o: wThe most common form of congenital adrenal
! B% _6 A' y) X$ k: f- e1 Shyperplasia is the 21-hydroxylase enzyme deficiency.0 j, H4 \$ b, b# W6 Q
The 11-β hydroxylase deficiency may also result in
8 \+ x/ R# f& g1 z2 q- A: {* f1 Wexcessive adrenal androgen production, and rarely,
, N( U2 Y( m2 c- @  G8 han adrenal tumor may also cause adrenal androgen( v8 l2 F/ V+ b) F
excess.1,3
: Z6 }1 g3 h% K: F& N4 z, b- V3 Rat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from& e- K4 S3 e- g
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007, r' W% |& |% x
A unique entity of male-limited gonadotropin-
! J1 y% c1 F1 y. x) Mindependent precocious puberty, which is also known$ Q3 r8 V. H& o2 J, f6 W0 u
as testotoxicosis, may cause precocious puberty at a
+ g+ Z/ `" ^' H% E$ {very young age. The physical findings in these boys
! R# T: T. D8 P0 X0 e& Fwith this disorder are full pubertal development,
* l! }3 m& j8 e" `: D$ J1 |* Sincluding bilateral testicular growth, similar to boys
0 m1 I* K% \  G$ I! nwith CPP. The gonadotropin levels in this disorder5 ]( B5 _& A) \
are suppressed to prepubertal levels and do not show8 @) D/ b4 u2 {$ H5 V5 v
pubertal response of gonadotropin after gonadotropin-
( z6 f' b" D3 K8 A' [releasing hormone stimulation. This is a sex-linked. S: Z& N9 _: L8 P4 e5 o" o0 g
autosomal dominant disorder that affects only
) z$ L- y7 W$ f6 _males; therefore, other male members of the family
  i  m+ y' D, j9 \. o. y; Smay have similar precocious puberty.3, S& s- l5 I9 \2 `
In our patient, physical examination was incon-; o! j1 ?7 d4 F/ \: g/ J
sistent with true precocious puberty since his testi-
2 S# T/ _4 ]! ~: X& d  z8 Lcles were prepubertal in size. However, testotoxicosis
& S7 d3 }' W/ ]" R6 O4 u4 J( l0 bwas in the differential diagnosis because his father" }& c6 J5 y# a. m
started puberty somewhat early, and occasionally,
' B& W+ z: s8 c! u$ Ptesticular enlargement is not that evident in the1 _/ d, K6 H! p2 _1 P' o( c
beginning of this process.1 In the absence of a neg-7 b# t# H# `' v% n; Y( y
ative initial history of androgen exposure, our/ X2 U: m  p9 J' C: b
biggest concern was virilizing adrenal hyperplasia,
- Q5 I, W2 h" t. o# D* X$ ]either 21-hydroxylase deficiency or 11-β hydroxylase5 @9 V) W9 m: k" D* h6 o
deficiency. Those diagnoses were excluded by find-
! Y% i, P6 ?0 \ing the normal level of adrenal steroids.
- D1 U6 J* B1 }9 A3 N# eThe diagnosis of exogenous androgens was strongly2 B8 ~/ g+ \0 r2 m, j2 M( Q
suspected in a follow-up visit after 4 months because, _6 p. h# @+ d7 N6 s* v$ A6 |& k
the physical examination revealed the complete disap-  G1 L3 N9 ~4 }* a: O( d& r# v
pearance of pubic hair, normal growth velocity, and
+ f) a; H7 l/ ~decreased erections. The father admitted using a testos-! p. _! m# f( m( c: t
terone gel, which he concealed at first visit. He was
5 s: b' a' {, T* o6 i0 e; }using it rather frequently, twice a day. The Physicians’& a! r* _. i  e
Desk Reference, or package insert of this product, gel or0 P. k- d' V# s! w; a6 T' F/ R1 c
cream, cautions about dermal testosterone transfer to+ ^" J+ H- ~8 T, a
unprotected females through direct skin exposure.( Z% L2 |1 m; F# k# |
Serum testosterone level was found to be 2 times the; b: _) V. G/ W) n3 y+ U% @
baseline value in those females who were exposed to1 s% Z3 a& g( U* C# U; T
even 15 minutes of direct skin contact with their male
: M. i$ V8 g) W0 [# @2 rpartners.6 However, when a shirt covered the applica-
+ u4 e0 I+ G5 l+ k0 X8 r/ dtion site, this testosterone transfer was prevented.
! ?. l$ B1 ^, y' N/ KOur patient’s testosterone level was 60 ng/mL,
  G, k6 q4 X: j' j( u. `( vwhich was clearly high. Some studies suggest that
7 }5 ]5 d% d$ w6 A2 w9 V  h; Zdermal conversion of testosterone to dihydrotestos-
7 o3 Z9 D+ s* ~8 p% A  R- eterone, which is a more potent metabolite, is more
5 Y1 Z6 x. K  u, @5 P1 x4 T+ ?8 q3 Vactive in young children exposed to testosterone* M* h4 v' l5 J$ p
exogenously7; however, we did not measure a dihy-2 Q6 \/ `$ p( V4 M
drotestosterone level in our patient. In addition to- y, I/ }, V3 N' C. ?
virilization, exposure to exogenous testosterone in0 j+ o7 H$ J4 {# z( {$ |
children results in an increase in growth velocity and
8 x( Z: P* e3 }+ s! nadvanced bone age, as seen in our patient.
7 F7 ^: j$ y3 d: zThe long-term effect of androgen exposure during
3 }* N6 S9 y) g5 e& _# |" Uearly childhood on pubertal development and final8 E4 M+ J- O. E# j2 J- B% C
adult height are not fully known and always remain# d% T9 H: F0 Q+ D
a concern. Children treated with short-term testos-8 h; y% N5 v9 V4 U* d
terone injection or topical androgen may exhibit some9 S+ W$ S8 |1 @+ O% g  b, V
acceleration of the skeletal maturation; however, after5 J' U. b# i1 T
cessation of treatment, the rate of bone maturation
) M1 B& w  f  c3 u6 I1 pdecelerates and gradually returns to normal.8,9
% _# i' Z  w6 I4 ~$ A: JThere are conflicting reports and controversy
( t% K) b0 _. F! w2 K# i; ?- j3 v  Bover the effect of early androgen exposure on adult7 i0 E7 m( p8 W6 P* @
penile length.10,11 Some reports suggest subnormal' k: u) ?' I# T; b. {% z! p
adult penile length, apparently because of downreg-
1 v+ A9 R1 Y1 o6 G# r* wulation of androgen receptor number.10,12 However,
- b7 J2 @2 G$ S. v# |Sutherland et al13 did not find a correlation between4 f: _$ S! c2 w6 {8 M
childhood testosterone exposure and reduced adult# b! x0 N3 {0 g6 T5 j; x
penile length in clinical studies.5 t' R4 p% }- d/ h+ t$ }
Nonetheless, we do not believe our patient is& v: B2 r/ F3 o8 @" W
going to experience any of the untoward effects from
, Q* g. t) Z/ E3 l( m+ ptestosterone exposure as mentioned earlier because
7 r2 O7 h- g+ j( Nthe exposure was not for a prolonged period of time.
: z5 N8 O. j8 ~& {: RAlthough the bone age was advanced at the time of$ U! I6 u0 a5 o: ?# E
diagnosis, the child had a normal growth velocity at
8 [* w2 t$ w7 c" Xthe follow-up visit. It is hoped that his final adult0 g( d* m  H4 A" F+ {  F/ p& h
height will not be affected.
0 }- q: Z6 R. A5 dAlthough rarely reported, the widespread avail-) w# e( y) ]" A( r/ E! k
ability of androgen products in our society may
. y8 j' s+ b" A8 W1 ~6 _/ Vindeed cause more virilization in male or female
# K& [1 w2 G4 h+ F: D, Rchildren than one would realize. Exposure to andro-& n; w8 ?2 Y+ y4 ^. p& B* m+ e
gen products must be considered and specific ques-
' @  ~/ l3 D. Btioning about the use of a testosterone product or
' {" W! c- L, Q1 H6 D* \4 j' K0 sgel should be asked of the family members during
: f7 ~3 G- C) Z* X- `2 c# z# zthe evaluation of any children who present with vir-
) J! _  _6 P; [* Zilization or peripheral precocious puberty. The diag-
4 W) p. U5 \. E( Y; R# Z" ^* Y$ b$ \nosis can be established by just a few tests and by
7 P/ x& Y5 ?' Q" v: M! jappropriate history. The inability to obtain such a/ d; ]7 y" \& ~& A
history, or failure to ask the specific questions, may& v* Z" v5 \7 i% ^5 u
result in extensive, unnecessary, and expensive6 A" }5 s/ g" C* P
investigation. The primary care physician should be
7 L5 E# ^( C9 n3 |+ ~aware of this fact, because most of these children
4 @2 O% \! C9 W2 q: F: Qmay initially present in their practice. The Physicians’3 O( y# C, [9 U+ X
Desk Reference and package insert should also put a
  K! N1 J2 k& E# G/ C3 {/ Y" ywarning about the virilizing effect on a male or$ W) h* K9 V  L0 f; |
female child who might come in contact with some-# u& h+ x- d  O1 f! e- ^+ W
one using any of these products.
, z/ ?& ~- ~8 E9 HReferences
' k# ^' g, D( \9 U& P2 p/ P+ n: I1. Styne DM. The testes: disorder of sexual differentiation; u8 z& h8 J7 N3 i$ ?% C/ B0 Y0 `
and puberty in the male. In: Sperling MA, ed. Pediatric9 V4 z1 K( \) o& j3 R
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;3 n+ G) V& D: K1 ^& O
2002: 565-628.
" l; Q2 E: i4 L2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
6 a3 d9 ]7 d# }" Y! C$ gpuberty in children with tumours of the suprasellar pineal
發表於 2025-1-7 21:59:43 | 顯示全部樓層
這個我收藏了!謝謝分享!WK的資源越來越豐富,這少不了大大的辛勞!
發表於 2025-1-10 10:43:39 | 顯示全部樓層
VIP精品區,資源無限好賺金任務區,輕松賺金幣
加入VIP,享受高級特權宣傳賺金又升級,超級棒
感謝大大的辛勞分享!我會繼續在WK關注大大的文章!
發表於 2025-1-11 22:18:01 | 顯示全部樓層
女厕偷拍辅导班主任尿尿老师的逼很嫩还有一点
發表於 2025-1-17 16:31:39 | 顯示全部樓層
VIP精品區,資源無限好賺金任務區,輕松賺金幣
加入VIP,享受高級特權宣傳賺金又升級,超級棒
4个什么样的?
發表於 2025-1-19 02:41:05 | 顯示全部樓層
' X; u0 R' |5 ^" M+ V
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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