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鄉下的妹子太便宜,一次四個都要了[12P]

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Sexual Precocity in a 16-Month-Old
" L, G$ ]' j$ kBoy Induced by Indirect Topical
7 W4 ?6 l# M2 k% h: DExposure to Testosterone, z, U& s9 i' ~0 \& W/ H! @
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2! W! m( K' X) h; A' I( x, Q
and Kenneth R. Rettig, MD1
2 v' y! d" y, {  T& ~) `9 KClinical Pediatrics
5 B- W. f/ R$ TVolume 46 Number 6
) T& a' d! K7 cJuly 2007 540-543
8 D8 _( o( T6 m( b4 ]+ v- r© 2007 Sage Publications; v9 A- R) E2 V8 L! g* O+ e
10.1177/0009922806296651
# G4 E2 G# o$ X3 ?" _http://clp.sagepub.com
! M" n1 b7 m9 ^. T4 ?5 ]$ e" Z) [hosted at9 A0 I/ F) h' {. c2 U0 O6 x; l
http://online.sagepub.com
' \# P& Q- m* c( Z: M5 ePrecocious puberty in boys, central or peripheral,
# l/ n4 T: e& y5 e% D( Nis a significant concern for physicians. Central/ z+ s% O1 I7 \* _" N5 B3 u
precocious puberty (CPP), which is mediated
2 k* K6 Z. o* i. a  F: C/ A9 athrough the hypothalamic pituitary gonadal axis, has
4 L# Q. t4 M" ^' va higher incidence of organic central nervous system8 _3 `9 \' A3 S8 Z* a( F
lesions in boys.1,2 Virilization in boys, as manifested
6 y' T3 {1 F! fby enlargement of the penis, development of pubic
, ~$ u0 d% M, ]- v# h# C; Zhair, and facial acne without enlargement of testi-
. m; P0 K3 l/ s3 Icles, suggests peripheral or pseudopuberty.1-3 We  R8 l2 r) e- m( s) u
report a 16-month-old boy who presented with the
. C1 v- w! s7 c3 Ienlargement of the phallus and pubic hair develop-& q" j0 Y$ K; i; _3 C' f
ment without testicular enlargement, which was due
, x' Q9 W& S, _( Xto the unintentional exposure to androgen gel used by
; g. _4 D/ Z1 p1 Y' @$ P( [7 zthe father. The family initially concealed this infor-
  P7 L4 O7 [$ H# f+ Jmation, resulting in an extensive work-up for this
* L5 [5 t) C3 L$ T* |child. Given the widespread and easy availability of& q4 E$ Q1 u, I3 [7 q5 a" M
testosterone gel and cream, we believe this is proba-" o- ~9 d$ Q5 q, r
bly more common than the rare case report in the
2 \1 k" f8 o) N% j# cliterature.4
/ O' Z4 o% Q* G# \Patient Report
& p7 s1 r: O9 D+ w5 {A 16-month-old white child was referred to the1 l2 Q/ q. }/ c1 }, y
endocrine clinic by his pediatrician with the concern& s% P! i* t* ]' M7 V* I9 R
of early sexual development. His mother noticed) J/ i) S# r$ x* C: V  u) C% g0 k9 N5 w  V
light colored pubic hair development when he was
/ e% h2 K. e6 X1 d* fFrom the 1Division of Pediatric Endocrinology, 2University of
- k2 z- z! N/ W; e- ?1 {South Alabama Medical Center, Mobile, Alabama.' D0 H2 I5 E) \- J7 \3 h8 o1 d
Address correspondence to: Samar K. Bhowmick, MD, FACE,8 d8 S" Q/ h3 w+ Z& N
Professor of Pediatrics, University of South Alabama, College of! Y# x& h& V9 c5 I
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
( Q& }5 @4 H; U* Re-mail: [email protected].
# R! q4 \8 ~4 F( Fabout 6 to 7 months old, which progressively became
: n; ]: y7 n5 H1 Q) k2 Adarker. She was also concerned about the enlarge-
* |* K3 p) M" J! M  H6 j, H) Gment of his penis and frequent erections. The child' n& q7 e8 G1 ]+ T
was the product of a full-term normal delivery, with5 T: B: |& S! [
a birth weight of 7 lb 14 oz, and birth length of
; K2 {# f- M% M8 |3 h5 u; F20 inches. He was breast-fed throughout the first year- }( y- _# X( v# p: n9 y7 Y. |+ R
of life and was still receiving breast milk along with
* ]; v2 _$ J5 }, _/ Msolid food. He had no hospitalizations or surgery,
+ @6 L2 r8 h6 Q* @: D- nand his psychosocial and psychomotor development4 u7 Y9 Y2 n3 i
was age appropriate.
! z8 u8 l: I: p0 N& h7 E9 {The family history was remarkable for the father,
( c  R+ F5 N* X8 i" I' rwho was diagnosed with hypothyroidism at age 16,
5 r$ B5 W8 N8 Rwhich was treated with thyroxine. The father’s
4 @2 E+ J' K* v7 O9 e' Dheight was 6 feet, and he went through a somewhat
: j% q8 R; a1 T+ Gearly puberty and had stopped growing by age 14.
' |, A9 Y6 e% Q, E2 G5 cThe father denied taking any other medication. The
( z! o, ^/ }" E/ n6 X2 x9 dchild’s mother was in good health. Her menarche
' F. z7 _( b" a+ I+ Awas at 11 years of age, and her height was at 5 feet4 T* w* q1 m; B9 _, @" X' R2 A
5 inches. There was no other family history of pre-: w# Y& B$ Q9 o
cocious sexual development in the first-degree rela-. I# h3 r5 Y+ i
tives. There were no siblings.
- T& W: Z% U0 a, JPhysical Examination
% t8 q% Y  U* e3 |9 ]* CThe physical examination revealed a very active,! k- N7 n' [0 x1 _; x) {6 X8 |; W
playful, and healthy boy. The vital signs documented  k! q5 p1 h8 K% U
a blood pressure of 85/50 mm Hg, his length was  n' B' \  R; ]9 f
90 cm (>97th percentile), and his weight was 14.4 kg
  N, n7 {7 {1 W- G3 s(also >97th percentile). The observed yearly growth; F/ \9 M2 m. Y
velocity was 30 cm (12 inches). The examination of7 \3 @$ {5 p0 z& B! }
the neck revealed no thyroid enlargement.
" y- v8 t  c+ e( BThe genitourinary examination was remarkable for
/ T$ y* ~, j' G, @6 j4 Senlargement of the penis, with a stretched length of
) k7 r9 w! [0 c7 b, Y8 cm and a width of 2 cm. The glans penis was very well3 \' d2 |$ L4 A4 _
developed. The pubic hair was Tanner II, mostly around# C9 R4 n( D9 J
540, @4 s! a2 r- A
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from9 y) f: J' q  Z6 e1 \
the base of the phallus and was dark and curled. The  i: O" h# Y( v* R3 R) H7 G
testicular volume was prepubertal at 2 mL each.
- E' y) Z3 d9 H! G$ JThe skin was moist and smooth and somewhat
, l% o- O1 H8 Ioily. No axillary hair was noted. There were no, Y0 p* F' E/ o& I1 J- R
abnormal skin pigmentations or café-au-lait spots.
) f* J- ^9 t0 L4 G0 Z3 rNeurologic evaluation showed deep tendon reflex 2++ |( v" K; C. B& ^/ E
bilateral and symmetrical. There was no suggestion3 v' I9 i2 n; w# E) ]- e. J
of papilledema.
% s- [3 q8 s9 q+ g% F$ `4 VLaboratory Evaluation
7 k; L0 e( S4 W# @" i# eThe bone age was consistent with 28 months by! Q. C9 A3 {- p
using the standard of Greulich and Pyle at a chrono-
9 n! g$ r! L# Rlogic age of 16 months (advanced).5 Chromosomal
3 \* |0 H1 s  l% Y7 w# A6 _! Pkaryotype was 46XY. The thyroid function test
: p: ?. a; e( i$ ~showed a free T4 of 1.69 ng/dL, and thyroid stimu-& @$ m+ M. ?& T  U2 n% }& B
lating hormone level was 1.3 µIU/mL (both normal).! I1 Y, X. u* o$ `
The concentrations of serum electrolytes, blood
/ @, O7 }) w: q! E" Zurea nitrogen, creatinine, and calcium all were
! y) E, t4 d) p. C5 Vwithin normal range for his age. The concentration
& g% q) t+ ?+ y6 `7 i$ U: d  Bof serum 17-hydroxyprogesterone was 16 ng/dL
6 x6 ?: q8 p& v8 g& I; m) q3 ^(normal, 3 to 90 ng/dL), androstenedione was 20: _# @$ `& U, I- b4 w
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-! w9 a, F+ c; v! ?8 X
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
/ U! Y$ {/ Q( u  t2 Xdesoxycorticosterone was 4.3 ng/dL (normal, 7 to. l9 T# R4 K% K3 e$ O/ w3 x+ P1 S( I
49ng/dL), 11-desoxycortisol (specific compound S)
4 w, _# s6 E/ M$ f* U, p. hwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
% F' r* l! r) `- o6 y. t& xtisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total/ P  j* r& |0 a9 `. H/ M1 K
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
+ ~8 O' |2 G7 \, ?and β-human chorionic gonadotropin was less than
" u) O5 E; Y5 R% s5 mIU/mL (normal <5 mIU/mL). Serum follicular
# ]% k" O7 u% Q2 a, C! }stimulating hormone and leuteinizing hormone' k: ]2 d3 d, ~& ?3 P
concentrations were less than 0.05 mIU/mL
* c7 [2 f" m6 ~# p, u(prepubertal).* a. e4 Y  _: Z- R
The parents were notified about the laboratory
2 m- E) D5 o% F# G, N1 {; h) a/ qresults and were informed that all of the tests were) G1 _; Q; X7 V. e- h9 m/ i
normal except the testosterone level was high. The8 s1 j# }8 b8 C4 k0 l( i( o! G
follow-up visit was arranged within a few weeks to
* U' Y8 y0 c! L' U! F2 f! g' iobtain testicular and abdominal sonograms; how-
3 W* J) W. Z5 t7 Kever, the family did not return for 4 months.& M7 u+ V5 c9 F1 F5 H& {1 J& c
Physical examination at this time revealed that the. N, o  G4 _( U3 v5 i9 _. @/ J0 X
child had grown 2.5 cm in 4 months and had gained4 j4 D$ }3 @% Z$ Y6 \3 X# K
2 kg of weight. Physical examination remained
# K4 j7 J# s, N, {% p2 X0 W8 q+ Zunchanged. Surprisingly, the pubic hair almost com-* @  l: A! c! D  y2 _; I  ?
pletely disappeared except for a few vellous hairs at1 G4 S5 t, \# y: v4 m% L
the base of the phallus. Testicular volume was still 2
7 H! B+ R0 p/ W0 UmL, and the size of the penis remained unchanged.
* M" ?  z9 ^, y- s, r) XThe mother also said that the boy was no longer hav-0 \; K$ @7 u- ]  d2 Q3 B
ing frequent erections.
4 ^3 m9 x1 o/ r  s/ IBoth parents were again questioned about use of
$ \0 a% b" [" _any ointment/creams that they may have applied to& i  S7 R( w7 h, O$ C- [1 O
the child’s skin. This time the father admitted the2 O/ W$ x+ S0 e
Topical Testosterone Exposure / Bhowmick et al 541
/ r6 n1 z2 ?, guse of testosterone gel twice daily that he was apply-
5 c9 x  A4 }: E- c4 h# @8 E& Aing over his own shoulders, chest, and back area for! {4 B# k5 P! P+ X1 J; j- [9 ?+ e
a year. The father also revealed he was embarrassed
0 C9 }& Y, d- d4 nto disclose that he was using a testosterone gel pre-
( {- p8 j, s; @# F2 n7 tscribed by his family physician for decreased libido
- d4 [* ]$ F1 ^9 y; Nsecondary to depression." s8 _; g. ~1 ?6 V5 C! H
The child slept in the same bed with parents.; w' r* [! a% _0 e
The father would hug the baby and hold him on his
1 i0 B3 O0 Q% X$ W5 k; j0 Lchest for a considerable period of time, causing sig-
% [- @) e+ w) a; _4 |5 snificant bare skin contact between baby and father.
& i- W  ^& @- z4 Q; RThe father also admitted that after the phone call,
( |0 w1 Y2 Z+ W9 S. Ywhen he learned the testosterone level in the baby
, ^4 l# v; `' Q: vwas high, he then read the product information
5 a& a  U: \# ]4 c$ U, C& p. hpacket and concluded that it was most likely the rea-% v# f3 a8 o8 t4 ^
son for the child’s virilization. At that time, they
0 w0 E) a( @9 x9 R5 F  Udecided to put the baby in a separate bed, and the
3 V+ v* Y8 h" X8 M9 _father was not hugging him with bare skin and had
. Y/ ~# K1 d9 l# Jbeen using protective clothing. A repeat testosterone/ |* I  L  G3 x! T# p9 W$ N- _
test was ordered, but the family did not go to the
* _' E6 N" |5 z& B% @1 Claboratory to obtain the test.
. H+ D9 h6 m) ODiscussion' [9 k% H* J- }7 \! A" V! G
Precocious puberty in boys is defined as secondary. T5 L& o4 x# P  J
sexual development before 9 years of age.1,40 S2 I/ Q+ I& A/ p( F; m
Precocious puberty is termed as central (true) when
  v" F% R& S( T  k$ Kit is caused by the premature activation of hypo-* k/ s+ p/ C: `# @8 p
thalamic pituitary gonadal axis. CPP is more com-% s, R: u3 H1 w3 ~
mon in girls than in boys.1,3 Most boys with CPP
3 S1 J$ K9 t* v5 n. q% l) mmay have a central nervous system lesion that is! v4 u+ b& N5 x6 ~* |
responsible for the early activation of the hypothal-
0 ^, ]$ O; E1 D4 c) g& camic pituitary gonadal axis.1-3 Thus, greater empha-
5 K2 j$ \  ]- |: _! Xsis has been given to neuroradiologic imaging in: C- `8 c* a5 l, g
boys with precocious puberty. In addition to viril-
- W5 e, P$ V5 N- h, Tization, the clinical hallmark of CPP is the symmet-
" b+ }$ ^2 [7 d& Srical testicular growth secondary to stimulation by
6 Z, ]/ t+ x9 A* tgonadotropins.1,32 f% Q+ z5 N7 l4 Q3 i
Gonadotropin-independent peripheral preco-8 Z8 M. o2 t3 y6 v' r. L! T8 |# z
cious puberty in boys also results from inappropriate0 c( f5 E' X. U+ F4 z3 L4 v% Y
androgenic stimulation from either endogenous or
3 f' H7 I5 _  t4 c3 I. n4 ^, `exogenous sources, nonpituitary gonadotropin stim-+ x$ }' V' v  J; Y
ulation, and rare activating mutations.3 Virilizing
, ?- K6 h' C5 y" @congenital adrenal hyperplasia producing excessive+ ?7 b3 `& x7 z
adrenal androgens is a common cause of precocious  u' I; M& k2 Y
puberty in boys.3,4
0 y: Y7 S: ^1 X/ Z; M7 z4 }7 OThe most common form of congenital adrenal4 Z+ E$ h6 @! s# P/ y
hyperplasia is the 21-hydroxylase enzyme deficiency.
- o3 B- X* R! LThe 11-β hydroxylase deficiency may also result in1 ~0 @! J% S7 R& v
excessive adrenal androgen production, and rarely,: R" Q* {1 J5 d( M
an adrenal tumor may also cause adrenal androgen+ R4 X5 K3 _& ]
excess.1,3
; ]2 e8 K7 d3 r+ L' B4 nat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from2 E2 F+ F) Y4 ^
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007% t0 M& q4 @8 ]* p4 ?- R; W9 g: A
A unique entity of male-limited gonadotropin-
% ^) Q! Y+ h0 k0 m( w. [$ dindependent precocious puberty, which is also known- o8 V3 J1 ?; b# K# _' i1 T9 p
as testotoxicosis, may cause precocious puberty at a
# L7 O! ~- }: [( Pvery young age. The physical findings in these boys) N6 G! x5 ^" Q- g: b) @) E
with this disorder are full pubertal development,5 x% }5 h# l. f( |) s4 t
including bilateral testicular growth, similar to boys
" s% P$ E2 k9 P) Twith CPP. The gonadotropin levels in this disorder
1 _) O+ R  c# |1 J! ^are suppressed to prepubertal levels and do not show
7 L  t0 e1 ^9 N2 _1 zpubertal response of gonadotropin after gonadotropin-- o7 ~" q/ u1 M9 _
releasing hormone stimulation. This is a sex-linked
# ?8 F9 O) F0 {autosomal dominant disorder that affects only0 P2 s! S% m5 a& |/ k
males; therefore, other male members of the family1 j; _/ _" ]4 I. a
may have similar precocious puberty.3
' n2 g0 P' h! R+ y6 XIn our patient, physical examination was incon-, ?$ v! G% F  c  Q: ?# j" w7 @0 J
sistent with true precocious puberty since his testi-, B) r% f1 g% J* W
cles were prepubertal in size. However, testotoxicosis/ \8 B" [- i! ?( g7 A* Z& G
was in the differential diagnosis because his father3 |4 A6 ^' k. O0 c
started puberty somewhat early, and occasionally,1 h* a+ v1 K; q6 `2 f: ^
testicular enlargement is not that evident in the
" x% J6 ]" y* S1 t) I6 A% e) z. Qbeginning of this process.1 In the absence of a neg-
9 ~4 ]% W; m  f* T5 V" Oative initial history of androgen exposure, our
- |1 I/ O- V, S* U  j3 W5 ybiggest concern was virilizing adrenal hyperplasia,
- u: c4 d- [$ n; heither 21-hydroxylase deficiency or 11-β hydroxylase# B; A7 w: e6 F  Z* ?: t
deficiency. Those diagnoses were excluded by find-3 U0 J% m8 P! f+ {6 x! P
ing the normal level of adrenal steroids.
5 S( G4 b% _# U: JThe diagnosis of exogenous androgens was strongly' I5 a" \5 o( Q& Q
suspected in a follow-up visit after 4 months because
3 z5 v, o4 ]! v( H6 q/ o% y& ithe physical examination revealed the complete disap-  |: C4 |( B" j/ X9 f) h
pearance of pubic hair, normal growth velocity, and' e+ r2 m) N' B% N! _0 l' I
decreased erections. The father admitted using a testos-+ Q% F$ M. B& `, i8 U2 g( Y
terone gel, which he concealed at first visit. He was. I  [% b, s0 I  R
using it rather frequently, twice a day. The Physicians’
/ S: o8 s+ h8 l6 VDesk Reference, or package insert of this product, gel or
! c5 D! Z9 Q4 H+ w) U, b! C, acream, cautions about dermal testosterone transfer to
5 g" U% X4 P5 k- h, O9 y9 M7 Funprotected females through direct skin exposure.
. R4 j. h" u# T4 w. O% p8 M* v# ^Serum testosterone level was found to be 2 times the3 `- o! m; g' ^) y) ~
baseline value in those females who were exposed to+ H* g/ `# b8 k# D
even 15 minutes of direct skin contact with their male1 T. f. t& U/ V# k
partners.6 However, when a shirt covered the applica-$ i/ c  F: z' g" M4 W
tion site, this testosterone transfer was prevented.
8 p0 ?5 p0 o4 b! x2 {$ C9 O$ VOur patient’s testosterone level was 60 ng/mL,4 S5 D+ l+ g- s: G* V0 v
which was clearly high. Some studies suggest that6 n0 }) l  a4 D2 k7 v( F
dermal conversion of testosterone to dihydrotestos-( N8 Z& l! d4 [- |5 M. O2 z
terone, which is a more potent metabolite, is more
, E4 q& K8 n+ {6 t  |$ Dactive in young children exposed to testosterone- M* O3 P5 _+ c
exogenously7; however, we did not measure a dihy-
' A' P8 W- ]' v# \9 l/ w9 y4 Mdrotestosterone level in our patient. In addition to
8 g4 s1 C8 o/ Svirilization, exposure to exogenous testosterone in5 D% P0 |# y7 I2 i4 q! Q0 {/ t' A& {
children results in an increase in growth velocity and
% A8 p9 B& p) _9 oadvanced bone age, as seen in our patient.! Y: J. x( e$ G, Y
The long-term effect of androgen exposure during4 h) }6 O5 ?9 G3 q+ s8 }
early childhood on pubertal development and final
; l! i7 r. N2 A7 N7 t8 H% X9 Yadult height are not fully known and always remain
, d$ H, S7 |7 \' z& l4 R$ oa concern. Children treated with short-term testos-+ Q: S) ]: y9 E
terone injection or topical androgen may exhibit some
" M! b' I0 D# |acceleration of the skeletal maturation; however, after+ {+ m, e9 [  x  X: }( c+ ?
cessation of treatment, the rate of bone maturation
1 S' l; V8 W/ F9 n. t" a6 Gdecelerates and gradually returns to normal.8,9
, }: N6 k! d! v) t  p! ~6 I7 G) l( pThere are conflicting reports and controversy
/ I, t; P+ _* a0 L- Qover the effect of early androgen exposure on adult! s4 k) a8 |+ x; {+ f, _- q
penile length.10,11 Some reports suggest subnormal
, ]4 o' A+ z0 e- c* c& madult penile length, apparently because of downreg-
4 h( V/ N; r+ C: w3 x( xulation of androgen receptor number.10,12 However,
' f! X; K7 r' [% U2 I' hSutherland et al13 did not find a correlation between
: x* Q! Y" l+ A% v0 {& B6 W" Achildhood testosterone exposure and reduced adult. |9 K3 k/ O9 O& r, E" A6 \
penile length in clinical studies.
- r: e" P7 k) \6 ]Nonetheless, we do not believe our patient is$ T% [* f& u, j) T0 K
going to experience any of the untoward effects from
7 L0 U, e% G! N9 h+ f0 U! Dtestosterone exposure as mentioned earlier because
) g( R8 z1 M4 \) B3 othe exposure was not for a prolonged period of time.
, g  |; w# `$ B) t3 d" T9 T% Q+ nAlthough the bone age was advanced at the time of
+ I# a1 T6 Z4 Adiagnosis, the child had a normal growth velocity at9 j/ Y$ y8 n9 {, r1 u3 B2 I
the follow-up visit. It is hoped that his final adult: H1 b5 i: j) \6 i; y8 K  A
height will not be affected.4 n( s0 ~2 C/ r1 N6 G+ H* d
Although rarely reported, the widespread avail-# I) e. o  u  J8 N- n' Z
ability of androgen products in our society may
; ]% R( A+ ~  Y( p4 @* ^indeed cause more virilization in male or female
9 W. F% g) I! Z5 s# \children than one would realize. Exposure to andro-# I+ }6 ~8 k9 f3 @& {& w; E8 u' t
gen products must be considered and specific ques-
/ v4 b5 Q/ w. s, o  T3 X' y5 ptioning about the use of a testosterone product or
/ K& C  u3 o4 R  P; Y' o0 Fgel should be asked of the family members during; b! H% s2 G: w& k
the evaluation of any children who present with vir-0 n. V& w" h9 |
ilization or peripheral precocious puberty. The diag-
2 @0 {; W' t3 m! |( ?nosis can be established by just a few tests and by
9 @5 X1 q! b, O% r: tappropriate history. The inability to obtain such a
& L" q0 q( u. z: }% S7 Lhistory, or failure to ask the specific questions, may7 _3 o- P( o- ]! W* B
result in extensive, unnecessary, and expensive
! Y; b* q5 T4 W0 ^+ H: p3 ~investigation. The primary care physician should be
- S, T8 v8 N9 |/ |% e9 C- ?; Iaware of this fact, because most of these children
! a! q, R: w3 c9 M. A( Emay initially present in their practice. The Physicians’7 q, t- u$ ?: v! s. i$ c% q$ [% m& r
Desk Reference and package insert should also put a/ s" t9 Z; O$ u3 q1 E
warning about the virilizing effect on a male or# [0 _; k* J1 ?! ~6 z5 s
female child who might come in contact with some-
1 J4 b6 o+ n# w7 W& z- Rone using any of these products., N& G& W, h" I3 G
References4 _9 K' e" ~' u5 O4 D' M2 t
1. Styne DM. The testes: disorder of sexual differentiation
/ [3 h$ B7 W' p3 I0 X) pand puberty in the male. In: Sperling MA, ed. Pediatric
4 X& E6 `- d' q; z; v, z9 bEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;& {; O  t! |, s5 v$ @; E
2002: 565-628.
: T* l& \9 A9 u* ?8 Q6 t2 c4 U2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
" ^# N: q" H- }  k5 j2 spuberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old3 G/ j! \& I0 s* T3 N' a  p
Boy Induced by Indirect Topical
. t7 I* o- f' {; D7 \, E( AExposure to Testosterone, i1 o8 f4 E  f+ _
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
3 `/ D& l' }2 rand Kenneth R. Rettig, MD1" z5 v8 p- @/ E* J8 e
Clinical Pediatrics
; p5 b; t+ Z! Z* tVolume 46 Number 6
% Q  n& z* a; X% Y& cJuly 2007 540-543
' e4 W. g5 {, }3 z© 2007 Sage Publications
% e7 D7 c" I, F% O' D, _2 T10.1177/0009922806296651
' [5 p- e" Z8 s% ^) Y2 ~7 g3 Bhttp://clp.sagepub.com
) n) J7 ^) j. k' D0 ~+ n- ehosted at6 \0 Q. _5 Q, ?
http://online.sagepub.com- _7 U$ a) N. a; m- X' l
Precocious puberty in boys, central or peripheral,& ~" a2 f* }3 {! d' [- [" {
is a significant concern for physicians. Central
  B) m& [3 @5 n" r4 D  I9 w; H8 hprecocious puberty (CPP), which is mediated
1 ~+ O0 w; G& c6 Pthrough the hypothalamic pituitary gonadal axis, has4 ?: l: B& v; x0 @2 i0 A$ n
a higher incidence of organic central nervous system
. R! G/ E0 V3 V2 v; h' q  elesions in boys.1,2 Virilization in boys, as manifested
! e' Z8 j4 U) s4 H2 Tby enlargement of the penis, development of pubic
3 \0 G; l  @9 _/ |+ }hair, and facial acne without enlargement of testi-) y1 `, E% U2 A7 Y
cles, suggests peripheral or pseudopuberty.1-3 We
1 @' ?) `/ F, p& Q5 Creport a 16-month-old boy who presented with the2 }% n8 V1 [; Y& S' h3 |" [( ]
enlargement of the phallus and pubic hair develop-
, U% j/ {8 O; j5 `4 m" U9 L1 Pment without testicular enlargement, which was due
1 G! [4 x3 f$ M( T7 t" Xto the unintentional exposure to androgen gel used by! a1 [. v# Y) S/ _
the father. The family initially concealed this infor-- M9 _" T" Q0 ]# U
mation, resulting in an extensive work-up for this
- O) W2 i  M6 B: p/ K! T9 Mchild. Given the widespread and easy availability of
4 R" k0 r: D% h5 U8 Qtestosterone gel and cream, we believe this is proba-
3 r% P. x, e( Q5 h- Z9 J5 H5 |1 sbly more common than the rare case report in the! i) B, Z% x5 U  s7 e5 Q
literature.4
7 ^2 d  h$ I+ j% d" ~# t3 o# oPatient Report- C4 Q/ ?  d  ^% T  A
A 16-month-old white child was referred to the
: i7 y% \3 o# h) e0 Oendocrine clinic by his pediatrician with the concern% X1 k( k: ?2 D- y
of early sexual development. His mother noticed$ f5 l, P: k( [* i; v8 W
light colored pubic hair development when he was$ l3 R! q2 i6 u" S( a, H) C
From the 1Division of Pediatric Endocrinology, 2University of' {- n% v: W& t8 w  @
South Alabama Medical Center, Mobile, Alabama.
- b: T, I8 J( }Address correspondence to: Samar K. Bhowmick, MD, FACE,% k- Z* s! ^* f: w2 K+ v
Professor of Pediatrics, University of South Alabama, College of0 r: U- a1 B8 L5 t: P
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
( b6 E% z$ q. ^. @0 T3 ae-mail: [email protected].8 n) f+ `0 B* Z! O9 P4 m
about 6 to 7 months old, which progressively became
" D* j7 k/ D" [/ Odarker. She was also concerned about the enlarge-" z# n9 |- F6 r3 r' T0 \
ment of his penis and frequent erections. The child
( ]1 w- A/ l! w7 S% j9 G0 }was the product of a full-term normal delivery, with
9 O# O7 Q; I% x  [* qa birth weight of 7 lb 14 oz, and birth length of" \% C; F% [9 @3 m, P
20 inches. He was breast-fed throughout the first year4 e( J* R  v1 v! V' M( K/ v8 Q$ H
of life and was still receiving breast milk along with3 j, s" q. ]1 f6 M7 d
solid food. He had no hospitalizations or surgery,
" `; C+ w0 ?+ {' D4 U, h; mand his psychosocial and psychomotor development, y2 r8 J" ^, K  ^
was age appropriate.
5 y  K3 N" @% d( s2 G- dThe family history was remarkable for the father,5 J% e: `2 K, m) f( M6 K
who was diagnosed with hypothyroidism at age 16,+ v! `- z6 y$ a5 p/ |1 S
which was treated with thyroxine. The father’s( V1 y. o, K( f$ o) A& A
height was 6 feet, and he went through a somewhat- p1 R0 O( i) P: a" P0 g
early puberty and had stopped growing by age 14." `# e( D" `. G1 p& D
The father denied taking any other medication. The' h4 a/ d! I) X5 L* V! t
child’s mother was in good health. Her menarche
, n1 u- ~3 W5 d4 }* Z/ {was at 11 years of age, and her height was at 5 feet% M* e) v" N  w
5 inches. There was no other family history of pre-% U( ]3 M/ z. v+ z7 `$ y: M$ X! y2 B
cocious sexual development in the first-degree rela-
  T, L/ S# l1 Ltives. There were no siblings.
1 y0 H  E3 Y7 R9 w- rPhysical Examination' p* |2 P# I3 J) V
The physical examination revealed a very active,
  |! i7 L) o/ J7 Qplayful, and healthy boy. The vital signs documented
' ^1 V" E! I/ E- Z  ]4 ]a blood pressure of 85/50 mm Hg, his length was
" i3 j$ _1 S+ @4 T1 K* o( M4 B90 cm (>97th percentile), and his weight was 14.4 kg5 K* C6 m! R7 [5 u1 T% K- _
(also >97th percentile). The observed yearly growth+ q+ z8 ?; T9 }* K
velocity was 30 cm (12 inches). The examination of
1 t* i5 y, ]; ?- o# athe neck revealed no thyroid enlargement.
* b. [. x* d  ?# t8 TThe genitourinary examination was remarkable for
1 ]  a% o- E- R6 p, u( g4 z1 penlargement of the penis, with a stretched length of
2 p. M5 w* F: ]2 z& }# u8 cm and a width of 2 cm. The glans penis was very well2 r/ F% P' s" T5 d5 f" ?- ^
developed. The pubic hair was Tanner II, mostly around9 |- _7 X9 x0 Q1 Z& V
5404 Z: z+ y7 S7 H& n
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the base of the phallus and was dark and curled. The
/ X( J2 J" G: u( N& ~testicular volume was prepubertal at 2 mL each.
9 q0 Y+ z7 z$ N$ m' M# n4 UThe skin was moist and smooth and somewhat/ s0 v% J/ N: L( M
oily. No axillary hair was noted. There were no
4 T2 m5 p& z+ o: m6 I, cabnormal skin pigmentations or café-au-lait spots.  |0 G/ b# G% t  O6 Z
Neurologic evaluation showed deep tendon reflex 2+" o8 o$ x( N+ Y. r; c5 A7 Z9 O
bilateral and symmetrical. There was no suggestion$ f1 N4 @5 J4 F
of papilledema.
# L9 `/ s5 Y5 W- v8 g0 [Laboratory Evaluation9 \2 {' _2 X1 V* N
The bone age was consistent with 28 months by
$ ]- ?- b9 l, I7 U1 V9 z, u3 f) Susing the standard of Greulich and Pyle at a chrono-
1 @1 ~# ]7 Q" s5 clogic age of 16 months (advanced).5 Chromosomal8 |) R2 ^, @  A# y# b- k
karyotype was 46XY. The thyroid function test  N. `& {/ x1 y2 W9 f9 ^* f# x# N7 L
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
  Q" d1 r' B' g. ~! s' H* Mlating hormone level was 1.3 µIU/mL (both normal).1 T2 b* d, R! ], m
The concentrations of serum electrolytes, blood
' b  k! w( y2 L& m$ O9 S  zurea nitrogen, creatinine, and calcium all were
; C' v7 n* U2 r) n, [9 `# _6 M/ lwithin normal range for his age. The concentration
3 s( o0 H" Q" ]- L' ^of serum 17-hydroxyprogesterone was 16 ng/dL
- t" f; D: _$ r, V4 t5 Q(normal, 3 to 90 ng/dL), androstenedione was 20
# H* J: E4 e! V- u& {ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-  `; Q! e3 n/ g. ^6 v: b/ c1 Y
terone was 38 ng/dL (normal, 50 to 760 ng/dL),' {: g+ D- u* c3 I( I" O" N
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
; N/ e' w' w4 W5 T49ng/dL), 11-desoxycortisol (specific compound S)) E5 J1 ^; S! [* E
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-' O+ ?7 m  n+ l. _
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total! H/ q' Y  ^! p. ~0 }+ s1 E
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
& u- Y& A" U. Q8 ]3 x& b" U1 Xand β-human chorionic gonadotropin was less than
& J( E9 z2 Z3 B4 h8 U$ {5 l$ G5 mIU/mL (normal <5 mIU/mL). Serum follicular
: _0 a" c( r. cstimulating hormone and leuteinizing hormone
. h, @" y4 J  Dconcentrations were less than 0.05 mIU/mL- G2 R8 t6 s+ Z9 Y, {
(prepubertal).
3 E4 E( y! W* A/ m: B% EThe parents were notified about the laboratory4 t2 D3 g) y. K/ p- Q
results and were informed that all of the tests were
' D7 j: }, y0 R; R9 D  [normal except the testosterone level was high. The
# O; `. V7 S  }8 M2 a* R8 w1 Yfollow-up visit was arranged within a few weeks to% i2 L7 Z* D/ |5 J
obtain testicular and abdominal sonograms; how-0 {: R5 o; o6 s  R1 V
ever, the family did not return for 4 months.
) E1 T8 y# R1 L# L# R* YPhysical examination at this time revealed that the2 J# U# c$ \: L& v  _! Y3 W1 l. l
child had grown 2.5 cm in 4 months and had gained5 n7 |% Z/ L  ~  x6 ~/ Q  P7 L
2 kg of weight. Physical examination remained6 R/ T. |3 [" a$ ]  h9 i
unchanged. Surprisingly, the pubic hair almost com-' R4 i5 v8 h4 e) {
pletely disappeared except for a few vellous hairs at
1 M8 ~2 d$ {& h! T$ tthe base of the phallus. Testicular volume was still 2$ l; G/ a7 ]! h, Z0 }7 L6 v
mL, and the size of the penis remained unchanged.
  D5 H: f& i, Z; {The mother also said that the boy was no longer hav-
, d/ x, e( N' l2 B7 }3 eing frequent erections.- V  j9 k  z2 b9 y# m
Both parents were again questioned about use of
# Q8 c# b' Q* c3 U+ O2 s$ x# B5 Yany ointment/creams that they may have applied to
3 h9 {% A1 n0 H% {/ dthe child’s skin. This time the father admitted the. J+ {0 z- s( o; y4 q. y9 m6 V
Topical Testosterone Exposure / Bhowmick et al 541$ Y) L4 {, E5 G: a1 _1 u) w7 P
use of testosterone gel twice daily that he was apply-
% I5 a  B" Q4 A# oing over his own shoulders, chest, and back area for( X+ y5 J! z' w
a year. The father also revealed he was embarrassed4 O; s* X2 d4 \  V$ F
to disclose that he was using a testosterone gel pre-# w. y1 ]2 C' D5 U  C. d
scribed by his family physician for decreased libido+ o, j; X, u5 [8 [/ e4 m; r2 }. {, q" Y
secondary to depression.
+ Y  [6 F7 I0 B+ F4 UThe child slept in the same bed with parents.4 N; Z7 q5 Q0 D) m0 V5 u% O; t
The father would hug the baby and hold him on his
0 H! L; P" ]/ h" jchest for a considerable period of time, causing sig-% w2 W3 c/ w2 D: n' }! B/ B0 O% S
nificant bare skin contact between baby and father.2 N# k) {* x# X
The father also admitted that after the phone call,; {( h2 a0 Y5 S8 i. }, [$ R/ t) Y
when he learned the testosterone level in the baby7 h- j7 V) g9 C) p( P# z
was high, he then read the product information* v8 u1 L4 n# L" W
packet and concluded that it was most likely the rea-9 G2 S. s: B* h9 _7 c  R/ B
son for the child’s virilization. At that time, they% p# B1 T7 O( C3 w" [; Z
decided to put the baby in a separate bed, and the
. Z* t  Y" Q- l9 J% f& u* ~$ \father was not hugging him with bare skin and had4 W8 v% B% @3 `) F  r4 C+ I
been using protective clothing. A repeat testosterone
& T+ ?0 {1 K  o5 G# M, ?test was ordered, but the family did not go to the. h7 f: U; s5 a5 j
laboratory to obtain the test.+ z6 b2 ^' ?" {6 p5 l
Discussion9 [7 j0 j- c2 T+ J
Precocious puberty in boys is defined as secondary& C8 f: b1 N  u- \, K0 S; @
sexual development before 9 years of age.1,4
9 f! |) y5 `' K  z" m- o2 NPrecocious puberty is termed as central (true) when, t) S$ H, |$ Z/ _/ x' C
it is caused by the premature activation of hypo-
' j& C! y% V0 h0 c, G2 D4 \thalamic pituitary gonadal axis. CPP is more com-# U; G) J8 _# ?* d5 }9 |. H9 W
mon in girls than in boys.1,3 Most boys with CPP
& \7 ~% S9 D' A( \0 v. ?# p$ Y0 k* ^may have a central nervous system lesion that is' u. M2 k1 Q/ m/ a* r6 C
responsible for the early activation of the hypothal-) t5 {% Z% x7 ^. T1 }
amic pituitary gonadal axis.1-3 Thus, greater empha-
# \) V4 P/ a# Z; r( U( }/ g- L- }sis has been given to neuroradiologic imaging in
$ m1 C* w8 r4 a7 ^boys with precocious puberty. In addition to viril-, g: k4 E6 F5 t# L3 s  G! A
ization, the clinical hallmark of CPP is the symmet-
$ d; J+ T+ Q6 ^) {( @. \' q4 [% xrical testicular growth secondary to stimulation by# ]! y$ X+ d/ p) I! i
gonadotropins.1,3" {6 f; I! X1 n4 d
Gonadotropin-independent peripheral preco-
5 t5 W7 J5 o* B, tcious puberty in boys also results from inappropriate
* Z; R" t9 M9 w3 `; M' Yandrogenic stimulation from either endogenous or
4 v! b$ C" q6 U% v! c" M1 Mexogenous sources, nonpituitary gonadotropin stim-
1 a3 N( r9 x% X& W% @ulation, and rare activating mutations.3 Virilizing
2 h+ A4 V! \5 x; Acongenital adrenal hyperplasia producing excessive
$ s) ~0 c# U+ t1 A% Padrenal androgens is a common cause of precocious
5 t' e# D$ e8 q& ], Dpuberty in boys.3,4- d+ G7 Q" E" l" j5 u; A  I  R
The most common form of congenital adrenal
1 Z: d$ c$ ~& Z2 j' p0 thyperplasia is the 21-hydroxylase enzyme deficiency.9 o; i0 U  F  J' S
The 11-β hydroxylase deficiency may also result in
! v. }+ p  Q: t2 |4 s# O, Yexcessive adrenal androgen production, and rarely,. D2 V% r3 n) @0 `
an adrenal tumor may also cause adrenal androgen4 |1 d) m2 q5 X; n- y7 A# g. g6 R! U- b+ X
excess.1,37 W; w9 c8 j8 T4 S# W
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
  |$ ]1 ]4 X4 Q* Y' s# f542 Clinical Pediatrics / Vol. 46, No. 6, July 20075 z6 v: K% q: Y2 X' k) j
A unique entity of male-limited gonadotropin-( e1 r  M; V. ]& I9 L0 a
independent precocious puberty, which is also known6 E) v2 T5 R7 u0 }7 a8 y0 d
as testotoxicosis, may cause precocious puberty at a+ [$ T; Y) w+ a
very young age. The physical findings in these boys
4 ^6 Y! z. a/ J6 Ewith this disorder are full pubertal development,
4 g' p, I7 E1 N" P# ~" C5 kincluding bilateral testicular growth, similar to boys0 @2 H: P+ o9 ?7 t! F: s
with CPP. The gonadotropin levels in this disorder
, H1 f& k6 E7 O5 T; C, X; |are suppressed to prepubertal levels and do not show
6 L' W4 v# p+ `; Y+ x3 z4 xpubertal response of gonadotropin after gonadotropin-
+ O) ~: {! K" F- Q3 H+ Wreleasing hormone stimulation. This is a sex-linked) [# O- |- p$ O
autosomal dominant disorder that affects only
3 t% B6 x% v7 P/ h0 gmales; therefore, other male members of the family
4 i$ `/ i2 d/ vmay have similar precocious puberty.3
; `: A) V  S9 V" N$ H' kIn our patient, physical examination was incon-8 W: s. @% N0 s2 ?; B
sistent with true precocious puberty since his testi-
6 ~, s5 ^0 X, Ncles were prepubertal in size. However, testotoxicosis: M% U$ f) F! ?. q) u9 D2 s9 F7 z) M+ ^
was in the differential diagnosis because his father
4 ~! K8 Q+ @4 estarted puberty somewhat early, and occasionally,
2 n' n: n+ v% S6 H, ltesticular enlargement is not that evident in the
4 k$ r2 |7 K  [; ~, z# G$ ?beginning of this process.1 In the absence of a neg-7 |' U+ }  h+ z- T. R
ative initial history of androgen exposure, our
: q' j6 f! y) H- L2 Z# B( vbiggest concern was virilizing adrenal hyperplasia,% W! y, y5 @6 P. Q* ?3 z3 D9 S- d
either 21-hydroxylase deficiency or 11-β hydroxylase
' g6 P% o8 t2 o* cdeficiency. Those diagnoses were excluded by find-
. E. v5 E, L- m; Ving the normal level of adrenal steroids.
7 x- P- y% Q1 X+ C: [The diagnosis of exogenous androgens was strongly
% C3 w0 O7 k5 J6 y+ \9 {suspected in a follow-up visit after 4 months because( L1 N# A8 h3 v* ]$ A+ e% o) h
the physical examination revealed the complete disap-" z; t$ O, z$ z3 I
pearance of pubic hair, normal growth velocity, and0 W2 J" C9 }! x* l* U5 C
decreased erections. The father admitted using a testos-
7 |" M$ w1 O; ]. ^4 ~( H  Y. vterone gel, which he concealed at first visit. He was
. J5 b: s/ M# N) g2 N, Susing it rather frequently, twice a day. The Physicians’, j) a: X' f, S; g6 s
Desk Reference, or package insert of this product, gel or
9 j$ Q/ V/ C3 tcream, cautions about dermal testosterone transfer to+ Q6 K4 _1 j0 A* \: z2 ~# {
unprotected females through direct skin exposure.4 u+ E' U# F$ `/ X. N3 s% J
Serum testosterone level was found to be 2 times the4 {, C* p$ O+ K2 m" D
baseline value in those females who were exposed to
4 u0 x0 R) ]9 q7 @/ [6 ^8 Zeven 15 minutes of direct skin contact with their male7 X9 [) H) L0 d) P
partners.6 However, when a shirt covered the applica-0 y; ~8 V0 @, B7 B( O% ]. o
tion site, this testosterone transfer was prevented.0 n2 a& r  g- E0 |! x5 D
Our patient’s testosterone level was 60 ng/mL,8 `" l% W" A( e5 G% F+ a7 u2 a
which was clearly high. Some studies suggest that$ p! T7 i4 |; ]; f
dermal conversion of testosterone to dihydrotestos-
+ b- ]" E" V* B0 H" Pterone, which is a more potent metabolite, is more! o2 F4 a% ?% \
active in young children exposed to testosterone
7 [8 Z* D* E0 M4 x6 G% Uexogenously7; however, we did not measure a dihy-
, h5 A8 Z: }3 f6 jdrotestosterone level in our patient. In addition to
9 \3 N/ B+ g* j+ `" d$ z# |virilization, exposure to exogenous testosterone in
& V0 g) q/ a' tchildren results in an increase in growth velocity and
+ g- [6 O$ w! d5 A, Y# madvanced bone age, as seen in our patient." x" I# H9 n) y2 e8 {, B: A6 k8 v
The long-term effect of androgen exposure during; ]) @. ?, B8 k- m1 j+ o
early childhood on pubertal development and final
% {; m5 C+ _' Y5 D. ]adult height are not fully known and always remain
0 [. k* G. B$ w0 {. _+ ja concern. Children treated with short-term testos-
9 O: q* h. X, y- \8 g' L* K* q0 Jterone injection or topical androgen may exhibit some2 o0 b1 h, L2 B5 Z% i, w7 _7 p
acceleration of the skeletal maturation; however, after7 f& L4 p( i3 Y; x; ?1 e; s
cessation of treatment, the rate of bone maturation' \9 w( P1 k2 Y
decelerates and gradually returns to normal.8,9
0 s& B% m/ W+ V4 L, h; ^( LThere are conflicting reports and controversy
2 ]+ m" d  e3 M% kover the effect of early androgen exposure on adult/ d2 Z  ]2 \4 h% ~6 i8 _* f( ^
penile length.10,11 Some reports suggest subnormal
( y( V' q3 ^1 d8 x7 P" d; k% Yadult penile length, apparently because of downreg-- j/ X! T2 W  a2 G2 v- u
ulation of androgen receptor number.10,12 However,
4 j; c  i9 J! c$ ~: v+ B7 w  ^Sutherland et al13 did not find a correlation between
; |- X2 h# V- i+ }! Lchildhood testosterone exposure and reduced adult
9 X; ?7 H" Q4 c: {) @( }1 |, @) tpenile length in clinical studies./ h2 o" a8 A/ [0 ~6 L, w% C
Nonetheless, we do not believe our patient is
5 g" q, K9 V& V0 Agoing to experience any of the untoward effects from. F' g& Q. U6 B' q
testosterone exposure as mentioned earlier because
" X$ V" U! ^, v7 Xthe exposure was not for a prolonged period of time.% z! Y6 h0 s; M0 t+ m7 {
Although the bone age was advanced at the time of
9 u" G9 I. I  ?) D! a0 [diagnosis, the child had a normal growth velocity at
  B! K" B& N# Y# S) y( ~3 xthe follow-up visit. It is hoped that his final adult( M) u. {7 P. N0 }- e" k4 F
height will not be affected.2 A  K) {. q- X( ^. {
Although rarely reported, the widespread avail-
, {$ ?0 T$ Z4 wability of androgen products in our society may
) z  T4 T3 a# t3 W1 Vindeed cause more virilization in male or female
! c- a, }" F9 @5 J' r* [children than one would realize. Exposure to andro-6 Q2 w. e0 L5 l: N+ P
gen products must be considered and specific ques-5 g3 V# _+ y% Z  A
tioning about the use of a testosterone product or
- V# n) s# O; W: Bgel should be asked of the family members during! k0 ^1 e4 C. X
the evaluation of any children who present with vir-
% {0 a4 ]# _  A" b7 E: Y3 M" Hilization or peripheral precocious puberty. The diag-+ l" @6 b2 ]1 N& b3 F. R
nosis can be established by just a few tests and by
( v4 _8 ]* z  @appropriate history. The inability to obtain such a" W; h# \. c* Q# j8 O  A0 \. ~) `
history, or failure to ask the specific questions, may
* `: F6 d( T& f' p( F, Uresult in extensive, unnecessary, and expensive
  a& B2 d. A( a6 ninvestigation. The primary care physician should be2 V. \5 B2 f0 }  b% v: F& d1 w! k
aware of this fact, because most of these children! }& F8 `/ _# G4 Q
may initially present in their practice. The Physicians’% b0 x. |& m$ f" H( K# A! p
Desk Reference and package insert should also put a5 O# y3 @( E3 W4 [
warning about the virilizing effect on a male or
7 C( T* S' o  K. H2 xfemale child who might come in contact with some-# Z( O" d$ R' k  Y2 d. ]( I
one using any of these products.
) _$ F% F5 W7 OReferences
. w1 n& C2 g1 @4 m: ]$ n  |, P1. Styne DM. The testes: disorder of sexual differentiation
+ N8 p3 L6 q! W- a; Aand puberty in the male. In: Sperling MA, ed. Pediatric, k% w8 M' U3 e7 f4 O+ U5 |, F
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
! R* v  b: U! H: v9 |2 L! U$ s2002: 565-628.
5 j7 q3 O9 H* q; l8 V% D* L$ [2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious  n: l5 N7 N: D2 }$ A$ E
puberty in children with tumours of the suprasellar pineal
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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
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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

8 ]; k6 Y/ {7 Z) \8 a1 A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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