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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-Old8 U0 r+ D( D& ~5 }) h5 b6 U3 G( z+ p
Boy Induced by Indirect Topical/ L* s' g' h( s/ i" X
Exposure to Testosterone+ ?" f6 X7 k# u/ _+ P1 y% g
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
  @- \1 y) J. j! _' Pand Kenneth R. Rettig, MD1$ t- ^  C0 U# f
Clinical Pediatrics  P3 L1 p3 ?$ X0 i" ?' M" J
Volume 46 Number 60 P" M+ r! [9 c$ R
July 2007 540-543& B& y& n$ x4 d  B$ d9 D
© 2007 Sage Publications% B  C8 m  F8 G$ [/ q$ l% D' q
10.1177/0009922806296651
( A% b% T# R3 }* w3 Y' [' t3 `http://clp.sagepub.com8 L' W6 D1 d# q7 }6 [8 r6 E
hosted at' r; Q# j, K5 m  f; y2 }! i5 E6 q
http://online.sagepub.com& t6 h$ q$ ^. U# a6 e# T
Precocious puberty in boys, central or peripheral,( h# V; o  c* Z$ y0 Z5 Y+ Y
is a significant concern for physicians. Central
( I7 T  W7 u* z) I1 F- c1 }, l$ Vprecocious puberty (CPP), which is mediated
, d$ H6 [# b3 M# hthrough the hypothalamic pituitary gonadal axis, has
2 i2 H3 S% L3 ?! O8 @7 Ya higher incidence of organic central nervous system
7 g' X1 O2 ?4 ]7 D  j1 J" ]lesions in boys.1,2 Virilization in boys, as manifested; n8 b( C8 `; d# e
by enlargement of the penis, development of pubic
7 S( R  i5 |! \6 a/ ?* chair, and facial acne without enlargement of testi-
( D( l; W. q7 _! ]8 Scles, suggests peripheral or pseudopuberty.1-3 We
5 N: h( O3 S; Q& \/ c( ~; yreport a 16-month-old boy who presented with the, Z! E% C& a9 g; T* G
enlargement of the phallus and pubic hair develop-/ S3 S$ ]! I- b& T7 g- Y5 y+ v& n
ment without testicular enlargement, which was due
7 G% o  P: D# i# g: j0 tto the unintentional exposure to androgen gel used by
2 l* _7 ?9 k) `the father. The family initially concealed this infor-
7 x# o/ M; s3 {# Amation, resulting in an extensive work-up for this
# [' i; n  ]6 N6 ^4 j7 \child. Given the widespread and easy availability of
% \- p. @6 T, I  S) M9 Xtestosterone gel and cream, we believe this is proba-3 Q) t! g; c) L5 F
bly more common than the rare case report in the
5 f' v" n! n2 kliterature.4
( y5 l/ p6 G0 x& ~Patient Report9 N1 }# |& l8 L
A 16-month-old white child was referred to the: l0 B- ^$ z6 z8 F1 N
endocrine clinic by his pediatrician with the concern& C4 V$ X, O) [) K5 [' U/ i
of early sexual development. His mother noticed
2 W1 r1 R; H; \  c& f9 P4 j* j7 Llight colored pubic hair development when he was4 c3 T, x. i. y8 {
From the 1Division of Pediatric Endocrinology, 2University of) M. n* n$ T) F1 c$ ^  z
South Alabama Medical Center, Mobile, Alabama.
' {% h6 F" o" IAddress correspondence to: Samar K. Bhowmick, MD, FACE,( X1 E2 T( @9 S2 F- s
Professor of Pediatrics, University of South Alabama, College of6 c7 m7 [2 I' q' D
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
! \2 ^" g" R. K/ be-mail: [email protected].
+ N( `9 s* f) tabout 6 to 7 months old, which progressively became
: M. W- y0 O. `, p- p& ydarker. She was also concerned about the enlarge-
0 S( ^+ d* @/ U4 W  z- q  W: Ument of his penis and frequent erections. The child
* h- G3 K8 z' o' S* _was the product of a full-term normal delivery, with
7 q& ^4 o+ T9 M' G* m  aa birth weight of 7 lb 14 oz, and birth length of
5 }6 p6 m* q7 x5 J6 Y, Z) c20 inches. He was breast-fed throughout the first year( {: P9 _4 H8 a: o/ `9 W3 n
of life and was still receiving breast milk along with
( `5 ^$ u9 K7 Z4 rsolid food. He had no hospitalizations or surgery,
; x5 V- h( Q! [; V3 }0 ?: P7 Yand his psychosocial and psychomotor development
8 t2 a8 l# `& E0 \3 Q5 k8 lwas age appropriate.* {+ L$ F# c' i; m  q. C$ O
The family history was remarkable for the father,
, E# T5 H! R4 u5 ~7 z& Q; h& k0 cwho was diagnosed with hypothyroidism at age 16,
( M: @9 l, a) Dwhich was treated with thyroxine. The father’s  I' I7 J. Q2 \0 G
height was 6 feet, and he went through a somewhat6 \2 l* |' ~/ V. P
early puberty and had stopped growing by age 14.7 _+ \$ D" b' s1 Y  x' O9 t* _$ \
The father denied taking any other medication. The0 v9 Q& Q6 c( ]( E3 F% ^
child’s mother was in good health. Her menarche
7 I& I: U: w6 \5 m0 ywas at 11 years of age, and her height was at 5 feet
6 j+ M9 _- a8 s" w5 inches. There was no other family history of pre-
: o) R$ ~3 I  ?cocious sexual development in the first-degree rela-
: v$ n- k: o2 Xtives. There were no siblings.2 N1 q9 ~0 Y1 ]( F  U- A
Physical Examination- X4 D+ Z& _% @1 ?# k4 F
The physical examination revealed a very active,. D- }. i, ?8 {7 S2 q! O
playful, and healthy boy. The vital signs documented& R" X/ r0 ^( i
a blood pressure of 85/50 mm Hg, his length was
: C* I6 u# P' _2 P90 cm (>97th percentile), and his weight was 14.4 kg2 `7 S3 O3 t+ U$ u- r
(also >97th percentile). The observed yearly growth. l9 Y) ^( p$ _5 p) F( M$ K7 y9 H
velocity was 30 cm (12 inches). The examination of( q1 Y/ |+ d3 X2 h4 b
the neck revealed no thyroid enlargement.
: V$ {9 i9 j" MThe genitourinary examination was remarkable for
% ?# t8 \: R3 ~6 \+ \  K$ Yenlargement of the penis, with a stretched length of
, s+ y9 \. `3 h2 S8 f6 X8 cm and a width of 2 cm. The glans penis was very well2 t, l0 A! H: g/ X2 U6 i5 ^( t
developed. The pubic hair was Tanner II, mostly around! ^0 }- s& e. b& j* c
540. O3 G. \$ ]9 H- f. w
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
" }1 r, Y" A3 G( athe base of the phallus and was dark and curled. The
) t% R' t# K5 W) @6 H$ x3 Wtesticular volume was prepubertal at 2 mL each.
8 y% I# h0 Z! o5 q8 y  }3 WThe skin was moist and smooth and somewhat
# K& R; Q1 M! M  y) hoily. No axillary hair was noted. There were no
9 m+ x$ n2 o6 t% R2 {! j4 y4 M0 gabnormal skin pigmentations or café-au-lait spots.
/ e, e% n' Y) N2 j$ P$ f+ lNeurologic evaluation showed deep tendon reflex 2+
4 P- \1 d1 E4 c0 d. fbilateral and symmetrical. There was no suggestion
0 x" f3 E+ M8 U* k, w3 |) p' nof papilledema.
: ?( \1 T9 i; q' e( d, YLaboratory Evaluation# B  o0 F6 ]4 R, K
The bone age was consistent with 28 months by5 E7 u1 ^' Y6 R( Q- M" {
using the standard of Greulich and Pyle at a chrono-
1 B7 Q7 d% z5 {* i# a! u( ^( ^logic age of 16 months (advanced).5 Chromosomal
; M. B& _6 x0 ]7 P- ?. Y- [* rkaryotype was 46XY. The thyroid function test
& c% l8 i  |& }1 V0 h' @& _% yshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
+ S' d  Y8 N# y3 m6 ~( ], K7 _) g- P0 }$ Slating hormone level was 1.3 µIU/mL (both normal).5 O1 O2 X; i4 _  ?5 V
The concentrations of serum electrolytes, blood
7 q% j- a4 `/ V: M$ @; ]urea nitrogen, creatinine, and calcium all were
  g5 G2 w0 O0 v: r& E# swithin normal range for his age. The concentration
7 e; f" k' d% k8 A3 D; gof serum 17-hydroxyprogesterone was 16 ng/dL+ P- x# X: B0 v: M
(normal, 3 to 90 ng/dL), androstenedione was 204 P4 O" z! P  s
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-6 N# [3 |- h4 |& [# V- J
terone was 38 ng/dL (normal, 50 to 760 ng/dL),, V; v; M0 R* O- F. K/ N2 Z4 B
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
# d0 T: ?* P! U* A49ng/dL), 11-desoxycortisol (specific compound S)
; V3 T4 g% x) v& _was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-" ?; ]7 b7 m  l: @# H! a3 t
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total$ a2 u! f* z% O* I! k  g8 J
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
8 ^7 d3 x8 X$ {, M5 Vand β-human chorionic gonadotropin was less than
& ^( O2 D! A' ~5 mIU/mL (normal <5 mIU/mL). Serum follicular5 h+ R( Q- j3 n, x, _
stimulating hormone and leuteinizing hormone1 w; z. z; D0 J6 f! z
concentrations were less than 0.05 mIU/mL
+ V' M" I" J3 d' B4 b. \(prepubertal).& A9 e2 [6 Q1 v& U3 |6 [! J
The parents were notified about the laboratory
1 I6 V! S1 I& G1 h9 w- Uresults and were informed that all of the tests were
! V( X' }! s% N$ h2 P! L3 G. Ynormal except the testosterone level was high. The
) i; b  Y. r; Dfollow-up visit was arranged within a few weeks to9 c6 \% Y9 k8 H) a% ?* j
obtain testicular and abdominal sonograms; how-
, ]3 T' K( _; H% r( m. }+ Y8 Xever, the family did not return for 4 months.! k& y5 H4 C+ }
Physical examination at this time revealed that the
' ^3 O: g1 s9 q2 v9 R- [child had grown 2.5 cm in 4 months and had gained1 j' y( A3 `. i. a- z# \$ z
2 kg of weight. Physical examination remained
+ ]8 c7 V# a( V' Cunchanged. Surprisingly, the pubic hair almost com-4 V& K! p8 E5 s  T+ w' @  [
pletely disappeared except for a few vellous hairs at
5 c* i0 K) Q! e  Q0 b2 ~the base of the phallus. Testicular volume was still 2
+ {! j1 M- Q- J, O( SmL, and the size of the penis remained unchanged.- ]+ Y  G6 ^) h7 F" m, m% }+ l
The mother also said that the boy was no longer hav-
# E! U2 L, H3 C6 n  s5 n3 Y/ bing frequent erections.
7 H% `0 g, T2 Y) Z( k2 gBoth parents were again questioned about use of: v/ z9 b+ x7 \$ u1 p! q& j& z
any ointment/creams that they may have applied to
4 n2 L( w& {" p- n1 D# tthe child’s skin. This time the father admitted the
" b. t2 q2 |: x2 t' KTopical Testosterone Exposure / Bhowmick et al 541
5 w, [% T2 u% p; {( huse of testosterone gel twice daily that he was apply-
5 O' a: y$ T" P- w/ p/ g  bing over his own shoulders, chest, and back area for
) U# T; X3 p/ J: R& _; [* Ua year. The father also revealed he was embarrassed; @% ~3 Z4 f- v4 }1 p
to disclose that he was using a testosterone gel pre-1 e7 G9 j6 p5 ]# k' f
scribed by his family physician for decreased libido3 K1 B! ]8 i$ Y8 Q! x) j# N
secondary to depression.
) n. a# f; _0 |; w; k/ nThe child slept in the same bed with parents.! K7 Q% h. a% A: B
The father would hug the baby and hold him on his
" s: R# V2 `: X5 h( bchest for a considerable period of time, causing sig-  e# l% c7 c* d- A, y
nificant bare skin contact between baby and father.3 x+ a( C2 P5 {/ {% _, F
The father also admitted that after the phone call,& T" }1 v6 t7 P4 X
when he learned the testosterone level in the baby& E/ d, o6 ?/ q6 S  o. z  O
was high, he then read the product information4 `$ e, u: g$ u( `  I9 ?; L( ], s
packet and concluded that it was most likely the rea-
& @$ N% B# T! D. _* g: M: T/ |son for the child’s virilization. At that time, they
' _) w  c3 `/ q* j1 X: @& w$ Zdecided to put the baby in a separate bed, and the
; n- Q6 l2 \! {3 ^! d4 dfather was not hugging him with bare skin and had
* f% I3 N5 I# c/ Z2 t6 O" Ybeen using protective clothing. A repeat testosterone
) g- V% ]" w: |+ T5 i5 f% d" ztest was ordered, but the family did not go to the7 H9 a! \8 L% d
laboratory to obtain the test., ^3 M2 `- k7 N2 I; U$ x7 H
Discussion' x# [- y% S: \" g' y
Precocious puberty in boys is defined as secondary
9 f% l9 A; v& B  W/ `# O6 c& o1 X9 Osexual development before 9 years of age.1,47 S! U7 i/ L! H; H3 j4 v; p
Precocious puberty is termed as central (true) when
( k* U6 }" b& g. {$ Iit is caused by the premature activation of hypo-
2 G1 F  ]$ z" b/ f4 m+ Nthalamic pituitary gonadal axis. CPP is more com-. C3 \, G' \4 R/ S  n* b: H8 x
mon in girls than in boys.1,3 Most boys with CPP
/ }5 \% N( N2 Omay have a central nervous system lesion that is
, X& `& E3 C6 Z5 `" g4 Oresponsible for the early activation of the hypothal-
+ |0 H& @6 h  o' K, Iamic pituitary gonadal axis.1-3 Thus, greater empha-  w+ L$ W# ^1 F8 {) G8 x
sis has been given to neuroradiologic imaging in2 B& K4 `( C# y% \: P
boys with precocious puberty. In addition to viril-
, ^! N' Z7 k% iization, the clinical hallmark of CPP is the symmet-
+ C5 t$ Q% J' l, _+ b! @rical testicular growth secondary to stimulation by1 [/ ?: `+ u* n8 }- h
gonadotropins.1,39 h( t9 e4 p9 C  i
Gonadotropin-independent peripheral preco-# @* Y9 y( l. S  r) F* @
cious puberty in boys also results from inappropriate/ K- ?6 }" V3 X, I
androgenic stimulation from either endogenous or
& B* i* y$ k, g+ j6 mexogenous sources, nonpituitary gonadotropin stim-. [8 _7 x2 h+ F0 B: m1 j6 W" v: I
ulation, and rare activating mutations.3 Virilizing: j) R" w. L- O( N- {( O5 K( l
congenital adrenal hyperplasia producing excessive
( ]( Q2 c' P6 j5 L2 b1 _adrenal androgens is a common cause of precocious
* ]* n! D* S6 \& h9 Q& Mpuberty in boys.3,4
. w  o- T* a9 |& [The most common form of congenital adrenal2 f0 [0 [# ?" W" [' Z
hyperplasia is the 21-hydroxylase enzyme deficiency.  w% U- S  [9 b, _" {* O
The 11-β hydroxylase deficiency may also result in% X5 B! N! _) B
excessive adrenal androgen production, and rarely,$ B4 |2 ^; `* o1 F- s7 L
an adrenal tumor may also cause adrenal androgen
# K, u- E6 m  |7 Z9 g9 l# xexcess.1,32 n$ M7 U. \- h6 n" b8 q# O
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
" Z! b! c% v: @# ^* w: b. B. r542 Clinical Pediatrics / Vol. 46, No. 6, July 2007: A6 C: }, o3 H, `* G5 I
A unique entity of male-limited gonadotropin-) R$ W  w6 `7 ]: _  f  n
independent precocious puberty, which is also known. k2 v! [$ l) @# Z
as testotoxicosis, may cause precocious puberty at a
+ P. V6 e* M. J, q/ k. t& u, ]5 Svery young age. The physical findings in these boys# z( D: G+ k/ K
with this disorder are full pubertal development,! c1 X, O9 E% U  U4 d
including bilateral testicular growth, similar to boys
/ ]4 v  Y  n& p: s1 k) k1 Wwith CPP. The gonadotropin levels in this disorder4 ^* Y' a6 t3 N' o
are suppressed to prepubertal levels and do not show
/ Q$ |; ]3 M4 M' x2 upubertal response of gonadotropin after gonadotropin-
6 v" Q& P$ f* f( Rreleasing hormone stimulation. This is a sex-linked: ^: W" a" B4 v
autosomal dominant disorder that affects only# b& ~. i8 G1 s% h3 l2 y+ z5 [' x
males; therefore, other male members of the family5 a. _( T7 l7 l: o3 M
may have similar precocious puberty.3* F8 K- M% V2 X/ q4 T
In our patient, physical examination was incon-
% s4 M. g1 i3 _) B  c$ v9 Csistent with true precocious puberty since his testi-
8 A* ?+ E" `- q5 O& T2 }1 ?, U3 ycles were prepubertal in size. However, testotoxicosis( O- x1 m6 R- U, l
was in the differential diagnosis because his father: r, [+ P5 y. a
started puberty somewhat early, and occasionally,
% C, y; n- C% ftesticular enlargement is not that evident in the- X+ O2 m9 {6 ~2 z
beginning of this process.1 In the absence of a neg-- Q7 V; h! e3 f. m, c; u
ative initial history of androgen exposure, our3 y, X+ u6 `( N0 y9 c# q# x  m
biggest concern was virilizing adrenal hyperplasia,# T' Y( C" R: y6 V5 S
either 21-hydroxylase deficiency or 11-β hydroxylase
1 s% l4 ?$ X% v+ udeficiency. Those diagnoses were excluded by find-
5 H6 f, |1 D  U+ x& K* Jing the normal level of adrenal steroids., u  p" i& @  a4 ?
The diagnosis of exogenous androgens was strongly9 i1 s: `+ g0 T% J
suspected in a follow-up visit after 4 months because
3 K8 r8 ^; A* |the physical examination revealed the complete disap-
. ]2 E2 S  O, _6 R, _; \! j$ Ypearance of pubic hair, normal growth velocity, and
' d' C5 V/ r% ydecreased erections. The father admitted using a testos-' U: `: g  b; o* k: ?- f( g7 L9 Y
terone gel, which he concealed at first visit. He was, m$ F; _% R4 u4 Y: d8 ]
using it rather frequently, twice a day. The Physicians’5 s2 r' _, i! E2 ~1 D, \* K
Desk Reference, or package insert of this product, gel or$ U4 M* o/ G  {# m& K
cream, cautions about dermal testosterone transfer to3 \* X; w7 f( C* C6 f
unprotected females through direct skin exposure.
( n8 R' S/ y. X1 eSerum testosterone level was found to be 2 times the
$ D  M$ j" ]* o+ z8 M) obaseline value in those females who were exposed to
1 G0 b% `4 I6 t5 \9 L2 v% r0 ]$ jeven 15 minutes of direct skin contact with their male- S5 Y0 R+ J: A3 ?3 r6 U
partners.6 However, when a shirt covered the applica-
2 b4 K6 s$ D8 k% n* ztion site, this testosterone transfer was prevented.
: I6 }. L6 m. ?! JOur patient’s testosterone level was 60 ng/mL,
- L3 m" u% j2 q4 ~which was clearly high. Some studies suggest that
  R; m3 K7 ]5 p+ V% t' sdermal conversion of testosterone to dihydrotestos-
$ Z) @. z, o1 G6 S! M# Yterone, which is a more potent metabolite, is more
1 g, p9 q. e# r7 Aactive in young children exposed to testosterone
  J3 N0 W$ }' @5 I% D. b4 Xexogenously7; however, we did not measure a dihy-
1 x" h. G- {: e7 Q; U2 jdrotestosterone level in our patient. In addition to  n& [+ T9 o# K8 `  K$ a% @
virilization, exposure to exogenous testosterone in
9 z1 ^+ R7 Q; G! r2 ~, }children results in an increase in growth velocity and8 N& M* m. o- N
advanced bone age, as seen in our patient.: O! v: e8 D( ^, x+ r
The long-term effect of androgen exposure during
, G- F" V* [5 K( ?" Jearly childhood on pubertal development and final
& J$ ~& n9 V- z" x8 V7 N0 Padult height are not fully known and always remain) x8 m, z; j9 I; I
a concern. Children treated with short-term testos-
$ ?6 o3 l+ r0 ]. f; _& fterone injection or topical androgen may exhibit some
2 w3 O# O9 U( M5 H! Iacceleration of the skeletal maturation; however, after  b  W& ]$ A( ^, ~' O* J0 a
cessation of treatment, the rate of bone maturation& r6 v5 y4 h6 F9 n
decelerates and gradually returns to normal.8,9
2 Q- ~( ~. y" {% a0 pThere are conflicting reports and controversy" R- H1 B8 T7 m+ S& n! R) {' T
over the effect of early androgen exposure on adult
$ Z: }, i9 D1 K1 ]- l3 [! _9 K* }+ wpenile length.10,11 Some reports suggest subnormal/ Q5 X' z# A6 A1 A# w7 c
adult penile length, apparently because of downreg-
; N' n6 `8 J' q  O) S- A5 ^ulation of androgen receptor number.10,12 However,6 V/ _6 w5 n" u; W8 N* o! C9 _
Sutherland et al13 did not find a correlation between
0 J$ _. Y: i1 B6 Mchildhood testosterone exposure and reduced adult6 V# F( @( S8 |0 L
penile length in clinical studies.1 t) g4 ?% t% G$ z  l5 u
Nonetheless, we do not believe our patient is+ q# u: d% I5 s# n8 t# ?" e
going to experience any of the untoward effects from
  q- w9 U1 p1 m; |% x! N/ Atestosterone exposure as mentioned earlier because
# k, y% b, C) ithe exposure was not for a prolonged period of time.
; U" V6 e) [; z. W* H4 Z, o7 F2 }Although the bone age was advanced at the time of
' e$ a/ ^; Y0 j4 \) H/ gdiagnosis, the child had a normal growth velocity at
3 K* @  i. _2 U1 A% w& tthe follow-up visit. It is hoped that his final adult
$ h' t# B; P) _. T+ o  r7 qheight will not be affected.* b% H! u8 R; ~. }( t
Although rarely reported, the widespread avail-
$ M7 e9 `* i3 z7 ~4 a  O$ Rability of androgen products in our society may
, n: g2 \; d% V& m9 z6 Mindeed cause more virilization in male or female
3 h' }. r8 o/ B' Rchildren than one would realize. Exposure to andro-+ n: }: h) v9 \8 n7 B
gen products must be considered and specific ques-
- h  m& s  k7 c' P3 t, M7 F, `9 btioning about the use of a testosterone product or
/ y1 P7 U" d! `gel should be asked of the family members during
6 z* u* o8 `9 othe evaluation of any children who present with vir-$ ?% g0 M' G) g1 n9 M% f
ilization or peripheral precocious puberty. The diag-' }3 t$ X- X/ g; x% T
nosis can be established by just a few tests and by7 ?" V) j( K( r( ~
appropriate history. The inability to obtain such a1 J  o4 m. J9 }% F0 i- b! _8 u1 g# X
history, or failure to ask the specific questions, may
4 U9 O! A+ ?4 w; g3 Presult in extensive, unnecessary, and expensive4 k7 g7 w: f( {* S2 n
investigation. The primary care physician should be
' ?; k  j) H: r  paware of this fact, because most of these children
0 b( b% b7 i) h, h, Cmay initially present in their practice. The Physicians’7 ]  `0 ~( N% W6 \3 H
Desk Reference and package insert should also put a9 \6 r9 E1 {9 p7 }+ E* E; L
warning about the virilizing effect on a male or, I! ^4 d" ?+ u' b
female child who might come in contact with some-
, a0 y1 v8 P7 z9 R, tone using any of these products.
; l; s1 Q' m+ S+ Q/ l9 D( lReferences+ X- h) u  I+ F* X$ J
1. Styne DM. The testes: disorder of sexual differentiation! x- K3 e8 q3 Q$ f. X6 n$ z6 ~
and puberty in the male. In: Sperling MA, ed. Pediatric
$ }! E/ t$ X$ e3 E$ R4 L0 bEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
3 G! B& i3 @2 X8 A2002: 565-628.. J5 P# V# d$ l# n6 s, B- O
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious, {: A3 r3 ?1 U# U: X
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
/ \* z4 J9 N' Z) x+ jBoy Induced by Indirect Topical
, u( B4 \+ G/ RExposure to Testosterone
9 u: n/ D- H8 J" W& PSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
& [: H) x' V) x: W9 U' w6 a: Fand Kenneth R. Rettig, MD1. ?; Q# e5 S( X" _. G& h5 e
Clinical Pediatrics
$ P3 {/ g; i+ P3 w' a& \' D( lVolume 46 Number 6
" S: Q- u% G) ?/ I0 T) yJuly 2007 540-543& Z9 E4 m( a6 I, V8 ?3 [
© 2007 Sage Publications
, Q* {, X7 `7 u, i" X4 ?1 t1 `10.1177/0009922806296651
; b& P% N. ]. C5 k7 N- @9 ?http://clp.sagepub.com
, }3 T5 i$ J# Q4 b6 w* Lhosted at
9 c* I7 J" f  L8 _9 F5 ahttp://online.sagepub.com$ }+ f, h) @0 W0 U) u  _: h
Precocious puberty in boys, central or peripheral,
$ k/ L9 _) S* ?& e! @6 X% z3 N/ Gis a significant concern for physicians. Central
) Y( F+ o/ @9 \% Wprecocious puberty (CPP), which is mediated, [5 ?% L, _4 i7 ~, P
through the hypothalamic pituitary gonadal axis, has
; ~- @" Y5 E& M" u6 h4 m! Ia higher incidence of organic central nervous system4 \# C$ g+ G: C3 B
lesions in boys.1,2 Virilization in boys, as manifested
& W3 T' @' D2 u- Oby enlargement of the penis, development of pubic
8 I4 _0 V" S/ r1 r( `$ f' dhair, and facial acne without enlargement of testi-* I; d# j/ j( x
cles, suggests peripheral or pseudopuberty.1-3 We9 P8 g8 {& j( O9 b
report a 16-month-old boy who presented with the) n2 c& P! [4 S# |9 }
enlargement of the phallus and pubic hair develop-' K4 _% I9 D) ^3 ~
ment without testicular enlargement, which was due
7 t) M9 X8 r& @' i" K. y' Uto the unintentional exposure to androgen gel used by
) G" g5 I6 k# U5 U; ~the father. The family initially concealed this infor-
0 K. T2 i8 W5 [mation, resulting in an extensive work-up for this4 a- E( B1 u4 d+ b9 E6 Q
child. Given the widespread and easy availability of
+ F: a9 M* f* u4 e. ~9 a+ |testosterone gel and cream, we believe this is proba-; R7 H; I4 {5 h) H/ k
bly more common than the rare case report in the
1 F) }1 d: r" w6 Qliterature.4
+ ~# f- d: K8 v( z$ G  J0 k- ~Patient Report# |4 {! a7 c2 ~5 T2 T$ K* s, ~$ R
A 16-month-old white child was referred to the6 d6 U. d6 D  f8 u# q
endocrine clinic by his pediatrician with the concern+ B5 u& z) I9 ]$ `: \% z
of early sexual development. His mother noticed6 T3 H$ }7 s6 \' L  H
light colored pubic hair development when he was
1 H- J' ~$ |+ `7 q. kFrom the 1Division of Pediatric Endocrinology, 2University of
9 X1 c1 X4 T( i% ]South Alabama Medical Center, Mobile, Alabama.
8 L' x' T" Z9 Q7 BAddress correspondence to: Samar K. Bhowmick, MD, FACE,* h; s1 {. W8 u# B9 U% h& H. j
Professor of Pediatrics, University of South Alabama, College of
8 t7 z3 J9 e  p( vMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;, @# M" B" y6 g) b) O# M& P$ j+ l- O
e-mail: [email protected].: l% ]. e# ~1 g& x) ^( r% x
about 6 to 7 months old, which progressively became
6 ^; h. r6 Y* e9 `& G! \  S( Ddarker. She was also concerned about the enlarge-
0 a# q  X& b1 G  _# M! rment of his penis and frequent erections. The child) p% |# Z/ a$ {/ w  M
was the product of a full-term normal delivery, with
# ]9 `; k( t+ V4 W- Q/ ya birth weight of 7 lb 14 oz, and birth length of1 B% a8 U8 E; p9 Z
20 inches. He was breast-fed throughout the first year
9 ]% Z# z7 |' r0 Aof life and was still receiving breast milk along with/ }# m+ f" w8 ?. R
solid food. He had no hospitalizations or surgery,
) o3 c& @. N% v. d) D: m) vand his psychosocial and psychomotor development
# m) g. O& S5 A1 T* wwas age appropriate.. l- _3 w! z6 o& @% W8 d
The family history was remarkable for the father,
( }$ g7 U, I. Mwho was diagnosed with hypothyroidism at age 16,6 h5 ]  D2 h; Z( W
which was treated with thyroxine. The father’s& r9 p. @3 T1 h+ b* E  ?
height was 6 feet, and he went through a somewhat
4 x. z2 C# o: v- s2 o4 Nearly puberty and had stopped growing by age 14.6 Z2 Z7 g; k: i! D9 w
The father denied taking any other medication. The
$ |( N. K4 I6 H- ^- \& Q$ j3 j6 dchild’s mother was in good health. Her menarche
5 M$ P& C5 G3 X; ^# Xwas at 11 years of age, and her height was at 5 feet" q% Z, Z: |, u- F
5 inches. There was no other family history of pre-
. |  ^- q: j0 x# o, t% O$ ]cocious sexual development in the first-degree rela-
6 u/ a. H. ^6 `tives. There were no siblings.+ G/ Z) q, N+ k& V& Q1 q
Physical Examination! Z. o8 A1 H  G" b7 z8 @
The physical examination revealed a very active,
3 ]8 _8 T* m6 t0 F' @# j( U# @playful, and healthy boy. The vital signs documented
5 z( r! g- [/ \  E7 u5 pa blood pressure of 85/50 mm Hg, his length was$ N- p1 }( U) y: P- x
90 cm (>97th percentile), and his weight was 14.4 kg
' `% E! J, e9 D0 |: z% d) l, Z(also >97th percentile). The observed yearly growth  H& x+ A5 G% p. y6 O6 W
velocity was 30 cm (12 inches). The examination of
. f# ]- H) |& y* o7 gthe neck revealed no thyroid enlargement.$ E. @7 t0 |. i4 O' d" c
The genitourinary examination was remarkable for
* C! p8 w* C/ Z9 Nenlargement of the penis, with a stretched length of
- K, r1 I# n8 F$ q; X8 cm and a width of 2 cm. The glans penis was very well
/ ]- I, `8 }# i: qdeveloped. The pubic hair was Tanner II, mostly around
* ~1 Z6 l* {- G* |  J5 r540" O4 u' H) B0 X* d' q
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
2 O" l. ]( y" D: w8 S4 Kthe base of the phallus and was dark and curled. The+ Q$ N% r' p. f% Q
testicular volume was prepubertal at 2 mL each.
7 w5 X" U1 d5 n6 i! _% M+ lThe skin was moist and smooth and somewhat- a/ Y3 R; ?) W" k$ B  u' }
oily. No axillary hair was noted. There were no
5 b1 _! a! [$ f# Jabnormal skin pigmentations or café-au-lait spots.
, o6 L5 k# F! H( b; P9 wNeurologic evaluation showed deep tendon reflex 2+
+ o4 i, D1 T3 s& O5 j! G1 R) T2 D9 Wbilateral and symmetrical. There was no suggestion+ J# K: l$ E' d( c' z( X
of papilledema.
& u5 g; x4 N5 J7 ILaboratory Evaluation
2 v4 T3 o  k0 }The bone age was consistent with 28 months by
% Q7 m% R! F* fusing the standard of Greulich and Pyle at a chrono-
3 e- n9 F6 e" w( q! |logic age of 16 months (advanced).5 Chromosomal
0 T5 H9 P* R" B: d* Y# l2 Akaryotype was 46XY. The thyroid function test6 Y) j9 J/ x; U, w; _: g
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
. y2 ]/ b" o! u. l: hlating hormone level was 1.3 µIU/mL (both normal).3 B% p4 _6 S* G4 y9 U
The concentrations of serum electrolytes, blood
% F8 g' A/ k6 \' |0 r" Uurea nitrogen, creatinine, and calcium all were- H% b% p+ d) h4 _+ b( J, {- H3 z
within normal range for his age. The concentration) C7 ]! i& u8 q+ \. b+ `/ K
of serum 17-hydroxyprogesterone was 16 ng/dL1 _  Q6 t3 }5 u, F) r, C$ L1 U
(normal, 3 to 90 ng/dL), androstenedione was 205 C4 e- H: g1 [7 z" F; Y( P
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-8 t3 g& j  K9 H. l% e. U4 E+ F( o, N8 `4 ^
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
. l# p0 p4 y7 u* |, D" Edesoxycorticosterone was 4.3 ng/dL (normal, 7 to
$ }* L- s9 W  ?49ng/dL), 11-desoxycortisol (specific compound S)
: ?; J4 C% V1 N- N" z: Hwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
+ @/ M  d  a% Q- _) t; qtisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total$ m% H0 B  O. O, G. f/ l; R$ O1 Y2 ?
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
1 T+ P/ q+ `6 p8 H, P+ o: R' r% Pand β-human chorionic gonadotropin was less than+ |5 g! \) {3 O8 t, M8 v: @
5 mIU/mL (normal <5 mIU/mL). Serum follicular
9 n6 R9 D( S6 Wstimulating hormone and leuteinizing hormone5 \+ T4 Y7 Y  G; _$ o- n, s. h
concentrations were less than 0.05 mIU/mL* ^7 q: T3 j; |$ m- V
(prepubertal).( a- Q! W# j: t6 `3 Z. c
The parents were notified about the laboratory
; z, [3 G* ?+ ~' v$ O7 kresults and were informed that all of the tests were
. u6 J5 i- P9 N5 y) _& u. gnormal except the testosterone level was high. The
; T/ ?1 K- o0 D6 @" C0 nfollow-up visit was arranged within a few weeks to
+ a# }* d& e2 ^2 G- uobtain testicular and abdominal sonograms; how-3 s6 k0 S! A, U- m8 V  e0 z
ever, the family did not return for 4 months.5 m4 f# U* F* Z7 k! v) w0 d* B
Physical examination at this time revealed that the
0 m/ I9 V/ V* R9 G) p9 o% gchild had grown 2.5 cm in 4 months and had gained
9 f; h# L/ C# O* [. b2 kg of weight. Physical examination remained0 t+ C! @4 r* N. c- }& k
unchanged. Surprisingly, the pubic hair almost com-$ T7 V9 X4 T9 C/ M/ \
pletely disappeared except for a few vellous hairs at
( j# i: R0 }% Othe base of the phallus. Testicular volume was still 2& V4 m  q; b$ F( S9 B# L
mL, and the size of the penis remained unchanged.+ ?/ g, a8 J/ v. G6 D
The mother also said that the boy was no longer hav-
! f4 t. o5 M+ |* f9 Oing frequent erections.6 b  A8 m: n5 t% I) B  H
Both parents were again questioned about use of
% ?5 X" c( Y4 tany ointment/creams that they may have applied to0 o2 m4 S& ^+ [: C6 b
the child’s skin. This time the father admitted the
6 y! `% Z) ?, ?1 `7 O  C* NTopical Testosterone Exposure / Bhowmick et al 541
2 X& r5 E% Q8 B6 E. Q5 puse of testosterone gel twice daily that he was apply-
+ s9 H& \7 \$ [5 R' A0 v: r0 \2 ^ing over his own shoulders, chest, and back area for( n. I/ G0 Z! \& N" u2 S
a year. The father also revealed he was embarrassed/ a7 S! I* R  Z2 s
to disclose that he was using a testosterone gel pre-. A- B6 F8 r2 I$ t7 {9 K
scribed by his family physician for decreased libido
0 B: `5 D3 P! M4 gsecondary to depression.  s! ^' h) P; l7 A; x
The child slept in the same bed with parents.
$ s& h3 N) {# q8 YThe father would hug the baby and hold him on his
  v6 m  I8 @; D# Q$ N: U; m# ~chest for a considerable period of time, causing sig-
9 W, ^' v  o2 o# |# ]. W1 Ynificant bare skin contact between baby and father.
8 o; ]; i5 x- a# f$ V: LThe father also admitted that after the phone call,' L7 d- J+ e: {0 U  P
when he learned the testosterone level in the baby
/ `3 b) z3 s9 x! d9 `was high, he then read the product information9 Z3 Z5 q$ r8 ?8 _) Q; h/ _
packet and concluded that it was most likely the rea-7 Z3 }4 U8 f* M) k2 e& ~
son for the child’s virilization. At that time, they
0 D, L( y4 B. |decided to put the baby in a separate bed, and the+ D, o" G' t. ]! ?( d
father was not hugging him with bare skin and had
4 F7 D6 @, u* y; Z% c6 ]been using protective clothing. A repeat testosterone8 N; q3 }* S# y. r' p
test was ordered, but the family did not go to the, X4 q- A2 s, ^7 `
laboratory to obtain the test.
2 j; ^6 _$ V$ a( Q: Z' Q/ wDiscussion
2 ^6 a$ g! G  X" v( X/ zPrecocious puberty in boys is defined as secondary
4 X8 o. n  @- h- T( Xsexual development before 9 years of age.1,4$ C& Q1 [7 D# |- V, {2 |* {
Precocious puberty is termed as central (true) when  u% Q$ x4 H1 s2 D" b4 U9 z
it is caused by the premature activation of hypo-, F4 I  r8 S) |8 w: _* X2 N
thalamic pituitary gonadal axis. CPP is more com-' Z2 Q4 f! `! G
mon in girls than in boys.1,3 Most boys with CPP
; j. R: G: J/ N4 e$ P3 A* ^may have a central nervous system lesion that is
( n& D  a& T5 D' @$ zresponsible for the early activation of the hypothal-. w% h; S8 C! H
amic pituitary gonadal axis.1-3 Thus, greater empha-5 R  Z+ v9 A5 _5 p, K% ]
sis has been given to neuroradiologic imaging in* p) H+ {+ x  {* \: P
boys with precocious puberty. In addition to viril-
* I  D1 L" {. U3 x  y, _! [ization, the clinical hallmark of CPP is the symmet-2 i8 \5 D2 \" x. P. \1 n. P- ^  T
rical testicular growth secondary to stimulation by* ]$ b4 q+ M9 M1 u& p0 u
gonadotropins.1,3
1 v; _- Y2 o, }9 @  ^/ p. j/ DGonadotropin-independent peripheral preco-" n, s% t' i, z2 D" T& _4 w
cious puberty in boys also results from inappropriate
- {3 [9 Y- W  s8 Z4 S9 Uandrogenic stimulation from either endogenous or
/ x! T3 ^1 y% y9 xexogenous sources, nonpituitary gonadotropin stim-
+ D& V, \0 B' c* F6 V, lulation, and rare activating mutations.3 Virilizing
2 W4 P/ O8 }% G& G/ Scongenital adrenal hyperplasia producing excessive# S$ B. o0 s4 j+ e  `9 e# }
adrenal androgens is a common cause of precocious) M) i/ m* m$ v
puberty in boys.3,4
( B7 |! A6 [( I6 `  G" _, _The most common form of congenital adrenal
: a4 h5 `7 u% _- L' xhyperplasia is the 21-hydroxylase enzyme deficiency.
! D1 D& a# d3 o8 }. Y/ |The 11-β hydroxylase deficiency may also result in/ g% k' C- W% X" Y1 e) e
excessive adrenal androgen production, and rarely,0 @% R! Z1 c+ P0 c  n
an adrenal tumor may also cause adrenal androgen
+ }. ?& k7 ?* w( J5 w- Zexcess.1,3
: M8 o/ x: j- q. Y) ^8 iat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
. ^# G' w3 @' e6 m* Q) c542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
% I( v0 Z% k3 m+ PA unique entity of male-limited gonadotropin-
* V( u. G& C9 q- }- Cindependent precocious puberty, which is also known
6 {  o8 N2 D, H: oas testotoxicosis, may cause precocious puberty at a6 u: K. I/ Z) o; m; x9 T
very young age. The physical findings in these boys
" {5 y9 s8 U, H$ Rwith this disorder are full pubertal development,9 ]7 h+ H8 h0 h% F$ i5 W) u& X
including bilateral testicular growth, similar to boys& M0 k' p3 [& m" f
with CPP. The gonadotropin levels in this disorder
$ K# f/ r% I# R7 h2 f, z, z6 Hare suppressed to prepubertal levels and do not show
* f3 a$ i, j, X; k  M. Fpubertal response of gonadotropin after gonadotropin-
6 h3 r+ p4 W- Y& W% rreleasing hormone stimulation. This is a sex-linked
( s* n; y2 P/ L  k- eautosomal dominant disorder that affects only
' R2 F5 J' t5 d4 F& ^  ?7 Zmales; therefore, other male members of the family# l1 R, q( e8 s
may have similar precocious puberty.3
1 I1 @, X2 G' F6 U  mIn our patient, physical examination was incon-
3 e( A/ S1 ]* ~( L: b# n# Vsistent with true precocious puberty since his testi-
1 i& \5 g7 P+ D0 o+ rcles were prepubertal in size. However, testotoxicosis4 A9 p  X: C1 U/ A; W& {0 y
was in the differential diagnosis because his father
/ U5 S5 I. ~6 S. }% y9 H' Q+ Dstarted puberty somewhat early, and occasionally,
: g/ |; w$ B) c$ g- e( Wtesticular enlargement is not that evident in the
- b" s% ?' c2 \# R# _beginning of this process.1 In the absence of a neg-
( \+ k6 h: h1 g6 V) Mative initial history of androgen exposure, our
0 |% z& O  r4 t$ V; l) vbiggest concern was virilizing adrenal hyperplasia,
8 v! x. ^5 A: Weither 21-hydroxylase deficiency or 11-β hydroxylase3 q) G/ N4 p/ h# L" b$ ?" o, ]& b
deficiency. Those diagnoses were excluded by find-. w* Z/ g+ A- }) U$ C6 y' a/ t
ing the normal level of adrenal steroids.
6 j. ^0 t6 Z2 w; X& u: t* a& UThe diagnosis of exogenous androgens was strongly
: e! }% M4 Y5 C" Fsuspected in a follow-up visit after 4 months because  ^, E/ V8 a; H. w& u' I2 D8 p4 `! D
the physical examination revealed the complete disap-4 a/ l+ T9 p( ?
pearance of pubic hair, normal growth velocity, and1 V8 S6 K$ x8 q) X
decreased erections. The father admitted using a testos-
* J, U7 Y3 g! u3 B8 eterone gel, which he concealed at first visit. He was
: r8 v( R5 D- Nusing it rather frequently, twice a day. The Physicians’
, s& n* {: [2 O2 E! y8 WDesk Reference, or package insert of this product, gel or% l- Q% M' `* V) l, s3 b
cream, cautions about dermal testosterone transfer to
/ f8 V! D. o& Y5 Munprotected females through direct skin exposure.0 L. b2 g2 Q8 h- T# W
Serum testosterone level was found to be 2 times the5 }$ n2 @$ z5 W0 `$ u' Y
baseline value in those females who were exposed to
8 I4 R" }* q* s0 ?* ?even 15 minutes of direct skin contact with their male+ D7 c9 \4 T  [
partners.6 However, when a shirt covered the applica-7 w7 _+ n7 u! H% P
tion site, this testosterone transfer was prevented.8 `- }4 Z) {; r  ]8 ]
Our patient’s testosterone level was 60 ng/mL,
; M" E; b4 n3 l+ d7 C% hwhich was clearly high. Some studies suggest that0 K: B+ F4 z* d' H& p" t
dermal conversion of testosterone to dihydrotestos-
. m% O9 h- w6 |& d0 Q% O; x0 vterone, which is a more potent metabolite, is more% ?3 Z5 n; M  t$ P# R% M$ H
active in young children exposed to testosterone9 ^# V& G6 l& m7 X2 ?! H/ G
exogenously7; however, we did not measure a dihy-
6 Q, Z4 l3 M/ P, o! ~1 W8 Y& gdrotestosterone level in our patient. In addition to) b; S3 m; U7 V, X3 j7 B
virilization, exposure to exogenous testosterone in% T: N* s8 B. ]
children results in an increase in growth velocity and
) ]$ a6 b. m6 n% Z# K! @- F' madvanced bone age, as seen in our patient.
# g; o- ~$ x0 N! ]  OThe long-term effect of androgen exposure during" \8 p8 R2 c2 q9 H
early childhood on pubertal development and final% O$ r9 g, j  |0 I% M
adult height are not fully known and always remain
: g3 @+ Y/ [* ^$ f: B3 Ra concern. Children treated with short-term testos-
5 j6 R: m4 f5 h$ m' j  |, P/ I) ]terone injection or topical androgen may exhibit some
2 Q; t1 ]+ F, [: Facceleration of the skeletal maturation; however, after
$ a% ?, L; b" dcessation of treatment, the rate of bone maturation  K& t! l6 _! m% R1 e: V7 O
decelerates and gradually returns to normal.8,9
5 X9 e  M) I! FThere are conflicting reports and controversy
% s2 H8 ?% T4 [# I" Q1 n; Yover the effect of early androgen exposure on adult
4 `& \0 A3 w- Vpenile length.10,11 Some reports suggest subnormal- W' H& N) C+ O! @9 f1 V  n6 S4 d# u
adult penile length, apparently because of downreg-! _/ _, w% e0 B' K# U9 C! B5 l
ulation of androgen receptor number.10,12 However,* G0 z; l( y- J* e
Sutherland et al13 did not find a correlation between
' C  i# \5 N  g& w. B! N( a8 Vchildhood testosterone exposure and reduced adult$ H- k8 g" l9 t' J; F0 ]9 Q  F
penile length in clinical studies.. }. q( |% I" ^
Nonetheless, we do not believe our patient is
5 a& L/ d* X; I4 H* ?' Q" ygoing to experience any of the untoward effects from
1 R2 x: E# G1 [; x( [6 A! }  Gtestosterone exposure as mentioned earlier because
3 z' f; D8 j7 L0 `the exposure was not for a prolonged period of time.2 X4 D' ^! V* f' N: v( B  d
Although the bone age was advanced at the time of
! n! |$ ~" s9 _. ]* h" ldiagnosis, the child had a normal growth velocity at! B) ]% y5 Y& j9 c- [+ s5 @1 Z
the follow-up visit. It is hoped that his final adult; i+ d# d- i7 _: O$ P& u+ e
height will not be affected.: k  f8 l/ Y9 d
Although rarely reported, the widespread avail-! e& E9 V+ `& x& a, l" z, k
ability of androgen products in our society may) O# a. U- _9 m
indeed cause more virilization in male or female/ _- B. I$ C8 e; X
children than one would realize. Exposure to andro-
! h% i0 S; x; W9 [4 q2 N- ygen products must be considered and specific ques-
6 t6 f3 s" B3 }8 I5 t9 @tioning about the use of a testosterone product or
; R0 p, |" M5 G# m- N$ c5 igel should be asked of the family members during
2 A2 U$ w9 v9 G$ B- Ythe evaluation of any children who present with vir-
0 W; k. H6 E. a, T. c2 g5 ]ilization or peripheral precocious puberty. The diag-
* x8 }* D& B  X$ @9 ~: Q% H* ynosis can be established by just a few tests and by
6 F; k' |( V- z0 E7 happropriate history. The inability to obtain such a
" x9 H5 E1 m& I* B, ^history, or failure to ask the specific questions, may3 t8 C6 y- |' H# C, h
result in extensive, unnecessary, and expensive. W! M$ u7 d% q" _3 }7 r7 N
investigation. The primary care physician should be
7 w3 t, P# F% Taware of this fact, because most of these children2 [$ T& R$ Z& A6 \; e$ r
may initially present in their practice. The Physicians’# a3 S0 l5 C; L
Desk Reference and package insert should also put a
) z$ u' k" ?0 F: `! dwarning about the virilizing effect on a male or
) Z6 S- I+ j8 N3 zfemale child who might come in contact with some-
6 C# K6 f; d& {! E3 [one using any of these products.# Q1 h6 V2 m! _$ Q6 w
References& k! u% z2 Q/ A
1. Styne DM. The testes: disorder of sexual differentiation
( i! V& E' S1 ?# F4 q$ rand puberty in the male. In: Sperling MA, ed. Pediatric
, o* {% B/ e2 ~: E8 r) J, o( K; [Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
2 U- Y: B- A/ S, J5 R2 g9 \' m( g  w# [2002: 565-628.
5 ~. k2 ?+ |0 f6 r, |0 y# z2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious. L  Y9 b# S8 K6 P0 ~
puberty in children with tumours of the suprasellar pineal
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感謝大大的辛勞分享!我會繼續在WK關注大大的文章!
發表於 2025-1-11 22:18:01 | 顯示全部樓層
女厕偷拍辅导班主任尿尿老师的逼很嫩还有一点
發表於 2025-1-17 16:31:39 | 顯示全部樓層
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
3 V. Z/ [% N) ]/ r
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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