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Sexual Precocity in a 16-Month-Old
7 @7 V; Q1 d, m5 c( O. @, fBoy Induced by Indirect Topical. U: _& W+ ?5 v( O
Exposure to Testosterone3 C" ]0 R. ~& Y" M
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2: P- b7 m! w: K7 \
and Kenneth R. Rettig, MD1
+ p1 l0 b5 }( P/ GClinical Pediatrics
' y, l8 P5 i6 \4 Z) zVolume 46 Number 6& y! v) s3 e' O" ?2 G8 c( T
July 2007 540-543
. ?6 x$ l4 g5 ~; \+ Q© 2007 Sage Publications* H6 q# C7 M  `$ I% b( v: z$ \1 R
10.1177/0009922806296651
4 N* k  I5 k7 ]% {/ \http://clp.sagepub.com
& w! I) c! ?: Y$ w1 X1 chosted at9 x4 V( f7 O1 o
http://online.sagepub.com: K8 y; n3 p) A# D9 {8 m
Precocious puberty in boys, central or peripheral," I" E2 ?# b( o8 [$ O2 l
is a significant concern for physicians. Central! `) `5 Z! ]2 }+ `  v  L
precocious puberty (CPP), which is mediated
$ s2 w; r4 D' K6 @9 i6 O/ J; qthrough the hypothalamic pituitary gonadal axis, has" ]  ~2 I, l3 K- V' f
a higher incidence of organic central nervous system: C: V: R* ^$ @0 {8 ?) s
lesions in boys.1,2 Virilization in boys, as manifested
4 a- a! l% O( N2 O0 iby enlargement of the penis, development of pubic
) g0 o. L5 _5 \hair, and facial acne without enlargement of testi-
4 d/ x7 w! V$ N1 E/ Lcles, suggests peripheral or pseudopuberty.1-3 We. G' \$ z( P3 e! O1 W( @
report a 16-month-old boy who presented with the$ C0 d! w% {5 X( U7 v* ?4 r0 y
enlargement of the phallus and pubic hair develop-
' S8 F% M" r/ Tment without testicular enlargement, which was due2 l4 S! O) N( X( n/ p/ V
to the unintentional exposure to androgen gel used by2 H" P' `2 g  ]7 n
the father. The family initially concealed this infor-
1 E: w6 k* k2 y! `mation, resulting in an extensive work-up for this  x9 R- @1 Q; d
child. Given the widespread and easy availability of
0 C' i! z5 X: d  otestosterone gel and cream, we believe this is proba-
9 k' N6 K' G6 o; @8 {7 J+ d5 ebly more common than the rare case report in the
+ ?& V& B, a3 j" D7 W, Y# dliterature.4
4 F0 S! V" W5 F# ?* b: IPatient Report. @4 [+ G- n, [, ?) i  }
A 16-month-old white child was referred to the
- _  g( A' P+ b+ eendocrine clinic by his pediatrician with the concern
5 M, z5 Y. W  Y5 l! t; Qof early sexual development. His mother noticed
( J$ T. J# M  [5 C" alight colored pubic hair development when he was# K5 n7 N2 ?7 W( S
From the 1Division of Pediatric Endocrinology, 2University of6 d* h5 I: m: U+ O
South Alabama Medical Center, Mobile, Alabama.
8 N0 w  [# \. {Address correspondence to: Samar K. Bhowmick, MD, FACE,% s' x! T- @8 G7 B* P9 e2 T) }0 ?
Professor of Pediatrics, University of South Alabama, College of3 K$ U' h7 X+ T+ R0 D- Y
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
: b% ~6 A: ^* le-mail: [email protected].
" L9 m4 M8 s2 q, q6 A! C, d5 e, s' xabout 6 to 7 months old, which progressively became9 H: S. L$ h. W' \% n$ \+ Q
darker. She was also concerned about the enlarge-
6 g/ m- v/ O9 R1 u% x# _5 iment of his penis and frequent erections. The child$ E- |  o% d0 N& S8 d0 t
was the product of a full-term normal delivery, with6 v, {. {0 F# e" c7 X  U
a birth weight of 7 lb 14 oz, and birth length of
/ G4 g. h8 \; \; g: |2 ?) v4 F20 inches. He was breast-fed throughout the first year% `( p. }% e5 y0 j" r+ u( x
of life and was still receiving breast milk along with( D- `6 [& K; c* ^' r
solid food. He had no hospitalizations or surgery," r8 T, x" [; x
and his psychosocial and psychomotor development
) E1 J  Z" |! ~" Hwas age appropriate." G3 \- E& ]- A
The family history was remarkable for the father,
7 n' b! v# @) _# I! Y' g! c8 Uwho was diagnosed with hypothyroidism at age 16,% u9 U- Q  |' b! l- Z. X
which was treated with thyroxine. The father’s
4 |9 M! O# b# l( a: Cheight was 6 feet, and he went through a somewhat
. J5 @# Z( G" W8 `0 gearly puberty and had stopped growing by age 14.( n% b; T; E8 s
The father denied taking any other medication. The* o* W( C1 O0 u* |
child’s mother was in good health. Her menarche7 z* ]" I, N3 s: m& s3 l
was at 11 years of age, and her height was at 5 feet# w% N% O& N5 m* P; D3 `
5 inches. There was no other family history of pre-2 Y3 p/ z1 A5 Q5 [: L6 ]6 A' u
cocious sexual development in the first-degree rela-( I( T. y/ V4 s( V( |' F
tives. There were no siblings.8 ]* t- F: W3 @) n8 k
Physical Examination) X: {& f9 J0 {
The physical examination revealed a very active,  G/ r1 R) U! |! C. R9 d& r
playful, and healthy boy. The vital signs documented; Q6 {& E5 ~' R7 k
a blood pressure of 85/50 mm Hg, his length was9 L2 P: f. q1 p) ]+ Y
90 cm (>97th percentile), and his weight was 14.4 kg3 ?7 A( e) ?2 w  V
(also >97th percentile). The observed yearly growth
% F9 \5 T8 J3 B9 n* G4 E. w6 Kvelocity was 30 cm (12 inches). The examination of' a$ E( i7 C% @1 Y5 l. X% R
the neck revealed no thyroid enlargement.8 s, s" ~. u) f. k6 V1 o
The genitourinary examination was remarkable for) X" z; g- B  A, O' H% G
enlargement of the penis, with a stretched length of
( x( p1 _! H" M" `9 |( y2 Y3 H8 cm and a width of 2 cm. The glans penis was very well
% q' r/ l8 _. t, b" L# Zdeveloped. The pubic hair was Tanner II, mostly around% r6 h% O1 ^8 O2 P3 ?
540! r9 d* `' g( a/ E; S
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from2 w# q$ w$ g- o# t% @! ]/ [+ D- X6 x
the base of the phallus and was dark and curled. The
5 {3 V- R! f2 E1 Ltesticular volume was prepubertal at 2 mL each.
( Y1 ~$ I) M( y( nThe skin was moist and smooth and somewhat
  e0 I$ Z8 ~: e0 G/ X! F( M$ noily. No axillary hair was noted. There were no: ?! Q7 N( V: K" m2 v
abnormal skin pigmentations or café-au-lait spots.6 O# x9 c8 H- v5 [) N6 o5 v- Q
Neurologic evaluation showed deep tendon reflex 2+
+ k( u1 z" X+ C5 C# L5 X8 Hbilateral and symmetrical. There was no suggestion
) o3 k1 ]1 c# c- w7 iof papilledema." ]7 \7 D9 @3 X
Laboratory Evaluation
/ _; Y: p9 t' P- IThe bone age was consistent with 28 months by5 W0 b- Z# k# p6 H2 l, K+ N; j
using the standard of Greulich and Pyle at a chrono-
9 \" y# q* m) f" b3 m1 B- m+ Llogic age of 16 months (advanced).5 Chromosomal
# D$ u& D; i) d# C4 I) hkaryotype was 46XY. The thyroid function test
5 p* k- q* F& [: v9 vshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
1 m3 [- c  B5 \* Alating hormone level was 1.3 µIU/mL (both normal).3 @, _2 v( o2 x- l) j8 o& T+ H, c
The concentrations of serum electrolytes, blood) }0 V7 x) \- O6 w0 R) x$ p
urea nitrogen, creatinine, and calcium all were
+ m  T  Z7 e' ^within normal range for his age. The concentration% H2 h, @% q( V- F
of serum 17-hydroxyprogesterone was 16 ng/dL
) m# W4 t  v- ](normal, 3 to 90 ng/dL), androstenedione was 20
. U# \9 @7 v; Jng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
9 x5 Q5 R" O2 aterone was 38 ng/dL (normal, 50 to 760 ng/dL),/ w5 T! N1 |! S( m
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
- E' F* N  Q0 w( U% K6 g+ O49ng/dL), 11-desoxycortisol (specific compound S)
0 Y3 ~3 Z; ?( m( D) B! R" {# hwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-! v) t# y/ W5 X+ @9 }7 q& m
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total: B( f# U+ L. A  ?, y/ E
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),' @4 i; v* `7 G; T+ _' c  B
and β-human chorionic gonadotropin was less than7 t( M  i5 [8 a. [/ R
5 mIU/mL (normal <5 mIU/mL). Serum follicular; V3 _# N* k% V" }3 L
stimulating hormone and leuteinizing hormone) G7 F2 o( M" z% B
concentrations were less than 0.05 mIU/mL
6 C# P' R" z( u# M0 E  z& X(prepubertal).
$ f  B% Q4 F; R  g! j1 hThe parents were notified about the laboratory- [# j0 g( U4 b; Z* T8 s2 ^( O
results and were informed that all of the tests were
, P8 y& A5 `  Q5 f5 D) pnormal except the testosterone level was high. The
( |, u- u5 s$ \& g) afollow-up visit was arranged within a few weeks to
9 e/ c! K+ o: W9 iobtain testicular and abdominal sonograms; how-: @2 p1 |& @) I' c. y
ever, the family did not return for 4 months.
$ g% [) Y% h- j$ O5 h$ fPhysical examination at this time revealed that the6 ~; B: g, u% t5 w4 Q4 B, ~
child had grown 2.5 cm in 4 months and had gained
3 e$ @# A' @- V% o3 Y3 `2 kg of weight. Physical examination remained" m* `3 b( i3 d; \& o
unchanged. Surprisingly, the pubic hair almost com-
* A! ~& f" }. |+ fpletely disappeared except for a few vellous hairs at4 r3 P2 T3 o5 U3 f6 \  _) x1 H
the base of the phallus. Testicular volume was still 2
* i, d! S: M! N: V+ s' H' vmL, and the size of the penis remained unchanged.( _1 O  `& k+ L7 m  F! c
The mother also said that the boy was no longer hav-& f0 W2 l+ R5 n0 f; V  i: Y4 c
ing frequent erections.5 `$ a, N& l3 [/ h# Z; m; h
Both parents were again questioned about use of' H: o9 K# n; X8 x- ]0 e* [
any ointment/creams that they may have applied to1 \0 e  q3 G& k6 Y' J; r  G
the child’s skin. This time the father admitted the
; q; z2 T% A1 n; t/ r' yTopical Testosterone Exposure / Bhowmick et al 541
* s0 D- k# F  k5 W, X: u  |! _use of testosterone gel twice daily that he was apply-" f% U# [* z  l+ j7 V/ w1 L- m/ L
ing over his own shoulders, chest, and back area for8 t+ D; ?, S; P$ @1 q2 z5 `. _9 k
a year. The father also revealed he was embarrassed/ ?. G' r7 T- U5 ^' E0 b( U
to disclose that he was using a testosterone gel pre-% g9 q7 ?3 C. R3 m2 g1 s: T: I# L
scribed by his family physician for decreased libido
9 y3 A1 s' ^  H3 ^2 q; \( Zsecondary to depression.
3 d: e/ T4 T; ?( R; }( q. ?The child slept in the same bed with parents.5 u( c, q7 `8 U$ y
The father would hug the baby and hold him on his+ U9 ~1 e' [7 R* h# M0 t6 y
chest for a considerable period of time, causing sig-+ H5 Z8 j" l/ s. f3 u/ I. f( [
nificant bare skin contact between baby and father.
' s' U9 H) j# V9 H3 m0 g+ O, cThe father also admitted that after the phone call,
7 d: Z* }& |; Owhen he learned the testosterone level in the baby
- H6 F! T- I+ @7 c" Q  c7 Ewas high, he then read the product information4 a6 z8 w( D# m5 s: p+ o* _
packet and concluded that it was most likely the rea-, z, w" N2 T7 r. n& |7 Q
son for the child’s virilization. At that time, they2 |) m" `& E3 Z& R
decided to put the baby in a separate bed, and the
4 F2 M1 m8 `: cfather was not hugging him with bare skin and had
) x; X5 Y5 D% j& ~, l& Nbeen using protective clothing. A repeat testosterone
* z9 m  i) x7 _test was ordered, but the family did not go to the
! M* e8 F/ c6 \0 Glaboratory to obtain the test.
7 c  d& e7 U! _9 V7 x) oDiscussion
+ N/ R' R' a- X) ?; R) T7 X/ q: {Precocious puberty in boys is defined as secondary/ \; f5 [& B+ Z$ P1 ]2 A
sexual development before 9 years of age.1,40 g$ C8 {6 v' |* s) m( Q
Precocious puberty is termed as central (true) when6 H  g4 ?2 y& A4 [9 g7 t( d
it is caused by the premature activation of hypo-
  T# ^/ i5 ]& K9 O. |7 W( Tthalamic pituitary gonadal axis. CPP is more com-
. {0 V% z$ a, e9 F3 ~6 F# M+ ^! n! }mon in girls than in boys.1,3 Most boys with CPP5 n! W* Q0 l0 P! Y' j* E" @/ {' y& R
may have a central nervous system lesion that is5 `" ~0 y: ^( ^" W9 ~- L
responsible for the early activation of the hypothal-0 E/ }9 Z* U+ x( C
amic pituitary gonadal axis.1-3 Thus, greater empha-
( Q" E6 W  Z% x4 {! N) z1 X8 H. ~sis has been given to neuroradiologic imaging in5 m; l+ D0 \- t2 o. H! q
boys with precocious puberty. In addition to viril-
3 Y' L7 {) [; g, eization, the clinical hallmark of CPP is the symmet-7 E/ `( b/ ^4 }$ J
rical testicular growth secondary to stimulation by$ U6 F9 h6 x* L: T
gonadotropins.1,3
- S: n/ ~' }# ~: KGonadotropin-independent peripheral preco-
7 j2 I0 ^% B& q# k% m2 C# u; Y" ucious puberty in boys also results from inappropriate0 n8 j5 o9 s: Q+ x/ H
androgenic stimulation from either endogenous or4 j! F7 e1 x* }9 Q  M
exogenous sources, nonpituitary gonadotropin stim-" w; i( q) T! h" c% d+ c8 t
ulation, and rare activating mutations.3 Virilizing4 o9 A; B4 h2 B% C2 H
congenital adrenal hyperplasia producing excessive
( U# L9 [2 W! L) ^5 P  y7 Tadrenal androgens is a common cause of precocious
# J) Y6 E# l- O* H3 Zpuberty in boys.3,4# l$ |4 U! d" k& X  h% W7 A" g
The most common form of congenital adrenal
5 n7 J; j* {' U" ~% K. ?2 |+ Ohyperplasia is the 21-hydroxylase enzyme deficiency.
$ T  i* I, ~& R& @' {6 c! aThe 11-β hydroxylase deficiency may also result in
3 z0 L4 c6 p# Y( H) g+ z4 Iexcessive adrenal androgen production, and rarely,% ?1 w& Z' W1 H, D
an adrenal tumor may also cause adrenal androgen
! {+ T1 j0 n" f9 A4 jexcess.1,31 v" I% z( y. Q
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from0 S( f9 D2 l: \6 P; R3 P% W" Z
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
  {$ s4 Y% [) L: u4 u5 I% ]. yA unique entity of male-limited gonadotropin-# Y& o1 L& V5 X# a" t: i
independent precocious puberty, which is also known
3 h, f2 ~- y  \+ V( fas testotoxicosis, may cause precocious puberty at a
" i7 \2 c. W) b: every young age. The physical findings in these boys
! @9 W) o5 x( U$ zwith this disorder are full pubertal development,
3 v9 |/ r0 s; O. Qincluding bilateral testicular growth, similar to boys( k1 i7 ^) d" b/ b
with CPP. The gonadotropin levels in this disorder& U) F: Y  f8 n5 {  r
are suppressed to prepubertal levels and do not show
. ~+ j  V- a$ w1 ]* X- {! qpubertal response of gonadotropin after gonadotropin-
* t7 F* v; g4 [+ M, Ereleasing hormone stimulation. This is a sex-linked* u, u. N, `1 o6 X: }0 C6 @( F
autosomal dominant disorder that affects only
: h2 Y! k9 [7 H: X4 o# j9 Wmales; therefore, other male members of the family
) t, c, L6 A+ g/ k$ L4 kmay have similar precocious puberty.3
" N8 K+ }" I1 T: _1 ]In our patient, physical examination was incon-5 }; x2 p* ~; G1 L  m* p$ P
sistent with true precocious puberty since his testi-
9 x7 a( a$ a7 j( k% ^cles were prepubertal in size. However, testotoxicosis* K0 j) e9 w6 \( T$ m6 U
was in the differential diagnosis because his father. l. J5 R8 F( W. d8 s8 P( n+ {0 ]
started puberty somewhat early, and occasionally,, Y1 _0 ~2 {: |
testicular enlargement is not that evident in the
5 N, a# W. g8 i; I5 ubeginning of this process.1 In the absence of a neg-
% W/ K9 k1 W0 s% n  `; Kative initial history of androgen exposure, our' l9 E) j& c0 g6 k
biggest concern was virilizing adrenal hyperplasia,
3 K3 @  U% X% j5 h, w; \- k2 w+ g: Ceither 21-hydroxylase deficiency or 11-β hydroxylase
% {0 b. b7 e* e2 j0 L' g+ e7 Ndeficiency. Those diagnoses were excluded by find-
8 y! Z, c; v  Y8 R) s/ T; k' w4 cing the normal level of adrenal steroids.
' `2 e4 Q8 v6 F3 n: D6 z9 `The diagnosis of exogenous androgens was strongly
# e. K2 ?, T+ @: t* `; wsuspected in a follow-up visit after 4 months because
% e. `9 m  B2 f& Y5 hthe physical examination revealed the complete disap-# a! G! t0 ?0 q2 l4 w+ \1 W5 I
pearance of pubic hair, normal growth velocity, and
0 ?* j  ]/ u; x: G5 ~/ Ndecreased erections. The father admitted using a testos-6 v1 O6 _0 n$ u0 T! w
terone gel, which he concealed at first visit. He was: n( R+ l9 C" `4 p6 B
using it rather frequently, twice a day. The Physicians’& O6 T; i# Z2 m- |# B5 @
Desk Reference, or package insert of this product, gel or/ p- o' u( l0 ?/ `3 l3 Z
cream, cautions about dermal testosterone transfer to" ]$ S0 m4 J4 n. y; D2 g; S
unprotected females through direct skin exposure.
5 j& u# `9 J: z, U& n; HSerum testosterone level was found to be 2 times the
: h9 P; @8 C7 mbaseline value in those females who were exposed to
8 }0 o3 B5 Y" P* D  z% S# Heven 15 minutes of direct skin contact with their male4 j; H1 ?# \& \8 y, m
partners.6 However, when a shirt covered the applica-$ p$ \! A( b, d+ J
tion site, this testosterone transfer was prevented.; @* j: e6 \& l, f
Our patient’s testosterone level was 60 ng/mL,
& v  r! M1 \5 t0 Ewhich was clearly high. Some studies suggest that
  t- ]/ T) j. m2 ~! g6 |9 e1 x7 k# Vdermal conversion of testosterone to dihydrotestos-
% J. b& W# Y3 X$ ]2 wterone, which is a more potent metabolite, is more
. o& N; r1 a% @! ^- @active in young children exposed to testosterone+ u4 J; \# N4 y) p, s
exogenously7; however, we did not measure a dihy-
. T" O, E* t( f$ v5 Tdrotestosterone level in our patient. In addition to
% s( _; k% ~1 ]+ I0 U% gvirilization, exposure to exogenous testosterone in! _9 ~4 C9 F* w3 p% Q+ H
children results in an increase in growth velocity and; q  `3 d# m% L* J! G  ^) B/ M, r
advanced bone age, as seen in our patient.1 K3 w% e5 }, I3 `& d- Y
The long-term effect of androgen exposure during
0 g  o6 W7 h) t: `8 |: learly childhood on pubertal development and final
/ B/ I3 Y9 O4 z9 \  A; K) xadult height are not fully known and always remain
. p$ x2 Z5 ^9 x$ @- ja concern. Children treated with short-term testos-
# K" l9 q& }6 O1 Z  h  P" Zterone injection or topical androgen may exhibit some
7 I' D* [: a8 v3 @; q% Qacceleration of the skeletal maturation; however, after- l8 k& y) \- }" n" |0 ~
cessation of treatment, the rate of bone maturation
  U( ?' M+ a$ J5 [3 Fdecelerates and gradually returns to normal.8,9
7 t6 ?: C$ h+ H- n7 |There are conflicting reports and controversy% g5 u$ S& @1 E: F  u3 a1 E: z8 Y
over the effect of early androgen exposure on adult5 d+ M$ z/ y9 |2 n
penile length.10,11 Some reports suggest subnormal
8 K$ E2 w$ A  }- w, x+ s! \4 Nadult penile length, apparently because of downreg-
/ G/ H; c) H( U  C! U, T% a% n: Yulation of androgen receptor number.10,12 However,
' ?5 S& N4 q3 C& ISutherland et al13 did not find a correlation between' O8 r. ~1 N; y8 `  I
childhood testosterone exposure and reduced adult6 ~6 l3 d; F8 Y1 s
penile length in clinical studies.( V' b: O. t! O3 V7 [# F7 M% p
Nonetheless, we do not believe our patient is
/ i0 @6 l7 {, p$ v; ]going to experience any of the untoward effects from
& q$ P& W/ m! u3 S: Ttestosterone exposure as mentioned earlier because7 y  L& b8 m7 M' R2 |
the exposure was not for a prolonged period of time.
+ p+ Z/ I( s5 g. j, uAlthough the bone age was advanced at the time of
$ ?7 H( m; E* c) I& Wdiagnosis, the child had a normal growth velocity at" O- a, y. k" h% y' r4 F
the follow-up visit. It is hoped that his final adult
5 R. r: l9 T; W+ f* Bheight will not be affected.% p: j! i: }: `1 K! h" h5 |3 y) i
Although rarely reported, the widespread avail-
- j6 u. E$ a1 b- H) x8 E4 Cability of androgen products in our society may( N, O2 H5 L5 l+ f) I
indeed cause more virilization in male or female- v, U$ t6 I; a) ~" K, U) S% m# V
children than one would realize. Exposure to andro-. J5 j$ d* o6 z4 P3 L5 U
gen products must be considered and specific ques-. I8 T" }& z, f
tioning about the use of a testosterone product or& I! S! |* ?1 }) F( i9 |! i
gel should be asked of the family members during
# r9 c2 r6 m: W- j9 xthe evaluation of any children who present with vir-
! P# q3 W& P/ p8 l- J/ @4 R1 qilization or peripheral precocious puberty. The diag-+ B' z+ }2 Y  O% _6 ^/ f8 V% ?1 L
nosis can be established by just a few tests and by
/ m, D8 F" b& _% f9 x$ tappropriate history. The inability to obtain such a+ D, W4 k( t0 [/ ^) ^
history, or failure to ask the specific questions, may
4 p6 Y5 @# F" P# L9 R' p# Y5 Wresult in extensive, unnecessary, and expensive
; b6 r/ h% @8 z0 I' U7 sinvestigation. The primary care physician should be
& {6 F3 o/ G! L. ~aware of this fact, because most of these children
- G7 ^$ F, L  ]6 Emay initially present in their practice. The Physicians’$ u+ d( M3 W8 t" A
Desk Reference and package insert should also put a( f6 x  s- g2 u+ ]) e" T( M7 g
warning about the virilizing effect on a male or% ^- k$ {% h$ ?! R: I2 S
female child who might come in contact with some-
& m& |* M2 L3 Aone using any of these products.
3 A) r" q, U& v  o+ c* G& ~, _& _References+ q% U. e" I* ^$ d
1. Styne DM. The testes: disorder of sexual differentiation
( y3 r- y5 E# ?# y& s4 f( Yand puberty in the male. In: Sperling MA, ed. Pediatric- R0 g1 v' z+ P* z. n3 y( h- _
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;, f3 {9 K' a& S3 z/ q9 R$ p& F8 Y
2002: 565-628.
6 M" T& I4 k) d: f5 U2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious2 D. B0 f4 x5 l* ^! E5 g: q
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old6 l: q* ?! X! f3 Y, I, Z
Boy Induced by Indirect Topical" O3 V7 b9 K% p% x$ `4 F2 n- g6 e
Exposure to Testosterone
" m5 `8 d% g9 f# I  ^0 m6 q' oSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2/ W& O0 a* E/ N8 f$ w
and Kenneth R. Rettig, MD13 Q5 a% ?8 T$ ?/ [
Clinical Pediatrics
2 g( o2 l3 T* ]- ^7 gVolume 46 Number 6
5 U5 {( I4 }) V) d$ a: P/ w+ @July 2007 540-5432 X  {* G* `1 o! O% S' k2 J$ f
© 2007 Sage Publications, G8 x5 i; \# c! t- z: ^6 d. b
10.1177/0009922806296651
9 W" P+ y  O! D: P' k! |3 Lhttp://clp.sagepub.com
  H% n1 r$ H. v3 T( Mhosted at; }" |( x8 u8 h, U6 ]5 N6 K1 Q- ?
http://online.sagepub.com
- h$ m5 L* @/ ePrecocious puberty in boys, central or peripheral,
. f' f, J4 L! ois a significant concern for physicians. Central
" T; G. z/ P3 j! r' Zprecocious puberty (CPP), which is mediated
" \# E4 P9 W4 G* u* Q' h) I5 Rthrough the hypothalamic pituitary gonadal axis, has+ Y$ I( k* C* W, G! y0 w
a higher incidence of organic central nervous system
7 T: t  K  z$ @9 F/ L; o/ flesions in boys.1,2 Virilization in boys, as manifested
5 r+ s7 K( G' Sby enlargement of the penis, development of pubic+ @9 j2 h, i5 C2 `# I
hair, and facial acne without enlargement of testi-
8 i# u% {5 ?6 q% M* kcles, suggests peripheral or pseudopuberty.1-3 We  P1 X7 W  g0 R) A0 D4 K7 s) r
report a 16-month-old boy who presented with the, L& }0 h0 Z3 l$ B1 @
enlargement of the phallus and pubic hair develop-& P# ^2 Q  [- N1 y. _5 v6 |$ Q
ment without testicular enlargement, which was due$ B. D# B2 C) \
to the unintentional exposure to androgen gel used by3 q( l+ n; Y$ S3 _
the father. The family initially concealed this infor-5 O3 a: U: }" g
mation, resulting in an extensive work-up for this( o! ?1 c: ]6 v/ l: D5 J0 b
child. Given the widespread and easy availability of/ G5 I! U4 s( i1 t% e
testosterone gel and cream, we believe this is proba-/ I9 Z! W' O) R2 {  M* q/ e
bly more common than the rare case report in the3 E; T- ~& W% P: g
literature.4: X. Q& ^$ T. U. _
Patient Report* S7 M# f6 w0 x6 y5 M6 c! ?
A 16-month-old white child was referred to the& G8 D" d: F% |# [. s% ^
endocrine clinic by his pediatrician with the concern2 j- I# M$ j8 C! N/ J
of early sexual development. His mother noticed
0 p! j7 b3 j% V* W) D" Elight colored pubic hair development when he was, O8 l! S1 Q7 |# Y$ X$ v. h' s5 w
From the 1Division of Pediatric Endocrinology, 2University of* |, I" i. k, o" z
South Alabama Medical Center, Mobile, Alabama.! P' i  V6 X0 Z: _1 D2 B
Address correspondence to: Samar K. Bhowmick, MD, FACE,
. w2 u1 B! Q% A; I6 i6 J& p! q! AProfessor of Pediatrics, University of South Alabama, College of  Z/ P8 U$ Z4 q- p8 X( e, O
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
: k) V2 v! [, a& O8 |; `* u4 q* Me-mail: [email protected].
8 F8 ^" a3 C7 x% r  ~' m# K# f4 h( babout 6 to 7 months old, which progressively became
5 d( d" N0 R2 Kdarker. She was also concerned about the enlarge-
# m' P' ^/ N- W% e) {% r$ mment of his penis and frequent erections. The child
1 v' ~) _+ Z* t! h5 [- N$ Bwas the product of a full-term normal delivery, with
8 l8 {$ ^& [- P* W. _9 B6 sa birth weight of 7 lb 14 oz, and birth length of/ n( i) D0 v1 S( e' }& Y- v  z0 B, h
20 inches. He was breast-fed throughout the first year, ?5 @4 s+ G, w* [
of life and was still receiving breast milk along with
' Q. J) M# ]0 V7 M/ Usolid food. He had no hospitalizations or surgery,
5 }( f& n0 V( T9 d- |and his psychosocial and psychomotor development( V/ N% @, m1 ^) m3 C
was age appropriate.. S# T3 c- y4 P) k+ `
The family history was remarkable for the father,6 B: f2 y; E7 b: s! a
who was diagnosed with hypothyroidism at age 16,% R) j: k; G* h) O' F
which was treated with thyroxine. The father’s
$ J: ?1 _, D. B! d+ mheight was 6 feet, and he went through a somewhat' R1 j4 C+ R* r. V2 J
early puberty and had stopped growing by age 14.  v6 s: _% C: F9 e1 j
The father denied taking any other medication. The# `+ V# f, m/ p/ V& G. J; [$ M7 T
child’s mother was in good health. Her menarche
' p. e$ \# _' q! r2 j) q2 vwas at 11 years of age, and her height was at 5 feet1 v0 {/ g. ~+ E* Z% r: T( ]* z
5 inches. There was no other family history of pre-5 j/ [. a0 ^9 R/ m2 l9 l- q7 u. Q
cocious sexual development in the first-degree rela-, ?% L6 m! i! P7 A
tives. There were no siblings.* Q* j$ @: y) B' @3 N
Physical Examination
1 r; e/ ^5 x, NThe physical examination revealed a very active,$ \& G/ d# [. ]; \% ?, I/ i3 G
playful, and healthy boy. The vital signs documented
" H* G1 S  y" M5 z/ o' ]a blood pressure of 85/50 mm Hg, his length was5 h/ Y) {+ z4 @8 L
90 cm (>97th percentile), and his weight was 14.4 kg
9 T! y2 x" `6 M; B& n(also >97th percentile). The observed yearly growth
+ f" e- V. N. zvelocity was 30 cm (12 inches). The examination of
' i# ]8 `! |: k5 A+ s2 ?- uthe neck revealed no thyroid enlargement.
  r- q3 I/ Q8 v; M9 PThe genitourinary examination was remarkable for
9 Q* B. H5 c. |& Y  _- Renlargement of the penis, with a stretched length of
7 w) f1 Q9 D3 I3 N8 cm and a width of 2 cm. The glans penis was very well
  v" U$ m; B2 W# U. cdeveloped. The pubic hair was Tanner II, mostly around
7 [* ~# s* T6 h540; c& T6 u8 \. k% n5 o2 p6 D8 r/ H
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from6 L! I+ Z8 S" D& F2 C
the base of the phallus and was dark and curled. The
; R6 ]) Y- A9 z8 K- e4 Vtesticular volume was prepubertal at 2 mL each.
* k* b1 `9 v. _4 m5 [! eThe skin was moist and smooth and somewhat
% T& Z+ S# V+ X* A4 R& doily. No axillary hair was noted. There were no
) P! A8 M, L" }0 b3 U4 @7 |6 iabnormal skin pigmentations or café-au-lait spots.* b: j9 R# W2 y# }' {7 N5 T
Neurologic evaluation showed deep tendon reflex 2+
3 ]# Z) T& ^7 y1 ]; q9 |bilateral and symmetrical. There was no suggestion
  C( E4 x7 R( c8 s0 T0 iof papilledema.7 A2 i" o& W: ^. T+ ?  h0 [0 c# X
Laboratory Evaluation
9 s9 A1 o6 |- V" t# `The bone age was consistent with 28 months by6 M$ ?/ W1 {6 j3 f$ ~( y
using the standard of Greulich and Pyle at a chrono-
  p9 Z& _6 K! P( D) Q. [1 Elogic age of 16 months (advanced).5 Chromosomal: U- z4 `) z9 a" G' w
karyotype was 46XY. The thyroid function test
0 E. C+ k- q0 v* l/ e, w( p7 Kshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
+ j3 g7 b7 p5 z4 R7 Wlating hormone level was 1.3 µIU/mL (both normal).3 {9 `7 ]# V% C; g% _) i7 y& P6 z
The concentrations of serum electrolytes, blood
" A1 o% A# M7 n7 p# q. C4 s2 lurea nitrogen, creatinine, and calcium all were. K9 [$ s: _; I( e
within normal range for his age. The concentration
7 }( I+ v7 m5 f& V3 N) r& Fof serum 17-hydroxyprogesterone was 16 ng/dL5 o% f! @8 v, b9 Q
(normal, 3 to 90 ng/dL), androstenedione was 20
4 C+ R3 i+ {# ~$ c9 Hng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-- E' C  D: R5 Z7 r
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
0 M  y4 O8 E! t( w& o9 Ydesoxycorticosterone was 4.3 ng/dL (normal, 7 to
4 {- b4 g" K3 [  B49ng/dL), 11-desoxycortisol (specific compound S), s6 L! e8 {. [
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-/ h0 |$ y% z0 g1 c) q; n
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
4 M7 E9 h; u& ~8 Etestosterone was 60 ng/dL (normal <3 to 10 ng/dL),& D3 l8 B2 X( g- j1 j; j
and β-human chorionic gonadotropin was less than% }) ]( C* ^# S9 l
5 mIU/mL (normal <5 mIU/mL). Serum follicular) }0 |; E7 J# \% H: F0 U; R" I
stimulating hormone and leuteinizing hormone
. i6 d4 b. k3 ]# \6 uconcentrations were less than 0.05 mIU/mL* g- ]: k  R; J4 t- _4 l& v% c
(prepubertal).8 s, P: i: w2 Y7 U5 x1 X! a$ ]3 L+ N
The parents were notified about the laboratory/ v' i  p7 ?, D+ O! z# H1 l( O
results and were informed that all of the tests were
+ G' ^9 a( |. e- M8 s$ Jnormal except the testosterone level was high. The
: B5 h& @9 D. N4 d4 w  m, i! }- qfollow-up visit was arranged within a few weeks to
/ ?+ z8 o9 N2 z* c$ {obtain testicular and abdominal sonograms; how-. P  ]% w+ t3 E, H% q% y( K* T+ ]
ever, the family did not return for 4 months.
, y! J: k& R  n. P& q% YPhysical examination at this time revealed that the1 H' B2 ~( e4 o9 t0 z) T. z% _
child had grown 2.5 cm in 4 months and had gained" m- }* K9 o) P7 q
2 kg of weight. Physical examination remained
; R5 {% D: K( u/ F9 k/ z. A' cunchanged. Surprisingly, the pubic hair almost com-
1 M! m$ T% [* u  b  n4 ?, _) rpletely disappeared except for a few vellous hairs at
' {) @& r  L" Q) Pthe base of the phallus. Testicular volume was still 2, e5 [7 i+ i) k5 q2 r) R! v
mL, and the size of the penis remained unchanged.
$ {) z* b. p1 U% x# n# o$ QThe mother also said that the boy was no longer hav-
; K. K2 U/ _$ d( k6 Ying frequent erections.& I3 L2 M$ l8 x# v& A. t. i7 |
Both parents were again questioned about use of
6 v' m7 f2 ]! Dany ointment/creams that they may have applied to# O! R' ?3 G% r0 O2 z* ^
the child’s skin. This time the father admitted the7 W8 \+ Q1 c. B7 B1 U
Topical Testosterone Exposure / Bhowmick et al 541
8 f# b0 F# T) B, |0 @; puse of testosterone gel twice daily that he was apply-
: ~- o9 P) C5 }  hing over his own shoulders, chest, and back area for
8 b% {, c( E- Na year. The father also revealed he was embarrassed) ?/ J* p9 I4 M* z$ C  z
to disclose that he was using a testosterone gel pre-
7 N! Y' B% ~3 n$ P9 H. xscribed by his family physician for decreased libido
# w* i0 E1 @1 S1 }/ W+ e1 `/ D8 Usecondary to depression.
! U1 ~$ ~5 {7 T; I+ r  x! V8 P) CThe child slept in the same bed with parents.
. ~! {7 ]0 Q7 j; SThe father would hug the baby and hold him on his( ^/ t  |6 n2 G) H6 H' W+ {
chest for a considerable period of time, causing sig-9 O' J' l2 |2 ]; S  x. U- ^, V
nificant bare skin contact between baby and father.0 w$ Q3 g1 V( [( C" d4 Z- w
The father also admitted that after the phone call,3 b/ j( f2 u1 u& w
when he learned the testosterone level in the baby
' |* G0 v0 s. U+ W6 B4 o" Dwas high, he then read the product information
1 X& L2 M, N% [6 `3 @- bpacket and concluded that it was most likely the rea-7 G' v7 S' v* T% O6 A3 |) s
son for the child’s virilization. At that time, they+ K* \1 d3 l9 Q8 l  M
decided to put the baby in a separate bed, and the
: N9 p, p0 `6 j+ _' {5 k2 D9 qfather was not hugging him with bare skin and had
" D& f- x( J) ^+ f- t- z" Ibeen using protective clothing. A repeat testosterone+ A( w4 d1 ]! c) ^
test was ordered, but the family did not go to the
; c6 D) A! j# _. q; `) Dlaboratory to obtain the test.
; E1 N8 e7 h8 X$ O0 Q; j2 p4 eDiscussion" Y$ ~  {( \' D. i
Precocious puberty in boys is defined as secondary( e: d5 O. W" e2 D1 O$ d  N& _
sexual development before 9 years of age.1,4
8 e3 K: A: Q. b0 _Precocious puberty is termed as central (true) when
! g+ G9 W. \8 v5 {: Git is caused by the premature activation of hypo-
" e/ C2 m% }7 ?: Y) _5 o  m/ z) D7 Qthalamic pituitary gonadal axis. CPP is more com-/ e# ~% ~1 B0 A3 r/ G
mon in girls than in boys.1,3 Most boys with CPP$ x, T# g( |- K  f! Q' j
may have a central nervous system lesion that is
/ b/ ]6 K4 i* q  D& b& `. p* }! Mresponsible for the early activation of the hypothal-, G, p8 M9 h: s# U6 j
amic pituitary gonadal axis.1-3 Thus, greater empha-
. L- V9 g8 |9 l3 E$ Z* usis has been given to neuroradiologic imaging in. v6 _  v& p9 i! i8 A$ p
boys with precocious puberty. In addition to viril-; ~# W* ^* k( e
ization, the clinical hallmark of CPP is the symmet-
7 u  ~1 \* i2 v3 p0 \rical testicular growth secondary to stimulation by
; o: Q) [7 j7 Q- {# |gonadotropins.1,3% S* {5 I* c4 d/ {- R% q- R/ K- R! V. r; j
Gonadotropin-independent peripheral preco-
3 T: S8 F( Z  M4 h2 C$ F% b( pcious puberty in boys also results from inappropriate3 {5 }# z0 ?& r( c' H
androgenic stimulation from either endogenous or
9 Z& Y7 i. w# M  n* kexogenous sources, nonpituitary gonadotropin stim-
8 K- b, X/ K" j# oulation, and rare activating mutations.3 Virilizing
+ ~: R* i2 I! J- C1 a8 Dcongenital adrenal hyperplasia producing excessive
. `  c" L% M2 E" Eadrenal androgens is a common cause of precocious4 s% b% J2 r% r! l# l
puberty in boys.3,4
7 P# t. _9 K, L% l, v) YThe most common form of congenital adrenal
$ w' z$ W0 _7 n+ a  J  [hyperplasia is the 21-hydroxylase enzyme deficiency.3 i7 h% Q% q5 T% `, t- u9 K' S
The 11-β hydroxylase deficiency may also result in. H, E# i/ J- R" Y, m
excessive adrenal androgen production, and rarely,& D& t+ s8 x: k# T
an adrenal tumor may also cause adrenal androgen# e$ V# N3 c% m2 @( i# G( n
excess.1,3
8 ^1 l0 @$ _! p2 Zat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from$ Q, v# {/ D$ v6 _1 ^) [6 Q
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007# `2 c! G6 t# l9 Z4 @5 p
A unique entity of male-limited gonadotropin-
4 D7 B7 c5 I8 Zindependent precocious puberty, which is also known
' n3 u. u+ T6 p0 U3 gas testotoxicosis, may cause precocious puberty at a
5 a% @$ G4 W, ~' D( B  y1 avery young age. The physical findings in these boys
2 d" ?/ {" \% `  Z% @, owith this disorder are full pubertal development,
) G9 u7 A: u5 rincluding bilateral testicular growth, similar to boys
, P' T5 `1 f( \with CPP. The gonadotropin levels in this disorder  M7 w, N' N) F/ h; V1 t8 b
are suppressed to prepubertal levels and do not show4 H# C/ r2 _% }5 m( X% A- }
pubertal response of gonadotropin after gonadotropin-0 E; n5 I& _2 s* u+ y
releasing hormone stimulation. This is a sex-linked& x; R8 E* K) r" \
autosomal dominant disorder that affects only* n3 c( y0 G6 e* G7 D0 T" H6 t: y) {
males; therefore, other male members of the family
# ]2 ?( }* ]0 T0 T3 [& {7 E2 `may have similar precocious puberty.3
2 Z' G! G8 j5 Z/ DIn our patient, physical examination was incon-* C; O5 P$ @# E" Q! T
sistent with true precocious puberty since his testi-) h' O# h* W) ?
cles were prepubertal in size. However, testotoxicosis4 W4 }# Y' I& s
was in the differential diagnosis because his father7 u. D5 ~6 x& q1 [: W& }5 p+ Y
started puberty somewhat early, and occasionally," K" |& a4 l  L" [. O
testicular enlargement is not that evident in the
% e; O& ^3 O3 y: ^4 q: Z( obeginning of this process.1 In the absence of a neg-3 y" z% V  @& c9 L7 c
ative initial history of androgen exposure, our
/ a+ r- _, m3 _% G7 T  zbiggest concern was virilizing adrenal hyperplasia,
0 b  b1 z2 Y2 |8 i3 M" d! [" heither 21-hydroxylase deficiency or 11-β hydroxylase4 |0 J8 l0 S$ n0 V4 D1 H$ c
deficiency. Those diagnoses were excluded by find-  C, Q& M* E: C- T( O4 _) [
ing the normal level of adrenal steroids./ f5 r4 ~- g( n1 U
The diagnosis of exogenous androgens was strongly
! ?2 O* \3 h0 o6 jsuspected in a follow-up visit after 4 months because
; e- _* M4 P8 O9 q/ a( kthe physical examination revealed the complete disap-
# U9 q, }( ]& ^* o0 b- t* ^7 B9 ppearance of pubic hair, normal growth velocity, and
9 a" n. U0 X0 S6 t+ cdecreased erections. The father admitted using a testos-
+ z) I# Y3 f$ s9 R9 r( Xterone gel, which he concealed at first visit. He was; e. M* u" s# Y& J: `. p2 T& X
using it rather frequently, twice a day. The Physicians’
0 I" m7 t6 y/ f* dDesk Reference, or package insert of this product, gel or( I+ S, a9 k; }* p
cream, cautions about dermal testosterone transfer to
/ l- P8 r8 f* e+ Z/ v. ounprotected females through direct skin exposure.5 s0 [& \; k/ E% I" K) q( L
Serum testosterone level was found to be 2 times the3 z$ R' y- h* h; {: S( Y/ ~2 m
baseline value in those females who were exposed to
: B+ q; X1 z1 M- ^  aeven 15 minutes of direct skin contact with their male
- s/ G2 ~4 J7 Ipartners.6 However, when a shirt covered the applica-# h+ ~7 B6 I1 N" [* @
tion site, this testosterone transfer was prevented.8 ]' `2 O, r% p- N8 {
Our patient’s testosterone level was 60 ng/mL,
7 ]' Q/ Q6 J, N  N! a" J; ~( wwhich was clearly high. Some studies suggest that& E5 Q- B5 r9 }" c! W) y
dermal conversion of testosterone to dihydrotestos-: D* r: o+ ^6 I: g; \# o$ U' n2 H7 G7 P
terone, which is a more potent metabolite, is more/ b* ?8 H7 |- l& P% ?
active in young children exposed to testosterone
; i! ?8 N2 I, F2 W3 @8 }" _exogenously7; however, we did not measure a dihy-
; t0 G. J2 R3 V7 ~2 L& K. c# ~' Cdrotestosterone level in our patient. In addition to+ i3 @; H5 c# q8 _0 H5 j
virilization, exposure to exogenous testosterone in0 O1 F7 y) m! u+ L
children results in an increase in growth velocity and
+ E1 Q, y& _) j# S/ B* C0 V( padvanced bone age, as seen in our patient.. J0 F5 X' q5 J5 t  s
The long-term effect of androgen exposure during
0 x5 A- o/ }' D; e3 B7 L* ]early childhood on pubertal development and final1 Y) N* N5 G. |" p
adult height are not fully known and always remain# E# i4 K% B% p( Q1 l' G
a concern. Children treated with short-term testos-3 I( u1 F1 N( s9 r5 Q; m$ p4 H$ k8 V
terone injection or topical androgen may exhibit some
: \" a- ?9 g/ c9 ~& w3 f5 h- b) H6 H+ \acceleration of the skeletal maturation; however, after
4 l7 z/ J3 [3 ^0 c0 E) Bcessation of treatment, the rate of bone maturation
9 F9 Z) ^* _6 G% V; S) [5 H' X/ C. Cdecelerates and gradually returns to normal.8,9' Z$ o$ U7 d  W7 @1 m
There are conflicting reports and controversy
8 L6 g8 t( j$ r$ M" }- L- w# Q( Vover the effect of early androgen exposure on adult
+ b1 Z7 X2 D; ypenile length.10,11 Some reports suggest subnormal! N$ M" F0 e8 M+ Y5 H
adult penile length, apparently because of downreg-! K' n; q* I: O" h6 n3 i
ulation of androgen receptor number.10,12 However,
, H' c/ r& O) D" q  U5 rSutherland et al13 did not find a correlation between2 l% e, l2 W! g0 [
childhood testosterone exposure and reduced adult
6 o; S7 Y* Y' bpenile length in clinical studies.0 @& k7 U" M4 h+ g
Nonetheless, we do not believe our patient is1 _" u+ `# H6 Y" ]
going to experience any of the untoward effects from8 h! X/ g9 d) a7 p+ Z1 }
testosterone exposure as mentioned earlier because
7 b: \# a5 G8 \6 b2 tthe exposure was not for a prolonged period of time.
4 n* |% w: b9 ]" k$ LAlthough the bone age was advanced at the time of
: B* C7 L) O. E7 R' |% M+ X: ~9 K' Bdiagnosis, the child had a normal growth velocity at
3 }' U& r5 O+ m+ L1 |1 G7 ^the follow-up visit. It is hoped that his final adult
" c) I0 t( h* ], t% v  K, Iheight will not be affected.
2 c- B* f" g9 A% q. lAlthough rarely reported, the widespread avail-
+ t6 u" t* q/ i7 K4 C/ [* k# y$ n4 bability of androgen products in our society may
1 \$ F& ?* d# ^8 Findeed cause more virilization in male or female
+ n5 J( P& g( {: p+ wchildren than one would realize. Exposure to andro-* R2 u9 K, L. _$ s5 Y3 o8 j1 \
gen products must be considered and specific ques-
2 h  X; V$ f. T! }! p& L. ~0 b) c! Ptioning about the use of a testosterone product or, I5 d9 x" a( P% \
gel should be asked of the family members during
: C/ K) B; f" r) g+ cthe evaluation of any children who present with vir-
( w/ ~5 t6 t6 ]( gilization or peripheral precocious puberty. The diag-
3 m5 r& h/ }7 dnosis can be established by just a few tests and by) k- v2 i6 }. C7 `: ~& A& O4 Y
appropriate history. The inability to obtain such a! J* l* v- G9 O( G$ c
history, or failure to ask the specific questions, may
' R- O: j1 ]' E( |/ W8 Yresult in extensive, unnecessary, and expensive
; o5 H% E5 ~0 v$ m. O% d1 r& x6 _investigation. The primary care physician should be
6 D- r# y. t) i$ s8 Oaware of this fact, because most of these children& H- q6 H8 c8 W) q* Q, V
may initially present in their practice. The Physicians’7 S  v9 P% Y1 M" a) U1 p2 g6 U! X7 r
Desk Reference and package insert should also put a2 g- D8 t% N$ \2 d; M+ {' I& q# k
warning about the virilizing effect on a male or
+ g/ i* v9 E, z$ P3 }2 U9 W4 mfemale child who might come in contact with some-
/ w; t3 J. M9 o3 ^8 \one using any of these products.- _! d% B9 k; C
References
  @, z6 t1 F* t# t! Q- }1. Styne DM. The testes: disorder of sexual differentiation$ v9 L" p' B# F  O$ b% z$ [$ C
and puberty in the male. In: Sperling MA, ed. Pediatric
! o0 i  H, L" j! [; O) z) `, Y+ R& L( XEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;3 I+ @2 `$ q/ @2 u
2002: 565-628.
; A2 x. t2 B- V4 y2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious  y# m: x" o# F  e% O4 e
puberty 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
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感謝大大的辛勞分享!我會繼續在WK關注大大的文章!
發表於 2025-1-11 22:18:01 | 顯示全部樓層
女厕偷拍辅导班主任尿尿老师的逼很嫩还有一点
發表於 2025-1-17 16:31:39 | 顯示全部樓層
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4个什么样的?
發表於 2025-1-19 02:41:05 | 顯示全部樓層
7 E$ _" ?5 r! T7 J# X1 b* o, n
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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