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Sexual Precocity in a 16-Month-Old8 |2 z3 Z5 V7 L+ n4 e8 R7 A, l
Boy Induced by Indirect Topical/ C5 Y. e5 Z, G
Exposure to Testosterone" e! X) o( E2 u( H3 a6 \
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,20 E$ k/ d1 E9 S
and Kenneth R. Rettig, MD1. w- p7 u2 A, Q& C) W
Clinical Pediatrics
. {" Q- t% X0 a& `; S. J  _Volume 46 Number 6
5 V+ |9 L* K" {! R" K0 ^* ?. ~3 C* IJuly 2007 540-543
$ s% h3 N5 ~& N: g( f© 2007 Sage Publications
7 ]! c- s, s3 O10.1177/0009922806296651
, |" y6 A2 H9 h/ z  N& H/ |http://clp.sagepub.com; W* k. T3 V0 }# a
hosted at
4 i7 M: q* X. _$ s/ P+ a4 \http://online.sagepub.com
; b: G* u; M1 w) `4 s+ iPrecocious puberty in boys, central or peripheral,
* Y' Y" S1 g+ F4 i! e$ s) H. {# K1 }: eis a significant concern for physicians. Central
7 ?. @0 m; G) J5 `: r+ Qprecocious puberty (CPP), which is mediated5 I# r2 k% w) c4 M/ Y3 G& ?2 f- w! W" y
through the hypothalamic pituitary gonadal axis, has
( d0 X! b' u7 a) C0 i+ p, Ra higher incidence of organic central nervous system# N/ j5 L$ k! y1 F4 g+ X  ?
lesions in boys.1,2 Virilization in boys, as manifested
6 n. T0 J$ R8 w" s# H/ w: D7 mby enlargement of the penis, development of pubic
1 k8 E3 l7 O; z* l: n+ U4 I5 g+ rhair, and facial acne without enlargement of testi-% ?* c# P) |& ^& k0 o" ^0 k' A
cles, suggests peripheral or pseudopuberty.1-3 We
# Q' W% f& b+ m7 x* z4 S9 t$ sreport a 16-month-old boy who presented with the
1 y4 O0 b8 K+ I  y: k1 zenlargement of the phallus and pubic hair develop-& `. |6 g4 }$ C) F: j
ment without testicular enlargement, which was due7 @& ]- O$ K' h$ w8 n5 ]7 w
to the unintentional exposure to androgen gel used by$ e/ S9 }. c7 }4 C$ H
the father. The family initially concealed this infor-+ Y" v) Z; S% ^* d3 z4 C5 ~$ Q
mation, resulting in an extensive work-up for this: p7 y; V6 E. b# h
child. Given the widespread and easy availability of
! b: N$ I* T$ O, t; Ytestosterone gel and cream, we believe this is proba-9 r3 D  i) ~0 R
bly more common than the rare case report in the1 i. o+ F: Q7 R0 F- x6 W/ _# P
literature.4' _' z. e$ e( F
Patient Report0 k( P% G' O0 O$ C/ _2 c
A 16-month-old white child was referred to the4 `8 b& D- N! B) y4 F
endocrine clinic by his pediatrician with the concern
. c; ^' T& n& K9 E6 `8 E3 Zof early sexual development. His mother noticed
* Q' J, m! `& x! ?6 ~8 Vlight colored pubic hair development when he was
% _: Z/ g! j* G1 rFrom the 1Division of Pediatric Endocrinology, 2University of
2 F0 {. ^2 L; {South Alabama Medical Center, Mobile, Alabama.
% I% z  n- C" ?: v' `( F" \; jAddress correspondence to: Samar K. Bhowmick, MD, FACE,8 j0 |+ S7 k9 z* g/ _# y
Professor of Pediatrics, University of South Alabama, College of: k9 S0 X: N9 n# y* }9 \
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
# O" v" ?3 W4 S4 \e-mail: [email protected].8 R+ L( j8 J! R& Y/ O6 \+ H6 r
about 6 to 7 months old, which progressively became( O' Y, @- e, s+ z2 ?7 o; @( T
darker. She was also concerned about the enlarge-1 q- v3 v' W2 s3 v! D' u( r
ment of his penis and frequent erections. The child) K  n6 S9 f2 K& f8 M1 X
was the product of a full-term normal delivery, with
# \( J( t5 v5 p# ra birth weight of 7 lb 14 oz, and birth length of
: }! C# c% y* Y$ w' V" Z; @4 k# X0 C20 inches. He was breast-fed throughout the first year
+ h) z7 b% m3 Y) m9 A( l! vof life and was still receiving breast milk along with( d/ K7 H% N5 ]% K3 r0 C* \# P
solid food. He had no hospitalizations or surgery,
$ `9 [. `, l5 V2 Qand his psychosocial and psychomotor development5 p5 ^7 F5 x- M/ d$ f
was age appropriate.8 \. w( C! s. m7 A- r2 p
The family history was remarkable for the father," l: m: Y8 e: i' `, r
who was diagnosed with hypothyroidism at age 16,
+ l6 G  i2 O6 S; _2 X. V9 Jwhich was treated with thyroxine. The father’s2 A6 B# E# s2 L5 `( c+ L, ^+ f
height was 6 feet, and he went through a somewhat
* [( L1 Y; z1 v9 @4 W" ]early puberty and had stopped growing by age 14.
$ f3 ?3 ?! c4 iThe father denied taking any other medication. The
' K' q+ y7 b' J! K3 x& hchild’s mother was in good health. Her menarche
  n- h! x* z: [4 E7 W( Nwas at 11 years of age, and her height was at 5 feet* g- D  w$ K0 B! L
5 inches. There was no other family history of pre-6 T7 g6 ]8 F) m& f( @8 V8 }+ [
cocious sexual development in the first-degree rela-  W+ q. M! O1 x) S, ?  r
tives. There were no siblings.
  F; T  m+ T" A  tPhysical Examination
5 G0 i5 c9 a0 w8 ?# i9 R+ CThe physical examination revealed a very active,! t. u. S  {( P* @( j1 i# q
playful, and healthy boy. The vital signs documented9 D2 H8 r; O0 |9 c+ x' J; C) C, {
a blood pressure of 85/50 mm Hg, his length was/ F5 W$ i3 t- M8 n  J9 O
90 cm (>97th percentile), and his weight was 14.4 kg
7 G, W, ~& O1 H(also >97th percentile). The observed yearly growth
% l" w, m( U) u' R$ V/ R  _velocity was 30 cm (12 inches). The examination of" d" I/ v% r  A& b# j
the neck revealed no thyroid enlargement.$ z1 j4 ~4 Z! [/ s' K# f3 [( F" U
The genitourinary examination was remarkable for
. Z" Z  A' O! g% menlargement of the penis, with a stretched length of+ {: W5 Y7 P9 e
8 cm and a width of 2 cm. The glans penis was very well
; @* L9 U+ r& y+ |  @2 I. ~/ xdeveloped. The pubic hair was Tanner II, mostly around0 G* F+ C+ u; S  Q& }% R
540
: v7 q4 {/ s" Y6 h  ]/ A5 }- \, T9 Cat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from( n! K. b' K  a2 p
the base of the phallus and was dark and curled. The
& y& m2 b9 e# i, p! {9 M6 ?9 I8 Ytesticular volume was prepubertal at 2 mL each.3 b* z7 p  p5 |! S0 P  n
The skin was moist and smooth and somewhat
: u1 V1 k6 i8 u5 u$ j: Goily. No axillary hair was noted. There were no1 k. E. J9 A1 @
abnormal skin pigmentations or café-au-lait spots.
& e0 f( S. k. n7 z+ ~: T) fNeurologic evaluation showed deep tendon reflex 2+/ t. `# }$ t$ G8 ?) c0 ^8 I
bilateral and symmetrical. There was no suggestion
% y. |" V# H6 O" W& yof papilledema.
, n- y  d* }1 w6 sLaboratory Evaluation
! u( O4 @, {2 C2 H/ b; y3 o! e( zThe bone age was consistent with 28 months by
1 S6 q' n& u6 l% f1 N: y9 F% yusing the standard of Greulich and Pyle at a chrono-
( S1 Y/ X) B  }: P8 w6 ulogic age of 16 months (advanced).5 Chromosomal
  ?, V6 N; |& [; S7 w0 O# Z& B- Rkaryotype was 46XY. The thyroid function test
9 ^0 i, P% R  ^( ]9 Zshowed a free T4 of 1.69 ng/dL, and thyroid stimu-5 n) y! v2 b. \' R  I6 A* b
lating hormone level was 1.3 µIU/mL (both normal).! {* h2 f6 i  n5 p" _
The concentrations of serum electrolytes, blood5 G4 [" W8 S: n/ K! Z! t
urea nitrogen, creatinine, and calcium all were  |  m$ W9 w; B5 K+ t! u9 d
within normal range for his age. The concentration
, ?6 R$ \8 _& G2 e; yof serum 17-hydroxyprogesterone was 16 ng/dL
" A! g, w' O( q5 l& e3 \. C9 b(normal, 3 to 90 ng/dL), androstenedione was 207 e' I  I1 u2 m  U5 J" I
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-6 ?6 y/ Y, v2 y8 l$ W6 L  X
terone was 38 ng/dL (normal, 50 to 760 ng/dL),2 f" h% V# E" ]6 i
desoxycorticosterone was 4.3 ng/dL (normal, 7 to6 S' f9 y6 _+ M$ u6 Z( C- D# C% f
49ng/dL), 11-desoxycortisol (specific compound S)# n9 }  _5 u: z- g+ `+ q
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-% e' L. N: Q5 R1 {4 n" S
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total) V! f$ Y; Y* [  g" {. e1 Q! t/ A* G
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),7 G+ \5 n8 k; _- O8 P
and β-human chorionic gonadotropin was less than; c" e9 T) N# n" `& S0 n8 h
5 mIU/mL (normal <5 mIU/mL). Serum follicular- j. c& k; I7 B" O  H: o5 H
stimulating hormone and leuteinizing hormone
% d  m; ~& Y, a: B% }concentrations were less than 0.05 mIU/mL
7 k, J7 L. n* K' \, ]2 D4 J(prepubertal).! S* \, a: h# w( D3 k) ^& k( S, r4 L
The parents were notified about the laboratory
$ ^3 P! R. V; r3 {% Mresults and were informed that all of the tests were
! F9 H1 w( F7 Nnormal except the testosterone level was high. The/ t' a+ k* X# _0 g4 n) c3 B8 X
follow-up visit was arranged within a few weeks to
/ |, s) B: `1 y4 D; I6 X3 n' Sobtain testicular and abdominal sonograms; how-) A9 l% j, g! t. T2 s' `% }
ever, the family did not return for 4 months.
6 g9 x8 l- ?3 w0 z0 X) FPhysical examination at this time revealed that the1 k, b, q# A* m) d
child had grown 2.5 cm in 4 months and had gained
$ f, F; P) x( J; }/ q: `2 kg of weight. Physical examination remained
  \1 P1 w5 \- x4 U9 Nunchanged. Surprisingly, the pubic hair almost com-
4 d7 M+ H: n3 f4 W0 o" xpletely disappeared except for a few vellous hairs at6 U. r% F" V# d& e/ i6 _. r
the base of the phallus. Testicular volume was still 2
0 x4 N) h; I  I1 y* z' ^7 xmL, and the size of the penis remained unchanged.
! }8 S: v. V3 f% N& q$ E5 BThe mother also said that the boy was no longer hav-9 e/ V* T/ g" y
ing frequent erections.
+ W+ U4 V" d' H1 a. w8 p; a2 JBoth parents were again questioned about use of
# ~/ J* d) G6 _% ?$ _+ Aany ointment/creams that they may have applied to
" S/ t1 `( P$ x1 o6 b. zthe child’s skin. This time the father admitted the$ d% {- K+ j! y1 ^2 W
Topical Testosterone Exposure / Bhowmick et al 541
4 A- H  f( X/ @8 M0 Q, W+ e/ o/ e3 A" C8 Nuse of testosterone gel twice daily that he was apply-8 W2 h2 @1 V) N! I7 k
ing over his own shoulders, chest, and back area for
, p$ h( I& p4 w0 y6 t. Xa year. The father also revealed he was embarrassed
! z3 U5 h0 W/ N4 R! T: X; i2 v: L6 [4 sto disclose that he was using a testosterone gel pre-: U6 C2 l, q9 ]. A
scribed by his family physician for decreased libido
/ P% x  s0 S' Q3 T& e, |* L; H- q( psecondary to depression.
) q) I, }! v, W6 U. f8 C5 ZThe child slept in the same bed with parents.
% W; R/ M0 }# H( s% l+ dThe father would hug the baby and hold him on his
2 E: B, K6 M0 k. h9 Jchest for a considerable period of time, causing sig-# k$ @: l7 R7 ^6 E+ C3 t
nificant bare skin contact between baby and father.
# q) @; B2 a. }The father also admitted that after the phone call,
/ p- {+ K& ~! ]# X" y+ uwhen he learned the testosterone level in the baby* k/ D6 F; l# d3 ]# `0 Y
was high, he then read the product information- G, s% h. ~* z9 o7 O
packet and concluded that it was most likely the rea-: ]& |6 ^) f# H' l, i+ V! b
son for the child’s virilization. At that time, they1 L* T& m  n+ }5 N3 P5 E: {$ e
decided to put the baby in a separate bed, and the
4 g3 A$ t; K7 j" M' X. S, }father was not hugging him with bare skin and had  k, o& h4 d9 l1 w$ b# F
been using protective clothing. A repeat testosterone; p3 c: v# Z" a/ B; M
test was ordered, but the family did not go to the, X; D& I" g( u  V7 Z3 t3 w
laboratory to obtain the test.
3 c; i7 q9 W9 q% n6 C# gDiscussion
* F) e% ^1 j; d  }) v! uPrecocious puberty in boys is defined as secondary
- o* S% f) D! J5 l- jsexual development before 9 years of age.1,4
" W* k3 \' `+ rPrecocious puberty is termed as central (true) when
; U2 N% I6 Q- wit is caused by the premature activation of hypo-
8 A7 L9 ]. Q/ H, x+ E/ lthalamic pituitary gonadal axis. CPP is more com-
! U6 k) o6 d# t  y# B5 zmon in girls than in boys.1,3 Most boys with CPP, C# a( K# [+ _
may have a central nervous system lesion that is
! X% ?; D( F% L4 g1 q; f8 k, v8 dresponsible for the early activation of the hypothal-
: E% S& D" x% P/ M6 bamic pituitary gonadal axis.1-3 Thus, greater empha-
1 k$ \) X8 [, ?$ ?& isis has been given to neuroradiologic imaging in" i  h& k& d% |7 _. i1 J
boys with precocious puberty. In addition to viril-2 d7 N6 h1 X! u3 Z' H) n- \
ization, the clinical hallmark of CPP is the symmet-
, z! P# y3 z6 u7 F# [rical testicular growth secondary to stimulation by* T# N) G" R" j' R
gonadotropins.1,3% D) C! e* F; C; A0 o$ r
Gonadotropin-independent peripheral preco-% n" w, ^) c1 w# Z) ^
cious puberty in boys also results from inappropriate
. \5 W9 P/ s( B7 ?androgenic stimulation from either endogenous or
7 h! H3 n: _( L4 N: I% qexogenous sources, nonpituitary gonadotropin stim-
+ ~% p8 B! T$ s( eulation, and rare activating mutations.3 Virilizing
1 F. ^% z! l- r0 X! jcongenital adrenal hyperplasia producing excessive5 S9 S& F) B: U5 D- y( N9 E
adrenal androgens is a common cause of precocious0 q% C( R- ]( Y0 T* ^  Y
puberty in boys.3,4
% r# z( s' [2 `2 MThe most common form of congenital adrenal( c4 C$ W$ r, C' {0 }4 F' ?
hyperplasia is the 21-hydroxylase enzyme deficiency.3 f# I5 i' H0 R0 z( z) |0 L
The 11-β hydroxylase deficiency may also result in0 m  J/ a6 v' m5 \
excessive adrenal androgen production, and rarely,( C9 c! A) V* C8 ]* G- d
an adrenal tumor may also cause adrenal androgen9 k4 Y3 L' s# f; k8 Z9 x, }4 Z
excess.1,3
3 m/ O- K" C$ ^at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
% C0 X* g$ a' a, z" z8 [542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
, v0 s  r1 Y# u, m" N( ?% ]: iA unique entity of male-limited gonadotropin-
7 a% }8 j- y3 d! d4 w- K; x( @independent precocious puberty, which is also known) [  m* w* B+ _4 e0 u
as testotoxicosis, may cause precocious puberty at a2 H. H* z/ {, W$ R7 @
very young age. The physical findings in these boys
1 s4 e+ h+ x3 U& |# Ywith this disorder are full pubertal development,
3 x  F( f$ I7 A4 z! i# yincluding bilateral testicular growth, similar to boys
* e3 c" t$ b0 x5 D. {, xwith CPP. The gonadotropin levels in this disorder: O! d- |( |& {: g! N5 L
are suppressed to prepubertal levels and do not show$ z% `- v. C$ H/ n9 p9 D
pubertal response of gonadotropin after gonadotropin-
0 [# k" V, N2 _+ C1 v& t2 {releasing hormone stimulation. This is a sex-linked
: s/ {, @' f+ u0 Y3 e; i. x' uautosomal dominant disorder that affects only
& t5 R2 ?' i+ D( b% J- W5 B6 B2 bmales; therefore, other male members of the family
, \. {! S5 ^2 h' V$ \: \may have similar precocious puberty.3
  r" p, O: [" RIn our patient, physical examination was incon-
" `: ?( S4 F# ^( `( Tsistent with true precocious puberty since his testi-
2 w) \+ f9 d4 M2 @7 q2 M# Q  Ycles were prepubertal in size. However, testotoxicosis
0 I, F+ ~( }' D- W& Ewas in the differential diagnosis because his father
8 y" Q# [2 a9 y5 Nstarted puberty somewhat early, and occasionally,
) @( \$ ~; w. d( Ttesticular enlargement is not that evident in the! k2 S8 P9 g2 p( i; Q8 n/ y. y
beginning of this process.1 In the absence of a neg-
6 _* l2 F7 D3 e/ }7 S0 oative initial history of androgen exposure, our% ~: ]; |; H4 C8 L% b& O
biggest concern was virilizing adrenal hyperplasia,
0 Z* G  ~0 U% j0 Yeither 21-hydroxylase deficiency or 11-β hydroxylase+ Q& T5 v$ M& s9 i% k6 p
deficiency. Those diagnoses were excluded by find-6 U" a# _- d7 i- \7 ~9 i
ing the normal level of adrenal steroids.9 }. b/ S8 {+ o) `6 P
The diagnosis of exogenous androgens was strongly5 _1 @. M1 [; t8 ~- v
suspected in a follow-up visit after 4 months because9 h" H4 [7 P# N$ q5 v
the physical examination revealed the complete disap-- I. p1 k# b+ M) |+ l
pearance of pubic hair, normal growth velocity, and
# B8 W: R+ s$ G7 d/ Edecreased erections. The father admitted using a testos-% n& r! \! |: ^4 G
terone gel, which he concealed at first visit. He was# @* ^: g; ~) Y5 \. h" y- `
using it rather frequently, twice a day. The Physicians’1 [2 w" y( t! O: x1 Z: U, e
Desk Reference, or package insert of this product, gel or
: y- ^4 L" w& t9 i6 v( fcream, cautions about dermal testosterone transfer to
* j& f( E" W+ w( s2 r  Wunprotected females through direct skin exposure.
8 R; h% [- j( V5 U3 c- y) WSerum testosterone level was found to be 2 times the
4 C, f- K* N3 L% V# D  Q5 v3 rbaseline value in those females who were exposed to( w) t+ Z/ A0 s4 Y5 F9 b
even 15 minutes of direct skin contact with their male  I" b8 f1 d7 `
partners.6 However, when a shirt covered the applica-3 u: G3 E. ^4 ^8 J! H
tion site, this testosterone transfer was prevented.
& P. w- g! b; @8 uOur patient’s testosterone level was 60 ng/mL,: X: a- z, N" E( a8 g3 T
which was clearly high. Some studies suggest that
# l$ w& W- u6 ^9 R" s9 odermal conversion of testosterone to dihydrotestos-
4 {7 M) L7 ^' |, `; |- Nterone, which is a more potent metabolite, is more
% A4 b# a" F: f+ E* ]: q+ Xactive in young children exposed to testosterone
9 H, V% a4 ?/ i% F: [  |1 ?exogenously7; however, we did not measure a dihy-
. [5 k( d! r# F6 k! k' Bdrotestosterone level in our patient. In addition to4 l3 ^; U: h) H: v6 c
virilization, exposure to exogenous testosterone in
+ {8 s6 G& B- {children results in an increase in growth velocity and' u1 ^% d5 C' C  p) B
advanced bone age, as seen in our patient.5 i9 ~' ^1 s& K9 j; W" o+ X" E4 m/ B
The long-term effect of androgen exposure during7 W  i) C7 V6 g/ m, T! l7 @
early childhood on pubertal development and final' b1 e9 w5 S4 v' T4 x, I! R3 ?
adult height are not fully known and always remain
1 p4 Z/ T3 }  q9 Wa concern. Children treated with short-term testos-
/ t5 t" b! I8 f: j8 B8 D% \, \terone injection or topical androgen may exhibit some
& W% o* `+ [: v; M$ _acceleration of the skeletal maturation; however, after  e& ]. n2 j) |1 c& |* l
cessation of treatment, the rate of bone maturation) }' `+ @, G6 N% o3 @/ J
decelerates and gradually returns to normal.8,9
3 G) \# ^& w2 ?8 j9 i. [3 u& BThere are conflicting reports and controversy  M( s& i! W' L3 @' x8 ^' {
over the effect of early androgen exposure on adult
2 X3 ~& k& K' F9 Wpenile length.10,11 Some reports suggest subnormal
0 V( S# u- ?7 A! `8 Xadult penile length, apparently because of downreg-
! u9 S& D1 }. V6 Tulation of androgen receptor number.10,12 However,+ {5 m1 k0 ], z$ _+ h
Sutherland et al13 did not find a correlation between
8 }, i' ~0 u) Ochildhood testosterone exposure and reduced adult
# p6 @/ r, W0 epenile length in clinical studies.
% V$ C& u+ J* ?4 |0 C0 c0 H2 _Nonetheless, we do not believe our patient is  ]) A2 q: R2 a( a2 k: u+ [, S; x, N
going to experience any of the untoward effects from3 Y# s" p7 ~" n4 i* u' o9 x
testosterone exposure as mentioned earlier because
: ?) y5 X+ Y  d! T, d$ c+ dthe exposure was not for a prolonged period of time.1 ]: }9 Q; h6 C
Although the bone age was advanced at the time of
, }2 O8 ^( w. D. y- h9 Wdiagnosis, the child had a normal growth velocity at
" T; e; y6 I+ N/ X2 u% I0 O- pthe follow-up visit. It is hoped that his final adult
' ?. o% N# F+ u/ H1 M1 m3 H1 o7 fheight will not be affected.
3 \# x6 I1 Z' J0 H/ q* I8 [/ L" KAlthough rarely reported, the widespread avail-
9 h" m. M8 \: P$ ]  ~. Vability of androgen products in our society may
" K/ T" S8 r: Y5 N0 e- ]% aindeed cause more virilization in male or female7 F# r: o  q, f& `
children than one would realize. Exposure to andro-+ c& P/ @$ {% I
gen products must be considered and specific ques-
5 e' j: w2 h0 k) O2 Qtioning about the use of a testosterone product or
3 ^, P3 n8 a8 L' G* Ngel should be asked of the family members during* @; N/ N" m+ P& t- b
the evaluation of any children who present with vir-, `; p4 T* v# r
ilization or peripheral precocious puberty. The diag-5 f  n$ }. D# E0 l- s4 ~) j
nosis can be established by just a few tests and by2 O: ]& D9 Y1 y: y
appropriate history. The inability to obtain such a' A$ u, T) ^# U/ n3 p
history, or failure to ask the specific questions, may
8 V) e4 W4 v5 l/ d' Cresult in extensive, unnecessary, and expensive0 j- A- E4 p+ e! Z7 \
investigation. The primary care physician should be
; c6 D" y  a2 s9 X& z) ?6 f( oaware of this fact, because most of these children
' ~" v* M/ S- @' ^may initially present in their practice. The Physicians’
6 Q. O' \4 U- @: ?+ G4 gDesk Reference and package insert should also put a- _" \: P  Y& {. f! c
warning about the virilizing effect on a male or; p  F1 W2 J' b# C7 ]
female child who might come in contact with some-
* F- }. {7 U9 uone using any of these products.: L( w' n+ g) l" R* L5 V
References
) w% P, z6 x( I( x: w) ?# W1 U6 h1. Styne DM. The testes: disorder of sexual differentiation) l( q* e; x- f1 c3 z3 A
and puberty in the male. In: Sperling MA, ed. Pediatric4 K4 Y/ U0 i0 s( F0 @4 A
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;$ H8 [7 m/ ~2 K4 r# b% a3 G
2002: 565-628.
1 W7 X3 A  t# b) {3 Z% R2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious& P% J+ n7 _3 C" D
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
3 B% }8 o& L. q! L0 sBoy Induced by Indirect Topical8 \6 [7 n7 a; e- O  P* r- ^1 ?4 R
Exposure to Testosterone
) @0 p: |$ Y* M; {' \2 PSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
8 a2 g0 U' _& I# y" e3 {# @$ @and Kenneth R. Rettig, MD1
# k+ s) d, c( ^0 m/ E) f0 KClinical Pediatrics7 f/ a# _, d# w" ?9 l1 u" t  L! Q
Volume 46 Number 6
$ G, m0 J+ U- E/ FJuly 2007 540-543
+ i$ X2 B1 J1 `1 Y+ _© 2007 Sage Publications
4 s7 a; G) E* L9 e. M10.1177/0009922806296651
% O! @6 f/ k4 r( u& bhttp://clp.sagepub.com3 Y, T5 H! E6 D9 \+ K6 ?
hosted at1 U3 M* ~- E" H! O
http://online.sagepub.com! y, [2 @- I* ~
Precocious puberty in boys, central or peripheral,
* j1 T' V+ r8 {, n' mis a significant concern for physicians. Central8 C& V9 M% v" z: I' `
precocious puberty (CPP), which is mediated: R2 g0 P0 e3 t: D. ], o
through the hypothalamic pituitary gonadal axis, has
  _( k5 h5 z$ p% }% [  la higher incidence of organic central nervous system
  H! B1 `  d# Y4 d5 R& blesions in boys.1,2 Virilization in boys, as manifested
: P8 [0 t1 Z% Q* Tby enlargement of the penis, development of pubic) S7 N$ c* ]- g" Z) T% P* H" _6 f
hair, and facial acne without enlargement of testi-. @( j6 K# {; a' O
cles, suggests peripheral or pseudopuberty.1-3 We
3 e9 s. G8 Z  G4 ~& f2 greport a 16-month-old boy who presented with the5 ~6 I7 [+ ~; Q$ E' O2 ^
enlargement of the phallus and pubic hair develop-
: Z  x9 ^  P# c* n) u$ M4 O% Mment without testicular enlargement, which was due
* e6 f- N9 P! ?0 Pto the unintentional exposure to androgen gel used by8 ], Q" G0 z: @  F. H7 v# u6 d0 U9 @0 l: F
the father. The family initially concealed this infor-( w$ J! f5 Y: q$ U+ h
mation, resulting in an extensive work-up for this
0 I0 l" }2 z$ A- y: fchild. Given the widespread and easy availability of3 N, o$ X' K  o1 ^( {4 u3 ~
testosterone gel and cream, we believe this is proba-
- p. e( q+ u- u6 V8 Sbly more common than the rare case report in the2 k% O' C# W3 a1 [
literature.4
/ a; C; v2 A3 [9 N' i- l& U0 B7 NPatient Report
- s0 t. }. V" F- oA 16-month-old white child was referred to the
7 H. m% T, @+ y6 D) [endocrine clinic by his pediatrician with the concern% c1 i* a  T9 @. u' H! {" x3 ]  f
of early sexual development. His mother noticed  y5 B* u9 ^5 P$ |( ]6 l2 c3 Z
light colored pubic hair development when he was
8 C7 O' i  y  r( dFrom the 1Division of Pediatric Endocrinology, 2University of& b- V# _2 O( n, S5 ^' B
South Alabama Medical Center, Mobile, Alabama.: }1 H3 o( Y- o1 ^: Y! O
Address correspondence to: Samar K. Bhowmick, MD, FACE,5 \+ a' J+ X% P' e/ m0 ?  s: V
Professor of Pediatrics, University of South Alabama, College of
6 ]) C: V4 A( C. t4 Q! A1 ~Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
$ F2 G5 `8 _* G' Y4 _5 W6 ]e-mail: [email protected].3 U3 u+ H2 d" F& G5 w' ^1 h- b; V
about 6 to 7 months old, which progressively became
0 J# G; d* n  [+ {5 u  ~darker. She was also concerned about the enlarge-
) _( B* @! y1 w0 s$ w0 y* K! U) Ument of his penis and frequent erections. The child% d7 Z/ M5 J* }' A+ w, N" E
was the product of a full-term normal delivery, with
1 Y+ W9 F: d% ja birth weight of 7 lb 14 oz, and birth length of9 O% L1 n' |9 p; h9 `
20 inches. He was breast-fed throughout the first year
* _% Y. e  n% Jof life and was still receiving breast milk along with
. g9 C. T& V* [% w: e- x9 i' G( nsolid food. He had no hospitalizations or surgery,
% o: R+ c# z/ N) Aand his psychosocial and psychomotor development0 e9 a9 Q) P% M  h/ |# o' @2 h
was age appropriate.0 Z# z2 A" w% t
The family history was remarkable for the father,4 }+ T5 J* Z( x. O' i! A
who was diagnosed with hypothyroidism at age 16,
( \- y5 i/ ]7 c4 H& a) Pwhich was treated with thyroxine. The father’s
6 \0 o8 ^9 p( L3 c; i' X& B" @height was 6 feet, and he went through a somewhat: [5 P& f0 W0 N4 [7 g! j
early puberty and had stopped growing by age 14.8 J8 L1 {5 m  S; u/ d' R( ^
The father denied taking any other medication. The' X; S2 ]1 V  {  Y* B' \
child’s mother was in good health. Her menarche
( {5 E- E; W$ `; c/ z2 cwas at 11 years of age, and her height was at 5 feet
( {8 A% K3 \  E5 inches. There was no other family history of pre-& E) Q' v# U' `
cocious sexual development in the first-degree rela-9 [# x( x2 {+ G0 v4 R: o$ d
tives. There were no siblings.
# t* Q5 x9 W& w- M- R* ]; i5 sPhysical Examination( Q- N( K% k$ _  K4 S  L
The physical examination revealed a very active,1 U& Z, I0 u8 r, x4 r  u  b% I( i
playful, and healthy boy. The vital signs documented$ H+ d( Y% x' W2 @! N% J0 {) M
a blood pressure of 85/50 mm Hg, his length was6 Z1 l- W6 x1 J% q
90 cm (>97th percentile), and his weight was 14.4 kg9 Z4 `2 S" b2 Q( n! [
(also >97th percentile). The observed yearly growth
, a: R9 K# R0 xvelocity was 30 cm (12 inches). The examination of
: l! o: ]6 c( P4 |7 gthe neck revealed no thyroid enlargement.
1 F4 R3 ^+ M% A  v. RThe genitourinary examination was remarkable for
, ~; n# D$ \6 i3 L+ v8 yenlargement of the penis, with a stretched length of2 u" R. N% v; ~( C- L2 q/ w- r
8 cm and a width of 2 cm. The glans penis was very well) B5 O. ]& X" E/ N7 X9 S
developed. The pubic hair was Tanner II, mostly around
: ]% }4 d* z0 O& |$ T540
" S; a, {/ W8 V5 ^1 nat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
6 Y; H  A( w' t/ M0 Hthe base of the phallus and was dark and curled. The
1 B8 E2 M* M: `; P2 }2 R- s. Dtesticular volume was prepubertal at 2 mL each.' a; M+ x% l$ o  }; h! s
The skin was moist and smooth and somewhat
+ C& X1 i% E% P  r& H/ ?' Y. voily. No axillary hair was noted. There were no: w2 ]7 \1 A6 v1 n2 u
abnormal skin pigmentations or café-au-lait spots.# C# _) P! t6 k5 P' w6 L5 M3 f
Neurologic evaluation showed deep tendon reflex 2+1 e: t9 Z& d* B0 s# T
bilateral and symmetrical. There was no suggestion+ T1 h, w3 T. Y) S$ Y+ M
of papilledema.; Z: T1 v! V# T3 M0 D$ ^; }" p
Laboratory Evaluation! R# E' ]2 |; u- l
The bone age was consistent with 28 months by1 }1 L) B; r+ U- _4 x$ F$ c1 ?$ n4 h
using the standard of Greulich and Pyle at a chrono-
. p( E4 G% Z9 C; s  v7 Flogic age of 16 months (advanced).5 Chromosomal
6 g$ ~+ d. l, ]- }3 S" xkaryotype was 46XY. The thyroid function test
, k- d0 d$ q) u; ?4 Q) D! @( a3 Ishowed a free T4 of 1.69 ng/dL, and thyroid stimu-5 s; `/ F$ U- ?2 y" G2 _4 Z, ^
lating hormone level was 1.3 µIU/mL (both normal).
4 F* H& {' i0 ^% P5 w7 x# |% ~The concentrations of serum electrolytes, blood% `  A1 ?( x# h# K
urea nitrogen, creatinine, and calcium all were
1 ]+ x5 r  x$ Q; }4 nwithin normal range for his age. The concentration
, ~0 k- o: f" p) w& g. [of serum 17-hydroxyprogesterone was 16 ng/dL
+ ?5 m; _& B+ H7 z(normal, 3 to 90 ng/dL), androstenedione was 20% U5 @+ o1 e& I3 F: C3 j
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-4 q' a4 ^& u7 v; z; X8 A6 t
terone was 38 ng/dL (normal, 50 to 760 ng/dL),* @3 Y, l0 f4 ?) }8 Q( D3 t* B+ C
desoxycorticosterone was 4.3 ng/dL (normal, 7 to0 g' u7 n' b& o- R0 F4 z6 q- @
49ng/dL), 11-desoxycortisol (specific compound S)
9 X+ `& R' X/ l4 ]9 pwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-* k0 b$ c7 I( r0 d& J& E
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total% T# e$ x0 m3 w8 W
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
$ W! ]4 t' ?- O7 K" @3 D3 gand β-human chorionic gonadotropin was less than/ w; B% g7 x1 C9 _
5 mIU/mL (normal <5 mIU/mL). Serum follicular1 `7 e$ D$ h, k0 C' u/ r
stimulating hormone and leuteinizing hormone6 O) W$ A: }- Q$ y4 U( d9 W8 b
concentrations were less than 0.05 mIU/mL4 U4 n* m& P7 Y4 k
(prepubertal).
. l7 U9 Z! R0 p  Z, pThe parents were notified about the laboratory
- ~) R! t) [: H; x2 Hresults and were informed that all of the tests were- N% d0 S. B, [* H% S8 Z: {
normal except the testosterone level was high. The1 _' e3 L. P0 W0 ~( k
follow-up visit was arranged within a few weeks to
# R7 s5 h& Z6 X# k0 xobtain testicular and abdominal sonograms; how-
1 ]/ C0 t' U4 S  N" ]4 g, w7 Eever, the family did not return for 4 months.' `1 w5 S7 ]" b( Q
Physical examination at this time revealed that the5 w5 Q% i' J& v7 ]; C4 _& _  K- B
child had grown 2.5 cm in 4 months and had gained. z0 w9 P( g+ z2 R. p
2 kg of weight. Physical examination remained8 e& }  i6 _1 H! G
unchanged. Surprisingly, the pubic hair almost com-
) R. H* j3 F% Z3 P# mpletely disappeared except for a few vellous hairs at
' G# r! P; O7 zthe base of the phallus. Testicular volume was still 2
. o7 S7 F- H+ T, C9 s# ]3 ~mL, and the size of the penis remained unchanged.
2 o: C- F# z  f, f5 `$ t1 gThe mother also said that the boy was no longer hav-
9 s+ G% L% D0 @' ?0 o! Fing frequent erections." ]4 h& P6 y# p, v
Both parents were again questioned about use of
* f+ X, M1 ~% P( Eany ointment/creams that they may have applied to: O2 X" i; }- b2 M5 ?0 n' G2 J9 J
the child’s skin. This time the father admitted the0 L0 a4 j& O( m3 r* @6 u# p/ \
Topical Testosterone Exposure / Bhowmick et al 541
" V/ M! s0 z0 _' A6 Duse of testosterone gel twice daily that he was apply-! i/ B! y* I3 Q* R1 B# E
ing over his own shoulders, chest, and back area for
  G1 C, h4 k& [a year. The father also revealed he was embarrassed& Y5 H- v6 G. V6 X/ v. m1 K
to disclose that he was using a testosterone gel pre-9 O9 ~) ]  k4 l+ ?+ s
scribed by his family physician for decreased libido
+ J1 ^1 C+ p$ csecondary to depression.6 [+ c5 S6 ]( g' T8 T( z
The child slept in the same bed with parents.6 C  J- ~& [1 }8 L# c
The father would hug the baby and hold him on his
( t( X+ ~1 }! D* ~, _- V5 fchest for a considerable period of time, causing sig-
$ z! _+ x1 m4 `nificant bare skin contact between baby and father.
# \  V; K/ U1 h0 J% x% a( ~! qThe father also admitted that after the phone call,
4 F1 B5 |7 L! Q0 ~0 v  ]when he learned the testosterone level in the baby' B8 L/ Q' R# Y/ {! \! c$ f
was high, he then read the product information
9 n) j+ B6 K' S  I. x0 Vpacket and concluded that it was most likely the rea-
1 X9 q0 n( Q" eson for the child’s virilization. At that time, they$ j! i1 w* t3 a& ~7 W7 Z
decided to put the baby in a separate bed, and the$ Z' g: x$ ~5 `
father was not hugging him with bare skin and had
- V3 L, L% s/ n, P; U- h; zbeen using protective clothing. A repeat testosterone: w" y3 l( a* `
test was ordered, but the family did not go to the0 |" r; l, J4 r6 W
laboratory to obtain the test.% R1 _( i5 d$ M( s* K
Discussion- X3 v; C6 P( ?# x# N
Precocious puberty in boys is defined as secondary' u) r% G. e9 v' f* b. M
sexual development before 9 years of age.1,4
) Z3 M' j4 P5 M8 s, m/ aPrecocious puberty is termed as central (true) when, x) I4 A/ ^/ ]1 e* j, ]! j6 D. C
it is caused by the premature activation of hypo-
6 D- W. H9 C  ~3 K: V- X; othalamic pituitary gonadal axis. CPP is more com-
: z+ H0 p+ {; Nmon in girls than in boys.1,3 Most boys with CPP  \9 z3 g8 B# l% W6 n# b' e
may have a central nervous system lesion that is' n# v( J9 P- }) D' v
responsible for the early activation of the hypothal-& ]: I# ^# G. Z
amic pituitary gonadal axis.1-3 Thus, greater empha-
% O0 }, z8 F" E  Vsis has been given to neuroradiologic imaging in
. q: q" N; _4 S% I& k* P7 Lboys with precocious puberty. In addition to viril-3 v( E, S; G$ v
ization, the clinical hallmark of CPP is the symmet-0 D, T+ X0 N+ p! F* V) p' i
rical testicular growth secondary to stimulation by
& e9 ]0 ?# S0 F2 h. t0 pgonadotropins.1,3
  ~, W3 @9 g( N$ V$ Y( B. X. RGonadotropin-independent peripheral preco-
6 H$ w5 [( U- a* w8 `8 scious puberty in boys also results from inappropriate
; {) t5 p/ @; s0 N- |/ _0 sandrogenic stimulation from either endogenous or; v/ a7 O: W( V1 z% k2 C1 n
exogenous sources, nonpituitary gonadotropin stim-
2 [' M* U4 a6 k/ [- C. |ulation, and rare activating mutations.3 Virilizing) @$ b8 l% r& U4 U
congenital adrenal hyperplasia producing excessive4 g3 G7 H- ?: ]3 c, {- Z
adrenal androgens is a common cause of precocious8 x& `& J) l* _- m: v" z$ F
puberty in boys.3,4
; {8 v( E# Z! u3 b! s7 BThe most common form of congenital adrenal6 ^" W. |. B7 h8 R9 _7 R
hyperplasia is the 21-hydroxylase enzyme deficiency.3 |0 _# U" f# j; X- i. o" c' [$ g
The 11-β hydroxylase deficiency may also result in
# f" K6 `. s: Gexcessive adrenal androgen production, and rarely,' Z! A$ S7 G+ X% w# i0 c
an adrenal tumor may also cause adrenal androgen8 \0 G6 P$ e- e3 c4 e
excess.1,3
; Q6 P  Z3 n8 Q) X4 mat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
) f7 r. D0 w6 _& `7 f: O542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
2 V1 W# a& u8 s# ^" K# A0 _A unique entity of male-limited gonadotropin-
3 ]& t& z/ F0 T6 @/ I; X! hindependent precocious puberty, which is also known
. v7 ?, U" _, T7 P, n1 K9 Was testotoxicosis, may cause precocious puberty at a( b; W0 F+ @$ g: y' r
very young age. The physical findings in these boys: B5 d+ c: g2 S
with this disorder are full pubertal development,$ T4 A, [6 E2 K7 x* V, @
including bilateral testicular growth, similar to boys& m5 ]& }2 h  q7 ]- ^( W" B
with CPP. The gonadotropin levels in this disorder
( d  I$ d! x2 {& I$ qare suppressed to prepubertal levels and do not show
2 m1 G, U; V; O2 ?$ h0 Wpubertal response of gonadotropin after gonadotropin-9 ]  g& ]  ?5 s
releasing hormone stimulation. This is a sex-linked1 U/ `7 B9 g$ ?! A  v# _  ^
autosomal dominant disorder that affects only
) ]5 j$ ?5 K2 d( t/ U1 |8 Nmales; therefore, other male members of the family8 D8 Q2 s6 ^% Y% {& U+ Z1 n
may have similar precocious puberty.3
0 A7 O0 ?$ ~8 ^8 Y- CIn our patient, physical examination was incon-
  T4 F/ X: L0 y$ p. csistent with true precocious puberty since his testi-8 H9 t4 b0 [* U9 N; T
cles were prepubertal in size. However, testotoxicosis2 E. S: ~7 d6 {8 P
was in the differential diagnosis because his father1 P2 |7 H/ f5 N; h& ?
started puberty somewhat early, and occasionally,
; R7 g: _0 C, Y* I4 K8 Ztesticular enlargement is not that evident in the
: R% w; A* S$ _+ [1 Mbeginning of this process.1 In the absence of a neg-0 L' H- U9 `! r6 \& V, |9 \5 o
ative initial history of androgen exposure, our
; O. S+ s. m3 O% H7 Vbiggest concern was virilizing adrenal hyperplasia,
& ]/ u9 Q3 T2 B& l; g% keither 21-hydroxylase deficiency or 11-β hydroxylase; f+ M) R3 H2 N4 s
deficiency. Those diagnoses were excluded by find-
8 O1 y* t- f% j& W8 Aing the normal level of adrenal steroids.
1 X2 j/ K+ I3 D0 w, o8 kThe diagnosis of exogenous androgens was strongly+ W  I2 C% d! }: u/ P8 N3 m5 U$ e
suspected in a follow-up visit after 4 months because
7 {- k, z' w  [) Jthe physical examination revealed the complete disap-6 l6 d; t% b0 C* o. [
pearance of pubic hair, normal growth velocity, and5 j/ n! ^% f+ q4 h: ^! O' i
decreased erections. The father admitted using a testos-
6 j9 h8 C) Q* V7 J. Oterone gel, which he concealed at first visit. He was, ?# L3 Z5 H0 E; p% W3 k' ?) f
using it rather frequently, twice a day. The Physicians’
% P. K- n3 W- U3 a' r) s' FDesk Reference, or package insert of this product, gel or' N; z& U4 B" C( v) j7 c- @) E: _
cream, cautions about dermal testosterone transfer to2 u9 Q; U# T3 ^4 }" l( [* A0 {
unprotected females through direct skin exposure.
! {8 R6 [6 L* z2 f& c3 Z) BSerum testosterone level was found to be 2 times the
6 i/ e$ [* E) L* g7 _baseline value in those females who were exposed to
& ]* N- v5 d! \; R0 Jeven 15 minutes of direct skin contact with their male
- i; H/ h4 X. y8 @8 J) L. S5 Opartners.6 However, when a shirt covered the applica-5 Y* |$ Z% x; }$ a0 Q6 T
tion site, this testosterone transfer was prevented.0 S' _* j8 F' c
Our patient’s testosterone level was 60 ng/mL,
. `! o+ h" t4 U% Nwhich was clearly high. Some studies suggest that3 v) T, t  u/ H4 |8 ]
dermal conversion of testosterone to dihydrotestos-
$ C& H8 Q- ~( H  q' {  u+ A% Qterone, which is a more potent metabolite, is more
  {- e2 I, X5 ]+ Tactive in young children exposed to testosterone
9 A5 ~5 A; y& ?4 _8 b! Gexogenously7; however, we did not measure a dihy-. B9 H6 E% P) {% c( F/ F( j# ^: `7 Y
drotestosterone level in our patient. In addition to5 d* {+ i5 H( {" o8 s( h
virilization, exposure to exogenous testosterone in
$ p( f6 g" P1 k' Lchildren results in an increase in growth velocity and
% G& p2 c( a! m& N( ]! f6 C9 }+ Radvanced bone age, as seen in our patient.
, }! s+ H6 |0 g, N, p$ ?0 ~The long-term effect of androgen exposure during# Q9 l% i* `; a" E# L7 _
early childhood on pubertal development and final7 J' x* H5 U6 R4 X
adult height are not fully known and always remain
0 s8 T+ i1 V9 G4 a$ ua concern. Children treated with short-term testos-
! p7 D$ C9 I- \3 ?9 q2 o8 s7 Kterone injection or topical androgen may exhibit some
. Z0 M/ G% [  `1 j; D1 P7 Macceleration of the skeletal maturation; however, after
! O, }  y( d6 D, q/ ~: D! |5 ^cessation of treatment, the rate of bone maturation4 D$ r2 u% K2 L  I" e: H8 s6 G
decelerates and gradually returns to normal.8,9
2 ~0 D, D$ b$ S3 T" q7 b8 yThere are conflicting reports and controversy. L; {( ?9 k. t. O! @4 ?, k
over the effect of early androgen exposure on adult
' i$ j2 @" u- c) }0 z) c. _. lpenile length.10,11 Some reports suggest subnormal
' i+ o4 W: e5 B' m9 X5 oadult penile length, apparently because of downreg-
2 v# s4 N- J" m; w' Z3 J0 Mulation of androgen receptor number.10,12 However,
* K6 o& `. }6 X" ASutherland et al13 did not find a correlation between! z* v" \/ w) z( b" p
childhood testosterone exposure and reduced adult
7 m; \  ]$ _0 f7 k$ \penile length in clinical studies./ U- a$ c# d5 s2 z; `2 w: t/ h( }8 }
Nonetheless, we do not believe our patient is+ e: J7 `( I) d3 o$ b
going to experience any of the untoward effects from
( m- X% X+ g3 i- [) P: ftestosterone exposure as mentioned earlier because
) X; N2 V6 V* W: i( S  Wthe exposure was not for a prolonged period of time.
+ l5 z1 f9 U  n8 G  Q, zAlthough the bone age was advanced at the time of  h' @, n( B, w& C/ t/ g
diagnosis, the child had a normal growth velocity at
- V' M+ a" N; Y6 l+ z1 k# Sthe follow-up visit. It is hoped that his final adult9 \# L2 Q& G4 n, w3 ]4 p: a
height will not be affected.- P' N# e0 B* A' J7 e6 Z; Z
Although rarely reported, the widespread avail-
/ L" `+ M6 ~6 y$ i4 Y6 W) uability of androgen products in our society may. X% E; ?* Q0 ?7 N# F: u, R
indeed cause more virilization in male or female
' j* d/ u- p/ P1 A0 Mchildren than one would realize. Exposure to andro-
$ Q0 A. U+ `1 ]gen products must be considered and specific ques-; X* y4 R. z& b. P9 y
tioning about the use of a testosterone product or
1 Y% v1 v  m9 y2 F7 ]* |" zgel should be asked of the family members during
& Y/ y  j; S/ q$ Bthe evaluation of any children who present with vir-: p$ N& T1 i! U2 h
ilization or peripheral precocious puberty. The diag-
, F: N/ M  j, Z' ~' S. Knosis can be established by just a few tests and by; o- h  e, W7 S; I9 \& n: ~
appropriate history. The inability to obtain such a
! a' c) B5 s' c6 phistory, or failure to ask the specific questions, may6 a% ?! I. e2 ]+ r4 x
result in extensive, unnecessary, and expensive
9 r# e+ W( ~! Y9 sinvestigation. The primary care physician should be4 o, A$ b1 J! B6 n: y8 h5 ^! f
aware of this fact, because most of these children
# I: R8 z7 U: B0 Umay initially present in their practice. The Physicians’
$ J! @/ x& T8 k$ N3 F2 _7 XDesk Reference and package insert should also put a
. p, k+ W  Y5 J; S$ n2 rwarning about the virilizing effect on a male or* C3 b9 e+ |/ g9 h, D6 i
female child who might come in contact with some-
; T& T- H4 E* ~8 n1 r" E/ ~1 d% h- Oone using any of these products.# g7 `/ H5 K' E: L0 J$ G! N
References
; |) b' I# n" c! D1. Styne DM. The testes: disorder of sexual differentiation( W& H; l* Q+ @- c$ W! z4 d) m, L
and puberty in the male. In: Sperling MA, ed. Pediatric( O+ q( ^& z/ }8 V* f) a, @
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;6 ^% E: \% }. P( N' u
2002: 565-628.
, t* i9 w/ b1 Q+ O/ _* _2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious0 w6 I7 c$ k: R) `, T: D* {
puberty in children with tumours of the suprasellar pineal
發表於 2025-1-7 21:59:43 | 顯示全部樓層
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發表於 2025-1-10 10:43:39 | 顯示全部樓層
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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
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

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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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