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Sexual Precocity in a 16-Month-Old+ f9 D3 Y6 z1 d0 b; ?, T2 E
Boy Induced by Indirect Topical
' f! w" [- _+ P; w  _) eExposure to Testosterone% T3 ~" S9 A. I  v# F* g
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2: F9 N' T4 s+ B" H) L. k1 J* F
and Kenneth R. Rettig, MD1% S  r) M; e2 h9 k% g( d6 ]
Clinical Pediatrics
  H: c: Y1 \- kVolume 46 Number 6
+ H9 `6 S. e& R9 _% E" P# m9 l3 FJuly 2007 540-543
9 y- I5 L5 N5 L© 2007 Sage Publications
2 P. p2 @6 k& a0 h" d( C5 j10.1177/0009922806296651+ n" F1 d, q7 Y% f
http://clp.sagepub.com9 S+ I3 ^6 g# e' {
hosted at% f- {/ t5 Q$ D; t- i' y
http://online.sagepub.com
2 H& ~$ b- l% nPrecocious puberty in boys, central or peripheral,& f3 R* r  j) J' b  x& S7 |5 U
is a significant concern for physicians. Central
0 Q8 m5 S6 A/ o5 i1 K1 ^precocious puberty (CPP), which is mediated. k  L5 ]. U. Y% Z
through the hypothalamic pituitary gonadal axis, has
8 s- H9 e0 I. s8 L7 K/ R& D! S& va higher incidence of organic central nervous system
% m$ g( H. y' A' d' h- N+ x+ flesions in boys.1,2 Virilization in boys, as manifested6 \0 @: F6 v9 a& |8 c0 K7 G% D% N- L
by enlargement of the penis, development of pubic& @: ?% H5 u$ W# n
hair, and facial acne without enlargement of testi-' g1 s7 d/ i$ o) i; E: z' s
cles, suggests peripheral or pseudopuberty.1-3 We: Z( e$ k* F, v; |2 C3 ?$ }% L
report a 16-month-old boy who presented with the
5 q' N. k& t' J& E; uenlargement of the phallus and pubic hair develop-
1 H* z1 z( Q& W+ @3 B7 lment without testicular enlargement, which was due
% j) C$ `! i, d1 S5 E9 y* T, p2 ^to the unintentional exposure to androgen gel used by
4 `) Q" Z( u6 E! n0 ?) G: y" Hthe father. The family initially concealed this infor-
6 j$ }& J" \9 I1 j: S5 m! ymation, resulting in an extensive work-up for this
) m4 a* u! S3 a0 z; Lchild. Given the widespread and easy availability of1 V4 o. j+ |2 [7 k
testosterone gel and cream, we believe this is proba-' E7 o9 c3 a/ O9 e; L/ B9 }
bly more common than the rare case report in the0 i  [, U& c' w/ m; d6 b
literature.4
1 T3 q# N  \0 F( V7 Q& }( rPatient Report' P/ Z1 X$ E3 t' [2 s6 c
A 16-month-old white child was referred to the: W5 I8 }& y0 G7 F6 T
endocrine clinic by his pediatrician with the concern
! s2 F$ C, }8 @of early sexual development. His mother noticed
* @. R0 }* }! @2 P/ F1 a+ d* olight colored pubic hair development when he was5 S6 |. b7 s8 O& W7 {
From the 1Division of Pediatric Endocrinology, 2University of
% f" t. ]+ q& g8 M6 |South Alabama Medical Center, Mobile, Alabama.+ j  |3 |0 ]. T2 U  c/ K/ e& [5 H- v
Address correspondence to: Samar K. Bhowmick, MD, FACE,
7 v# ]* h* f* \  p) }5 oProfessor of Pediatrics, University of South Alabama, College of: }5 T/ q( s/ {3 F
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
+ @2 v+ G. Q# d( K1 `/ ke-mail: [email protected].
: r, l8 w! z( D9 `/ b6 o* Cabout 6 to 7 months old, which progressively became  M7 }& g" ]$ f3 K% S/ u
darker. She was also concerned about the enlarge-
5 l! {. Y- S$ Q  vment of his penis and frequent erections. The child3 [7 Z! }* n; h, K3 w# |4 R
was the product of a full-term normal delivery, with
; @. x2 `4 ?/ v% V" {a birth weight of 7 lb 14 oz, and birth length of' z0 r* H) @. @5 |; U+ b" b
20 inches. He was breast-fed throughout the first year" I3 ]. ^1 h. a! q% Q
of life and was still receiving breast milk along with
  s- A" Q4 b8 F6 ?3 jsolid food. He had no hospitalizations or surgery,
3 A) _2 \6 D7 p) Y2 Q/ Zand his psychosocial and psychomotor development
4 t/ I8 a; f: M0 i" H$ u, Rwas age appropriate.
' i# g+ Q+ N3 G* X, {The family history was remarkable for the father,0 ?3 P2 {- }7 H! z- e$ v; Y
who was diagnosed with hypothyroidism at age 16,
4 d7 F, Y" k+ N& n3 r( ?# I: Q. cwhich was treated with thyroxine. The father’s) l. t* R3 T2 S7 Y. x. K5 g
height was 6 feet, and he went through a somewhat
1 A+ ^+ W1 z8 {) [6 A0 hearly puberty and had stopped growing by age 14.) m# N5 [4 T+ V. {
The father denied taking any other medication. The1 ?: \8 K- {0 y; ]# g5 i0 q
child’s mother was in good health. Her menarche
( c! Y5 Z# F& H  N5 w4 Wwas at 11 years of age, and her height was at 5 feet
. G2 l# G0 q: S" ~  h5 inches. There was no other family history of pre-+ f9 G  ?0 l* j
cocious sexual development in the first-degree rela-: h+ I2 N& S- D5 _( ~
tives. There were no siblings.  {6 w/ S6 b2 Z7 b6 L2 `9 I% ^
Physical Examination- D  ~. ^9 P8 f% R1 h. B
The physical examination revealed a very active,
' _* X3 W# L3 v# Yplayful, and healthy boy. The vital signs documented
" C4 Z/ s8 _, t! k! |! V/ ua blood pressure of 85/50 mm Hg, his length was
6 w* h- s0 D5 P$ d. k! `" d90 cm (>97th percentile), and his weight was 14.4 kg" A) g/ l! d  o. q9 w2 U
(also >97th percentile). The observed yearly growth/ X) y0 w3 Z0 r
velocity was 30 cm (12 inches). The examination of
3 k! E2 Q3 x* H/ C6 rthe neck revealed no thyroid enlargement.
' R. u6 j4 i* [+ Z( U9 ]) pThe genitourinary examination was remarkable for6 x2 s9 Q' X5 u! z; U2 Q2 Y
enlargement of the penis, with a stretched length of
& b7 Y$ F2 u8 o) o, I8 cm and a width of 2 cm. The glans penis was very well& X3 p! Z. }1 s% T5 k
developed. The pubic hair was Tanner II, mostly around
; _5 G3 S% T7 M; m7 N+ u540: ?, ?1 t. Q6 [0 y$ t6 |
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from2 y: u. r2 K3 {! ~- B6 C8 D
the base of the phallus and was dark and curled. The
) S1 K( N6 w+ e$ C% Ptesticular volume was prepubertal at 2 mL each.5 A. y0 ?8 z$ d. R# F- D, x7 B0 {
The skin was moist and smooth and somewhat  g" a8 Q' G# p  B% `7 [7 G
oily. No axillary hair was noted. There were no% A' B' G! {# y+ u7 m7 r$ l
abnormal skin pigmentations or café-au-lait spots.' E5 {" r, |- _$ d6 o' q; Y7 G
Neurologic evaluation showed deep tendon reflex 2+
' q* w3 V# R9 Ebilateral and symmetrical. There was no suggestion% K" j8 g+ h  s! n! l# v+ F& Q
of papilledema.% E& e- R& i: K% H6 i1 F/ V2 _
Laboratory Evaluation
; U) E; Z4 D1 c8 G  jThe bone age was consistent with 28 months by$ S7 Q) U$ D# V* Q2 T$ v
using the standard of Greulich and Pyle at a chrono-
$ X+ a7 X3 s2 a/ q5 S2 e0 q5 n  hlogic age of 16 months (advanced).5 Chromosomal
5 p1 B" y  h% V6 lkaryotype was 46XY. The thyroid function test
6 z. M5 Z9 y( K/ Dshowed a free T4 of 1.69 ng/dL, and thyroid stimu-3 }+ S& Q* @5 v( w& y0 G4 T6 e
lating hormone level was 1.3 µIU/mL (both normal).+ e9 z& Q, I- @- N! y4 u+ P
The concentrations of serum electrolytes, blood
8 v+ W: }4 i, f3 y1 x  Furea nitrogen, creatinine, and calcium all were
0 G3 b0 U- x0 O0 p& R' B, C2 A; swithin normal range for his age. The concentration# K; M* b- A, m- r2 {& r
of serum 17-hydroxyprogesterone was 16 ng/dL
! K+ u1 ]3 N$ P( X(normal, 3 to 90 ng/dL), androstenedione was 20' B- n4 Y, B8 C
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
8 o4 n; M; i! z1 M* eterone was 38 ng/dL (normal, 50 to 760 ng/dL),
2 d* s' U8 z: @5 q: ]desoxycorticosterone was 4.3 ng/dL (normal, 7 to; J: r& b6 I' e; J. |" E
49ng/dL), 11-desoxycortisol (specific compound S)' b3 b% x7 L3 A$ ]7 j9 s; I
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
5 \$ \7 @/ i$ m& D3 S- I! ptisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
: h7 }" M6 q; F' g7 }  F2 G6 D, ?testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
, w+ b0 w2 n+ a; u9 g, F$ I, ?" Eand β-human chorionic gonadotropin was less than
1 e# n; Z, r6 y* R2 h5 mIU/mL (normal <5 mIU/mL). Serum follicular( t7 F5 [$ ^. N0 `2 g. p
stimulating hormone and leuteinizing hormone9 u! G3 a0 @& ~7 j( }/ A+ s% ~
concentrations were less than 0.05 mIU/mL9 L9 Y/ T. D3 X- K/ R" n: W9 K
(prepubertal).
; q( F$ g4 N  P2 ]The parents were notified about the laboratory! i1 q% H3 q: h8 ~% D' j
results and were informed that all of the tests were
0 C( q  }& o' D8 ]( unormal except the testosterone level was high. The
$ `" K* W" h- B( b2 o3 T# zfollow-up visit was arranged within a few weeks to
. t, V. Q  e; Z. Nobtain testicular and abdominal sonograms; how-+ L% ?$ Q7 z0 A& D6 _* e' E6 j
ever, the family did not return for 4 months.; s- s2 t, a! |* f
Physical examination at this time revealed that the5 o- ~! ^) o% V7 p
child had grown 2.5 cm in 4 months and had gained
  C, K) Y# X6 b: @* M/ R- X$ i' L. G2 kg of weight. Physical examination remained( |" q6 I/ |$ I
unchanged. Surprisingly, the pubic hair almost com-
- M, H# ?$ q; v- I  l* z9 b, npletely disappeared except for a few vellous hairs at
$ p# i4 V) h8 b/ vthe base of the phallus. Testicular volume was still 2/ r$ @' t* A  \6 \1 G+ H( ]
mL, and the size of the penis remained unchanged.
9 `. e! z& x6 n9 UThe mother also said that the boy was no longer hav-
6 C/ k7 k7 ?( N9 A1 _3 {0 ting frequent erections.  t0 F0 c+ Q2 w7 u& {: P, l
Both parents were again questioned about use of& ^1 E8 f% t6 p) G0 W9 N8 x
any ointment/creams that they may have applied to8 R5 s% \/ v1 {& l8 B/ i! K
the child’s skin. This time the father admitted the& C% ]" ]  s0 c, |; }0 L3 r
Topical Testosterone Exposure / Bhowmick et al 541( B( b$ X9 p  a- S
use of testosterone gel twice daily that he was apply-/ G. x, h0 P' ?6 \, O8 C- u2 J
ing over his own shoulders, chest, and back area for
$ z5 m. }, x# z2 x9 ba year. The father also revealed he was embarrassed( B0 s" h% l: A0 w. I: S
to disclose that he was using a testosterone gel pre-
! |+ D/ T. ^6 y3 ]  d6 Mscribed by his family physician for decreased libido  g4 R" I# J7 {. u# Z
secondary to depression.& A% h) H. u! s2 o8 E2 f
The child slept in the same bed with parents.
" n  @( A. l- R0 a1 I. K. LThe father would hug the baby and hold him on his
% x! w" y* |4 G5 Q1 Vchest for a considerable period of time, causing sig-1 |! x7 w# r1 M# b/ l  T
nificant bare skin contact between baby and father.
2 `* [) e' T; P  ]: V9 zThe father also admitted that after the phone call,. ]2 |5 i0 a6 G) m6 Z  w6 }
when he learned the testosterone level in the baby
5 X) j* T% o% Q5 m0 N. @  \2 cwas high, he then read the product information+ G5 c. H2 ?* e6 ?9 m
packet and concluded that it was most likely the rea-
/ Z/ I4 r$ m2 n8 n1 g: l$ Qson for the child’s virilization. At that time, they
4 b' k& |7 [, }3 I3 e0 j3 R* Adecided to put the baby in a separate bed, and the
  Z: m3 O& d- u: {% z* i3 M' Gfather was not hugging him with bare skin and had
* F8 ^! m9 o; Q% U9 Pbeen using protective clothing. A repeat testosterone8 ?: W. i% i( L) Y1 Z1 p' I! y
test was ordered, but the family did not go to the
* Q3 c8 a, v* L5 z/ P) llaboratory to obtain the test.
1 Z/ t7 l+ y; g/ I9 k( NDiscussion3 n% \( o) k% g" o( ~0 O
Precocious puberty in boys is defined as secondary
+ m7 o/ ]7 g2 H" F8 [/ J: asexual development before 9 years of age.1,4" L. E! ~, [2 I! Z& L+ h0 B
Precocious puberty is termed as central (true) when
4 c+ ^# U% O# o. k# hit is caused by the premature activation of hypo-4 \% ^3 i' z: z7 O8 c
thalamic pituitary gonadal axis. CPP is more com-1 F7 z& _4 R+ ^7 N# R% e
mon in girls than in boys.1,3 Most boys with CPP
7 d: N$ t+ }6 Bmay have a central nervous system lesion that is
# \: g) V: m4 {- Tresponsible for the early activation of the hypothal-
, l( O2 u; R5 \% G9 ~, M0 U% \amic pituitary gonadal axis.1-3 Thus, greater empha-
6 N" ~" L" R* _! Ksis has been given to neuroradiologic imaging in
6 Q/ S" z" r" ^boys with precocious puberty. In addition to viril-- p- a: u3 N$ T6 O) I; \
ization, the clinical hallmark of CPP is the symmet-( n; t- P4 }; I1 q6 B0 |: b
rical testicular growth secondary to stimulation by
+ k) b" w/ c4 agonadotropins.1,3
5 d& j8 J5 }5 W5 w; v4 A' xGonadotropin-independent peripheral preco-+ K+ E$ z$ R( ^: L# g; P5 j9 W+ v
cious puberty in boys also results from inappropriate
8 y/ E' l, j6 t& ~* q- A4 T# ~androgenic stimulation from either endogenous or
/ _$ q& Y) ^! b' |: oexogenous sources, nonpituitary gonadotropin stim-6 r& A* I1 z& a/ L9 n% d; s
ulation, and rare activating mutations.3 Virilizing) z* j  C, L! p! p  V9 ^- t
congenital adrenal hyperplasia producing excessive
/ g, U6 u5 J! aadrenal androgens is a common cause of precocious
7 @: d8 I) }' D$ @3 Y- L; Ypuberty in boys.3,4' Q2 |; V+ J8 _9 a
The most common form of congenital adrenal- b# Z8 ^) d( N& @) K
hyperplasia is the 21-hydroxylase enzyme deficiency./ m6 G* Q% F& c3 L5 t
The 11-β hydroxylase deficiency may also result in
* h+ @! y) a. D- I0 K- yexcessive adrenal androgen production, and rarely,, e0 Q: N2 s6 g* L
an adrenal tumor may also cause adrenal androgen& v: Q" i8 j5 s' n2 Y  X3 ~( f6 _
excess.1,3
/ \: B6 g. m2 M0 aat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from; v  _* h) a6 V9 K" `
542 Clinical Pediatrics / Vol. 46, No. 6, July 20078 c$ g5 D. k3 m/ Z- m
A unique entity of male-limited gonadotropin-* Q  ?' W: z5 M* c! B
independent precocious puberty, which is also known. ^! i' Y8 M, z% I9 j
as testotoxicosis, may cause precocious puberty at a2 [1 {' z4 a) _" @
very young age. The physical findings in these boys/ t8 A. Z9 U$ {  O+ l( ?
with this disorder are full pubertal development,9 r$ y$ u0 w' b
including bilateral testicular growth, similar to boys
5 W% ]# f- {8 O+ Xwith CPP. The gonadotropin levels in this disorder: e# Z# v# N% B. `" P0 P0 a2 r
are suppressed to prepubertal levels and do not show/ i, A$ x- |) C: I9 l5 \6 r
pubertal response of gonadotropin after gonadotropin-
& f# T: u4 l( z. u6 X' [+ k& X4 `- i* wreleasing hormone stimulation. This is a sex-linked
% G/ E+ z9 @. J  O2 E2 }% h- hautosomal dominant disorder that affects only: ^) p* x& _4 ^& L8 M' Q
males; therefore, other male members of the family
( o4 Z9 `$ }; w# |! }2 h" U1 Kmay have similar precocious puberty.3! }5 A' g, k% _0 |" h  C5 l
In our patient, physical examination was incon-1 N! P) n7 b6 `: K1 P$ V6 ~2 W, z
sistent with true precocious puberty since his testi-
/ Y0 Y! u! K" ]7 qcles were prepubertal in size. However, testotoxicosis6 y% g4 {! N% y
was in the differential diagnosis because his father9 g& f3 Z( s& m9 a8 v
started puberty somewhat early, and occasionally,1 N9 }. Z- M7 y
testicular enlargement is not that evident in the# L& u' |4 x+ d; O5 m1 s
beginning of this process.1 In the absence of a neg-
6 v9 T( X1 P) [8 V' I7 I. r0 Cative initial history of androgen exposure, our- n% q$ [2 ]' b1 B- }
biggest concern was virilizing adrenal hyperplasia,
2 P$ H6 M  M4 g4 F! i3 beither 21-hydroxylase deficiency or 11-β hydroxylase' v6 b2 ?8 ?9 P% Y; ?" r7 p: d
deficiency. Those diagnoses were excluded by find-+ k! h. J( I, a) K/ f" j
ing the normal level of adrenal steroids.2 J9 f1 ?$ a- ]  n
The diagnosis of exogenous androgens was strongly4 }1 ?, |. J$ _+ c( {
suspected in a follow-up visit after 4 months because
: W1 `  k6 a! J; [1 P: Q5 Mthe physical examination revealed the complete disap-, a& h8 E* t4 u4 a5 m$ e/ Z' ]
pearance of pubic hair, normal growth velocity, and9 X0 e( j  O* r7 x% Q6 I+ t2 x
decreased erections. The father admitted using a testos-/ t0 H; z0 G3 l
terone gel, which he concealed at first visit. He was
" N6 k" v6 a9 xusing it rather frequently, twice a day. The Physicians’
6 E+ H% g1 N: s# h$ _% i; m$ wDesk Reference, or package insert of this product, gel or1 }' x6 ~" P6 D, r# y, n
cream, cautions about dermal testosterone transfer to1 M& j+ Q7 {2 i# s. ~0 B" ?
unprotected females through direct skin exposure.
+ s+ |9 c8 L/ E* C0 rSerum testosterone level was found to be 2 times the$ O5 l/ a- b! e" e  x
baseline value in those females who were exposed to
1 D. `6 M9 h5 I& o0 K: beven 15 minutes of direct skin contact with their male
& L# |8 l  _8 u" W7 d  ]partners.6 However, when a shirt covered the applica-
; B7 l. V8 A, t% R6 etion site, this testosterone transfer was prevented.+ M6 \- W" l9 d6 E9 d
Our patient’s testosterone level was 60 ng/mL,
# I* ^% I# e2 f. c4 fwhich was clearly high. Some studies suggest that2 T; {9 C( W1 A1 W
dermal conversion of testosterone to dihydrotestos-9 K' i$ L+ @6 e
terone, which is a more potent metabolite, is more
1 U5 B' Z+ ~9 P/ @0 q: O7 {3 d7 H1 Oactive in young children exposed to testosterone3 R' d1 s3 y6 F$ A/ ^8 g( x
exogenously7; however, we did not measure a dihy-
+ N4 V( \9 ?. v7 Ldrotestosterone level in our patient. In addition to
+ D3 E! ~$ ?7 g5 Tvirilization, exposure to exogenous testosterone in
$ a! S. B, I! ?5 {6 _! H$ u7 @children results in an increase in growth velocity and7 m6 z/ ?' v0 {3 q- S! V0 X9 z
advanced bone age, as seen in our patient.' J% ?, z2 b% c, q
The long-term effect of androgen exposure during! k- J. f8 j+ E' [; H' ~5 _$ V6 }
early childhood on pubertal development and final) p8 [3 g- [! y" V
adult height are not fully known and always remain
6 O+ ?4 e" a3 S' s, Fa concern. Children treated with short-term testos-1 i; H* v: Y4 H- o+ p0 [) L
terone injection or topical androgen may exhibit some! }( {. ~) _+ F- _9 b: \
acceleration of the skeletal maturation; however, after
2 u* H2 P' F& v0 V+ K" ]cessation of treatment, the rate of bone maturation6 }, {: K' P9 F
decelerates and gradually returns to normal.8,9  k' ]1 R% P- E3 A" E
There are conflicting reports and controversy2 _9 W! Q, x( a  J" _
over the effect of early androgen exposure on adult
/ o: C* u3 i% G! \) |penile length.10,11 Some reports suggest subnormal
% s- S$ ^  W2 t" N3 hadult penile length, apparently because of downreg-( a# d) Z3 {) v0 \! [  N0 }
ulation of androgen receptor number.10,12 However,
' u9 c0 a! l' _! ?& ~. C, L' hSutherland et al13 did not find a correlation between3 r' p+ r: X# v' E0 J
childhood testosterone exposure and reduced adult
' q& @( i0 n7 Y! ^: b. ipenile length in clinical studies.6 P! P+ k7 t* W- i7 v! t
Nonetheless, we do not believe our patient is& w6 A, Y' t: n1 M5 v
going to experience any of the untoward effects from4 L6 A0 t/ }9 ~) W9 K5 b: o. p  o
testosterone exposure as mentioned earlier because
1 d! _7 |, \/ C2 R: l% dthe exposure was not for a prolonged period of time.3 r3 z# a$ p' f
Although the bone age was advanced at the time of
) V2 m6 D# a, Y" }3 K' Q3 fdiagnosis, the child had a normal growth velocity at/ W$ i: R3 c1 r% _( W6 G- [7 Y: Q
the follow-up visit. It is hoped that his final adult8 T. D: R4 g2 j/ K* V) T6 i) h
height will not be affected.
  h' E8 Q9 L4 D$ B/ f5 Q, @Although rarely reported, the widespread avail-1 F! z4 {4 G# A  g$ o' B; _
ability of androgen products in our society may
* l5 @* U+ \0 Z  X% a$ _$ [9 vindeed cause more virilization in male or female2 l- K" ^8 B' I! {! V0 i
children than one would realize. Exposure to andro-
4 i0 B8 m$ d; M' E8 agen products must be considered and specific ques-
7 i& e; _# s5 w% Ytioning about the use of a testosterone product or
: Y2 ^/ _/ d3 {! {3 Wgel should be asked of the family members during
; h  P8 C! Z. q# x1 Uthe evaluation of any children who present with vir-8 z% b* y# l7 v, M" M
ilization or peripheral precocious puberty. The diag-
" n" a( d5 M* E. |" nnosis can be established by just a few tests and by
7 R" P- ~, f  A6 s* jappropriate history. The inability to obtain such a
' [& K: @, o; f) Hhistory, or failure to ask the specific questions, may% B5 a# }4 x8 H* {. e
result in extensive, unnecessary, and expensive
" e: y' w3 x' Q5 H# Winvestigation. The primary care physician should be
: x( L6 x5 X+ g! k" S* d) Paware of this fact, because most of these children3 @2 u9 R8 j; v4 g- v
may initially present in their practice. The Physicians’( G  D0 i7 u- n; S# p
Desk Reference and package insert should also put a
3 m1 J. ]' I  F, t; T4 d6 Mwarning about the virilizing effect on a male or6 \+ N$ o5 C2 S; G: \3 i- `
female child who might come in contact with some-
9 j3 Q0 y8 i) g1 A/ k) zone using any of these products.  z9 d2 N4 L2 W2 W
References
2 x3 ^8 A3 d% m4 K1. Styne DM. The testes: disorder of sexual differentiation
* B3 n9 A& W- c) R# c& E' sand puberty in the male. In: Sperling MA, ed. Pediatric0 [) K1 I" a9 L. k! U6 w
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
3 r+ z  e  w) I, [  H9 C2002: 565-628.
' _0 k0 W" ]+ v/ E: ?0 V2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
' q) k. c. h, t! w4 ]! Npuberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old3 n5 a# U# _$ O7 p3 F' [
Boy Induced by Indirect Topical
) h# N  W) K, w# J5 EExposure to Testosterone
9 E; r2 h; F* r' \Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2; `  N; v/ H4 I) t$ R
and Kenneth R. Rettig, MD1, t5 j+ w& s( h2 w  L
Clinical Pediatrics3 Q* V& h9 \& t; f) }# |7 N
Volume 46 Number 6" x" O! ~8 i# z4 @7 I/ l4 {
July 2007 540-5434 a: Z& i- h" _$ I
© 2007 Sage Publications6 ]4 S5 Z. p1 z2 V
10.1177/00099228062966512 F) n3 v: B; R5 |5 A
http://clp.sagepub.com
- h" B5 I) E; xhosted at
" G% q2 ~7 Z" \: o/ R+ V7 Mhttp://online.sagepub.com
. K' X. R# t# N) NPrecocious puberty in boys, central or peripheral,
  c  y0 B' S& o: e& |$ Q0 iis a significant concern for physicians. Central& T$ F( p$ [2 t. r1 A
precocious puberty (CPP), which is mediated
; U% d( m4 f( h9 U& ~& p( L2 jthrough the hypothalamic pituitary gonadal axis, has0 X0 F# i/ h( u& T# N
a higher incidence of organic central nervous system
3 M# c" m7 i' u$ p4 ]2 t$ k1 ?lesions in boys.1,2 Virilization in boys, as manifested
5 Z& s$ V% m; V+ P3 K" Q' Mby enlargement of the penis, development of pubic
, s3 t! Z; @- O# e& J" D" Ihair, and facial acne without enlargement of testi-
' ]- R" p- ?' T  z- D7 [cles, suggests peripheral or pseudopuberty.1-3 We
: j/ X' f* j; n8 M! U& creport a 16-month-old boy who presented with the2 e3 y% U3 D: {: Y
enlargement of the phallus and pubic hair develop-% c& d2 m3 O( W! Z! R
ment without testicular enlargement, which was due5 o3 l2 M5 M% u( R5 `, R/ `. n
to the unintentional exposure to androgen gel used by
! U6 d$ V* C6 @3 \2 Q5 N  ]3 A, ?the father. The family initially concealed this infor-* e" M3 i/ x' z2 U/ o2 z
mation, resulting in an extensive work-up for this, u" K* g! W$ L4 J5 ^% W9 S+ y& K
child. Given the widespread and easy availability of- k4 n0 C$ U6 I/ @7 }' U5 r
testosterone gel and cream, we believe this is proba-
/ v3 L+ D' F0 s5 |$ f" c3 h- y4 kbly more common than the rare case report in the
: q! E* ~5 u( f! U3 P) N8 nliterature.4+ n3 H/ Y: ^) g) G6 ?: f/ C
Patient Report
7 r& Z0 A; T( ~4 o. W4 ~A 16-month-old white child was referred to the0 K. z1 T8 j; p
endocrine clinic by his pediatrician with the concern
4 t/ u3 m4 `+ Rof early sexual development. His mother noticed
. j: s5 ]- \8 L, `  Zlight colored pubic hair development when he was+ X7 [: h) k, l  Y
From the 1Division of Pediatric Endocrinology, 2University of& h, E9 Y8 F9 w0 x3 z2 R  L' X  Q
South Alabama Medical Center, Mobile, Alabama.
! L% C, v- k0 QAddress correspondence to: Samar K. Bhowmick, MD, FACE,2 p8 d( |. }/ s7 K, R; M
Professor of Pediatrics, University of South Alabama, College of
# O6 d/ R* f# l: I, i9 WMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
8 \0 f# N, D& X9 Y) ?e-mail: [email protected].6 s6 b' i; i- n+ z) w1 F! n+ f
about 6 to 7 months old, which progressively became
3 s# U& e6 I) f. ~6 l' _darker. She was also concerned about the enlarge-( N2 k( r+ m  n- v/ v' h
ment of his penis and frequent erections. The child, l" k% h! f. P9 `
was the product of a full-term normal delivery, with, V' z; N8 Y0 N: H5 }$ Z# M4 u
a birth weight of 7 lb 14 oz, and birth length of% A5 p" e: E: A! D5 b
20 inches. He was breast-fed throughout the first year
4 G$ x7 Q& @3 A9 w! O2 |1 Eof life and was still receiving breast milk along with3 e0 E: ]- G. [, \7 s& P" v
solid food. He had no hospitalizations or surgery,7 u) h6 n3 ^' b: A" {8 p) r
and his psychosocial and psychomotor development
' s2 N% K# c9 z. ^1 ?# v. b6 Bwas age appropriate.% e; u( n7 Q& Z8 Q9 d' T9 f+ }
The family history was remarkable for the father,
+ m( U: V  x, |- S/ |who was diagnosed with hypothyroidism at age 16,
8 h& N+ f0 m) m' f* ]4 d! [* Fwhich was treated with thyroxine. The father’s
0 C0 @' ~0 L! j& f2 O/ Pheight was 6 feet, and he went through a somewhat
- O& }/ U8 l( Y9 Kearly puberty and had stopped growing by age 14.. ?. a$ X5 v0 i& z' L2 t
The father denied taking any other medication. The3 X1 r4 ~3 z7 A2 e% W: s7 y) ?
child’s mother was in good health. Her menarche
8 H9 z0 T3 Q" |was at 11 years of age, and her height was at 5 feet
2 h+ d: {. l" i/ ^3 R3 e3 B, q5 inches. There was no other family history of pre-( {, X$ j& _6 O; p% k/ _5 e
cocious sexual development in the first-degree rela-* ?- E% S! c! h1 A. E
tives. There were no siblings.
+ y" K( o  G8 N$ {7 n2 e  OPhysical Examination
! @% B. Z, a4 TThe physical examination revealed a very active," x9 [4 v2 Y& J& I
playful, and healthy boy. The vital signs documented
9 c! v5 b0 W$ ?! ra blood pressure of 85/50 mm Hg, his length was
& `% Z! h3 M1 ^+ z90 cm (>97th percentile), and his weight was 14.4 kg
$ l1 i  D" D, P1 k(also >97th percentile). The observed yearly growth* O5 @% P3 ]( b- o$ f0 [/ j
velocity was 30 cm (12 inches). The examination of
) X: l/ @0 ]* c1 }0 T# Y  ithe neck revealed no thyroid enlargement.
+ a6 Q) o0 A0 w9 r2 W+ j. P) tThe genitourinary examination was remarkable for! k* v" d, }8 J+ M  X9 V- K
enlargement of the penis, with a stretched length of  X6 |/ N# |6 P' K+ q% o1 [
8 cm and a width of 2 cm. The glans penis was very well
1 e& V- |! o: [9 p: ideveloped. The pubic hair was Tanner II, mostly around
7 }  `" P+ Q3 T7 p9 C! Q540
, G2 g8 t; t  @0 C# B, j+ I: ?# Iat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
3 q- v5 j; g2 {  F" B, ]the base of the phallus and was dark and curled. The
  S. g4 r' _* |5 _/ l4 n3 Qtesticular volume was prepubertal at 2 mL each.0 X+ Z+ v% W5 n5 M
The skin was moist and smooth and somewhat
3 @! m' n$ ^; \oily. No axillary hair was noted. There were no
/ p$ ?5 R3 T  J' u7 q% }abnormal skin pigmentations or café-au-lait spots.
1 ^5 N5 ]2 b0 D9 w2 {; cNeurologic evaluation showed deep tendon reflex 2++ y7 g4 f: i. L- w0 |3 j  Y9 V
bilateral and symmetrical. There was no suggestion
7 s% V7 I( ?% [3 N4 Bof papilledema.) P" ?6 g0 q' R+ a3 ^1 ?
Laboratory Evaluation" Q: f0 H$ V, j8 x' {+ D% w
The bone age was consistent with 28 months by
7 M; ~* N7 Q- N) D+ S2 l& cusing the standard of Greulich and Pyle at a chrono-" H! I4 r) d# D+ m
logic age of 16 months (advanced).5 Chromosomal
) x& |" `4 B: o# c+ R- Gkaryotype was 46XY. The thyroid function test
. K- I  @1 C5 A1 k! sshowed a free T4 of 1.69 ng/dL, and thyroid stimu-" k# P0 O5 O2 d  t3 [% E0 l! z% _
lating hormone level was 1.3 µIU/mL (both normal).
' p! W& B' d# j2 ]The concentrations of serum electrolytes, blood! T0 B1 g- f$ F# k
urea nitrogen, creatinine, and calcium all were. u& t$ u& v6 X/ E# @
within normal range for his age. The concentration3 F) M2 M/ U- z. `
of serum 17-hydroxyprogesterone was 16 ng/dL
, }: J5 Y- @  L0 O/ b( v(normal, 3 to 90 ng/dL), androstenedione was 20
2 }+ B. p# a" }8 }; mng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
/ b) y5 T# o! p6 `terone was 38 ng/dL (normal, 50 to 760 ng/dL),
' c( H. @0 j/ C! }% k+ {' H6 tdesoxycorticosterone was 4.3 ng/dL (normal, 7 to
4 w% q4 }! {( x9 t# |7 W49ng/dL), 11-desoxycortisol (specific compound S)
5 X. P  H" N& f4 k1 h3 Swas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
: |1 C  O& ?  |/ d' @/ x* c! rtisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
; |4 |+ `7 B/ O1 [6 Ytestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
. t3 B6 @9 ?5 q! V( k$ Z$ iand β-human chorionic gonadotropin was less than* A" @8 e+ |6 {0 l8 j/ l( @9 X; i, `
5 mIU/mL (normal <5 mIU/mL). Serum follicular
$ J+ j9 ~& _' }/ P* o/ Y( Wstimulating hormone and leuteinizing hormone$ R  W0 k9 ?+ V* M
concentrations were less than 0.05 mIU/mL
* Y' d/ a% C" V5 G( v(prepubertal).
, J* ~8 K; O: M: v  B- n. DThe parents were notified about the laboratory; ]* ^; z; X8 }6 b* {
results and were informed that all of the tests were1 ^1 e) F* ?. D% o' N6 ~
normal except the testosterone level was high. The: y, J1 v# |2 }( G+ N8 Y0 Z( q3 B
follow-up visit was arranged within a few weeks to
/ c$ x+ `! d  G. q! Hobtain testicular and abdominal sonograms; how-# L" @# d- t' ?* h
ever, the family did not return for 4 months.5 o7 |; t; d7 ~% ~+ u
Physical examination at this time revealed that the
: P9 k* H7 w# S2 |1 g8 wchild had grown 2.5 cm in 4 months and had gained) C, {2 x  r2 B" d* g' C+ P0 G
2 kg of weight. Physical examination remained
5 {7 o: o, y' i; Z7 munchanged. Surprisingly, the pubic hair almost com-
" s0 V5 H! A% c- U6 }3 r. G$ U8 l. Spletely disappeared except for a few vellous hairs at+ V3 c& i) m( p* Y- b" X5 }
the base of the phallus. Testicular volume was still 2
! c; A1 ^; \) F6 ^mL, and the size of the penis remained unchanged.1 c2 G' f+ L2 v1 Q
The mother also said that the boy was no longer hav-
' ?4 S% ]. X6 R! ying frequent erections.
/ [. T: |7 }9 z9 j* ~$ H- \Both parents were again questioned about use of6 L! f/ h' o& Z6 P" e/ Q6 a: e
any ointment/creams that they may have applied to3 G- E- K- a; o2 m. T% k3 j
the child’s skin. This time the father admitted the
2 g/ G( I) p6 VTopical Testosterone Exposure / Bhowmick et al 541, G6 i  N; f- N; g9 {9 n
use of testosterone gel twice daily that he was apply-6 J$ J5 p! F$ }. g7 x- U
ing over his own shoulders, chest, and back area for0 \) x$ b, h  S4 R5 r
a year. The father also revealed he was embarrassed
0 c/ z( `" R5 Vto disclose that he was using a testosterone gel pre-1 s5 q; \9 [. r  y9 a
scribed by his family physician for decreased libido
( Y& s' I3 U  Q4 s* Isecondary to depression.5 \9 p$ h; z  v9 Z2 I- S& O, ~
The child slept in the same bed with parents.
. p/ i& q0 d" s: j/ PThe father would hug the baby and hold him on his
7 O: F* l4 y* vchest for a considerable period of time, causing sig-
! |$ X) t# {' K: C8 |nificant bare skin contact between baby and father.1 q7 J3 M6 c4 y6 L
The father also admitted that after the phone call,) F) h, I6 P9 J# f4 x2 @( ~8 ?- h" D
when he learned the testosterone level in the baby
2 P; ?. x( a9 Q, f) s- F* qwas high, he then read the product information
" G. Q8 P. W/ l  wpacket and concluded that it was most likely the rea-
" y2 g6 q: K! R- @6 `son for the child’s virilization. At that time, they4 _% r# T- T2 g- r9 i
decided to put the baby in a separate bed, and the7 I  ~: r# x9 ^3 ^0 H
father was not hugging him with bare skin and had
6 ], |  t, L9 n" ~0 ibeen using protective clothing. A repeat testosterone  _6 E1 P- v& z- ?  ?) Z: P& C
test was ordered, but the family did not go to the
5 E' R, Y; Q! _! D3 R( Flaboratory to obtain the test.
. |* D' i% p5 q! uDiscussion" Q! B0 v) i' z
Precocious puberty in boys is defined as secondary
: t# H1 q& |4 I: {6 ^: zsexual development before 9 years of age.1,4+ o3 A0 M% ~/ w; l4 l
Precocious puberty is termed as central (true) when1 s, v7 Y% R$ V5 T6 W
it is caused by the premature activation of hypo-( {! y5 M& t+ y' }' s8 ?
thalamic pituitary gonadal axis. CPP is more com-1 f4 b, K  u) j& B% I# x/ J
mon in girls than in boys.1,3 Most boys with CPP( _) O1 c' @( T' Q' g* [. f( Z
may have a central nervous system lesion that is* I  Z; Z8 K3 q! ]! e& n
responsible for the early activation of the hypothal-6 |$ [" v! k! f7 S8 e9 L. I
amic pituitary gonadal axis.1-3 Thus, greater empha-
& g9 [! z& C* y2 ]3 Bsis has been given to neuroradiologic imaging in
# _0 x2 h4 q* N5 N# |; aboys with precocious puberty. In addition to viril-
. j6 F  E; \; a3 z' `9 eization, the clinical hallmark of CPP is the symmet-
( u" A* ~0 Z. N5 A. x8 R6 rrical testicular growth secondary to stimulation by% R; ?4 x+ O3 B0 _. y
gonadotropins.1,3% W3 p- m% R* v0 V1 ?: |1 c
Gonadotropin-independent peripheral preco-# i( K6 I! P& n9 r4 t
cious puberty in boys also results from inappropriate
! ]+ ^7 P& v; n7 T* R! Oandrogenic stimulation from either endogenous or! P7 u& D7 p8 ?# l) q0 R
exogenous sources, nonpituitary gonadotropin stim-0 u- U  l% E: C7 a  i# n5 ~2 j5 h
ulation, and rare activating mutations.3 Virilizing! Y( p* T5 f/ _% u7 t5 p/ z
congenital adrenal hyperplasia producing excessive
! `8 H3 j  W, l8 `% q& t8 g8 [9 qadrenal androgens is a common cause of precocious
+ d- `" J* G5 x; spuberty in boys.3,4: O  }! Y$ v0 p- D' h
The most common form of congenital adrenal5 O) H; M' ?; ~+ T" \7 t5 d$ z
hyperplasia is the 21-hydroxylase enzyme deficiency.
, a4 F( o3 d1 P: g1 k: x- fThe 11-β hydroxylase deficiency may also result in- T3 N& I3 ^6 W# ?/ {- j
excessive adrenal androgen production, and rarely,
& I: g2 c1 G% o2 s: _an adrenal tumor may also cause adrenal androgen+ X* _6 c: F% ^& @) U
excess.1,3$ B$ N7 u( U, d0 u
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from/ X6 K' ?4 x+ N: [% [
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
. J' Q) m- \: R) j$ cA unique entity of male-limited gonadotropin-
$ U0 z  T# L: Y' uindependent precocious puberty, which is also known
& T" J' c0 N' T3 U& `as testotoxicosis, may cause precocious puberty at a
. S6 c( e- Q9 J9 Cvery young age. The physical findings in these boys4 C. H0 H; C, k0 K& e! k3 R
with this disorder are full pubertal development,
0 Z9 T+ O4 o: ~' ]including bilateral testicular growth, similar to boys
/ L) W* e$ X! \# t3 u0 A9 C! Bwith CPP. The gonadotropin levels in this disorder& f5 Q0 y& h6 g% F; O1 r
are suppressed to prepubertal levels and do not show* J. R+ y, X7 K% n: b' l
pubertal response of gonadotropin after gonadotropin-4 U7 t8 W  [; U9 A  o, K  V; j
releasing hormone stimulation. This is a sex-linked5 j$ B# G4 s" T( E* C
autosomal dominant disorder that affects only
5 |3 X" y  u7 ?, R( F. ^1 zmales; therefore, other male members of the family: o% O/ t" m4 z* o
may have similar precocious puberty.3
; [. A0 r' j0 I: LIn our patient, physical examination was incon-8 w8 y6 k# d1 M1 r
sistent with true precocious puberty since his testi-; f7 `. `0 I7 h
cles were prepubertal in size. However, testotoxicosis8 N. [' [2 O+ e0 l0 z
was in the differential diagnosis because his father
8 g* l7 p. K/ t$ E( ]started puberty somewhat early, and occasionally,: C- _, J  ^; Q1 |7 ?" {
testicular enlargement is not that evident in the1 K; u1 b$ ~0 U3 e! W
beginning of this process.1 In the absence of a neg-
* F( X$ v. |" t# B, bative initial history of androgen exposure, our, y# }& z  O9 C6 C* @0 B
biggest concern was virilizing adrenal hyperplasia,# p0 @5 ?! k, v
either 21-hydroxylase deficiency or 11-β hydroxylase3 Y, F2 {5 s( T' F) V! q; Y7 r% }
deficiency. Those diagnoses were excluded by find-% D5 o4 z8 D( V) z! `2 O: y
ing the normal level of adrenal steroids.
% Z' n3 n1 k0 Y# IThe diagnosis of exogenous androgens was strongly, S2 v* v; X4 [/ T. J6 @4 v2 ]! y
suspected in a follow-up visit after 4 months because. f& d# U+ B$ V" x, G! ?: V6 |/ V! I
the physical examination revealed the complete disap-
/ Q  X% S: r4 N& o/ C, J5 l& `pearance of pubic hair, normal growth velocity, and  N6 \6 r: u/ i1 \% ]
decreased erections. The father admitted using a testos-
9 O! K' \( I# B% Gterone gel, which he concealed at first visit. He was
! R* _, d/ p3 z9 W5 X1 musing it rather frequently, twice a day. The Physicians’
+ D' T9 r% s( `& D. h6 }Desk Reference, or package insert of this product, gel or5 n. C1 Y# i) B6 f5 b+ ~& i8 M' x; X
cream, cautions about dermal testosterone transfer to3 j% Z9 a3 I5 m* o0 m. r% [$ g
unprotected females through direct skin exposure.
2 c4 l, X% w: o$ ^2 ySerum testosterone level was found to be 2 times the
0 e+ D  B5 G, ~+ lbaseline value in those females who were exposed to
  N5 U) G( {! t% @- V: yeven 15 minutes of direct skin contact with their male8 G( T& p7 T2 W) }7 e/ E
partners.6 However, when a shirt covered the applica-
5 Z7 ]' V9 F5 P  ?; G' m' otion site, this testosterone transfer was prevented.
2 o3 k! o* J: [' |, vOur patient’s testosterone level was 60 ng/mL,0 Q7 }" e; z3 R
which was clearly high. Some studies suggest that- \8 g$ m! t% u( M: k
dermal conversion of testosterone to dihydrotestos-" r2 c$ |) x, W0 v7 o6 b$ |/ v
terone, which is a more potent metabolite, is more( w) K4 e# L+ v$ ~2 _4 N
active in young children exposed to testosterone
" ~1 @+ _2 v# R. y8 Nexogenously7; however, we did not measure a dihy-
/ C7 E6 c; y0 {1 |0 G* B* g6 Fdrotestosterone level in our patient. In addition to9 {0 ~; G/ z' L+ @" o% L
virilization, exposure to exogenous testosterone in
* ~% |( R8 s: A/ l% m' ]children results in an increase in growth velocity and
1 u0 b2 }* d4 ^; s$ v7 wadvanced bone age, as seen in our patient.5 q3 \5 X% l$ D3 l
The long-term effect of androgen exposure during
$ s8 {" J9 e/ I+ Tearly childhood on pubertal development and final
0 }$ E. T* Q0 a. iadult height are not fully known and always remain
4 O' |) \. e# K/ d2 c1 s; q) Xa concern. Children treated with short-term testos-8 W! t, ^  P$ O3 V$ D  y1 V+ ~
terone injection or topical androgen may exhibit some
" I' Q( h7 t4 p* T( A! X: u+ r4 Bacceleration of the skeletal maturation; however, after
( k; M' z" k6 ~2 M7 F* P- b0 kcessation of treatment, the rate of bone maturation! x; q/ [; |# Y; u/ Y* s
decelerates and gradually returns to normal.8,9
( J/ ^+ |: j/ M2 A0 j" B7 lThere are conflicting reports and controversy# i' a1 D6 p) k6 B5 p4 r# Y8 y
over the effect of early androgen exposure on adult
- H4 q' N% P5 m7 Xpenile length.10,11 Some reports suggest subnormal
2 k1 j7 m8 R% q8 ladult penile length, apparently because of downreg-
9 B. B  d/ O! n) f) Oulation of androgen receptor number.10,12 However,
# i" |5 q/ ?6 @* WSutherland et al13 did not find a correlation between
6 K. p4 ]& z9 j7 N, K, C$ v+ h0 Ichildhood testosterone exposure and reduced adult" V, |0 A' g- t8 E  v7 o$ w
penile length in clinical studies.! r& X* x- |9 {$ a
Nonetheless, we do not believe our patient is
& G* E- U7 L8 @4 wgoing to experience any of the untoward effects from
4 [% c- n- P. K5 htestosterone exposure as mentioned earlier because
0 v/ J" G& |: Y& s% p  Zthe exposure was not for a prolonged period of time.
2 Q/ D. I8 a% ?* n" G4 tAlthough the bone age was advanced at the time of" u9 C% n4 Z% ~+ N7 I4 |4 F
diagnosis, the child had a normal growth velocity at: [9 i+ }4 W- B0 D6 E' Q
the follow-up visit. It is hoped that his final adult4 `0 S* _! Q+ J7 c9 @' v1 z
height will not be affected.5 [8 S( t$ u8 f
Although rarely reported, the widespread avail-
! ?& c3 W2 d& x. b# u1 Zability of androgen products in our society may
3 N5 q" e% F$ l" T  findeed cause more virilization in male or female
1 T% c# C0 O5 i" Hchildren than one would realize. Exposure to andro-- @$ D0 A) r7 |) k9 f# R, G* M
gen products must be considered and specific ques-
$ C/ o2 {, |$ N) B! \tioning about the use of a testosterone product or& B4 ^! i7 B( ?1 P5 z
gel should be asked of the family members during
: w' X( B8 e- V" ^the evaluation of any children who present with vir-
( Q2 q2 \; ~; C" B" |ilization or peripheral precocious puberty. The diag-9 R7 x+ x  y, g/ x
nosis can be established by just a few tests and by
# {( |& _/ P5 m7 h' ]0 ?( Mappropriate history. The inability to obtain such a
7 t" G& t1 N( R+ H( e% ~# }history, or failure to ask the specific questions, may
$ t: X( |/ {- ]5 ?result in extensive, unnecessary, and expensive, E8 f* C8 i. u; @
investigation. The primary care physician should be1 }. n0 ]( Y1 b8 `& ^
aware of this fact, because most of these children
) _4 X+ V$ }  }% N2 ]2 ?0 `may initially present in their practice. The Physicians’/ v6 t' T6 d2 ^7 f3 e8 ~
Desk Reference and package insert should also put a
* V' y$ A4 e+ [2 w( l- d* G8 N* Mwarning about the virilizing effect on a male or6 n4 t4 m! ~7 C( R+ b
female child who might come in contact with some-
7 h% f% |' ]/ ~one using any of these products.
7 `, R9 {9 w& U$ e: Q$ b) z# NReferences
7 x4 J7 d1 Q; n- f# f1. Styne DM. The testes: disorder of sexual differentiation
2 g* K) P8 p3 `8 T& }. a$ u; Yand puberty in the male. In: Sperling MA, ed. Pediatric
$ W) X/ ]2 U& ]3 q# t) A( `* Q. mEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
5 n0 H$ W9 N% v; T$ e) t: Q2002: 565-628.
4 c' Q& h2 n& [5 ~) k5 d2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious$ h  ~4 p7 f+ p' ~$ @- W
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
VIP精品區,資源無限好賺金任務區,輕松賺金幣
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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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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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