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Sexual Precocity in a 16-Month-Old
* j7 w- l( o' B5 a+ Y$ [7 E. {Boy Induced by Indirect Topical
. g9 `& ~6 X/ g# YExposure to Testosterone! `( U0 L$ E! N7 i  i, w
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
( G. Z0 n4 d- ^! p- Z# z' oand Kenneth R. Rettig, MD1
1 ~/ p7 F1 y1 {' f# a3 [Clinical Pediatrics
; x7 |, `' U6 d6 c3 F4 IVolume 46 Number 6
, \  [# n+ D' X6 RJuly 2007 540-543
+ Z# Q6 V; ]0 V" S* q* V  h, _© 2007 Sage Publications
* I& s' ]+ j1 i! o, B4 z" C10.1177/00099228062966517 S7 S8 L: }( i  p" {7 [
http://clp.sagepub.com0 M* h/ \( w! `, ?  j9 Y& }
hosted at
9 H1 |( R% u. c! Yhttp://online.sagepub.com0 P& m6 {# X7 B/ H, s) N7 O7 k
Precocious puberty in boys, central or peripheral,
$ @4 d1 i/ P: cis a significant concern for physicians. Central
: q  }9 c1 [) V# I, y4 S  V0 [precocious puberty (CPP), which is mediated
/ @: V/ f. x# j8 \2 [through the hypothalamic pituitary gonadal axis, has
. k$ \5 A; S" |) M% _' b8 Ea higher incidence of organic central nervous system, A- ~0 `4 ?* Y& P& K' I* W, k4 a
lesions in boys.1,2 Virilization in boys, as manifested# b* }( t/ \, x) _
by enlargement of the penis, development of pubic
4 j& B4 e2 s* t& {( Nhair, and facial acne without enlargement of testi-
5 E+ U' C# c5 J; b6 |) U; rcles, suggests peripheral or pseudopuberty.1-3 We
0 z$ I4 Y* h; T7 I' Ireport a 16-month-old boy who presented with the
& a! p) E+ ~$ j& a0 q" penlargement of the phallus and pubic hair develop-
6 p  o0 S9 m! E& [, m" B+ }5 vment without testicular enlargement, which was due
0 U2 {4 o+ f! W* _+ @6 |to the unintentional exposure to androgen gel used by
7 z# k  a3 N4 zthe father. The family initially concealed this infor-
1 L/ _2 k. S$ Vmation, resulting in an extensive work-up for this7 b& G( I0 t. R, E* E4 [
child. Given the widespread and easy availability of
' [. T, @4 R8 d6 qtestosterone gel and cream, we believe this is proba-
" }% y# F0 P1 A. U7 Nbly more common than the rare case report in the2 U. X' W9 c' k
literature.4
1 u, j$ [! b2 c- Q) KPatient Report  I! \$ v" Q) E4 c7 [& R. H7 V
A 16-month-old white child was referred to the
4 S* z0 Z- J' ^3 h* ^endocrine clinic by his pediatrician with the concern% v8 x; x9 W+ s& b- L! ~
of early sexual development. His mother noticed  x7 z! n+ _5 w" O6 D
light colored pubic hair development when he was
2 M- x7 v2 M5 e- ~# s( s/ |( @From the 1Division of Pediatric Endocrinology, 2University of
& q; m. T8 e  G0 }/ g3 X5 FSouth Alabama Medical Center, Mobile, Alabama.* f7 h, I/ b5 [, G. E# P' j
Address correspondence to: Samar K. Bhowmick, MD, FACE,8 L1 O: i2 d9 Y8 A0 Q
Professor of Pediatrics, University of South Alabama, College of
6 J0 ]4 L+ y- |) ~3 Y# K! ]3 S' uMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
: i% {4 z! m4 x6 J# t5 i' c4 be-mail: [email protected].
- D, m1 d5 i' s7 \4 K% ?* oabout 6 to 7 months old, which progressively became
7 }; b9 r8 M: Ldarker. She was also concerned about the enlarge-* ^# ?+ i, Y# l# A5 p0 j2 P
ment of his penis and frequent erections. The child5 ^6 M8 i( K; q: G
was the product of a full-term normal delivery, with
) g0 Q+ |: r) d8 F9 Q8 za birth weight of 7 lb 14 oz, and birth length of
' K, x* p+ M0 U- ^20 inches. He was breast-fed throughout the first year( J& q2 ?7 d+ W, x. m
of life and was still receiving breast milk along with
0 g- y$ `2 ^% F+ v4 d4 l, {0 @4 v0 csolid food. He had no hospitalizations or surgery,) x8 l; C- `; e: M1 U' @# h# D
and his psychosocial and psychomotor development
: f9 \2 g) X8 L& a9 X+ m4 dwas age appropriate." D4 T3 R7 D, |1 K
The family history was remarkable for the father,
* `; }, l1 {# S$ ]1 p0 ]/ ~who was diagnosed with hypothyroidism at age 16,; \1 J6 m3 j4 I8 W& Q
which was treated with thyroxine. The father’s
, C9 E2 L- [  z7 F9 B4 \height was 6 feet, and he went through a somewhat
  D6 m- R' Z0 G* K$ Yearly puberty and had stopped growing by age 14.
$ j) G  }- G1 I7 q- J8 r: fThe father denied taking any other medication. The
2 n* _7 |2 E. @6 g! R9 g# ]child’s mother was in good health. Her menarche# [( }6 X  t) y9 S
was at 11 years of age, and her height was at 5 feet8 G- `9 ?. c0 L7 U
5 inches. There was no other family history of pre-
9 F1 {0 F6 _6 Q$ @! a# F8 {cocious sexual development in the first-degree rela-
( c8 k- r. S" [% r. m- d4 d, t1 Utives. There were no siblings.
7 L0 `1 W0 _4 I% wPhysical Examination3 d0 R% H9 N& n; @7 o9 r) T2 p8 ~
The physical examination revealed a very active,
+ R0 z9 e; X- A8 g& \: p  Splayful, and healthy boy. The vital signs documented
# t6 E$ {0 Q5 q: A) i, Ja blood pressure of 85/50 mm Hg, his length was, R. D. d. b4 r3 A6 }4 _9 d) O
90 cm (>97th percentile), and his weight was 14.4 kg1 Y* W3 v" z/ h+ u+ }. h+ Z
(also >97th percentile). The observed yearly growth1 R9 O  e% e$ f- {3 B. H) H. t& a
velocity was 30 cm (12 inches). The examination of
+ B, ~* C6 t- N) c% k0 q' tthe neck revealed no thyroid enlargement.
: g: y' ]+ z' G& M, }9 Y8 E9 IThe genitourinary examination was remarkable for$ A; j  c7 j- M/ ~, |
enlargement of the penis, with a stretched length of
& b8 q. m: t; w! D! N$ x8 cm and a width of 2 cm. The glans penis was very well
& A4 H9 y5 c" ~+ K2 z% P- S- H3 }7 adeveloped. The pubic hair was Tanner II, mostly around8 _/ w* [! ]& G; o$ @8 ?
540$ h, e" n8 D/ V% _
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
. M0 |9 A& E9 Q- i) Y/ ]the base of the phallus and was dark and curled. The' C  N5 X) |9 V% k: y3 F( A% V7 ^
testicular volume was prepubertal at 2 mL each./ ]3 F, M- I3 T' t1 C
The skin was moist and smooth and somewhat
) f5 w5 e% |1 ^. H2 ^oily. No axillary hair was noted. There were no" y! Y6 ?( B/ P7 z# t
abnormal skin pigmentations or café-au-lait spots./ W5 S: E0 {( a! A/ f
Neurologic evaluation showed deep tendon reflex 2+6 T. u, M' u2 d
bilateral and symmetrical. There was no suggestion
& p" D, B6 j- @) a8 m6 {of papilledema.. C7 e$ W$ @* ?( ?$ M- c# p* `' [
Laboratory Evaluation6 ^- B/ s2 G+ a
The bone age was consistent with 28 months by/ s7 W) X2 d3 E& `* F% F
using the standard of Greulich and Pyle at a chrono-5 q0 L+ N4 O+ k% K. V7 t6 J
logic age of 16 months (advanced).5 Chromosomal. Q6 T- v) E  s  b
karyotype was 46XY. The thyroid function test
# j- h6 @- N& Q' Bshowed a free T4 of 1.69 ng/dL, and thyroid stimu-1 I, l# e$ T# R" v$ B$ P
lating hormone level was 1.3 µIU/mL (both normal).
& T; R9 z3 R$ T! x5 J& }5 x  EThe concentrations of serum electrolytes, blood# f' Q- |( K2 ]) d; |! v
urea nitrogen, creatinine, and calcium all were$ i3 G5 T* c) w2 b) }2 J
within normal range for his age. The concentration( b7 w4 W# B! C" v- p% ^: d3 v
of serum 17-hydroxyprogesterone was 16 ng/dL
0 R: }& E4 W$ v9 T(normal, 3 to 90 ng/dL), androstenedione was 20* g% P. g% `$ _* m
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-  p% d2 r! d- q! C5 d
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
, {3 p4 `* j! d4 Xdesoxycorticosterone was 4.3 ng/dL (normal, 7 to& u6 J$ V! D7 S, h
49ng/dL), 11-desoxycortisol (specific compound S)
& Q2 ^) N# l% U1 O, G% Qwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-# K. X% m) N/ M2 w1 O+ ?6 P
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total. J( Q& L; G( K
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
; s0 F. p  D$ g- U( K7 Cand β-human chorionic gonadotropin was less than2 n: ?2 n" C5 C7 `: w
5 mIU/mL (normal <5 mIU/mL). Serum follicular+ i& L/ O/ r' A$ C
stimulating hormone and leuteinizing hormone
$ W9 M6 d& j. \' ^0 Y$ }concentrations were less than 0.05 mIU/mL  |  \7 u" n& m( M! d: I8 b
(prepubertal).0 F$ z- I4 U8 H6 s' L! z' V
The parents were notified about the laboratory
+ S2 {1 \6 V7 v! iresults and were informed that all of the tests were
) S8 v+ T( ^+ j: e& v0 O' rnormal except the testosterone level was high. The
& P" ]# ?/ F4 ^5 z" E$ ?follow-up visit was arranged within a few weeks to& |5 F" ^( C/ S5 O. H' o6 }( a$ K
obtain testicular and abdominal sonograms; how-+ c: d+ L  D) b! ?, V. b
ever, the family did not return for 4 months.
" F8 |+ V3 i& @Physical examination at this time revealed that the
' \- O! E. O2 D: a7 R& l( _8 ^child had grown 2.5 cm in 4 months and had gained9 r/ v4 g+ u- d; S
2 kg of weight. Physical examination remained+ h* c) r4 S5 H7 A6 {* A
unchanged. Surprisingly, the pubic hair almost com-
+ _4 U5 f! _/ i6 ^0 `. F9 ]pletely disappeared except for a few vellous hairs at4 N6 A1 z1 r* `) q/ y
the base of the phallus. Testicular volume was still 2
% b$ j1 t4 e# }# R/ N; i  q9 rmL, and the size of the penis remained unchanged.5 |* A. U9 y1 \! n0 A* |
The mother also said that the boy was no longer hav-
( d8 T' T. s: [6 X# Iing frequent erections.
* x7 v. D/ U$ `! U- r: j6 Q1 |Both parents were again questioned about use of
1 \! n( |. |- L: Rany ointment/creams that they may have applied to/ P6 Z+ Y* u, N" D' V# G
the child’s skin. This time the father admitted the
" J& W4 J: w: ^* kTopical Testosterone Exposure / Bhowmick et al 5414 v) Y; \! L8 _0 t
use of testosterone gel twice daily that he was apply-
1 \; q% ]  H% S+ z; l+ _7 D$ aing over his own shoulders, chest, and back area for
0 ?- m0 k$ U$ j! P4 K5 ma year. The father also revealed he was embarrassed
3 T  |. N! I3 v1 A# F" e& Zto disclose that he was using a testosterone gel pre-
3 @& u, h% \  l" r, V( Cscribed by his family physician for decreased libido) [1 P/ q" r( a* H) \, D! t$ Q
secondary to depression.7 Y3 v  z  m2 c" e. t  k2 ]
The child slept in the same bed with parents.
" [: h# s+ h0 J3 G2 C" ~2 MThe father would hug the baby and hold him on his/ \' r- n6 o( [4 e. f
chest for a considerable period of time, causing sig-6 d+ z" C: @9 i; [& l5 Y; W- L
nificant bare skin contact between baby and father., u3 {6 u/ C: X* o( h
The father also admitted that after the phone call,
' ^9 m! S/ U* D3 `2 Dwhen he learned the testosterone level in the baby: h9 o( p$ ]/ x
was high, he then read the product information$ t  f, K1 v; Y3 ?
packet and concluded that it was most likely the rea-
0 o1 ^+ M& O" Fson for the child’s virilization. At that time, they
' \# [- i& b: udecided to put the baby in a separate bed, and the2 D8 i: h# p" A, K4 v& [& d; ^
father was not hugging him with bare skin and had# S* ]( c, i; m5 ], B9 I' D2 n" s
been using protective clothing. A repeat testosterone4 `; a; J: q5 B) N$ g6 g3 m2 B( n- z
test was ordered, but the family did not go to the
& S. e! Y' O& e. X1 Mlaboratory to obtain the test.3 o; \; E5 A6 b1 U5 q* p
Discussion! f6 n) J) Q! `
Precocious puberty in boys is defined as secondary
+ U! i* F6 t( x) z! Fsexual development before 9 years of age.1,49 K! C  H% m& r/ u- g$ P
Precocious puberty is termed as central (true) when
8 D# X  R7 D. n  {0 x5 X" X7 jit is caused by the premature activation of hypo-  c; z8 ]5 ]) D# E/ P
thalamic pituitary gonadal axis. CPP is more com-: [$ M. c5 l0 s: D
mon in girls than in boys.1,3 Most boys with CPP7 v* u' H! a/ N" H9 |
may have a central nervous system lesion that is
* J' F8 G! N2 |/ O+ a0 Aresponsible for the early activation of the hypothal-
0 U# Y2 G. w6 z) Z2 k! _amic pituitary gonadal axis.1-3 Thus, greater empha-
- G% X% p" B- K$ g- Z: H9 Dsis has been given to neuroradiologic imaging in
4 `8 u5 H& b+ j8 v7 U8 P2 Vboys with precocious puberty. In addition to viril-4 I; c. F# Z2 l. @% z0 V
ization, the clinical hallmark of CPP is the symmet-' \5 {6 F7 V0 N7 i& p8 B5 \2 y
rical testicular growth secondary to stimulation by
  p# c1 ?- ^6 bgonadotropins.1,3
: }' K# A: }( k: ]" M0 rGonadotropin-independent peripheral preco-- w% h5 o  f4 k- G
cious puberty in boys also results from inappropriate
" D# M$ k- Z, |# h; u  Dandrogenic stimulation from either endogenous or
/ f2 I6 D, b$ s9 Uexogenous sources, nonpituitary gonadotropin stim-7 j; L7 A& O& {" Q
ulation, and rare activating mutations.3 Virilizing9 a* x. f2 M7 I
congenital adrenal hyperplasia producing excessive
, a, `* v7 q2 c& V8 Z4 t: m" Iadrenal androgens is a common cause of precocious
& W+ c4 T) ?# k1 `, fpuberty in boys.3,45 ^* k' l2 c4 Y+ u8 r; o9 n* A( c
The most common form of congenital adrenal. I) |; b2 P8 j+ L' u
hyperplasia is the 21-hydroxylase enzyme deficiency.
% i1 O5 F3 W- j; I9 aThe 11-β hydroxylase deficiency may also result in, \9 N9 L* a7 t$ f0 V
excessive adrenal androgen production, and rarely,
8 N* a: z8 n6 x# F+ `  {an adrenal tumor may also cause adrenal androgen) K/ X- E0 r# b# g+ P% a" j
excess.1,33 i3 I, l4 K% \$ O7 Q
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from6 `1 t5 ~7 R/ m9 ^$ `
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007" I  d" D3 H* i( G, J( ^
A unique entity of male-limited gonadotropin-
6 R3 q5 |! p4 O: ?& j& H! uindependent precocious puberty, which is also known
& ]) Z9 z8 T2 b6 a# k6 ^& tas testotoxicosis, may cause precocious puberty at a
) L9 r7 J# r" |  X* z1 ^5 ^% Gvery young age. The physical findings in these boys
; N! E% c4 J  ~, y. Awith this disorder are full pubertal development,( ~# C& f- u7 e1 f5 ^& i. p! Q
including bilateral testicular growth, similar to boys8 k. O& ?; I) B
with CPP. The gonadotropin levels in this disorder
$ ]! `- X, ~' ], yare suppressed to prepubertal levels and do not show
1 s! P: \3 f1 t: g) f; vpubertal response of gonadotropin after gonadotropin-. |. {4 ?, V' f5 J8 }$ f; N: O$ j
releasing hormone stimulation. This is a sex-linked$ S+ T  J# _3 F( ]  w3 w
autosomal dominant disorder that affects only
$ X+ k; s* a7 e% d* Vmales; therefore, other male members of the family
% V9 b2 p- C1 lmay have similar precocious puberty.3
5 ^" w6 C& r$ @" s: S4 iIn our patient, physical examination was incon-
1 A! q: o/ Y* q: R5 xsistent with true precocious puberty since his testi-
* j& j1 ^& x% J7 ~2 ncles were prepubertal in size. However, testotoxicosis3 q% t' R# {! G- A6 C
was in the differential diagnosis because his father
6 ]& t4 e8 V% M4 s+ [started puberty somewhat early, and occasionally,0 a3 y4 }/ {- W0 T$ V
testicular enlargement is not that evident in the+ D7 Z9 j2 q1 @# A+ h9 Q) @  \
beginning of this process.1 In the absence of a neg-! f$ `* o' a% [
ative initial history of androgen exposure, our& _/ x, n& X; ^  z7 O" E$ g" l& p
biggest concern was virilizing adrenal hyperplasia,
/ S! U  K  l0 T. heither 21-hydroxylase deficiency or 11-β hydroxylase( P" n4 z+ z  d9 _
deficiency. Those diagnoses were excluded by find-. m) Q' s; L6 M% @) `, ?7 R1 J; f. s
ing the normal level of adrenal steroids.
' l1 e1 [9 r, f! ~1 eThe diagnosis of exogenous androgens was strongly$ M8 b. x4 l7 O$ N: ?
suspected in a follow-up visit after 4 months because
. ^8 q! L2 B# V! E  Nthe physical examination revealed the complete disap-
5 x+ u2 z6 t7 y$ ~4 n4 h/ rpearance of pubic hair, normal growth velocity, and
. I5 q+ H, `# {  sdecreased erections. The father admitted using a testos-
3 N; p9 i/ Y2 k, wterone gel, which he concealed at first visit. He was/ t$ _2 n6 V! ~4 c- h
using it rather frequently, twice a day. The Physicians’8 @* ^7 m. @% Z
Desk Reference, or package insert of this product, gel or
1 ]+ q7 h& D& rcream, cautions about dermal testosterone transfer to; a  t2 p4 g* U5 v5 Z8 g: ?
unprotected females through direct skin exposure.
  |6 m1 i# _6 L* pSerum testosterone level was found to be 2 times the
9 K/ _+ E% \6 Y; A' Dbaseline value in those females who were exposed to
" h7 G! M" \5 e; o* [even 15 minutes of direct skin contact with their male
5 z5 K5 e4 D6 Q. S5 k/ l6 Kpartners.6 However, when a shirt covered the applica-
" {( s; ^% a( k; P9 Q6 f0 c8 Btion site, this testosterone transfer was prevented.
3 V4 v1 y1 P+ a" [Our patient’s testosterone level was 60 ng/mL,
9 ?7 Y+ b+ K0 c: a& J9 Pwhich was clearly high. Some studies suggest that6 p4 d: l* T- D+ h7 e
dermal conversion of testosterone to dihydrotestos-
$ e0 I1 a' @8 {3 b: @terone, which is a more potent metabolite, is more! M, A7 t) }. V$ M1 h* X7 i
active in young children exposed to testosterone
- N- w9 t9 e- ]exogenously7; however, we did not measure a dihy-
5 @7 `9 j! N+ b* i. z& A( V& `0 D1 Zdrotestosterone level in our patient. In addition to) j( d1 h, S3 p
virilization, exposure to exogenous testosterone in- J* ^; H1 _1 i) @( _% C* c, M  H
children results in an increase in growth velocity and, E  g3 i- d+ j) k; k" a4 D$ ^
advanced bone age, as seen in our patient.9 v% B7 m+ D# d
The long-term effect of androgen exposure during# o* q  S+ ]3 f: `7 c1 e% \
early childhood on pubertal development and final6 ]9 n3 Y3 v+ Q4 Q
adult height are not fully known and always remain
: d. o' S. i+ t$ p+ N9 r7 L$ s+ pa concern. Children treated with short-term testos-$ x6 x( H4 g3 z% Q
terone injection or topical androgen may exhibit some, ^+ {+ @' A0 [# o5 C! g0 X6 `
acceleration of the skeletal maturation; however, after! i7 C1 g$ c( H
cessation of treatment, the rate of bone maturation
7 S+ I6 n1 ^! J  z( x, B- udecelerates and gradually returns to normal.8,9
: u  K& O0 w! `8 {. h. n* F5 [+ cThere are conflicting reports and controversy/ Y/ V" b4 \1 k* E  a  [
over the effect of early androgen exposure on adult
7 \4 ^6 S+ `- A" A% B) r3 Upenile length.10,11 Some reports suggest subnormal
. L; L+ \7 H  f$ padult penile length, apparently because of downreg-
) i! Y" J" x9 k+ D+ x2 m4 mulation of androgen receptor number.10,12 However,/ D9 b2 x5 y% P$ u
Sutherland et al13 did not find a correlation between: S9 t4 \* @& K; a( T9 I
childhood testosterone exposure and reduced adult
9 s- a3 q) B* R( G3 g0 qpenile length in clinical studies.
- B4 o) E+ M5 F' g( H1 R2 r8 YNonetheless, we do not believe our patient is
' U3 \! P" r2 m' C) dgoing to experience any of the untoward effects from0 t$ r' C+ v3 D5 G) a* r
testosterone exposure as mentioned earlier because
3 m0 u  c3 n2 l- ^7 tthe exposure was not for a prolonged period of time.+ V( A0 c2 p- D$ X7 K$ m
Although the bone age was advanced at the time of/ e, g7 [, Z( E4 F- [4 I
diagnosis, the child had a normal growth velocity at
* C9 F% _: `( G1 M( rthe follow-up visit. It is hoped that his final adult  \* @+ p, B5 ?9 z6 V
height will not be affected.
$ r3 U8 ^1 y, I$ NAlthough rarely reported, the widespread avail-3 l" s6 m/ a# n3 G( G& J
ability of androgen products in our society may9 J& L8 a' U* n2 q
indeed cause more virilization in male or female2 b, j& S  C9 ?8 L) x
children than one would realize. Exposure to andro-
+ X0 y. U, f. z5 }' K  rgen products must be considered and specific ques-
  Z- U$ w( m( Xtioning about the use of a testosterone product or6 N2 w, s$ S; c6 {2 J# q
gel should be asked of the family members during# L$ Q8 p. f; `; E4 v
the evaluation of any children who present with vir-% R$ Y' j/ N3 u( c/ T/ ~0 @
ilization or peripheral precocious puberty. The diag-
' B8 j9 D- v5 S4 H2 D4 vnosis can be established by just a few tests and by0 y" c7 i7 k$ |' b" E3 R3 U! ?# f4 ~& H
appropriate history. The inability to obtain such a7 Y( H' c1 b% v/ Y% i8 G
history, or failure to ask the specific questions, may1 A& i$ m5 Q/ z$ U
result in extensive, unnecessary, and expensive
4 n# n+ w9 X/ e! c" ^/ J+ X" T% e2 hinvestigation. The primary care physician should be
8 [) L8 f4 P- y8 taware of this fact, because most of these children5 N5 L1 h2 R7 H9 T
may initially present in their practice. The Physicians’% }& q6 Y; t! w3 b5 L: z! q) D
Desk Reference and package insert should also put a" |9 {5 n2 a7 D$ ?* g
warning about the virilizing effect on a male or' p- P: K$ \! g0 a8 c
female child who might come in contact with some-
, y0 K2 g- l1 n# G% v1 _one using any of these products.7 L3 g# [9 }2 {; w; C: I& \
References
8 r1 i& G% B8 `" J' ^1. Styne DM. The testes: disorder of sexual differentiation
9 F4 A) U  x0 o8 cand puberty in the male. In: Sperling MA, ed. Pediatric, v- t5 q. {1 Y- q
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
4 X4 m5 z. [1 Q2 H2002: 565-628.$ f- e9 M/ O# M: E, t! O% E7 B/ `
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious: s# Q4 n7 _( X' Z% c! |
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old; u7 n: r" s0 d* l  M# v
Boy Induced by Indirect Topical
0 @, j1 Y, B* b# _; dExposure to Testosterone- X. ?- C# V3 o, Z( f5 f" I7 ^
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2  N5 o! F* O% i: |* ~
and Kenneth R. Rettig, MD1
7 s2 v5 A. g$ u' ?' p2 Z7 l9 b% TClinical Pediatrics9 a4 I7 N/ H, t1 y6 v, Q
Volume 46 Number 6+ T  w% l! _1 p: O6 s
July 2007 540-543
% r( `" F3 v& [  R© 2007 Sage Publications
9 O" e4 \9 t6 A: ?' a10.1177/0009922806296651
4 p" u* O0 t+ ^3 c" hhttp://clp.sagepub.com5 L( \; P7 a0 v2 n% }3 m$ X
hosted at6 j: O  y5 }9 q/ s
http://online.sagepub.com' |( c1 a- f% [/ R
Precocious puberty in boys, central or peripheral,; ~4 r% F: L  E) R* w( ^
is a significant concern for physicians. Central
) R: S4 {* P7 x( p3 qprecocious puberty (CPP), which is mediated5 o5 j8 D  o- M
through the hypothalamic pituitary gonadal axis, has  Z& I  ]* u1 r& T. M
a higher incidence of organic central nervous system7 @' S) q5 S- }) l3 |" @
lesions in boys.1,2 Virilization in boys, as manifested# q" `' O# q! |" Y2 M' b
by enlargement of the penis, development of pubic
  F* c: U4 i( V- o* }7 Y4 {! Zhair, and facial acne without enlargement of testi-4 q) ~) l" x4 _% @- }: {: m1 R* s; G
cles, suggests peripheral or pseudopuberty.1-3 We/ ?1 A# V2 N* ~9 a0 u9 w
report a 16-month-old boy who presented with the0 R( x: }7 F1 n: l7 r
enlargement of the phallus and pubic hair develop-& y% K# c: S, C0 M) F. x
ment without testicular enlargement, which was due
% T2 {) `7 z7 \2 m& G1 S  cto the unintentional exposure to androgen gel used by' R0 i- W* c4 y! ]
the father. The family initially concealed this infor-7 C; k8 u: t  ?2 i5 M) `" Q
mation, resulting in an extensive work-up for this' S7 @* k% s$ l7 ?/ m% ]' @" z! P
child. Given the widespread and easy availability of
" z7 L2 b4 i. Ttestosterone gel and cream, we believe this is proba-
  E# [; y8 \( x) Z1 f- x4 x- ibly more common than the rare case report in the& y, Y  p( Y4 ~, f4 X# i  I
literature.4- @: v# l+ J+ T
Patient Report! O$ s5 Z/ t& u2 B
A 16-month-old white child was referred to the6 k/ o' q) K' r5 ?
endocrine clinic by his pediatrician with the concern+ u" `4 S$ m0 u$ D7 i) n+ U+ G
of early sexual development. His mother noticed
' P. @) l8 q; Z9 v8 flight colored pubic hair development when he was' p# F! m1 k; y0 D- w8 Q! w
From the 1Division of Pediatric Endocrinology, 2University of- o% G& ~  W. P& z: d. s% x+ o
South Alabama Medical Center, Mobile, Alabama.. t* n) \2 d# E" N; I% L
Address correspondence to: Samar K. Bhowmick, MD, FACE,4 |  t6 f9 X) N7 s- X5 [4 _4 z5 d
Professor of Pediatrics, University of South Alabama, College of' O4 d. H$ |) z; c3 u5 B' K; ~
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;% v" z+ [" |, f' d2 G2 T( H
e-mail: [email protected].
/ m2 G7 c) T3 vabout 6 to 7 months old, which progressively became
) e0 P8 P/ H4 F6 F% pdarker. She was also concerned about the enlarge-
9 S: _* t. P7 _6 a* sment of his penis and frequent erections. The child# h, B  _1 R$ g- [/ N
was the product of a full-term normal delivery, with% J* `$ ]7 q1 U, V( O
a birth weight of 7 lb 14 oz, and birth length of
9 z% `( `1 I1 D5 l3 W) T20 inches. He was breast-fed throughout the first year
8 E0 H" _9 D+ d9 F5 z6 w" lof life and was still receiving breast milk along with; U4 L1 }  p9 i- a
solid food. He had no hospitalizations or surgery,/ F/ Z  a9 r0 ~( W. h. e- C. _
and his psychosocial and psychomotor development
. K# G: t- V5 {0 O- d% ^% mwas age appropriate.
. u# c, p) s7 C2 Z4 _1 l5 d0 AThe family history was remarkable for the father,) s0 D1 @5 k* T: X" o: i; E
who was diagnosed with hypothyroidism at age 16,
/ m9 R: d; r! d. C4 }* k9 `  iwhich was treated with thyroxine. The father’s" Q8 r0 v* a2 V: u5 o* F
height was 6 feet, and he went through a somewhat
# ~7 |- g. }, S$ G! iearly puberty and had stopped growing by age 14.- G$ ^2 D# F& J8 f. g  w3 f/ `
The father denied taking any other medication. The' t! R: G2 Y2 O6 ?+ L5 x! J
child’s mother was in good health. Her menarche* U8 }  Z$ T" u+ x0 H) }
was at 11 years of age, and her height was at 5 feet
% l3 d8 A/ Q% p8 @5 inches. There was no other family history of pre-. ~5 M. }2 O2 K) e/ c9 h
cocious sexual development in the first-degree rela-
1 }# }7 F$ X' _' |tives. There were no siblings.
8 v, \& w) S- L1 fPhysical Examination
( [' K9 _0 j5 L' hThe physical examination revealed a very active,% m0 ]5 _! U$ T( Y" I2 B
playful, and healthy boy. The vital signs documented9 n  P) x  I* Y# a. N8 E& V
a blood pressure of 85/50 mm Hg, his length was9 }7 u8 l) C. u8 v* t
90 cm (>97th percentile), and his weight was 14.4 kg
$ Z) I# |5 v. a0 X(also >97th percentile). The observed yearly growth
% z6 p( L4 @/ d, U8 e- Wvelocity was 30 cm (12 inches). The examination of  @4 Y9 F- T4 H, P1 ?, \8 F
the neck revealed no thyroid enlargement.( G: f4 V1 X' a# l. W4 h. D5 m6 F6 a
The genitourinary examination was remarkable for
5 c  [$ Z+ Y2 L8 T0 I( H  n! K5 L# renlargement of the penis, with a stretched length of2 W, n) w, b; q3 o2 ]  b+ W3 n! K
8 cm and a width of 2 cm. The glans penis was very well
: ?0 w8 D/ [: S; x3 tdeveloped. The pubic hair was Tanner II, mostly around
% N3 X! f. _6 ?3 k6 X540
' \" a& A8 g% c& {" p: Lat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
3 t" ]9 ~0 f6 i* e$ i. d6 hthe base of the phallus and was dark and curled. The8 t0 o1 X# T- Y) A) M, i7 ]8 ]
testicular volume was prepubertal at 2 mL each.
! H4 I1 ]3 X' I9 K, v/ JThe skin was moist and smooth and somewhat
& S+ f: b7 f4 yoily. No axillary hair was noted. There were no
* F- c/ J) e" I/ Nabnormal skin pigmentations or café-au-lait spots.% m0 B5 ^# ?7 V
Neurologic evaluation showed deep tendon reflex 2+
7 t' H' H$ t! ?1 ]8 Abilateral and symmetrical. There was no suggestion5 S/ y$ y! q  A: w' e4 u2 r
of papilledema.
* d  z/ Y6 K/ I! oLaboratory Evaluation4 M6 l8 l% s! c
The bone age was consistent with 28 months by. |4 l! M/ @5 ?3 {- u" P
using the standard of Greulich and Pyle at a chrono-
! Q+ a9 d( T7 C. f: i2 O/ s, \logic age of 16 months (advanced).5 Chromosomal
5 g) `5 s2 ?4 V; s# N( okaryotype was 46XY. The thyroid function test4 G3 a: q. F9 q8 ?+ J9 I7 Q# k7 N
showed a free T4 of 1.69 ng/dL, and thyroid stimu-( O# q( Q4 U8 ?6 @4 r$ r! m
lating hormone level was 1.3 µIU/mL (both normal).7 T) A2 `0 H8 h4 d/ S9 `' N; E
The concentrations of serum electrolytes, blood
' I  x* U# y- V  P6 L0 c9 gurea nitrogen, creatinine, and calcium all were. |5 u0 h1 _3 m1 M" k2 b; }
within normal range for his age. The concentration9 \- }8 Z4 |2 |9 Y
of serum 17-hydroxyprogesterone was 16 ng/dL3 W( D( z9 o: L$ s3 X* z* @
(normal, 3 to 90 ng/dL), androstenedione was 20
1 o  W/ c( f; [* j, y  Png/dL (normal, 18 to 80 ng/dL), dehydroepiandros-: H: J/ u8 o- W5 E2 f
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
3 z) V. P) \, M4 U, F4 G: ~" b; kdesoxycorticosterone was 4.3 ng/dL (normal, 7 to9 R0 G, A' u: C0 H/ g% O
49ng/dL), 11-desoxycortisol (specific compound S)
  |" ?# Z4 G0 C, ?was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-1 S2 {- z3 c* O  r5 _: P" e
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
+ c, @5 R  S) v( {testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
( o& E7 x( v) f  T2 |" l- Eand β-human chorionic gonadotropin was less than
2 G; G$ N; [" c* L0 l& R5 mIU/mL (normal <5 mIU/mL). Serum follicular
. L" P+ f' o( ]5 p- estimulating hormone and leuteinizing hormone
3 K  {  E) z2 y/ a& l& K- Rconcentrations were less than 0.05 mIU/mL
8 Y7 e  u/ ~# t8 h' B, t5 G- C/ P$ u( B(prepubertal).
: e, ?0 w& b& A% H* D! }# z9 `The parents were notified about the laboratory5 O& k  ]: {3 ^
results and were informed that all of the tests were
0 W- q2 [* j  ]) _% K; O- enormal except the testosterone level was high. The
+ P8 O% m/ u& J5 M3 |3 yfollow-up visit was arranged within a few weeks to8 i/ W8 G7 P; m6 Z$ m7 N( Z
obtain testicular and abdominal sonograms; how-
( ?, l# ?1 Z4 f9 b, [2 aever, the family did not return for 4 months.4 ~; ?2 [' P' U/ R
Physical examination at this time revealed that the
$ v2 Z5 \* P: wchild had grown 2.5 cm in 4 months and had gained6 p  k5 e( Z+ G4 q
2 kg of weight. Physical examination remained
) I- j) u) R" L" }7 k+ G; d# Hunchanged. Surprisingly, the pubic hair almost com-
8 a9 r- A+ Z  b' mpletely disappeared except for a few vellous hairs at
' y- v# F7 M8 g1 `5 Pthe base of the phallus. Testicular volume was still 2
9 h* d' I" k" y9 }mL, and the size of the penis remained unchanged.
% J$ o6 c" s: r" n4 W7 D$ x2 DThe mother also said that the boy was no longer hav-
9 o" x) e* a' L0 h$ D, V3 ~ing frequent erections.
5 z  t- _9 f' z* ?- M" nBoth parents were again questioned about use of
; N& y% l$ C  a% kany ointment/creams that they may have applied to
  {9 ^2 ]% P! A  _" p3 Gthe child’s skin. This time the father admitted the1 |" Q2 \' o  D2 h6 S4 l
Topical Testosterone Exposure / Bhowmick et al 5419 N# [6 `* ]3 Z9 x
use of testosterone gel twice daily that he was apply-& q$ x, p) h0 _
ing over his own shoulders, chest, and back area for
/ c  [& r5 A- ~% ?3 ?% ]9 Ha year. The father also revealed he was embarrassed
' p! x6 \! G1 tto disclose that he was using a testosterone gel pre-
7 O4 ?: h, g- T* [2 N% q5 P- @scribed by his family physician for decreased libido5 }; N0 L6 O- L' b$ x, L$ [
secondary to depression.
1 V/ Y2 ?4 }( v0 f# CThe child slept in the same bed with parents.
* U  H% j. w9 K  Q) f9 XThe father would hug the baby and hold him on his
# ^9 I, ?% _( c+ E0 l1 Kchest for a considerable period of time, causing sig-6 D% V& l  v- ~, a
nificant bare skin contact between baby and father.
* s7 K& a3 a+ s; l0 W( M' a8 UThe father also admitted that after the phone call,
6 e4 B" F1 J! _/ y5 Dwhen he learned the testosterone level in the baby/ w" G% t+ a, O" c' b" t3 {4 }
was high, he then read the product information' B1 x0 B; G' v7 s, N2 f! `2 d6 r
packet and concluded that it was most likely the rea-8 v+ v& H; r9 W2 q: U! m
son for the child’s virilization. At that time, they8 s$ z4 n& {. Q4 @; k: _' E5 x
decided to put the baby in a separate bed, and the7 I& j' j" s  m( ?4 b
father was not hugging him with bare skin and had/ d# @7 Y  J; P) l% p" ~
been using protective clothing. A repeat testosterone
: s* j5 _; n2 c7 P* E/ Q: K# Ztest was ordered, but the family did not go to the8 j0 g9 D0 i* @0 Y
laboratory to obtain the test.( v" ?5 o! A, a; M; m" `- o. f
Discussion
: @" B% Z3 Q9 c8 s/ @* I6 rPrecocious puberty in boys is defined as secondary
  {# v( Q0 A4 v, ysexual development before 9 years of age.1,43 c) `& l: M3 b: ~# V+ S" q6 c
Precocious puberty is termed as central (true) when
7 I( L9 I1 M8 K* b" U1 Zit is caused by the premature activation of hypo-
$ B  z8 a# O8 u9 \$ d  xthalamic pituitary gonadal axis. CPP is more com-( u, }: g, r" I; V0 s: g; \2 k
mon in girls than in boys.1,3 Most boys with CPP' i1 I# @2 A: c) I, G
may have a central nervous system lesion that is9 t" z+ u, m1 \+ A2 O6 E+ j6 N
responsible for the early activation of the hypothal-  |  f; k) L: w6 |0 t3 ]
amic pituitary gonadal axis.1-3 Thus, greater empha-5 U1 r: E8 a- _/ t5 K$ j0 w
sis has been given to neuroradiologic imaging in' C7 S* ?/ i) ~2 g! f4 u0 T2 c" _, K
boys with precocious puberty. In addition to viril-$ Y: P, Q0 M$ F$ C$ `$ T5 G1 g
ization, the clinical hallmark of CPP is the symmet-; ^/ A+ d8 h$ B8 ^2 }- g3 Q
rical testicular growth secondary to stimulation by+ p; y3 t, P, G  C
gonadotropins.1,3
4 P- w$ V" O# Y$ RGonadotropin-independent peripheral preco-
. \' o  y" {. lcious puberty in boys also results from inappropriate4 o' e0 n5 M; Z  o
androgenic stimulation from either endogenous or
( j4 x1 M- G+ C( D4 mexogenous sources, nonpituitary gonadotropin stim-6 \1 S# W! [0 g. z% Q
ulation, and rare activating mutations.3 Virilizing
& d; ^9 |0 E' c# |: ?congenital adrenal hyperplasia producing excessive
- q8 c+ Q. D5 M  ~adrenal androgens is a common cause of precocious8 f: ~0 W; `; Y; S2 G
puberty in boys.3,4$ |8 r7 U: m8 C$ I5 U3 M6 n
The most common form of congenital adrenal
) X0 @* ]8 \) _hyperplasia is the 21-hydroxylase enzyme deficiency.9 m! ~! R  T1 x1 b) {' o- Y  m
The 11-β hydroxylase deficiency may also result in5 d, R  a7 y& w9 O( o' l
excessive adrenal androgen production, and rarely,
# u# j% c" y6 W0 Y8 a; f* Zan adrenal tumor may also cause adrenal androgen* @' t, Z4 w% D( Y2 z( R6 @
excess.1,3
" F* A3 V1 A( @3 {0 hat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from; M+ w# N: B+ p& X+ H
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007+ T5 N8 h/ w: I
A unique entity of male-limited gonadotropin-. s9 {5 U4 {- ^) L7 D1 d
independent precocious puberty, which is also known
# W8 \" W9 N1 J) jas testotoxicosis, may cause precocious puberty at a( O' c9 Z" V! a" c5 S
very young age. The physical findings in these boys
& `4 H  a8 V: z* l) _& B5 L/ |with this disorder are full pubertal development,
, M) o' X- d% l! lincluding bilateral testicular growth, similar to boys
& K7 M- y% P! y* G# Bwith CPP. The gonadotropin levels in this disorder
0 Q/ B3 Z) l, Q1 Pare suppressed to prepubertal levels and do not show
% e- D7 `- |) O+ Opubertal response of gonadotropin after gonadotropin-2 M1 _$ Y4 z% L- b1 O7 R
releasing hormone stimulation. This is a sex-linked
  T! Q, ]# Y* R3 [0 o5 mautosomal dominant disorder that affects only
2 b, W1 M: G; K3 pmales; therefore, other male members of the family
& i0 X! c7 L! n6 w. T* ^may have similar precocious puberty.35 d- u+ Y. i" `9 _6 K% H  Y4 R1 X5 w
In our patient, physical examination was incon-' q( h3 f; d0 A  [' a: E3 e
sistent with true precocious puberty since his testi-, w/ O! m4 V5 ~# Q* [5 I
cles were prepubertal in size. However, testotoxicosis
, O0 ^% v6 y5 {' w* g- R6 P+ xwas in the differential diagnosis because his father' Z, O! l9 i; S  m0 W1 h" R
started puberty somewhat early, and occasionally,' \. w6 S* p- h; z/ {- e6 c
testicular enlargement is not that evident in the
+ ^0 i. _2 E2 L% d9 [2 ubeginning of this process.1 In the absence of a neg-
) {* z$ t+ W, m1 yative initial history of androgen exposure, our8 K& k8 E" w0 A% G
biggest concern was virilizing adrenal hyperplasia,
0 A# S. ~7 E. ]0 T- c% Meither 21-hydroxylase deficiency or 11-β hydroxylase; t0 m/ U6 i& I
deficiency. Those diagnoses were excluded by find-, V; @* T& ?+ b) x* i& a
ing the normal level of adrenal steroids.
- ?. r8 {. b& q$ s9 eThe diagnosis of exogenous androgens was strongly0 ]( h7 @5 X; \* \( H) q
suspected in a follow-up visit after 4 months because
7 b. L" L, A: t% i9 j9 ethe physical examination revealed the complete disap-
: N. Q! R6 `: `. |  O6 fpearance of pubic hair, normal growth velocity, and9 C* E: m( w( o1 }
decreased erections. The father admitted using a testos-* G0 i) w$ w( E$ q- N+ c
terone gel, which he concealed at first visit. He was
% o; o0 p  w) _+ w; Iusing it rather frequently, twice a day. The Physicians’9 E; P/ }) c8 e2 P
Desk Reference, or package insert of this product, gel or/ ~# }. o3 l) P( a! ]9 J2 y" d
cream, cautions about dermal testosterone transfer to4 g+ e8 b/ `% `, x& ?/ p7 R+ h
unprotected females through direct skin exposure.! L) k0 u) {9 Y
Serum testosterone level was found to be 2 times the
( @: ^% D; y# m+ _baseline value in those females who were exposed to; B: m) N, S/ d  l
even 15 minutes of direct skin contact with their male
  [) e4 Q+ I; a  }$ J" T  T* Jpartners.6 However, when a shirt covered the applica-
; l9 E# P7 C2 m# e+ ^# l$ H+ }tion site, this testosterone transfer was prevented.1 R) }4 y3 o0 V- K
Our patient’s testosterone level was 60 ng/mL,+ V7 U1 c/ m, _# i" K+ ]' u
which was clearly high. Some studies suggest that
% {7 b5 w5 s9 I1 C0 \8 d- g+ gdermal conversion of testosterone to dihydrotestos-
$ a8 M  B, u2 H8 W; S5 nterone, which is a more potent metabolite, is more
/ I% ^4 Z: s! Q5 e/ H+ n0 D2 `active in young children exposed to testosterone# f, z+ ]4 z! f% l. h, K
exogenously7; however, we did not measure a dihy-
# Z, Z7 T+ [- c" R$ I& |) ydrotestosterone level in our patient. In addition to2 [0 a% C: Q( C0 ^, H+ [$ F3 a4 ?
virilization, exposure to exogenous testosterone in
3 o- x5 D2 t7 q4 G% \  x: _children results in an increase in growth velocity and1 H; q% Q, b8 M! k' S% j
advanced bone age, as seen in our patient.7 p+ A. _: `8 r+ T( \& V. K+ z  b) }5 T
The long-term effect of androgen exposure during; ]) o; F+ \2 F, i/ X  m
early childhood on pubertal development and final" O6 Y# U4 g3 j# ]7 N
adult height are not fully known and always remain
7 u; e3 W$ X$ N" v$ Qa concern. Children treated with short-term testos-
7 u- M( O  h8 n( Kterone injection or topical androgen may exhibit some
& M; G0 ]6 _* \0 H4 W: F5 x* y- j: zacceleration of the skeletal maturation; however, after# m( H+ J; @( n; |+ G. \
cessation of treatment, the rate of bone maturation4 U1 `& Q; G" {& I$ X8 }
decelerates and gradually returns to normal.8,9) p/ f; A) _# Y4 _) p* I2 s4 F, C
There are conflicting reports and controversy
3 J: w) K, p& P0 J6 Oover the effect of early androgen exposure on adult
+ `1 U1 B3 e8 P6 w0 e6 {penile length.10,11 Some reports suggest subnormal
  h: p- h; u* g/ Iadult penile length, apparently because of downreg-. }7 L9 `- r2 i$ }4 R
ulation of androgen receptor number.10,12 However,* G2 z- b4 v. P3 h* N
Sutherland et al13 did not find a correlation between5 c: X! i4 I) f  L
childhood testosterone exposure and reduced adult
0 D8 q: K& w6 z1 J; k! p: cpenile length in clinical studies.
7 c) ]" z8 q8 K) cNonetheless, we do not believe our patient is- O7 m% [. s% |4 Q- {4 a# ~! b; J9 t
going to experience any of the untoward effects from
/ P4 u% i$ B$ a3 p) P' X" u# ztestosterone exposure as mentioned earlier because
% i  t- w/ J( n$ ]# n* fthe exposure was not for a prolonged period of time.* j/ J: e/ Y% C8 Y; {1 n
Although the bone age was advanced at the time of& x9 I. \7 u- x7 D  F1 V5 {/ |0 G
diagnosis, the child had a normal growth velocity at
3 Y6 @  a8 T( I; k' _2 ^6 P+ Q2 s8 l6 hthe follow-up visit. It is hoped that his final adult
: j. ]6 d/ F6 E3 t. `! `( eheight will not be affected.
1 @) I) }( w' `8 iAlthough rarely reported, the widespread avail-
3 @- ^7 z$ ?7 p* Uability of androgen products in our society may
' }/ D+ H9 ~0 p: r( W6 J1 v0 Xindeed cause more virilization in male or female! |6 r% j3 N" j' X
children than one would realize. Exposure to andro-
3 d8 g& e! ~2 J9 E" }1 }3 Lgen products must be considered and specific ques-
6 H1 E, R; \1 j! _; C0 Itioning about the use of a testosterone product or
# `0 D$ y! c. @$ ^+ D' cgel should be asked of the family members during9 ^* I  f/ d+ m/ Q& ?4 J0 B4 B
the evaluation of any children who present with vir-
4 q/ L3 |6 L% D, e! P) u7 }ilization or peripheral precocious puberty. The diag-
& s% x' I9 J. Xnosis can be established by just a few tests and by! }2 S, y+ m1 F: }
appropriate history. The inability to obtain such a
. v; k0 }& ?( n5 p+ L, y+ a: ahistory, or failure to ask the specific questions, may
$ T0 \& n1 R% E9 wresult in extensive, unnecessary, and expensive
& j6 W7 k7 u" cinvestigation. The primary care physician should be" b4 p* l2 D$ y7 m3 Q- ]5 W
aware of this fact, because most of these children! x" u) O( C$ A; ~" T+ p8 R' M+ }
may initially present in their practice. The Physicians’! c$ J8 t  f$ N9 W# s( [
Desk Reference and package insert should also put a3 f/ Y& Y) n5 P5 [4 n  z# O
warning about the virilizing effect on a male or2 Q+ [; G7 E( ]% i7 h7 \0 |
female child who might come in contact with some-' c& H  Z# t3 ~0 \# _6 ~  g  l( j& M$ U
one using any of these products.
7 E3 n8 }: I1 YReferences) [6 ^+ e& B$ }' B' ]9 L+ n
1. Styne DM. The testes: disorder of sexual differentiation
3 v* `! g0 \# r2 b0 }2 _  ?9 @( Cand puberty in the male. In: Sperling MA, ed. Pediatric
/ s7 T  W- N4 A7 C$ E, Q# U- b) YEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;  M2 [- S  X1 p8 \4 U
2002: 565-628.0 N. A& I: j9 X: P
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
3 J0 E$ F, [7 j; B* @puberty in children with tumours of the suprasellar pineal

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