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Sexual Precocity in a 16-Month-Old* ~3 Y2 ?8 `3 r+ f0 i6 \% i
Boy Induced by Indirect Topical- P9 D# T9 w# `1 Z; r) k
Exposure to Testosterone
3 k2 @5 \/ v4 ?1 h& y+ wSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2, ?! V' U8 ^% }- j0 o3 t4 N
and Kenneth R. Rettig, MD1
, P' U- ^+ q8 {# |0 aClinical Pediatrics/ U& Q" Z% ]+ g; s# _( b7 Q3 E
Volume 46 Number 6
) P4 c8 {& L( n4 }: M8 m: x5 D0 mJuly 2007 540-5435 q$ H$ G7 ]- i& z H$ x2 B, F
© 2007 Sage Publications! _- Z j& d L6 m. A4 \
10.1177/0009922806296651
+ E# c1 ?' m' B# y2 ]http://clp.sagepub.com
# i$ I$ w4 s9 ?. p5 ~* @1 Ehosted at
( G3 |& @( e) A5 {* T. n) l- |http://online.sagepub.com
2 t* w% ?: V- v. e4 R( LPrecocious puberty in boys, central or peripheral,
( Z: [7 U1 Y% n2 H% His a significant concern for physicians. Central0 H) Y6 h7 y& ~6 U7 [/ h
precocious puberty (CPP), which is mediated- R/ F9 V$ t) f8 Z8 R2 P
through the hypothalamic pituitary gonadal axis, has
/ }7 T- }5 N! L2 {3 }a higher incidence of organic central nervous system7 E5 d- z m2 _. q; {7 v( X, X
lesions in boys.1,2 Virilization in boys, as manifested
# \7 S5 V" p4 _. yby enlargement of the penis, development of pubic3 y4 }; O/ ?. @2 n! i* A
hair, and facial acne without enlargement of testi-' d" _0 O) k$ L- Z
cles, suggests peripheral or pseudopuberty.1-3 We
4 d2 h+ K6 q, z# g: x% S( Ireport a 16-month-old boy who presented with the
" [+ u" F+ r" n3 M; |( \enlargement of the phallus and pubic hair develop-. c6 b" V. H1 M0 t/ H
ment without testicular enlargement, which was due
8 z) l# |+ Z2 I+ t6 v- Vto the unintentional exposure to androgen gel used by
0 t$ n* |3 `; b; k! i2 hthe father. The family initially concealed this infor-
3 [1 o# u- Y* e8 `mation, resulting in an extensive work-up for this
5 G; o8 C0 t/ Qchild. Given the widespread and easy availability of# O5 o. {: r; F' p% Y; t8 H
testosterone gel and cream, we believe this is proba-# f' U" _3 r% B" E
bly more common than the rare case report in the
* Q% F' _+ e7 S8 G" i" w. W$ jliterature.48 y/ Q3 T, [+ F c
Patient Report
7 t' o2 ?. X; M( S9 t% j1 WA 16-month-old white child was referred to the/ y0 i- y8 [7 ~, m! ~2 o; B2 z9 B
endocrine clinic by his pediatrician with the concern. t3 a6 K8 \1 ~# I l- `2 K
of early sexual development. His mother noticed
+ A" _! y$ v; T0 t3 Nlight colored pubic hair development when he was6 D7 d. b w' e1 `1 }
From the 1Division of Pediatric Endocrinology, 2University of
s: X- Y+ ^' C% L- E+ x0 FSouth Alabama Medical Center, Mobile, Alabama.
& o; o. d& b5 f8 |0 [Address correspondence to: Samar K. Bhowmick, MD, FACE,
6 c/ G) }" u8 g% iProfessor of Pediatrics, University of South Alabama, College of" Q4 Z% N( d: A) ^3 [6 f
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;3 U; l7 ]% Y2 J
e-mail: [email protected].8 X8 f* m% R8 Z- q3 s$ J
about 6 to 7 months old, which progressively became
% u! U& F/ T. o3 J5 z& e1 Hdarker. She was also concerned about the enlarge-
; C' [# j8 a5 u' s0 Cment of his penis and frequent erections. The child
, E! E$ k1 f1 t1 w. Z" S# _; a+ jwas the product of a full-term normal delivery, with) N. e' D0 X+ T [% `
a birth weight of 7 lb 14 oz, and birth length of+ N1 X: L J8 b& Q
20 inches. He was breast-fed throughout the first year
7 k' l& |+ X* @: |' t/ Vof life and was still receiving breast milk along with, O3 k) p" b' {' V5 e
solid food. He had no hospitalizations or surgery,
, g( y- w: J- |+ G9 Jand his psychosocial and psychomotor development( g, s* w* ^. X2 Y3 g B
was age appropriate.8 y- l& F, n$ m: G! X! b
The family history was remarkable for the father,6 N4 c8 a) `5 \$ L' K% W2 C6 \
who was diagnosed with hypothyroidism at age 16,; [; ^+ C# t: Y3 d, a1 m, D
which was treated with thyroxine. The father’s
- J/ L; Z7 v1 K4 U9 i5 C- Mheight was 6 feet, and he went through a somewhat5 l0 I0 A$ I. u4 P3 G: r- e
early puberty and had stopped growing by age 14.2 U" g, a0 V* L1 K
The father denied taking any other medication. The1 D6 D2 E0 N+ `: Q% ]6 g; v
child’s mother was in good health. Her menarche# l; L8 Y" C! m2 l2 x: u; v
was at 11 years of age, and her height was at 5 feet7 o6 d. S+ S# T' j1 x
5 inches. There was no other family history of pre-5 r# l$ o9 l( F
cocious sexual development in the first-degree rela-' r9 H; W7 |6 I' E" i
tives. There were no siblings.
$ q, w+ [1 w# Y W( H! APhysical Examination
7 k/ |8 F) |; Y" G7 p; T# X* DThe physical examination revealed a very active,
1 W' h+ B6 i/ K, H4 M3 \/ y) X9 Gplayful, and healthy boy. The vital signs documented) I/ D7 @2 a8 ]
a blood pressure of 85/50 mm Hg, his length was
`0 D, K% g, L+ I90 cm (>97th percentile), and his weight was 14.4 kg9 c" Y) J+ z I! l
(also >97th percentile). The observed yearly growth
. A" A# p0 |5 Q6 o1 t; _1 w9 D0 Hvelocity was 30 cm (12 inches). The examination of
3 }# W% D. Z& d( E9 Kthe neck revealed no thyroid enlargement.
( P: w) m! r$ S qThe genitourinary examination was remarkable for
8 s% O$ o6 `! D) J/ b! v8 Tenlargement of the penis, with a stretched length of
$ K& V- L1 r3 C8 z8 cm and a width of 2 cm. The glans penis was very well* m+ f/ Q u6 L7 ?
developed. The pubic hair was Tanner II, mostly around
, y. G* D0 \! V- A- Q# v& ]& _540
Q( N; j5 i1 c" uat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
: N6 ~1 Y5 ^! h, s3 }6 ^4 ?5 n! qthe base of the phallus and was dark and curled. The: ]$ v) X2 c( E( ?
testicular volume was prepubertal at 2 mL each.
6 l/ t& C3 B3 f9 j: rThe skin was moist and smooth and somewhat
5 l4 B9 R9 V) v. M1 U9 }oily. No axillary hair was noted. There were no/ [: Z' E' O8 z6 V. a
abnormal skin pigmentations or café-au-lait spots.
- u* \3 p" C# L. q" b7 i/ Y( K5 nNeurologic evaluation showed deep tendon reflex 2+
; e* V; P$ M9 J; {( j* \* W# I( \0 ibilateral and symmetrical. There was no suggestion! a g' w- p' J- D. h
of papilledema.0 l4 l& Q x: C& p6 R3 ?8 c# h
Laboratory Evaluation
6 J' d. \4 j: r6 U) R* g. _The bone age was consistent with 28 months by
}# \2 l+ s% _3 k; Z% I1 {8 jusing the standard of Greulich and Pyle at a chrono-
4 R- }) G" x3 \4 Ulogic age of 16 months (advanced).5 Chromosomal
. o8 H; k8 W; skaryotype was 46XY. The thyroid function test, ?% W7 Q$ a" D' q/ v
showed a free T4 of 1.69 ng/dL, and thyroid stimu-9 I# F+ L. w6 l8 B# z$ I
lating hormone level was 1.3 µIU/mL (both normal).
6 a# v) F; T: l( D+ n; o' FThe concentrations of serum electrolytes, blood T$ _7 x/ L9 T' ^+ k0 }
urea nitrogen, creatinine, and calcium all were
& S% [) Z, }1 P0 f$ Zwithin normal range for his age. The concentration3 f" K3 a6 R6 D4 X2 N
of serum 17-hydroxyprogesterone was 16 ng/dL1 A! q o# u5 ~, j: Y: m) G% y+ v
(normal, 3 to 90 ng/dL), androstenedione was 20 [& A- D1 y7 Q
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-6 R/ H$ `: ?9 ^* f- K
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
7 O/ r+ y- @( r3 b9 {" i: v; h2 T9 }desoxycorticosterone was 4.3 ng/dL (normal, 7 to' m$ I/ p+ H1 \# t' |) ^
49ng/dL), 11-desoxycortisol (specific compound S)
7 g6 T' U e, A) Twas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-. S, q/ c- v$ y9 I( z7 O
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total- r$ N* [# s, V" x: I% |1 V% q1 V4 I
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),9 F; Q+ h" v' ]& m9 b: X
and β-human chorionic gonadotropin was less than1 z I* X' @/ s) \" w
5 mIU/mL (normal <5 mIU/mL). Serum follicular' v" x! v3 |$ j5 f0 j6 G
stimulating hormone and leuteinizing hormone
: Z& A- K9 k/ R1 a% H: S% y! Jconcentrations were less than 0.05 mIU/mL8 C, V- L, W3 ?$ N
(prepubertal).' I! ?- f7 h/ I; S
The parents were notified about the laboratory
. Y3 v# v0 ~, T5 L& Uresults and were informed that all of the tests were
0 D9 p- D1 i; K7 K1 \2 Q! }; O& Wnormal except the testosterone level was high. The
* W' `5 _4 {5 x0 Ifollow-up visit was arranged within a few weeks to
! _5 ] M$ {7 Q6 Y2 ?3 Uobtain testicular and abdominal sonograms; how-' v' x8 T. N3 O4 d& G9 C
ever, the family did not return for 4 months.4 {! N4 N2 ^! M6 }
Physical examination at this time revealed that the
: k+ y1 s/ Z8 K2 n8 k+ R2 ?child had grown 2.5 cm in 4 months and had gained
- t- z! [7 f9 H$ _* m* Q2 kg of weight. Physical examination remained
) A- @& n$ O' A q; Dunchanged. Surprisingly, the pubic hair almost com- b. R* S2 L/ z5 V/ e3 K7 s7 C
pletely disappeared except for a few vellous hairs at
. D7 F) u) T! L/ I6 Z4 |8 Cthe base of the phallus. Testicular volume was still 2
9 y4 f6 y- @# \6 \3 DmL, and the size of the penis remained unchanged.
a, i: Z5 s) V- q! y3 u3 N, [The mother also said that the boy was no longer hav-
' |) L! x8 J' E6 l3 |. W) Ging frequent erections.; ~4 K6 R! i A/ X0 `0 |; C, y4 a3 l5 l
Both parents were again questioned about use of
2 z9 P! i* q# v2 n/ [9 kany ointment/creams that they may have applied to
$ c7 ]1 k9 Z9 Rthe child’s skin. This time the father admitted the
3 T6 w3 z6 G s" G$ V7 @Topical Testosterone Exposure / Bhowmick et al 541+ Z8 Y) o, `$ O2 Z2 l6 y& o" `
use of testosterone gel twice daily that he was apply-! B7 C. V/ [1 @) k1 ?% Z/ f$ d
ing over his own shoulders, chest, and back area for7 g) }2 ^, o4 Z5 u' ]8 _2 D8 b2 n
a year. The father also revealed he was embarrassed
/ P2 b1 l5 b! y: ]to disclose that he was using a testosterone gel pre- N" b' [5 Z8 R* t
scribed by his family physician for decreased libido
, a. j5 M" D/ Ksecondary to depression.
' ]. @2 T6 W; P. k2 T( D# ~; ?) DThe child slept in the same bed with parents.
; M5 A( V5 ^- u) IThe father would hug the baby and hold him on his/ L( |9 O1 d: l/ n1 _; i+ |; _6 z
chest for a considerable period of time, causing sig-
# X9 |% D) |# ` f% vnificant bare skin contact between baby and father.
# Z1 Z, b- K5 b: ^: n6 V6 YThe father also admitted that after the phone call,( M" z+ }7 B5 x( E% \6 q. W
when he learned the testosterone level in the baby
5 l5 k$ |4 S5 P6 xwas high, he then read the product information ?6 H7 w- ?7 D( m% w+ \: m5 R
packet and concluded that it was most likely the rea-
5 A0 S6 O. j/ E- @- ^( Y7 ?son for the child’s virilization. At that time, they7 n8 I `) u; O7 O9 {
decided to put the baby in a separate bed, and the
7 R; r l8 R l7 C) i* Tfather was not hugging him with bare skin and had9 K+ f& f% ^- A$ A* l0 Z R% F
been using protective clothing. A repeat testosterone( U6 X' u/ `1 ^+ q! }; S( ]
test was ordered, but the family did not go to the! X3 E* g g" |, [- S
laboratory to obtain the test.
2 A8 J& r+ O: C5 sDiscussion
3 r5 [) `; e+ n6 W7 p. ]1 T# }- @Precocious puberty in boys is defined as secondary- B. u) Z C& ]1 o+ u! Q, S$ O
sexual development before 9 years of age.1,4
3 M7 q2 m, `2 \: ]: O7 yPrecocious puberty is termed as central (true) when1 E7 p9 P0 a* Y" m% F, a) m7 ]
it is caused by the premature activation of hypo-
* }/ u7 Z8 f! Wthalamic pituitary gonadal axis. CPP is more com-3 R( _3 |1 `6 m5 l `/ Z
mon in girls than in boys.1,3 Most boys with CPP
. G! G* S, E+ I/ ~& O3 E7 Umay have a central nervous system lesion that is2 [# W" m9 H6 {0 A& W0 P
responsible for the early activation of the hypothal-; ~5 ]. K% @3 q3 F; K4 {. I
amic pituitary gonadal axis.1-3 Thus, greater empha-( O! W8 T, U- o5 s9 k0 b
sis has been given to neuroradiologic imaging in
8 @, Y/ Y( a+ t6 p$ L% bboys with precocious puberty. In addition to viril-* L( q- r" @% F- f U' n3 @
ization, the clinical hallmark of CPP is the symmet-
: q6 K/ a3 O5 g; F& Crical testicular growth secondary to stimulation by
" K* J/ c/ G: `/ ogonadotropins.1,3$ W* B0 L5 c7 W2 u) E& j! k, w6 D
Gonadotropin-independent peripheral preco-0 E9 ~: v4 A1 T( u3 @
cious puberty in boys also results from inappropriate+ Y* k7 J- P3 b, [3 H4 J2 F( ~$ ~7 h
androgenic stimulation from either endogenous or5 [, b; g1 @: C
exogenous sources, nonpituitary gonadotropin stim-. X. F7 w5 D; Z* {6 ]( Y
ulation, and rare activating mutations.3 Virilizing. x. h+ y7 g% L2 w
congenital adrenal hyperplasia producing excessive
9 v1 ?' y$ z" L8 M8 _adrenal androgens is a common cause of precocious
) ]# R+ f* ~$ k" p$ S/ }puberty in boys.3,4
' \ G, m f$ {; L' C8 b( ]The most common form of congenital adrenal
" W$ w1 P3 I0 `% phyperplasia is the 21-hydroxylase enzyme deficiency.
1 H2 |* F: o0 _% E& VThe 11-β hydroxylase deficiency may also result in9 H: H$ o4 N* h
excessive adrenal androgen production, and rarely,
c( a* s |3 }6 p, Wan adrenal tumor may also cause adrenal androgen
% z6 c/ p3 J& Q+ vexcess.1,3
' [) y! b" V5 b3 t) l. Fat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from# s1 z2 O5 M: M3 M1 u$ K( }8 Q% b
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
) X, Y0 p; J+ \" v/ P" X" ?A unique entity of male-limited gonadotropin-$ q/ P% m* u. `2 d& R
independent precocious puberty, which is also known
4 F% U2 J% L* D; K( b( T2 L+ sas testotoxicosis, may cause precocious puberty at a+ m( t: m! Z, b7 R5 k
very young age. The physical findings in these boys
' z; D7 M1 ^2 a+ z4 fwith this disorder are full pubertal development,; L; T1 B/ R0 P, Y+ h% f- O# ~
including bilateral testicular growth, similar to boys
$ [0 r7 x' q1 _5 Q5 A {2 ~with CPP. The gonadotropin levels in this disorder
4 d. }5 e# Y( }3 l& b% [are suppressed to prepubertal levels and do not show
/ Y' J: I8 E) s7 i d, ~1 kpubertal response of gonadotropin after gonadotropin-
$ K8 g1 X; z* T) z# ]releasing hormone stimulation. This is a sex-linked
; t( ?$ T0 a; \6 e' f. Aautosomal dominant disorder that affects only
X/ R, D9 C+ R/ _5 @( b1 bmales; therefore, other male members of the family
9 H$ n; p7 z8 @. ?! _may have similar precocious puberty.36 f0 k/ t) L9 v
In our patient, physical examination was incon- L4 m" {3 y' ^# e4 \' q$ ]2 p
sistent with true precocious puberty since his testi-! x0 Z3 ]+ M5 ?7 K- v1 s, I7 M
cles were prepubertal in size. However, testotoxicosis
& w" ?+ s8 p# `was in the differential diagnosis because his father
' q; z3 J6 n/ J! a9 ?started puberty somewhat early, and occasionally,
/ T$ I$ G" J* z6 n; Z0 i7 utesticular enlargement is not that evident in the
% N$ l! g% b8 f" Zbeginning of this process.1 In the absence of a neg-
7 a- _7 a8 t0 \$ |8 rative initial history of androgen exposure, our
~! f( D2 L7 y; ]4 r5 J& t- q- Z2 ubiggest concern was virilizing adrenal hyperplasia,
4 P6 M& S$ c- ^1 t3 p, _either 21-hydroxylase deficiency or 11-β hydroxylase* R6 Q/ I& @# e5 j9 D& h
deficiency. Those diagnoses were excluded by find-
; C4 Z+ |$ n6 d, n8 }0 n% i* ting the normal level of adrenal steroids.
2 S: m' ]3 ]3 JThe diagnosis of exogenous androgens was strongly% k/ R s9 u# K9 ^) t' v8 d
suspected in a follow-up visit after 4 months because7 \ J! @" u0 {( I
the physical examination revealed the complete disap-
) e( u+ f+ L( Z* N8 ipearance of pubic hair, normal growth velocity, and" p- ]/ X# a2 |( o5 U5 u4 {
decreased erections. The father admitted using a testos-; Z. i8 C" Z' q* v* a6 V. F# r' a
terone gel, which he concealed at first visit. He was
( B1 n; y5 r8 y: s5 v! R4 Yusing it rather frequently, twice a day. The Physicians’
; ~* t: S8 x* iDesk Reference, or package insert of this product, gel or- Q" Z% j" A# m8 r) C! a, R: y
cream, cautions about dermal testosterone transfer to" {1 s, N. c* R- A" i
unprotected females through direct skin exposure.
# Z% k' M5 ~5 i. c! ?& GSerum testosterone level was found to be 2 times the% o$ C' V, L% |6 D0 l- l
baseline value in those females who were exposed to
+ I# _* e0 S. `& R4 _8 R% @6 H0 Veven 15 minutes of direct skin contact with their male
* `9 F1 b. `" ^8 M& t ?partners.6 However, when a shirt covered the applica-1 t, H2 i1 A6 O2 |9 X
tion site, this testosterone transfer was prevented.* I e- ]7 ~$ H) I0 L/ [
Our patient’s testosterone level was 60 ng/mL,
8 ]( H5 P! U. W, n* b! r) iwhich was clearly high. Some studies suggest that: O7 Z4 {$ Y' z% h1 H
dermal conversion of testosterone to dihydrotestos-% \5 X* j! C5 [: l" V& B8 \+ e
terone, which is a more potent metabolite, is more
. U4 W- r% l0 d+ w3 t' u. Factive in young children exposed to testosterone
/ ^ K6 [5 x/ n% ~exogenously7; however, we did not measure a dihy- i% ~/ s) Y5 B" r$ \$ A
drotestosterone level in our patient. In addition to
4 s3 N$ ?5 [5 ]2 ]virilization, exposure to exogenous testosterone in- I3 H3 _ \; B$ ^# K
children results in an increase in growth velocity and
+ k$ B- R. U$ P! o, q6 c d { eadvanced bone age, as seen in our patient.
6 y/ t) C. U% ^( JThe long-term effect of androgen exposure during
. J& H- }+ x& z7 [early childhood on pubertal development and final
: l! ]$ |/ I, d/ ^ dadult height are not fully known and always remain
# A. `3 ~4 {/ y- xa concern. Children treated with short-term testos-
8 S4 f' s" \2 Q4 m" n0 F2 Q& gterone injection or topical androgen may exhibit some0 E) A$ {$ b& v
acceleration of the skeletal maturation; however, after
! X, _& _" S Q+ L, Kcessation of treatment, the rate of bone maturation8 T& k% a5 t0 h
decelerates and gradually returns to normal.8,9: n, W) _$ R8 M: V- o5 f
There are conflicting reports and controversy- k* |$ T" b; I' I+ T
over the effect of early androgen exposure on adult" R3 V1 d6 i% S+ t7 x1 O
penile length.10,11 Some reports suggest subnormal
: l, Z5 j) _/ p% {8 p/ W5 gadult penile length, apparently because of downreg-
! @0 _3 X5 g' m: r7 P/ m9 z; Wulation of androgen receptor number.10,12 However,
# Y1 N8 c+ I1 d1 c! v, `Sutherland et al13 did not find a correlation between
" q$ v4 c1 \9 p. _, M, @0 ?$ Mchildhood testosterone exposure and reduced adult
7 k1 J8 M3 [( a2 h3 U2 apenile length in clinical studies.
* Y/ N" L( E1 k9 QNonetheless, we do not believe our patient is
$ G9 o b5 B9 b3 {1 m; ]going to experience any of the untoward effects from
' s' k' x5 z, atestosterone exposure as mentioned earlier because: h+ Q h) G; ~' A1 ?+ x
the exposure was not for a prolonged period of time.
7 X& V- ?+ n E- PAlthough the bone age was advanced at the time of: ?$ F3 L: v8 {' S
diagnosis, the child had a normal growth velocity at
: I" X: t6 B! C( q0 f S" b; J* ~: ^3 kthe follow-up visit. It is hoped that his final adult
) T) E% I0 _: h( K# c( f5 qheight will not be affected.
* L8 |: {! P# E+ W# M/ ~Although rarely reported, the widespread avail-
) V4 O/ o/ b3 m1 o, Hability of androgen products in our society may
. p& k# J- W+ _ j- ~indeed cause more virilization in male or female5 V7 o0 h9 R7 L6 I0 a
children than one would realize. Exposure to andro-
0 [. `) c3 Z3 N5 G# P8 @gen products must be considered and specific ques-
: W, H# `3 y8 Jtioning about the use of a testosterone product or7 j4 Q& H- v" e ^+ |3 s
gel should be asked of the family members during
6 J1 h7 u9 N% L& Y. Z- E# _; {# ithe evaluation of any children who present with vir-/ d( n9 q" g2 O. ?3 [9 I
ilization or peripheral precocious puberty. The diag-" a. q' w. j, A
nosis can be established by just a few tests and by
' Y: A" a$ a5 J9 e& c+ \! F7 oappropriate history. The inability to obtain such a# x2 a/ Q% q2 g/ n% B* g" o
history, or failure to ask the specific questions, may% R( f4 y, Z. h% U: W: _/ v
result in extensive, unnecessary, and expensive
8 \: R* a' V: k: }4 R: einvestigation. The primary care physician should be
% E T/ B; _& v; r! [aware of this fact, because most of these children
. R3 Q, g+ v+ W7 B! Q0 ^may initially present in their practice. The Physicians’9 Z( s) x' Y' A- m W4 N5 |. V
Desk Reference and package insert should also put a8 T! E# @! F- l) d- a
warning about the virilizing effect on a male or& H5 v# |6 S1 k$ S8 {- j6 T
female child who might come in contact with some-
5 w% c) o+ a2 ]( ~8 q7 aone using any of these products.
+ W+ O1 q$ Y% R: |9 T4 xReferences
, N1 J+ h7 j8 w2 \7 p8 x5 V1. Styne DM. The testes: disorder of sexual differentiation
+ A4 { a: W# x, }and puberty in the male. In: Sperling MA, ed. Pediatric
$ [# q* [$ H- K- h% jEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
* s4 r1 o. d1 R* q2002: 565-628.! q- [2 `! O* o- X7 Q
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
- ^2 u; n2 w# L U6 Z8 Zpuberty in children with tumours of the suprasellar pineal |
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