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Sexual Precocity in a 16-Month-Old, f- \0 s" g' H' r& \
Boy Induced by Indirect Topical
+ P/ H& V/ V0 l. ]0 ]% M, c" @Exposure to Testosterone
9 |% l M5 D1 _* vSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2- M5 k; N, H! `
and Kenneth R. Rettig, MD1
" ~; G+ n9 C/ d1 \! b7 FClinical Pediatrics
" n' v. G/ Z* _$ r( k; SVolume 46 Number 6
! ]8 _2 J% @1 S8 DJuly 2007 540-5432 u3 w+ g5 v8 l- \6 s7 w ^: y
© 2007 Sage Publications
6 ?6 Y: x: ~6 P10.1177/0009922806296651
6 K- N9 h6 W- E# s$ E$ E1 ?7 q0 rhttp://clp.sagepub.com
, Z. H0 H3 Q: q) p n2 [: ]hosted at; R/ G& u' x5 w3 S+ w* F
http://online.sagepub.com* l: t: n. b" L& `7 P+ M
Precocious puberty in boys, central or peripheral,
) ~" F6 @5 h4 z! ?: @& t/ r( Gis a significant concern for physicians. Central! i' h/ r5 H9 \ M# t
precocious puberty (CPP), which is mediated) F Q$ Y7 a, @9 S. I! w! S* C1 W
through the hypothalamic pituitary gonadal axis, has
6 D7 w+ l' M2 a2 T2 G4 r; |a higher incidence of organic central nervous system! ^# y4 e( X# P. ?. y+ g" n
lesions in boys.1,2 Virilization in boys, as manifested
4 @+ W. _9 G$ T9 P$ nby enlargement of the penis, development of pubic" }/ q. C5 w" z4 j
hair, and facial acne without enlargement of testi-9 e: B4 Z5 ^4 \4 Z4 C: I
cles, suggests peripheral or pseudopuberty.1-3 We
0 }' i3 C0 x# N. Mreport a 16-month-old boy who presented with the; b1 P/ \1 U3 }9 ]5 d% S5 e* G
enlargement of the phallus and pubic hair develop-
$ R E) j0 Y4 P8 M& ament without testicular enlargement, which was due, l6 B0 `: W ]3 j* l& r, k
to the unintentional exposure to androgen gel used by6 @" T9 E# b+ L: k3 C3 X. K
the father. The family initially concealed this infor-& p+ L% F$ M5 w M' V) ?
mation, resulting in an extensive work-up for this
' t) i3 f/ g6 O5 i: @) |0 Wchild. Given the widespread and easy availability of W: B) G4 J! U" y
testosterone gel and cream, we believe this is proba-# B+ ~8 X! W$ z t; F6 F" L
bly more common than the rare case report in the, e7 |. ~# x0 h* ]9 g8 U3 F
literature.4: h8 {( D. }6 l$ o
Patient Report3 D# Q& t$ t7 J6 w% ^2 x
A 16-month-old white child was referred to the
# q0 c9 |7 k+ m* G2 [6 Dendocrine clinic by his pediatrician with the concern
- _, T2 S, U% j B/ f4 h- W$ ~of early sexual development. His mother noticed
2 r1 G" g! D2 E6 J3 A( v. Q% n0 ]& ~light colored pubic hair development when he was* l6 t8 [- `2 v# G$ f' n4 S& a8 a
From the 1Division of Pediatric Endocrinology, 2University of, B, C6 N' ?& z0 Z: V
South Alabama Medical Center, Mobile, Alabama.
: P. d t5 |/ G+ FAddress correspondence to: Samar K. Bhowmick, MD, FACE,6 F8 ^& L$ l5 a
Professor of Pediatrics, University of South Alabama, College of' m) L( N4 \/ z7 j I, h4 _
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
- \. a$ t$ F& k A2 x8 ^2 p* C* x" fe-mail: [email protected].
8 f6 L9 ~5 n- v. c! g! Babout 6 to 7 months old, which progressively became
- n( n0 D- C ydarker. She was also concerned about the enlarge-) l* B. Q6 m/ G' W
ment of his penis and frequent erections. The child
) V/ R, q0 h' bwas the product of a full-term normal delivery, with
- t9 K- K/ r6 i* c7 q; P% }a birth weight of 7 lb 14 oz, and birth length of( \) d& ~8 i i d2 ?* H: h
20 inches. He was breast-fed throughout the first year
( U+ ]9 j# ? Wof life and was still receiving breast milk along with
% h: u0 N7 j& F; \2 `/ J/ Qsolid food. He had no hospitalizations or surgery,
0 _/ C1 D5 E! S5 C4 L2 L* W0 {and his psychosocial and psychomotor development" H' S1 M# @3 |7 u/ W0 o
was age appropriate.
/ t: I* c) x3 g. @2 }5 WThe family history was remarkable for the father,2 c/ D+ k; I; u! |* g. }6 |, \
who was diagnosed with hypothyroidism at age 16,
8 {: g6 B$ Y4 N0 gwhich was treated with thyroxine. The father’s5 F* [+ E; ?! e( R8 N8 J
height was 6 feet, and he went through a somewhat6 I8 R% w8 ?* I
early puberty and had stopped growing by age 14.& }: E7 R" a3 U& a4 l4 _
The father denied taking any other medication. The
1 P6 G6 I! t9 M5 nchild’s mother was in good health. Her menarche
2 C/ K& ^, D$ C! E. ~6 [( E* Nwas at 11 years of age, and her height was at 5 feet* ?! l9 A/ m) v- b' `' | `
5 inches. There was no other family history of pre-" Y7 x4 N4 g) m( ?+ m
cocious sexual development in the first-degree rela-
7 @" a) O7 I$ \' M' g' C: k3 d( rtives. There were no siblings.
/ d M' g/ L7 Q3 APhysical Examination* m! a; W7 W ~+ p' G, O
The physical examination revealed a very active,5 n n$ F0 {8 K
playful, and healthy boy. The vital signs documented
, _: @, R5 M% X1 w. B0 q: da blood pressure of 85/50 mm Hg, his length was2 \0 B' V; f# U7 s2 |5 Y( b9 \
90 cm (>97th percentile), and his weight was 14.4 kg$ H& b2 Y1 _) `7 ?! c
(also >97th percentile). The observed yearly growth
4 G4 Z4 p- {# V( j( U9 v% Kvelocity was 30 cm (12 inches). The examination of
$ A$ d, R) {( K* ithe neck revealed no thyroid enlargement.
, L2 y* W6 p9 r; F1 J5 UThe genitourinary examination was remarkable for
# f/ l* z1 x: [enlargement of the penis, with a stretched length of
1 U! V5 f! h3 o8 cm and a width of 2 cm. The glans penis was very well# K- ^* N# M" N- c) l3 [$ X
developed. The pubic hair was Tanner II, mostly around
. \( V3 F' h1 r9 `# ?/ l540
! b2 w6 Y. c+ r2 }at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
1 \) S5 j" P4 [* K( K0 g( ?$ ]the base of the phallus and was dark and curled. The
- a) V% b% }8 ^6 E0 jtesticular volume was prepubertal at 2 mL each.* Y( L9 l* A# Y X- h3 N0 w! w
The skin was moist and smooth and somewhat/ G; _0 N$ V8 G/ F9 A
oily. No axillary hair was noted. There were no$ ~* I) r6 D7 ?0 L) A) W' Q/ S) Z- F
abnormal skin pigmentations or café-au-lait spots.
: ?2 i% O6 q& m3 r8 s) M4 ]Neurologic evaluation showed deep tendon reflex 2+
, X6 h$ q' ?" Ubilateral and symmetrical. There was no suggestion
3 a" b( M+ Y5 \( p. |: h) |% Sof papilledema.
0 d2 T- n( k3 X- q; M0 M! ZLaboratory Evaluation
* o& E; p/ f7 H, m7 _. t! m2 `The bone age was consistent with 28 months by
5 \& R, X/ u0 ^ p {$ A* X5 n5 L% Busing the standard of Greulich and Pyle at a chrono-
6 Y3 B" {$ s: ^, H7 c; ^+ X, a9 zlogic age of 16 months (advanced).5 Chromosomal& m: N( f- B [/ z# y3 e# Z* j
karyotype was 46XY. The thyroid function test$ S6 \5 r7 v0 q+ b" o, W+ s/ W
showed a free T4 of 1.69 ng/dL, and thyroid stimu-( O1 I3 _/ X; t2 `0 ~4 ^
lating hormone level was 1.3 µIU/mL (both normal).
( Z3 R: g9 }3 b( x# W. j8 D PThe concentrations of serum electrolytes, blood
; r7 S# k0 g3 z* W8 f0 W$ {urea nitrogen, creatinine, and calcium all were
6 ]" c- x; D+ n, J. J$ g7 _ fwithin normal range for his age. The concentration6 M8 e0 l7 p5 f& Z' F/ g* l
of serum 17-hydroxyprogesterone was 16 ng/dL
# l$ c1 A5 g/ V0 ~4 {5 t(normal, 3 to 90 ng/dL), androstenedione was 205 n8 a+ a' C5 s- g' w; u8 i
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-, {7 Q5 K3 z% H x
terone was 38 ng/dL (normal, 50 to 760 ng/dL),2 z) L$ A- o9 L: @2 H1 d
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
8 I3 P. [' L) ^) @; U4 F, f49ng/dL), 11-desoxycortisol (specific compound S)
9 q0 S9 V; w% D2 k7 Awas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
! |8 V6 v+ B F2 V& ~tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
?, D* u+ _6 B6 l( n; X+ Gtestosterone was 60 ng/dL (normal <3 to 10 ng/dL),3 r2 ~0 A9 E5 j/ q* n8 Y7 j
and β-human chorionic gonadotropin was less than
8 p! O& z; I5 V# s5 mIU/mL (normal <5 mIU/mL). Serum follicular
; u& C9 }5 d, qstimulating hormone and leuteinizing hormone
: }( e* q7 s3 b: F) O5 }" kconcentrations were less than 0.05 mIU/mL
! f" P% P! Z8 Y! [- t$ p4 v(prepubertal).) u' L6 N6 Q- u$ @! n# j+ `
The parents were notified about the laboratory# L5 P& x8 C6 h5 s
results and were informed that all of the tests were
7 M5 H# E( i$ o* h5 V: `normal except the testosterone level was high. The( n5 [, W- S1 F, U
follow-up visit was arranged within a few weeks to
1 V5 S6 E' W. T: k( @obtain testicular and abdominal sonograms; how-1 r/ T7 G/ s* ^- ], T7 y) m
ever, the family did not return for 4 months.
6 Z: \! r9 v! I5 v4 g8 c6 MPhysical examination at this time revealed that the2 y+ G H9 `6 ^" ?) R6 S
child had grown 2.5 cm in 4 months and had gained
o( j/ Y2 u, e8 P# }3 s2 kg of weight. Physical examination remained
2 e7 Z z8 u' m+ `) @1 ounchanged. Surprisingly, the pubic hair almost com-
- N9 k: ? [2 D5 n! \pletely disappeared except for a few vellous hairs at# |- S' E, J" L9 e; \
the base of the phallus. Testicular volume was still 2" q- N1 W6 j/ r7 ^
mL, and the size of the penis remained unchanged.
( w. k/ z7 |) Q( gThe mother also said that the boy was no longer hav-5 `2 Y! p2 J+ j' S) h# G
ing frequent erections.9 j& i7 I! ~! L+ O! q
Both parents were again questioned about use of
d O" C9 [; cany ointment/creams that they may have applied to- r0 O! a# B$ U0 O& J
the child’s skin. This time the father admitted the
$ T$ d3 K7 R( f$ ]. rTopical Testosterone Exposure / Bhowmick et al 5415 T7 i8 I- `) k* s
use of testosterone gel twice daily that he was apply-
* h6 l% T. K( u+ [0 E8 |: S3 ^ing over his own shoulders, chest, and back area for
1 W' d# {& Z" Ba year. The father also revealed he was embarrassed
# L6 n( r2 s# k0 ~+ lto disclose that he was using a testosterone gel pre-, F- ~5 r! q4 \- r! l8 x7 G
scribed by his family physician for decreased libido
1 i6 G! w: H. ~$ k4 isecondary to depression.
) y0 g7 N* ?! C2 r4 s6 @) RThe child slept in the same bed with parents.
. g: y' T$ N' q! |% B" ]5 z! CThe father would hug the baby and hold him on his
) F4 c7 b. Y9 i0 ?; X# Ochest for a considerable period of time, causing sig-; ^- X' A& O3 z7 v3 h+ T7 c
nificant bare skin contact between baby and father.2 H% k# m% P% m1 t# i* E
The father also admitted that after the phone call,6 n& Q: T+ m4 a* @, l& [& ]/ n
when he learned the testosterone level in the baby& ]$ M9 _9 f% J8 D# z2 ^9 z2 l
was high, he then read the product information
% g% N3 M3 C* u0 i/ r& Gpacket and concluded that it was most likely the rea-/ s( n) O4 j% n
son for the child’s virilization. At that time, they6 o3 u/ X# Q2 T8 H$ |; i0 g3 x
decided to put the baby in a separate bed, and the
& r1 O" `9 D" U, K, |: v2 hfather was not hugging him with bare skin and had
4 n/ s2 C, N8 v) {& K5 U) G% `been using protective clothing. A repeat testosterone3 f& e# s; ~. c% C7 t6 ?
test was ordered, but the family did not go to the3 K0 E* F) k- n. N5 ~- N8 I
laboratory to obtain the test.
, c8 }) g$ r5 v! UDiscussion+ n7 m0 C) W* z) P. R
Precocious puberty in boys is defined as secondary8 W6 t- i4 j7 m W3 n8 i% p' ?
sexual development before 9 years of age.1,47 @8 g. Z8 ?, ?2 J- I. W1 r7 I
Precocious puberty is termed as central (true) when0 c; y6 ?! k4 l
it is caused by the premature activation of hypo-- v# j% e6 Q4 A$ l2 N I
thalamic pituitary gonadal axis. CPP is more com-
9 B% y4 _8 O5 h6 nmon in girls than in boys.1,3 Most boys with CPP
- m G! u5 B' w7 l- e3 C' ]may have a central nervous system lesion that is( q8 [% R) [# [
responsible for the early activation of the hypothal-
; q' B: t9 d8 v9 O7 ?$ h+ K- ^amic pituitary gonadal axis.1-3 Thus, greater empha-; r$ d) X, L! H8 N# s
sis has been given to neuroradiologic imaging in5 z, ]# v) N- W
boys with precocious puberty. In addition to viril-
- p* v$ ~' w! Z" Dization, the clinical hallmark of CPP is the symmet-% {" W% k* t* f+ n
rical testicular growth secondary to stimulation by) X7 V" A. i1 V- [$ r- e
gonadotropins.1,3 o6 G. u4 y) c8 y S
Gonadotropin-independent peripheral preco-
% z9 G! n, N( R. c% F; |cious puberty in boys also results from inappropriate9 i1 w+ D; N# ]; I, N
androgenic stimulation from either endogenous or9 t/ x4 K! Q* r. o x: m6 i6 q
exogenous sources, nonpituitary gonadotropin stim-
3 w! u' j$ X- g0 x& _% ?ulation, and rare activating mutations.3 Virilizing' N {; v1 X1 M6 T/ o8 ]% l
congenital adrenal hyperplasia producing excessive
# {, z2 U0 K3 k, ]+ z* B2 Xadrenal androgens is a common cause of precocious
- b/ u& x% ~2 g2 Gpuberty in boys.3,4
+ u! p4 Z5 ?( d6 k% ^The most common form of congenital adrenal
) \8 b, Y$ L! ^% \; h! ~/ i' W" \hyperplasia is the 21-hydroxylase enzyme deficiency.
7 F! B2 N; F+ t8 {* @8 x! K6 RThe 11-β hydroxylase deficiency may also result in* J: r1 V' w9 \$ Z- D) i1 @7 S
excessive adrenal androgen production, and rarely,
. Z8 f; J, K) z% t% x v: L: s0 Man adrenal tumor may also cause adrenal androgen
! ]; o; s# X, u/ M8 @) R5 ~* dexcess.1,3
% \# Q- t9 m- p% W! ]3 V7 Uat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from$ s9 K: z, u6 W4 E/ k! p; ?3 R( W
542 Clinical Pediatrics / Vol. 46, No. 6, July 20076 }/ h- C" v" c9 |
A unique entity of male-limited gonadotropin-, {) A( Y5 J3 [
independent precocious puberty, which is also known
. O) K6 {. ~, {% j, s0 Bas testotoxicosis, may cause precocious puberty at a
1 T' L* G' h4 E$ ~0 overy young age. The physical findings in these boys3 ^2 f* M# B8 c8 p5 L0 i* ?
with this disorder are full pubertal development,8 I7 C5 ?2 I: a+ u3 E
including bilateral testicular growth, similar to boys
- F2 ?3 e% f B) ~. r% O* |+ U gwith CPP. The gonadotropin levels in this disorder- h/ ~$ S4 x9 ~3 t) N
are suppressed to prepubertal levels and do not show
4 C9 i2 s" `6 J1 Cpubertal response of gonadotropin after gonadotropin-
2 B. J* O" {: F, areleasing hormone stimulation. This is a sex-linked) L% _2 p8 A% m5 ?6 y, I9 _& ^
autosomal dominant disorder that affects only% Y& e { I0 j5 M! U3 u4 J
males; therefore, other male members of the family$ W! ^. Z4 c3 h* U9 _0 \+ p
may have similar precocious puberty.3
! m6 E% X' w. S& P7 V3 b7 i8 HIn our patient, physical examination was incon-7 H! {. D4 H# m- \/ `, s: X
sistent with true precocious puberty since his testi-' e T2 P+ l/ u$ e2 `6 Z u
cles were prepubertal in size. However, testotoxicosis
( ^' p# Q/ `0 M- b- _. t1 ?was in the differential diagnosis because his father& d$ S ^% C1 z2 P5 U" |! z6 {" z
started puberty somewhat early, and occasionally,6 h1 |/ ?' J' O
testicular enlargement is not that evident in the
/ ?' N) t# p, w! i3 l; Wbeginning of this process.1 In the absence of a neg-
; T% f1 u- I G( v- Q" Mative initial history of androgen exposure, our
& c0 s! j) I' C" W- R N% Vbiggest concern was virilizing adrenal hyperplasia,2 z( ^' s: e1 r' `9 u, l8 z/ G: O
either 21-hydroxylase deficiency or 11-β hydroxylase
* h. Y; T" J/ o+ E9 T& c! X- N- Ideficiency. Those diagnoses were excluded by find-2 Z4 w! t& j8 p9 j2 u- F# b
ing the normal level of adrenal steroids.
& g9 A; L% d" t4 O9 B: ]7 h aThe diagnosis of exogenous androgens was strongly* C- O: n% ~5 {3 }: y! U
suspected in a follow-up visit after 4 months because2 ]/ \ W1 |4 Z' r
the physical examination revealed the complete disap-
4 M1 d* ]2 x1 S3 C: gpearance of pubic hair, normal growth velocity, and
# M: `& b/ ?# {5 j) mdecreased erections. The father admitted using a testos-! J% j% {9 x8 I3 E8 f; n& L
terone gel, which he concealed at first visit. He was
! z5 e" C* @% r: Z, v9 Z/ vusing it rather frequently, twice a day. The Physicians’0 {! Z3 f) Y; D1 m3 m9 A5 `
Desk Reference, or package insert of this product, gel or
; Y, z, K4 @/ h8 T; jcream, cautions about dermal testosterone transfer to
# |7 X3 D j( ^6 l, u% P5 k( ^4 Wunprotected females through direct skin exposure.
5 G& _' n8 Y! G6 a, @, vSerum testosterone level was found to be 2 times the, ]4 O$ _8 L% k, X4 f
baseline value in those females who were exposed to4 j# H7 G0 L% o" ^' b% n3 u
even 15 minutes of direct skin contact with their male& ~8 y4 V/ v+ U
partners.6 However, when a shirt covered the applica-
) |) t n& {1 l0 ~0 D& \% M" F9 Jtion site, this testosterone transfer was prevented.) X* v6 n5 ]2 u) M7 v/ {' h7 G* ^
Our patient’s testosterone level was 60 ng/mL,# j/ ^4 b' I5 e
which was clearly high. Some studies suggest that
" L" o( m$ p, J, w# o; c; sdermal conversion of testosterone to dihydrotestos-
. Q7 X+ Y( A" g" mterone, which is a more potent metabolite, is more
+ B3 [; \& }0 t/ U3 J: ractive in young children exposed to testosterone
3 f, ^- `5 p: f! i2 b& bexogenously7; however, we did not measure a dihy-& f$ g) Z8 F7 A: t6 [9 @
drotestosterone level in our patient. In addition to" D- m& ]6 g9 r) g( |7 J/ n: t
virilization, exposure to exogenous testosterone in5 G# h$ ]2 `5 U4 H
children results in an increase in growth velocity and
8 q1 T5 @+ h" fadvanced bone age, as seen in our patient.$ L! E: G% o2 `4 J# C6 F
The long-term effect of androgen exposure during
4 v7 v: t j0 R/ z4 i% O* K! L/ jearly childhood on pubertal development and final
: m8 Q3 v8 ]' I' [, `adult height are not fully known and always remain! ^: B7 k# O" T
a concern. Children treated with short-term testos-
# H" d2 Y2 ^. a$ r" T9 }terone injection or topical androgen may exhibit some. Q8 N; B; G- o5 V6 W4 T6 i
acceleration of the skeletal maturation; however, after' ]' h% R& e) i+ b4 b
cessation of treatment, the rate of bone maturation# d$ Y9 U- o2 X0 U; H
decelerates and gradually returns to normal.8,93 n0 G; E* k/ r4 p9 S4 r5 f
There are conflicting reports and controversy5 J$ M' |# j& k/ @
over the effect of early androgen exposure on adult% w% f1 b2 B. q b4 M, i
penile length.10,11 Some reports suggest subnormal
: n W) z# A% s; S. \( Tadult penile length, apparently because of downreg- A# a. c& t" A m ~/ w
ulation of androgen receptor number.10,12 However,
8 X% @1 H4 @: d OSutherland et al13 did not find a correlation between
; b9 [8 S6 b( {" p3 M7 w: Ichildhood testosterone exposure and reduced adult5 L# L" k0 p+ x6 S. H& `
penile length in clinical studies.
6 J' f' ?. [. y8 ]Nonetheless, we do not believe our patient is
" J2 G1 A1 b4 b& S% n6 [/ h% ^4 xgoing to experience any of the untoward effects from
. ~8 c0 l6 { x: |% t Xtestosterone exposure as mentioned earlier because
5 F5 s2 a3 W% R7 T$ O) L9 cthe exposure was not for a prolonged period of time.4 c( P" Y4 S0 `, F
Although the bone age was advanced at the time of0 @, A: s$ i- M& d+ O0 v
diagnosis, the child had a normal growth velocity at
* U$ `% M# r& M& @& lthe follow-up visit. It is hoped that his final adult+ H" V+ p( n9 D$ F3 l2 V. H) u
height will not be affected.' g( H5 M3 p. l D: R' A5 [
Although rarely reported, the widespread avail-4 I# n9 K. [9 m9 U6 \4 R
ability of androgen products in our society may
5 z) ?5 s# Z& a; d; b/ x" hindeed cause more virilization in male or female' E, N& y" n9 b. D2 L, E
children than one would realize. Exposure to andro-
. q Y$ T. C) C8 H! @gen products must be considered and specific ques-
3 {& _6 x( Z, F9 e& {+ ationing about the use of a testosterone product or
% Z$ R }- [- Ggel should be asked of the family members during* X+ D3 ^0 W3 W
the evaluation of any children who present with vir-# [. k/ x& G4 ? K( L, M& Y% [
ilization or peripheral precocious puberty. The diag-
% h) u+ u) X6 Y8 r. N! C7 qnosis can be established by just a few tests and by8 @) m# b4 ]+ Z1 H! p, b
appropriate history. The inability to obtain such a( ^$ W5 M+ V H5 a0 R5 @
history, or failure to ask the specific questions, may7 s3 ^+ W% ?6 w) U& G
result in extensive, unnecessary, and expensive$ G+ k6 n7 k& Q+ f' V
investigation. The primary care physician should be, C9 p5 {3 i/ \$ q# b M" T
aware of this fact, because most of these children& b" i( R8 q/ Z" ^
may initially present in their practice. The Physicians’
. d& U' O' \ F: l( x- \Desk Reference and package insert should also put a" ]& G- V! f& Y$ P; g k
warning about the virilizing effect on a male or3 B5 G' v: \4 [. G
female child who might come in contact with some-8 f' n }( J4 q; ]
one using any of these products.
# V! S+ Q5 B2 z* `7 {0 q b( l" W; bReferences8 i; U8 b$ L4 R2 F! C6 ?1 I* N
1. Styne DM. The testes: disorder of sexual differentiation
8 V7 ?& ]) V2 ?. ?; O% `3 Xand puberty in the male. In: Sperling MA, ed. Pediatric
, s$ z2 e, }! W$ z% }4 pEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;8 o9 F/ v0 R& ]
2002: 565-628.
- w5 P' |) P0 p2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
1 t7 a8 G+ d. j: o$ R" F' E P5 gpuberty in children with tumours of the suprasellar pineal |
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