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Sexual Precocity in a 16-Month-Old& K* e( E! l7 Z7 \9 F" Q
Boy Induced by Indirect Topical* Z: _% k. W6 E, b
Exposure to Testosterone
3 Q5 Y; C; F0 f CSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
7 x" X. V: C5 Qand Kenneth R. Rettig, MD13 C- P$ c9 T$ v: |# u1 Z! X
Clinical Pediatrics! [: ^) t" Y' R; O/ l2 y7 n
Volume 46 Number 6
* u; x" p: K8 _2 Y! [2 g5 x/ k$ vJuly 2007 540-543+ t7 [7 O9 j. T
© 2007 Sage Publications" B* O, A, s5 d: K+ j: c
10.1177/00099228062966512 w8 z9 y% M4 k8 A: u
http://clp.sagepub.com
" x3 A( H( }2 U: ]# a2 N# h; Whosted at
: s# G8 E- H- {. q x; Dhttp://online.sagepub.com8 [+ U! g: _* h `+ n5 ^
Precocious puberty in boys, central or peripheral,5 g+ x9 {( Z6 V
is a significant concern for physicians. Central; W2 v4 R4 [* a H, D# P/ e
precocious puberty (CPP), which is mediated+ [$ m7 C0 X/ _+ A5 l
through the hypothalamic pituitary gonadal axis, has5 b+ K, Y% D. Q; l, S0 `' A. l W
a higher incidence of organic central nervous system$ x$ \* m% |$ W/ F2 S
lesions in boys.1,2 Virilization in boys, as manifested
+ p) Z! Z1 v4 E& }( o p! G2 Gby enlargement of the penis, development of pubic
( i/ m: M$ J7 w( thair, and facial acne without enlargement of testi-
2 V% M3 D& U R& h; r3 L9 Ucles, suggests peripheral or pseudopuberty.1-3 We
8 v' T2 N- [, t; Z1 a2 }report a 16-month-old boy who presented with the
# p- r1 {! I, l, fenlargement of the phallus and pubic hair develop-' H6 P6 P: A2 H3 D
ment without testicular enlargement, which was due
! |2 n( L- O8 rto the unintentional exposure to androgen gel used by
5 C; V/ B5 [% H& t& F" E: Fthe father. The family initially concealed this infor-, {- u2 c5 O4 _/ K
mation, resulting in an extensive work-up for this. l: {; g3 G( N+ F. y
child. Given the widespread and easy availability of
/ ?; B/ n) O( f* N/ `testosterone gel and cream, we believe this is proba-
6 Q* b: P) Y% a4 q6 s: Qbly more common than the rare case report in the
' r* z# g% d( g. [! Jliterature.41 Z: a2 I1 }$ ?, ~/ Q$ t
Patient Report
; |+ i# }" |# ~9 X% I+ p- DA 16-month-old white child was referred to the* Y7 z* e A j9 |
endocrine clinic by his pediatrician with the concern% T, H6 T1 q2 M4 m
of early sexual development. His mother noticed8 Z* W+ }8 k, U% ~) s, |. \" v, m
light colored pubic hair development when he was
* {; i+ n8 Z! C& o8 OFrom the 1Division of Pediatric Endocrinology, 2University of" B" r- J2 y% O+ Y2 ]! c% X
South Alabama Medical Center, Mobile, Alabama.5 D: H+ p8 M; |
Address correspondence to: Samar K. Bhowmick, MD, FACE,0 C5 h* k" r. K) M# R6 E8 \
Professor of Pediatrics, University of South Alabama, College of
: Q9 B2 L' R( s" x& _Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
\3 |7 _: ]4 |e-mail: [email protected]." u: F" v0 \+ J% j8 c
about 6 to 7 months old, which progressively became
- X2 V3 K7 _) h$ r& [darker. She was also concerned about the enlarge-- B, W R+ R5 B$ | m% C
ment of his penis and frequent erections. The child" z, V, G) G+ |7 J' ]# {
was the product of a full-term normal delivery, with
' ~6 n5 d; H. i* y$ M# Ba birth weight of 7 lb 14 oz, and birth length of
" a5 W9 s: Z0 q7 [( ~20 inches. He was breast-fed throughout the first year9 J* r0 |1 }" V& ]( ~
of life and was still receiving breast milk along with
! L) ~ L; @7 T9 Y) isolid food. He had no hospitalizations or surgery,
& J. x5 W' p( O9 hand his psychosocial and psychomotor development8 N8 \: w; l% x, C" m
was age appropriate.2 O t8 I, {$ z+ }2 `7 _
The family history was remarkable for the father,1 x/ j2 U( s6 ]. L/ c
who was diagnosed with hypothyroidism at age 16,$ u/ {# Q8 G5 x
which was treated with thyroxine. The father’s- ^ Y! a! [3 l0 r/ c0 K: Z/ l
height was 6 feet, and he went through a somewhat
/ {8 Q* ]1 t! K3 z( {early puberty and had stopped growing by age 14.
; E% F, a2 N, T& E, e& y! eThe father denied taking any other medication. The
3 ]/ \* n/ f& J8 _- S0 ?child’s mother was in good health. Her menarche
! {) Y( J1 V$ D0 ~1 y& ~ B& W8 f0 Vwas at 11 years of age, and her height was at 5 feet1 @- P- o/ `3 p6 W+ M- U/ V' p
5 inches. There was no other family history of pre-
" V. [8 k9 c6 ~% O' p6 zcocious sexual development in the first-degree rela-4 ?6 S1 F1 G' b) S) s8 |
tives. There were no siblings.
4 C. s8 q& {: x+ e; F- M, @Physical Examination/ _6 m, B# w" w, Q
The physical examination revealed a very active,6 T1 z' b: K2 k1 r- s4 M. B
playful, and healthy boy. The vital signs documented
3 t9 ~& T! g( pa blood pressure of 85/50 mm Hg, his length was
8 i8 D' G; Q: P: I. ?( w* _& s& `90 cm (>97th percentile), and his weight was 14.4 kg2 g% H- t, l$ ^3 L
(also >97th percentile). The observed yearly growth9 e3 X/ u: m2 O2 Z+ q; N
velocity was 30 cm (12 inches). The examination of. G& |) d# I6 w
the neck revealed no thyroid enlargement." y( X% [: c- v6 S4 }! R# Y
The genitourinary examination was remarkable for; }- z! P: Y7 S) L8 s4 g
enlargement of the penis, with a stretched length of, m1 @. X6 Z \, ?1 e. k
8 cm and a width of 2 cm. The glans penis was very well
8 k. u: r o4 W; A1 Ndeveloped. The pubic hair was Tanner II, mostly around; A" Y* J8 J: b; \5 y3 j
540' i8 [2 M S m* {( i0 \1 W: ?7 q
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
9 W/ ^8 e7 w/ n5 sthe base of the phallus and was dark and curled. The
( l' y/ J/ ?6 r" R. G ztesticular volume was prepubertal at 2 mL each.
# s+ W. T( p) X1 @6 IThe skin was moist and smooth and somewhat
5 c9 f5 P; ?5 f1 ]# ~( p. qoily. No axillary hair was noted. There were no
/ g* {% J2 i! m3 ?abnormal skin pigmentations or café-au-lait spots.
1 A. {7 o* i4 {* U3 PNeurologic evaluation showed deep tendon reflex 2+/ e2 X4 I f! s* P2 n6 ~6 h
bilateral and symmetrical. There was no suggestion
8 p# _" i( {: {1 X+ ?% U& ^of papilledema.3 W* f7 i" d$ ~4 ]# N
Laboratory Evaluation0 Z8 G Q" o3 P# G
The bone age was consistent with 28 months by
! b0 M; {8 Q' ~9 Kusing the standard of Greulich and Pyle at a chrono-
3 L7 C( o2 ~) rlogic age of 16 months (advanced).5 Chromosomal
; m+ g( j: _" R9 s) x& Lkaryotype was 46XY. The thyroid function test+ @# c8 D1 z7 H) ^, b8 s( B# l: k, ]
showed a free T4 of 1.69 ng/dL, and thyroid stimu-3 {# O% @+ ~0 @$ e9 L. C; H( _
lating hormone level was 1.3 µIU/mL (both normal).8 T8 n# y" e3 U/ ?4 A4 U' i
The concentrations of serum electrolytes, blood
! s; F( c: N- q$ p. x0 V' G& ourea nitrogen, creatinine, and calcium all were
2 U0 d. l3 {1 R1 f5 b5 S9 `within normal range for his age. The concentration, _# A6 h* R. L+ S. d6 q
of serum 17-hydroxyprogesterone was 16 ng/dL7 R3 Y8 G" Y% V" C7 b
(normal, 3 to 90 ng/dL), androstenedione was 20" S5 }, E" }7 p
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-3 @% n0 i. E, O: e8 `0 E" M* H+ h
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
8 B, d7 ]5 p2 ^( Q3 ldesoxycorticosterone was 4.3 ng/dL (normal, 7 to
{( T& E, d M- T5 E+ Z49ng/dL), 11-desoxycortisol (specific compound S)# b: N% M2 L; Z. ]- L
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
3 J2 q$ ?$ O6 Z* l( n' G. r+ Htisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
4 w9 c( K$ i, {( w0 xtestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
+ E7 g2 X6 d% h8 L, I8 v- |and β-human chorionic gonadotropin was less than0 W" N+ Q5 D8 g* [
5 mIU/mL (normal <5 mIU/mL). Serum follicular
& ]0 i( s4 x9 Rstimulating hormone and leuteinizing hormone
3 u+ l4 l4 d( k/ Gconcentrations were less than 0.05 mIU/mL
$ a( K2 I3 E! ]( r) W(prepubertal).
; x/ N9 U4 p, F3 N6 q, I. E6 EThe parents were notified about the laboratory* s0 ?% L* o0 s: F6 @" F) z
results and were informed that all of the tests were
8 O( Z/ Z9 \; E$ E$ {5 }4 {normal except the testosterone level was high. The6 y) t- f+ }' N
follow-up visit was arranged within a few weeks to% v: s% L6 Z) W- J) o) E( s
obtain testicular and abdominal sonograms; how-* c9 F+ m( Y8 I$ p; P% ?, L5 N& M. S3 s
ever, the family did not return for 4 months.
2 x" L. B& J* D( e+ MPhysical examination at this time revealed that the/ s8 _' Q2 [# j0 G2 G
child had grown 2.5 cm in 4 months and had gained
" o( N% d( C1 u! q" h& g# t2 kg of weight. Physical examination remained) h( r' F$ V h. N" T
unchanged. Surprisingly, the pubic hair almost com-; x' Z6 I, L( k
pletely disappeared except for a few vellous hairs at# @) t8 ?: k r* z# H( x7 H3 q
the base of the phallus. Testicular volume was still 26 n/ u; H3 T/ ^, X8 w! i
mL, and the size of the penis remained unchanged.* q$ Z' l5 Y9 A8 k! a5 V( U1 m# m" P
The mother also said that the boy was no longer hav-" d) W) H2 Q4 O2 R6 @1 T6 T
ing frequent erections.7 f& C5 t: }& d, F1 Q8 o
Both parents were again questioned about use of. M7 y$ w/ p# Q+ e- Y1 A
any ointment/creams that they may have applied to
, T6 z# P& f* y$ _: \9 r1 _# wthe child’s skin. This time the father admitted the
u5 y7 H2 M# {2 V* z, NTopical Testosterone Exposure / Bhowmick et al 541
% \, I) s0 }. N3 V. a" G% y! kuse of testosterone gel twice daily that he was apply-
4 i* K$ E' a5 C' o6 D# w+ Q- ging over his own shoulders, chest, and back area for
`' T/ u. ~5 F$ w# B% J. k/ \a year. The father also revealed he was embarrassed
0 D& I4 B) e5 {9 H8 {1 i5 z6 H# Lto disclose that he was using a testosterone gel pre-
3 ?' E- f+ B: ^$ X6 i+ Y+ r! s. V5 tscribed by his family physician for decreased libido% Q2 o5 c8 t! ^8 ~' f. m9 q/ H) t$ }" q
secondary to depression.5 E/ k3 M1 b- M! l# p6 s4 i
The child slept in the same bed with parents.
. S% I3 V( [" Y7 D" K# N( AThe father would hug the baby and hold him on his/ W- f& E8 y; c& T5 p. J$ b: [; i2 R
chest for a considerable period of time, causing sig-& e! a' O2 v3 k" i% }2 P9 z
nificant bare skin contact between baby and father.
$ Y, F- E, r/ H% F3 p, YThe father also admitted that after the phone call,$ w: V3 d& x2 Y. N6 I, \& g' O
when he learned the testosterone level in the baby; U' z' W, | P; w0 z: c! ?
was high, he then read the product information
# K2 V& C7 U3 r" W7 c3 J! o+ opacket and concluded that it was most likely the rea-
$ X6 ?3 _$ y% i5 K# k) u* E2 ?son for the child’s virilization. At that time, they1 x! O) T5 z) e8 j2 C( H
decided to put the baby in a separate bed, and the
0 \& h" G2 \! Z3 e* F7 wfather was not hugging him with bare skin and had+ H7 y5 k! p- U+ j5 g4 h5 R. a6 B+ ^
been using protective clothing. A repeat testosterone
! X, z0 u0 Q" y! k! mtest was ordered, but the family did not go to the
/ Q" \. _/ ?( H: k- Llaboratory to obtain the test.
4 b* O' y+ _0 r# ?, n( ], t/ bDiscussion
! u/ A5 }& B1 \# IPrecocious puberty in boys is defined as secondary
5 X7 d6 r2 V. i" f5 P0 w0 hsexual development before 9 years of age.1,47 t: r5 {+ Q0 T1 E8 r
Precocious puberty is termed as central (true) when
3 d7 q a8 S3 G: Oit is caused by the premature activation of hypo-* m5 O0 \" X* y
thalamic pituitary gonadal axis. CPP is more com-
6 v; h; |1 g; r/ o4 Y% ~$ u" zmon in girls than in boys.1,3 Most boys with CPP& z7 I; D" [# n9 V. k( @# K# t$ J. w
may have a central nervous system lesion that is
7 Z7 d# v# U3 V4 Oresponsible for the early activation of the hypothal-2 P1 i) x# Z# v) v# @! x
amic pituitary gonadal axis.1-3 Thus, greater empha-1 \# n- f) \4 [
sis has been given to neuroradiologic imaging in
$ Y3 T" H% Y0 [! y3 x1 A; w2 iboys with precocious puberty. In addition to viril-
7 s. m) G! n, G2 M5 m& Tization, the clinical hallmark of CPP is the symmet-8 i* ~3 |. u$ n2 i! D; A9 w) p
rical testicular growth secondary to stimulation by
% z" _& R% Q7 h" h2 y$ U* r& |gonadotropins.1,3
* r+ ^% h. ?8 D( z q/ JGonadotropin-independent peripheral preco-
; l& U N* I4 E! o- j( d& I' p% S" Lcious puberty in boys also results from inappropriate
$ {# B% m9 p! u; d; H) j$ ^androgenic stimulation from either endogenous or" }! w( H: f/ x8 c; ~- @
exogenous sources, nonpituitary gonadotropin stim-+ M8 G) a" Z! A1 ?7 c7 W L; I( i
ulation, and rare activating mutations.3 Virilizing" y5 F' S8 O8 c1 d' b: P3 G
congenital adrenal hyperplasia producing excessive
. o0 e$ V$ L! ~2 o7 L! Q9 n2 }adrenal androgens is a common cause of precocious* x2 _7 a' ^& B( K4 M
puberty in boys.3,4
- A4 d0 I( R7 y! hThe most common form of congenital adrenal
# D8 m/ |% n+ p2 dhyperplasia is the 21-hydroxylase enzyme deficiency.
. q8 B% P$ B7 V5 ^The 11-β hydroxylase deficiency may also result in
* ^. n$ E& i) m' O# F/ N5 `( b) g: oexcessive adrenal androgen production, and rarely,
0 F0 u R. r; han adrenal tumor may also cause adrenal androgen
' V6 A1 n% n5 F7 L0 u; hexcess.1,3
0 [( ]: ^5 ?7 k% \at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
, j' ]( @: F) F2 }' l( p% _/ a542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
% x- ^5 I# ]" [; @5 @9 OA unique entity of male-limited gonadotropin-
2 @) }% [$ E% ~& S8 O! xindependent precocious puberty, which is also known
' t f# S* Z$ _as testotoxicosis, may cause precocious puberty at a$ t+ p+ u: F& G7 y- p0 M+ ]# q* q
very young age. The physical findings in these boys
2 ?' T! b* P( R n+ F6 H- M, ]with this disorder are full pubertal development,& J! ]/ O7 }9 L9 K# I
including bilateral testicular growth, similar to boys. U& Z( A7 p( G
with CPP. The gonadotropin levels in this disorder
3 A8 O6 P8 x( D! T8 Z! yare suppressed to prepubertal levels and do not show
2 M8 @( [8 r5 N, S$ Lpubertal response of gonadotropin after gonadotropin-9 T' ~+ s2 s; K6 l1 O* n! r( A9 A; d" F$ b
releasing hormone stimulation. This is a sex-linked5 Z) c; S" D' Z' F S
autosomal dominant disorder that affects only
3 h0 Q% O9 p+ l/ u$ ?2 D% u* ^males; therefore, other male members of the family: c; h C) y0 Z3 K' Z
may have similar precocious puberty.3
4 g ]4 F; Q, [0 A& t/ s# _In our patient, physical examination was incon-* T; E- @3 y- h7 H- U) t y
sistent with true precocious puberty since his testi-
3 f- E" ^# S, G; Rcles were prepubertal in size. However, testotoxicosis
0 a1 H4 i' u/ }3 jwas in the differential diagnosis because his father
2 n5 k+ U. h, j- a% a, g, k( Vstarted puberty somewhat early, and occasionally,/ D, E2 j4 g# P
testicular enlargement is not that evident in the
. E4 Y# d h$ o5 [3 [beginning of this process.1 In the absence of a neg-5 X. X( S* y- T7 N0 a$ u) u
ative initial history of androgen exposure, our; C. ?# R6 Z G. r
biggest concern was virilizing adrenal hyperplasia,
" R9 _, V! j/ K6 r# leither 21-hydroxylase deficiency or 11-β hydroxylase. Y3 {& s* p5 w+ ?+ N2 r" y2 Z3 [
deficiency. Those diagnoses were excluded by find-9 _: T( N. T- @: _" {
ing the normal level of adrenal steroids.( W) m9 c2 z8 O) ~ U
The diagnosis of exogenous androgens was strongly
' v) {, b' u; ~- R. p5 l) r+ tsuspected in a follow-up visit after 4 months because
& C/ \$ ]" P1 m( g) H; h* X# athe physical examination revealed the complete disap-
5 K/ Y, M7 A/ a- v2 r& G0 Gpearance of pubic hair, normal growth velocity, and3 m" i( M( I' v- { A% @' D% f
decreased erections. The father admitted using a testos-0 e E u' ^# j4 \
terone gel, which he concealed at first visit. He was
: o- Y9 D4 V6 l3 G3 g, g0 J0 }using it rather frequently, twice a day. The Physicians’
4 F& W3 k2 j" w7 g9 RDesk Reference, or package insert of this product, gel or# r! ~; R( d4 z4 }# s7 C
cream, cautions about dermal testosterone transfer to
! R$ ?& a: v! y1 ?5 zunprotected females through direct skin exposure.. N6 r9 ^+ S) O. V' ~
Serum testosterone level was found to be 2 times the# |& `0 E5 I% { y2 g
baseline value in those females who were exposed to
; [4 l1 Q; c p9 a. c( z, \# |even 15 minutes of direct skin contact with their male
G3 `; Z; I$ s- I& M, Q, M+ Cpartners.6 However, when a shirt covered the applica-! c" y. A) U! U0 z/ U1 R* `
tion site, this testosterone transfer was prevented.
4 S, V8 m8 _" tOur patient’s testosterone level was 60 ng/mL,$ I4 v# l7 b8 [' N* n
which was clearly high. Some studies suggest that8 `% @1 K- [" x) L9 Q" g( n$ F
dermal conversion of testosterone to dihydrotestos-" n$ K, O' k$ ?9 Y; G" L0 S
terone, which is a more potent metabolite, is more/ A# P) ?+ A" I$ }: a0 r" {" Z& B% s
active in young children exposed to testosterone2 Z6 R3 c/ @* R! R" e
exogenously7; however, we did not measure a dihy-
1 e8 o: [- Q* g+ y3 Y; g) ]drotestosterone level in our patient. In addition to
3 ]1 P( u. J: v$ m# d' kvirilization, exposure to exogenous testosterone in
+ B* Y9 T5 P: I. u1 Y2 H Ochildren results in an increase in growth velocity and9 a- `. @) K8 ]9 R+ B0 X& z
advanced bone age, as seen in our patient./ N; K( x! H9 F6 n: p
The long-term effect of androgen exposure during
* h m4 }/ U' F% mearly childhood on pubertal development and final2 U; w" a+ x; B0 [! W, W9 `' v7 x
adult height are not fully known and always remain% T* u( n, P% M
a concern. Children treated with short-term testos-/ M2 r/ I, n# p. p
terone injection or topical androgen may exhibit some
& P/ X5 |& L+ ?acceleration of the skeletal maturation; however, after$ K, ^' u' Y! W* B4 B
cessation of treatment, the rate of bone maturation
4 A) B4 j, g6 q% z5 \1 qdecelerates and gradually returns to normal.8,9. s* `* O. X3 U5 Q
There are conflicting reports and controversy0 z: w% E3 Z* G% N9 A% j3 }
over the effect of early androgen exposure on adult- }. I$ x# a7 _1 r. ^3 K
penile length.10,11 Some reports suggest subnormal# B! g( K& g" f: t8 {& ~. ~
adult penile length, apparently because of downreg-$ w/ G; g- y/ N
ulation of androgen receptor number.10,12 However,
3 t" X3 D- C9 E5 {9 CSutherland et al13 did not find a correlation between
5 S. @+ P+ R: F# p; C; Kchildhood testosterone exposure and reduced adult
, u$ C7 F6 a+ j+ w) vpenile length in clinical studies.
- a% a n! v/ Y) d$ O9 vNonetheless, we do not believe our patient is
/ v9 F& T4 K4 ]: \8 V( Ggoing to experience any of the untoward effects from* G8 A& E# t9 D. a ~1 H
testosterone exposure as mentioned earlier because
5 u3 ]3 \0 D2 Dthe exposure was not for a prolonged period of time.) s: }0 X& ~3 h( G5 \7 C2 ^3 k& B
Although the bone age was advanced at the time of$ ?: Y0 V/ n, J4 q6 b* l
diagnosis, the child had a normal growth velocity at1 S+ v2 X" i5 q0 M
the follow-up visit. It is hoped that his final adult
- X4 l4 f+ a' G! sheight will not be affected.
# s7 ]; [" h. x0 f, ]: nAlthough rarely reported, the widespread avail-
/ |+ X3 d2 }& ?5 K- P/ g6 q. h6 tability of androgen products in our society may9 D# V$ J; W$ S' x/ q
indeed cause more virilization in male or female
: `8 d; Z2 o0 @children than one would realize. Exposure to andro-7 D* k; @! q% f t! @. i0 K' H
gen products must be considered and specific ques-8 E* A3 \3 l' F# t+ _6 F
tioning about the use of a testosterone product or. M* v& a& O+ C9 k2 V% J y& B* \
gel should be asked of the family members during; [3 w% x( f$ F! F0 \3 H2 Z- R8 Q) ~
the evaluation of any children who present with vir-
/ N" F4 m/ e5 C$ `ilization or peripheral precocious puberty. The diag-
4 ?2 I" l* u0 R) U4 O# o& dnosis can be established by just a few tests and by( ?4 z% S8 ^1 }0 I
appropriate history. The inability to obtain such a
+ z |7 p6 k! _# P7 ]6 `history, or failure to ask the specific questions, may0 e) s' _8 h$ P a
result in extensive, unnecessary, and expensive7 j$ d0 `' _5 B
investigation. The primary care physician should be5 u, ^1 q1 a9 A, s. Z1 k* t
aware of this fact, because most of these children
3 V! y" n& L/ qmay initially present in their practice. The Physicians’4 V9 d+ W( Q1 ~& _/ c
Desk Reference and package insert should also put a
( \: K4 x2 \/ u( |! j7 ]! dwarning about the virilizing effect on a male or
1 o6 I; D. t" T: A7 v. q2 Tfemale child who might come in contact with some-4 p% N4 e( V5 w6 z6 @9 L: |
one using any of these products., e7 g3 Y4 [" [2 k; d
References9 D& L2 d- O4 `8 ?: r6 V( r
1. Styne DM. The testes: disorder of sexual differentiation2 [- n& E" N# S% ?) j
and puberty in the male. In: Sperling MA, ed. Pediatric
# z3 D# o% { E" {Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
! O2 B1 V5 w* l. w0 b, e" a2002: 565-628.
; Z5 R, l3 g: r) [2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
4 z3 R2 y+ R q. N/ ~5 @puberty in children with tumours of the suprasellar pineal |
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