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Sexual Precocity in a 16-Month-Old
9 D4 C; M+ H. _7 |+ P( { sBoy Induced by Indirect Topical
" ]6 s# j- o5 A% F: JExposure to Testosterone5 p. y6 g, ^; r( }; G
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,26 p" S z5 D4 O2 E0 p$ o' ^( w
and Kenneth R. Rettig, MD1
2 j/ b& n0 @& W" b0 |2 nClinical Pediatrics: g8 `) Y$ S2 K+ g& r) w/ L
Volume 46 Number 6
" g3 B ` f0 sJuly 2007 540-543+ v4 ]; s& ?5 E) y* D7 @3 @
© 2007 Sage Publications
, z7 N+ o# ]; G0 r1 a! ?10.1177/00099228062966519 G; j2 [. T" U; `7 S
http://clp.sagepub.com* n, S! }! @% P+ E# d6 i
hosted at
5 A1 U& @# O* b7 Z5 jhttp://online.sagepub.com
, @/ M) i( W, X1 |2 ?) gPrecocious puberty in boys, central or peripheral, P2 K9 H' j: p) P! P7 h
is a significant concern for physicians. Central( U+ r+ G1 b4 r* }- c
precocious puberty (CPP), which is mediated
9 P$ A' G* K0 U# ythrough the hypothalamic pituitary gonadal axis, has
x, u& U! A% B! o& w; ]" N" [7 |a higher incidence of organic central nervous system; [7 g' I3 M7 z# h
lesions in boys.1,2 Virilization in boys, as manifested
, A% Y0 T8 n0 B9 A) r, wby enlargement of the penis, development of pubic
& N0 _1 I1 Q$ y7 d: Whair, and facial acne without enlargement of testi-; `) {& G" C W% y, y; m
cles, suggests peripheral or pseudopuberty.1-3 We
0 g2 @$ o1 N! K5 u8 f8 C+ ^report a 16-month-old boy who presented with the
: Y# ^3 `; Z" c0 k, R% X3 Z9 [9 E9 C1 Denlargement of the phallus and pubic hair develop-
2 }. \2 }4 o t2 L2 ^ment without testicular enlargement, which was due
% e1 L: _9 i2 ?. t% k+ {7 _2 oto the unintentional exposure to androgen gel used by
0 k) Y! {" Y( @+ T/ mthe father. The family initially concealed this infor-, L8 t. X+ T) h5 U2 X4 E; y
mation, resulting in an extensive work-up for this+ h5 {6 o8 y9 W! U, ~) Y
child. Given the widespread and easy availability of
' p0 g2 `% D; _, s/ ztestosterone gel and cream, we believe this is proba-
4 B8 F Y3 @# [' Y- wbly more common than the rare case report in the. c7 D5 i* H; |( g7 z
literature.46 A3 u$ B# f. O6 i/ _) o x% i
Patient Report) S9 Y6 t' c" @" W8 I ~
A 16-month-old white child was referred to the
2 q) c- j$ O, P3 b( rendocrine clinic by his pediatrician with the concern" F- W8 A- W7 t6 x$ k
of early sexual development. His mother noticed
! c" x" Y! n2 n5 \: ?light colored pubic hair development when he was& \ o: M6 Z2 j" w' P1 @+ a& x
From the 1Division of Pediatric Endocrinology, 2University of
* H$ J3 a$ J0 VSouth Alabama Medical Center, Mobile, Alabama.$ k; s; J: K; J/ e9 ^; ]
Address correspondence to: Samar K. Bhowmick, MD, FACE,3 @& p$ p% R8 l) v- O% y9 \: I
Professor of Pediatrics, University of South Alabama, College of
, }& h' l3 n0 b; ]! t8 {Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
' V. y) c2 v$ I% t6 `e-mail: [email protected].
7 q2 @" x4 V7 V* B5 pabout 6 to 7 months old, which progressively became
: @9 E; V3 ~, h. s& b1 A* ]8 p( ^darker. She was also concerned about the enlarge-2 ]1 @& S# l6 j) l0 T/ Y
ment of his penis and frequent erections. The child% q' k# \3 v/ U# H3 g
was the product of a full-term normal delivery, with
: ^: Y* Y' B" \0 I( Sa birth weight of 7 lb 14 oz, and birth length of
1 |4 O4 O2 j; E; y7 X& |( s20 inches. He was breast-fed throughout the first year
! y+ n" X) l; v" W b1 ]* w- e7 ~of life and was still receiving breast milk along with. g- X4 a5 p6 N2 J4 F2 V1 s
solid food. He had no hospitalizations or surgery,/ a) U: Y y% S) {/ r8 w" V) p
and his psychosocial and psychomotor development
, r4 @& V) i% hwas age appropriate.
1 I( v" D! }/ n% i9 E& W7 ]# q" \The family history was remarkable for the father,
+ V6 i5 ]6 y% G1 Vwho was diagnosed with hypothyroidism at age 16,, g: Z7 p- \$ h+ z
which was treated with thyroxine. The father’s% }2 F m" n% C: g2 m4 X* }
height was 6 feet, and he went through a somewhat! F3 \9 [0 M& H$ o
early puberty and had stopped growing by age 14.
5 j7 {- q/ k" |( _1 lThe father denied taking any other medication. The/ J) [, U! `+ H5 j3 g1 l# q
child’s mother was in good health. Her menarche) v# N0 n% I. G5 N/ E
was at 11 years of age, and her height was at 5 feet8 {+ }9 i: D; |% x/ v/ z2 b
5 inches. There was no other family history of pre-+ S3 a; d8 Y& z2 n4 j5 y8 g& ]2 f
cocious sexual development in the first-degree rela-
: V4 J$ w# O ^ y% v0 Jtives. There were no siblings.
3 ]7 P" ^* a: k' iPhysical Examination
( X; i& c8 Z$ b- t6 o5 A1 t7 D$ cThe physical examination revealed a very active,3 d- X4 J9 C d) F: P( v
playful, and healthy boy. The vital signs documented& g. W4 J: [2 Q' p; y
a blood pressure of 85/50 mm Hg, his length was
4 O! L9 ` i+ U3 V! L2 u3 M90 cm (>97th percentile), and his weight was 14.4 kg v' K" T3 ~9 E; X8 T; @* D! r4 ^
(also >97th percentile). The observed yearly growth+ q0 @6 B, C* t; S7 w" o" q
velocity was 30 cm (12 inches). The examination of( p1 I* H, z! a6 H1 e
the neck revealed no thyroid enlargement." l1 t9 J3 x9 M
The genitourinary examination was remarkable for
8 c, G% ^. |$ y! Q, ?& {2 q/ lenlargement of the penis, with a stretched length of
2 @: C K' v9 T) B8 _6 C/ h8 cm and a width of 2 cm. The glans penis was very well" T6 s0 A& J0 P/ G
developed. The pubic hair was Tanner II, mostly around
/ @& h# r, t) _" C- s. i3 q' z540
. @8 A' S" _! B4 d% K) {at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from) y% B8 V9 z( b* x8 x" h2 H. P
the base of the phallus and was dark and curled. The
$ C8 }) `! l V2 T2 ]& K- y7 [testicular volume was prepubertal at 2 mL each.
% G; L7 W, ~& {1 c' G: \The skin was moist and smooth and somewhat
# w/ e F3 [. joily. No axillary hair was noted. There were no5 q* N! N1 H5 \0 ~7 v
abnormal skin pigmentations or café-au-lait spots.
7 W, l8 C( R6 i& D. p; fNeurologic evaluation showed deep tendon reflex 2+7 X3 t+ B" t7 N b, A* O4 T$ C
bilateral and symmetrical. There was no suggestion
5 F- F3 c/ ~1 r, j6 nof papilledema.9 d% u. h! W) x% c
Laboratory Evaluation3 k G% ^ A8 f4 D' r1 u9 L5 O
The bone age was consistent with 28 months by2 W' ?/ c$ r5 _" o
using the standard of Greulich and Pyle at a chrono-; Q8 I' X- l, W0 h7 {) y
logic age of 16 months (advanced).5 Chromosomal
4 J- b/ |+ _ r2 }) zkaryotype was 46XY. The thyroid function test0 c! H4 v7 ~' L, ~. _; X8 k
showed a free T4 of 1.69 ng/dL, and thyroid stimu-- I( @+ i; l e- O6 N. \5 U( B
lating hormone level was 1.3 µIU/mL (both normal).
' T: ?0 Z2 }7 g- N4 l4 z) h, DThe concentrations of serum electrolytes, blood- C! r) Y6 T! a5 S0 j. N* c* o
urea nitrogen, creatinine, and calcium all were8 l% z* ]( [9 J, ?6 j/ s% o( w$ M: X- r
within normal range for his age. The concentration
4 p0 o2 R& M8 { Sof serum 17-hydroxyprogesterone was 16 ng/dL
$ x7 \/ F$ W. T5 I' \/ }/ g' r8 \- z(normal, 3 to 90 ng/dL), androstenedione was 20# ?4 H/ v0 `1 l! f6 A' @
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
- ~$ f. B1 c" Uterone was 38 ng/dL (normal, 50 to 760 ng/dL),
" t4 e) b# w- K! u; Zdesoxycorticosterone was 4.3 ng/dL (normal, 7 to( e0 u }% ?' h0 {
49ng/dL), 11-desoxycortisol (specific compound S)( A# U- B" K# C) h: @
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
' G1 U! P# y9 `/ G8 y: Dtisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
`' w: Y& S) i, b( atestosterone was 60 ng/dL (normal <3 to 10 ng/dL), ^9 B7 a2 B' ~6 D% A2 \4 s
and β-human chorionic gonadotropin was less than; z$ C' r+ B( Y5 m/ A
5 mIU/mL (normal <5 mIU/mL). Serum follicular. l% o3 F! ]$ b. i4 k! ]
stimulating hormone and leuteinizing hormone
; f0 a! H. n7 \% m2 aconcentrations were less than 0.05 mIU/mL: U1 E Y. E' @1 Z1 x r- g
(prepubertal).
4 ?( W) n- G* }, }7 A" \3 e kThe parents were notified about the laboratory
, r- |) k* p# e- T- r! {) n8 Qresults and were informed that all of the tests were; }1 j9 Q3 F: h
normal except the testosterone level was high. The4 O; g2 j7 M5 w
follow-up visit was arranged within a few weeks to3 R2 Q6 U& y9 ` K" l' H
obtain testicular and abdominal sonograms; how-
: m0 S. p$ i1 d% f9 @' zever, the family did not return for 4 months.
j" ~6 n" x; R. R9 DPhysical examination at this time revealed that the
# t9 z6 g( j/ L/ p' B$ mchild had grown 2.5 cm in 4 months and had gained4 B) {6 C$ b# D# c
2 kg of weight. Physical examination remained
4 p( o9 ]3 R0 M4 {& b( ^unchanged. Surprisingly, the pubic hair almost com-" f+ a2 S e9 i6 U7 _6 D
pletely disappeared except for a few vellous hairs at* @+ }1 V# B: f2 e/ m
the base of the phallus. Testicular volume was still 2/ Y8 M) ]$ m+ Z! m
mL, and the size of the penis remained unchanged.
4 \7 K) |* G6 [+ U/ GThe mother also said that the boy was no longer hav- H: S6 d9 Q% A* F s6 c
ing frequent erections.. ^# R$ D) }3 B7 `& o
Both parents were again questioned about use of9 o& Y/ y* f( ^+ n
any ointment/creams that they may have applied to
2 j4 j, k% d0 q \( dthe child’s skin. This time the father admitted the
2 y0 ]7 u0 J* @/ F0 ZTopical Testosterone Exposure / Bhowmick et al 541
; L. U9 m& s3 b; s7 h. \use of testosterone gel twice daily that he was apply-6 O! I1 t" r1 ? V+ U8 C/ f
ing over his own shoulders, chest, and back area for
* q, j: G$ Q0 d& g* l* p! \* Wa year. The father also revealed he was embarrassed
2 C7 ?0 e+ Y- A8 Q7 m4 Fto disclose that he was using a testosterone gel pre-
. R, d* `: U, @% Ascribed by his family physician for decreased libido
6 d. x+ j& v% L+ T4 isecondary to depression.
3 l, v$ T5 i$ R, `) A6 p/ \8 aThe child slept in the same bed with parents.; q% H5 u0 m7 _/ V
The father would hug the baby and hold him on his
0 w. _$ N% V! H1 {8 lchest for a considerable period of time, causing sig-/ N. _" ^2 p$ G6 ` D; d' Y
nificant bare skin contact between baby and father.& c- U7 H0 ]) k( e* t9 ~; H; N3 V
The father also admitted that after the phone call," y; D4 [7 c( f% ?/ f+ @- n
when he learned the testosterone level in the baby5 _: ?( d7 R4 r9 B/ y g3 U6 a1 ?. }
was high, he then read the product information
/ J6 q4 z' }, [: p( xpacket and concluded that it was most likely the rea-$ ]$ w; ^6 H7 z$ y3 m9 K
son for the child’s virilization. At that time, they i! q* k; q* b
decided to put the baby in a separate bed, and the! x2 h3 `) U# H- r* [
father was not hugging him with bare skin and had3 [" z7 [4 |1 o: X* e; H$ i
been using protective clothing. A repeat testosterone& Q# Q. c8 D: N2 O7 C/ `3 ]
test was ordered, but the family did not go to the
" N- W9 n, ?* v. q7 v: _2 Blaboratory to obtain the test." \/ Z4 j8 J/ m
Discussion
( G _# e" E/ [$ G9 uPrecocious puberty in boys is defined as secondary
; n w/ e2 y7 |$ Nsexual development before 9 years of age.1,4% T" q; c& q$ i) V! \& i8 y, Z, ]
Precocious puberty is termed as central (true) when" z( p: a8 m9 s6 `! x1 c
it is caused by the premature activation of hypo-$ d) j9 K2 I. K! p6 Y; B& Y: w( c
thalamic pituitary gonadal axis. CPP is more com-
& R4 q& t, V+ _+ Nmon in girls than in boys.1,3 Most boys with CPP6 {8 c$ |5 d& k: e
may have a central nervous system lesion that is
4 P- a9 h" g. o( v1 I5 H1 Tresponsible for the early activation of the hypothal-
0 \0 J1 J! l9 }. b. P2 ~amic pituitary gonadal axis.1-3 Thus, greater empha-5 [4 O/ w4 ^9 H
sis has been given to neuroradiologic imaging in
! z* E+ L6 Y: u1 d# Q' W: _boys with precocious puberty. In addition to viril-
+ [( V& `3 u9 e7 G M) N" q. bization, the clinical hallmark of CPP is the symmet-9 D3 v- h- F( a7 }
rical testicular growth secondary to stimulation by! B5 C9 {2 V S7 d
gonadotropins.1,34 Q4 m- J* N! R+ E# y5 s
Gonadotropin-independent peripheral preco-
- L: F# J4 E1 I( o. x1 Icious puberty in boys also results from inappropriate3 {7 G5 k( {6 G$ r2 K) ~/ [& ~
androgenic stimulation from either endogenous or
8 J' f$ w* e" A# F; c' m0 ~exogenous sources, nonpituitary gonadotropin stim-
5 b, N- D' g8 H/ ^3 }2 Iulation, and rare activating mutations.3 Virilizing$ O3 d; _$ D$ B" p' `0 x4 P
congenital adrenal hyperplasia producing excessive: I, Z: d$ `" Z; h; s3 O5 t
adrenal androgens is a common cause of precocious4 N; u) f- m, u/ l
puberty in boys.3,4; c! H* o$ X1 E9 ?$ e( y6 E
The most common form of congenital adrenal
# `3 o, v8 p+ lhyperplasia is the 21-hydroxylase enzyme deficiency.. x/ u/ s% U; L* [; Y; `. o( k
The 11-β hydroxylase deficiency may also result in# [7 k5 ]( R5 M. w1 M
excessive adrenal androgen production, and rarely,
- O' q; w& Y& M$ T3 @+ _! y. yan adrenal tumor may also cause adrenal androgen
4 M' e" U0 ]; D4 Jexcess.1,3. s6 Y! o3 _" T& D% k p. R9 Z
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from& ]" U4 j4 f. P) K& k- c
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
5 x, j0 m! P# D* x5 T& M ZA unique entity of male-limited gonadotropin-
7 U3 f8 i7 ~4 L+ d( m: a6 E1 q# F2 tindependent precocious puberty, which is also known. D8 F8 } Y3 F8 r+ }5 t, x- U6 W, i: s
as testotoxicosis, may cause precocious puberty at a2 o2 R; W. ^- g5 _3 ?
very young age. The physical findings in these boys
4 s/ X/ A6 S' }with this disorder are full pubertal development,
) P9 w) n0 H$ Z" ?* iincluding bilateral testicular growth, similar to boys
1 j7 u+ q8 L/ M& Gwith CPP. The gonadotropin levels in this disorder
9 f1 R2 e9 c8 D) H) nare suppressed to prepubertal levels and do not show
0 x) k z; a3 V+ P, Tpubertal response of gonadotropin after gonadotropin-: z1 ~ P2 ]7 q2 d4 Z
releasing hormone stimulation. This is a sex-linked$ f) S- Z& N- b
autosomal dominant disorder that affects only) g- G; C; o& i' S3 m" V! j* z- D
males; therefore, other male members of the family) x; Y7 [. {/ h# B) N
may have similar precocious puberty.3
4 z0 l" {* d# L2 Y5 s2 DIn our patient, physical examination was incon-& Y# e. p: W4 e* o4 f
sistent with true precocious puberty since his testi-) U# Z$ ]5 h. P6 e
cles were prepubertal in size. However, testotoxicosis
3 t" `6 \( H/ I6 C& ]: Vwas in the differential diagnosis because his father% x2 U+ `: r2 O N: f$ h
started puberty somewhat early, and occasionally,3 A' C: X( ?: ?1 u1 A! U* I( t
testicular enlargement is not that evident in the
4 {9 d, @' Y& O1 t: Qbeginning of this process.1 In the absence of a neg-6 _* G6 e& F+ j: n* |+ m( e& N
ative initial history of androgen exposure, our4 O; W+ T8 y3 L' p& r
biggest concern was virilizing adrenal hyperplasia,
, |: e# j, u" ?7 O9 q' keither 21-hydroxylase deficiency or 11-β hydroxylase% a" b* q4 \# s" j$ d0 F E" ^; A1 x
deficiency. Those diagnoses were excluded by find-: \8 l; I2 I( U! @' v+ q2 E% c
ing the normal level of adrenal steroids.
& b5 p K" D3 D. JThe diagnosis of exogenous androgens was strongly
k! @* f8 Z8 k* W* esuspected in a follow-up visit after 4 months because3 b. C% m% J+ s3 x& t; u; B
the physical examination revealed the complete disap-
( U' t) S; M7 N! rpearance of pubic hair, normal growth velocity, and/ p+ f5 ?, ` ?& l# C
decreased erections. The father admitted using a testos-$ i' `, ?- s2 b0 u
terone gel, which he concealed at first visit. He was
) [9 E; Z. S. L. n6 X# ]& Musing it rather frequently, twice a day. The Physicians’
% ^" l/ _: S& m- ?2 z/ C, oDesk Reference, or package insert of this product, gel or# |7 k q, B! o0 ?- a* ~* p5 \
cream, cautions about dermal testosterone transfer to" B8 r7 }$ P4 w; {
unprotected females through direct skin exposure.
* n! d0 u$ x6 I6 D8 V1 P s" l' z* V! WSerum testosterone level was found to be 2 times the
! S5 U' r8 w' D& K1 a) `6 ^baseline value in those females who were exposed to3 X% R; }; R* `! r+ x/ C% y
even 15 minutes of direct skin contact with their male" f) ~% A+ ~' Z E8 }! h
partners.6 However, when a shirt covered the applica-* A7 X% J1 M# t- v
tion site, this testosterone transfer was prevented.* C* A$ \1 Z. U/ f: M5 I- M0 w. Q
Our patient’s testosterone level was 60 ng/mL,
- n/ k, u7 i3 {6 }* j" dwhich was clearly high. Some studies suggest that+ n+ m+ v5 f% w& ^) ^/ @! [5 e
dermal conversion of testosterone to dihydrotestos-+ n. r2 t4 @/ Y6 P' K
terone, which is a more potent metabolite, is more
+ n, i4 X8 g) o( T- B9 E8 yactive in young children exposed to testosterone, a8 S O1 c1 v y( D7 Z" Z! [
exogenously7; however, we did not measure a dihy-
% `) }' X8 x. C1 }1 Wdrotestosterone level in our patient. In addition to! V/ j3 O# S7 _0 i, B5 z+ i
virilization, exposure to exogenous testosterone in' B5 r/ m5 L- g* |) I) y; ?
children results in an increase in growth velocity and
8 }4 B6 M% E7 X& Tadvanced bone age, as seen in our patient.
% Y" B. S* w2 V& e' j. t% C& @1 SThe long-term effect of androgen exposure during( t8 q) O/ d" B1 u: a
early childhood on pubertal development and final
8 Z% x3 w! _, D. p) R9 ?* Cadult height are not fully known and always remain
2 k9 x" N& l y4 Ba concern. Children treated with short-term testos-+ K( m4 C0 z! ~6 e1 i/ O$ \2 `, Y
terone injection or topical androgen may exhibit some& f# _7 N' c# Y' s+ o
acceleration of the skeletal maturation; however, after' B" ~* H; S' P. o7 P! `$ B, W
cessation of treatment, the rate of bone maturation
! t8 }+ V, P- y! bdecelerates and gradually returns to normal.8,9
X1 G$ y2 Z- B: z7 A& h0 |There are conflicting reports and controversy
~0 A, I* Z' Lover the effect of early androgen exposure on adult
& B3 d0 b5 R. [: I; Epenile length.10,11 Some reports suggest subnormal- W. I8 I; k8 ]
adult penile length, apparently because of downreg-6 U& C! a W! Z0 r& Y S$ g
ulation of androgen receptor number.10,12 However,0 d0 A6 |3 J' K- O; ?
Sutherland et al13 did not find a correlation between
' D0 m& i Z1 Tchildhood testosterone exposure and reduced adult
$ e+ d) z7 ]7 `) p$ w* m! s4 kpenile length in clinical studies.
5 U" c0 `2 I/ Z9 u# _Nonetheless, we do not believe our patient is( H& i0 k! y. H3 y" p
going to experience any of the untoward effects from
6 R+ c) _: V2 ]5 X- g1 z9 htestosterone exposure as mentioned earlier because/ V: @, l. B* t7 `
the exposure was not for a prolonged period of time.2 i* n5 @6 i `& ]2 Q. I
Although the bone age was advanced at the time of2 A& [. v' d% ~6 H4 E2 Q" {
diagnosis, the child had a normal growth velocity at. ^) h- s+ ]. X) [# M
the follow-up visit. It is hoped that his final adult
" m7 R. x4 ?) R, ~$ v) hheight will not be affected.
8 r' ^# I- m. O2 J, D! LAlthough rarely reported, the widespread avail-
3 X2 |, d& `" l3 V: eability of androgen products in our society may0 s% U+ w h" }3 Q8 t9 R1 Y; t/ E
indeed cause more virilization in male or female+ a- g! [ s; L) i' o; Y2 {1 ?, G
children than one would realize. Exposure to andro-6 W4 z& E8 w) ?& s: \" d1 h
gen products must be considered and specific ques-6 S! U0 J% t+ N: n/ h. X! z
tioning about the use of a testosterone product or
# m- h! e( C' g' i6 R' Q( B# ggel should be asked of the family members during
$ c5 E* R' a9 |' Othe evaluation of any children who present with vir-
6 `/ P+ I, u" Q4 L2 P% yilization or peripheral precocious puberty. The diag-
$ y# J0 T. M! q, M5 }2 Jnosis can be established by just a few tests and by
$ C+ ]# y5 z. t6 ] M5 Iappropriate history. The inability to obtain such a
! W2 }0 ~: ?/ j+ Phistory, or failure to ask the specific questions, may
$ n* _! D: X, i8 tresult in extensive, unnecessary, and expensive
- n+ y E+ n& x1 Iinvestigation. The primary care physician should be
& n" q C. E2 \$ P% Z) c8 baware of this fact, because most of these children/ ]: N0 ?! @( B9 j( e
may initially present in their practice. The Physicians’/ Z# M y% q% ~- d/ j0 Y: _
Desk Reference and package insert should also put a/ S5 G% U" [, ]8 S$ V
warning about the virilizing effect on a male or
- G+ s& a- l5 z1 {3 |) \2 wfemale child who might come in contact with some-8 P* [& l8 Q: w% c. e
one using any of these products." _+ C" L A$ `3 n- G
References8 ^1 q& ?7 y) k }, M+ s# C& m" H0 v
1. Styne DM. The testes: disorder of sexual differentiation
0 q r& Z+ C8 C! \and puberty in the male. In: Sperling MA, ed. Pediatric7 K$ s; r8 d5 h& F# i& G! u8 }
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
: L7 g) G, O" e0 e0 j2002: 565-628.8 Q! R* B3 R6 H" j* k# v
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
- P" c$ r+ e G- i' }puberty in children with tumours of the suprasellar pineal |
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