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Sexual Precocity in a 16-Month-Old; u2 G1 ?( E# w+ c
Boy Induced by Indirect Topical: y- D% G& ? P' @) x4 v- h
Exposure to Testosterone2 M9 p3 y9 n& j' S: c
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2# Z0 Y3 z' q" \2 P) P0 } X: S0 f
and Kenneth R. Rettig, MD1
! v# V2 S; `2 T/ R9 r5 {! HClinical Pediatrics3 `' N9 v1 K5 I) l; E+ s
Volume 46 Number 6: u& R: X. \+ e; m6 s
July 2007 540-543- a1 e0 q1 J6 M) Y7 t% { C; A
© 2007 Sage Publications
) B- A" a6 `# \6 }3 h5 P10.1177/0009922806296651
6 z/ c0 j' r" S9 A, @http://clp.sagepub.com
' q3 r7 O9 o; D6 I% Q3 jhosted at' |5 }% ?7 s5 }# b$ \- w6 q
http://online.sagepub.com
& D8 A' S; b9 jPrecocious puberty in boys, central or peripheral,
5 }/ u, T5 A: [* Qis a significant concern for physicians. Central
5 k+ n5 | N( b4 _) b" pprecocious puberty (CPP), which is mediated# r& F6 h, L, H% D+ J* |- J
through the hypothalamic pituitary gonadal axis, has
; [6 s7 H6 p$ H% A5 X9 Q& M, I; | ]: Pa higher incidence of organic central nervous system
0 a" `2 p( u ~8 T% c6 ?lesions in boys.1,2 Virilization in boys, as manifested/ p* Q% _9 Z0 A; t0 z/ ^6 j
by enlargement of the penis, development of pubic, I+ q- Z/ I: N, b3 x0 a( J
hair, and facial acne without enlargement of testi-
9 A/ M. e! X) m. D5 j8 zcles, suggests peripheral or pseudopuberty.1-3 We: y% j4 Y# h) D
report a 16-month-old boy who presented with the0 L* E' `- K5 d% H3 ^
enlargement of the phallus and pubic hair develop-
: ~# m7 P7 s$ E8 w& p4 R6 C4 Mment without testicular enlargement, which was due
) Q; R3 ^$ Y h, ~to the unintentional exposure to androgen gel used by
4 t1 o. X% R1 cthe father. The family initially concealed this infor-
, [: @% j4 M! \" I# u l5 W8 A+ fmation, resulting in an extensive work-up for this
, t; t. J# R) E" t5 H4 zchild. Given the widespread and easy availability of
1 w7 n" k# |6 J- H4 k" f0 Ptestosterone gel and cream, we believe this is proba-# t6 C, c6 m, v) a# |1 s. ?
bly more common than the rare case report in the: Z3 o7 y1 l+ ]4 M5 J6 P
literature.4! ]1 O4 p" A+ C
Patient Report
) Q5 @6 c! p0 B: RA 16-month-old white child was referred to the
: i' X: X& _+ V3 W. E% c6 z7 F0 vendocrine clinic by his pediatrician with the concern
& P. t( |! L7 Q' K$ T6 _6 ~- C% fof early sexual development. His mother noticed
: X: t3 e7 C$ t8 k: ^light colored pubic hair development when he was b, Z) g# Z* i0 t+ A; s2 D4 t
From the 1Division of Pediatric Endocrinology, 2University of2 \9 p2 a- t/ N- Z+ G+ }* N
South Alabama Medical Center, Mobile, Alabama.
# i/ p! F' u+ R+ w0 \Address correspondence to: Samar K. Bhowmick, MD, FACE,
% A/ W+ G/ J5 eProfessor of Pediatrics, University of South Alabama, College of# S, X# [# R5 _, P- G
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;7 {8 h: E6 c' @6 W' H9 w
e-mail: [email protected].
0 ~8 u% }# [+ H8 F# ?3 Eabout 6 to 7 months old, which progressively became
7 H3 G% k1 v# R# g/ s' i# f; Q( Ldarker. She was also concerned about the enlarge-
- U# F; k9 _; l% B2 |( {5 {ment of his penis and frequent erections. The child* @" s6 U) t) ~, b j6 _
was the product of a full-term normal delivery, with6 j" f1 J4 t; E% q3 n3 u
a birth weight of 7 lb 14 oz, and birth length of7 J) |8 n( e7 q7 v' H, s9 C
20 inches. He was breast-fed throughout the first year& P: A4 ]0 M: s( X: G, F$ u3 r
of life and was still receiving breast milk along with- a j& P; \* J1 [9 J) f% E
solid food. He had no hospitalizations or surgery,* g/ A" `, }7 M0 V
and his psychosocial and psychomotor development
3 }/ X" m0 ~! y* X( w, Bwas age appropriate.
4 i8 F# S2 ^0 [6 ~9 u/ m1 m( }The family history was remarkable for the father, W/ }) ^2 R" X5 O: [' T0 \. v
who was diagnosed with hypothyroidism at age 16,
" B* A% `/ s7 n4 x! n% [4 F( @which was treated with thyroxine. The father’s
/ C7 Y' p+ Z. T7 g; Iheight was 6 feet, and he went through a somewhat) X& p6 P. {9 t9 U: s9 q
early puberty and had stopped growing by age 14.
d' G2 E# ]: K( p, b) [The father denied taking any other medication. The& ~ T+ e H/ o0 w( [5 r
child’s mother was in good health. Her menarche) v0 }6 K4 o% h6 h9 @: u
was at 11 years of age, and her height was at 5 feet, s5 d1 Y2 k+ ?
5 inches. There was no other family history of pre-
~5 u% d) u9 icocious sexual development in the first-degree rela-" G2 D, N9 F% M0 T# r: t K9 \
tives. There were no siblings.8 l) \3 f& y) A/ `8 j
Physical Examination
' w, w4 p& C2 t; k6 ^- zThe physical examination revealed a very active,+ v$ H5 v p' |0 G3 n# H
playful, and healthy boy. The vital signs documented
+ x: p/ s" A% \( z. e% l8 V9 Xa blood pressure of 85/50 mm Hg, his length was* f% n; d: K% x1 v
90 cm (>97th percentile), and his weight was 14.4 kg; i$ ~/ s9 c( m- U/ Y5 | L
(also >97th percentile). The observed yearly growth
$ l J) p# T' Yvelocity was 30 cm (12 inches). The examination of
& Y" x; H5 w4 R; Y: ^the neck revealed no thyroid enlargement.7 I3 N8 U8 n, P. Z- F9 N, y) z
The genitourinary examination was remarkable for. \. l6 C. m, @) G' B& o r1 `
enlargement of the penis, with a stretched length of" x2 c4 {6 E+ U0 g& \- F* o: C
8 cm and a width of 2 cm. The glans penis was very well; J/ {% n7 O/ J
developed. The pubic hair was Tanner II, mostly around5 g! | }! I. w
540
2 c8 c% m( ]$ @+ q9 ]0 Oat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from: Y4 p: t' \2 R# s3 }
the base of the phallus and was dark and curled. The
" @/ C! K+ ]& q- M: c& F( Ztesticular volume was prepubertal at 2 mL each., m& ~$ c! r! ]
The skin was moist and smooth and somewhat! i0 |6 K9 H3 `. J9 q
oily. No axillary hair was noted. There were no, S* Q. j' u& s; q" g% A! _
abnormal skin pigmentations or café-au-lait spots.
8 q1 [# N; M( x, m3 k. t: H, GNeurologic evaluation showed deep tendon reflex 2+
% t! w( p2 z _2 ~/ Ybilateral and symmetrical. There was no suggestion
& x$ @2 W. ]/ m/ P( Qof papilledema. q* u5 k& n# X- m
Laboratory Evaluation z% U) _: Y/ \8 S6 ^
The bone age was consistent with 28 months by
2 c9 k/ O6 }: T) L" R4 u) o, Lusing the standard of Greulich and Pyle at a chrono-
( p) |! A# D* J9 J+ |) o7 `logic age of 16 months (advanced).5 Chromosomal" M& g1 s3 l4 [* m. O
karyotype was 46XY. The thyroid function test u o/ p% m' T% {% I ]) Z, W. ?
showed a free T4 of 1.69 ng/dL, and thyroid stimu-: b' d7 z; M! M( c9 h' c
lating hormone level was 1.3 µIU/mL (both normal).% e1 _! a) \8 H( U( D" Z2 E2 \
The concentrations of serum electrolytes, blood- }1 @7 H5 r$ `+ F
urea nitrogen, creatinine, and calcium all were
5 z3 d! `! x5 zwithin normal range for his age. The concentration
5 c+ L3 h- a* c$ eof serum 17-hydroxyprogesterone was 16 ng/dL
$ g$ j# M* ^3 P$ u(normal, 3 to 90 ng/dL), androstenedione was 20
/ q4 H2 o( D* C: \- z Wng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-9 L( n1 ?* W% [8 f/ q
terone was 38 ng/dL (normal, 50 to 760 ng/dL),3 G6 o2 \! d: k
desoxycorticosterone was 4.3 ng/dL (normal, 7 to+ s4 }2 z* C6 B7 }/ {# g% U5 P
49ng/dL), 11-desoxycortisol (specific compound S)) d- I; B4 ~# j/ a4 E
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-- N" k" B$ K8 K7 D
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total# o( @! d2 P" C+ }- R: @
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
4 u; N1 e7 P: gand β-human chorionic gonadotropin was less than
6 x& X0 W$ k8 O: J5 mIU/mL (normal <5 mIU/mL). Serum follicular
1 T* e+ C! j4 \8 {# |& i- q6 Mstimulating hormone and leuteinizing hormone
3 S$ V6 l7 G$ U! ? Z9 N) Aconcentrations were less than 0.05 mIU/mL; t# V3 Q/ f& N. k' ]3 H# h
(prepubertal).
& t- K! ?* ]$ D& _! _0 l, DThe parents were notified about the laboratory1 z |" V. D$ @! r/ Z0 \; s: t
results and were informed that all of the tests were* k2 Z- j; P& p
normal except the testosterone level was high. The+ L9 k! s; x/ ]- V8 x6 |) r
follow-up visit was arranged within a few weeks to
1 S4 K! m* j4 v7 T. r( F8 O4 aobtain testicular and abdominal sonograms; how-
& k2 ^. V* W% aever, the family did not return for 4 months.
$ U6 t0 E2 P+ K6 ?# ~Physical examination at this time revealed that the# t2 o0 J+ n" |8 T$ m
child had grown 2.5 cm in 4 months and had gained
: B, a% G- g: Q6 l+ u2 kg of weight. Physical examination remained
: U: `* ]- N8 }1 @. @' I5 Sunchanged. Surprisingly, the pubic hair almost com-
8 `! W$ ^5 `6 X9 A& O- tpletely disappeared except for a few vellous hairs at/ N( _" @9 ~% L' J; r
the base of the phallus. Testicular volume was still 2+ E- E2 ~6 L$ t) D" x: Y+ i
mL, and the size of the penis remained unchanged.
; H. _* y2 B$ H: h& k" {* ZThe mother also said that the boy was no longer hav-
" l E- K1 p7 R& v/ b' Z3 T eing frequent erections.
& P @0 M" `# g5 f- WBoth parents were again questioned about use of
# A- l5 [ K9 Z: }9 G. {( Cany ointment/creams that they may have applied to
5 ]: k& y. J) z. N# q1 h$ P4 i4 {the child’s skin. This time the father admitted the
4 x1 C3 b' Y+ c8 b% wTopical Testosterone Exposure / Bhowmick et al 541
4 s3 C( } a* O9 Y) e, |9 L- I( Ause of testosterone gel twice daily that he was apply-! S! U+ F9 h8 ]! i8 x" E* u
ing over his own shoulders, chest, and back area for a( M5 g' N/ U$ g4 S; \' j% b, V
a year. The father also revealed he was embarrassed! ^: O$ e( r* h( P
to disclose that he was using a testosterone gel pre-
9 M7 B {0 l2 q. Hscribed by his family physician for decreased libido
B. E' q2 g% e7 R, d vsecondary to depression.
/ S5 T$ b3 A4 H: H. wThe child slept in the same bed with parents.
3 v; x+ q6 A/ x; L; qThe father would hug the baby and hold him on his
% ]& \' x h: z: n P. s% ?4 Q" W* {chest for a considerable period of time, causing sig-
1 ~2 _. |4 P: z! U- ^6 W3 enificant bare skin contact between baby and father.
: h2 Z9 ^! ]. J4 ^. Y/ a# UThe father also admitted that after the phone call,
1 O1 H2 j& U- f( p! Uwhen he learned the testosterone level in the baby5 ^' [) t1 J# K, u' P7 L' a
was high, he then read the product information
4 c! L# u! g4 I% {- A4 Ypacket and concluded that it was most likely the rea-
. a, G2 e R5 T" U% @; e/ }# nson for the child’s virilization. At that time, they: x8 g& `4 S1 Y& _8 w9 N/ l
decided to put the baby in a separate bed, and the2 h2 F0 @7 L2 H" |% b# D3 `; g; G/ ~) `
father was not hugging him with bare skin and had
. s1 ]1 J( \+ K1 m8 {been using protective clothing. A repeat testosterone% m6 i* |0 c) \4 I
test was ordered, but the family did not go to the
& T. Z( ^' B9 e* R/ ylaboratory to obtain the test.. s- D. F! T* Z0 J! i
Discussion3 I( V5 M9 ~/ J$ z" F: u9 E7 ^
Precocious puberty in boys is defined as secondary
+ C i( i9 d7 R1 Q3 ^7 Z: ksexual development before 9 years of age.1,47 x# N: `% ]2 H* j. w9 T# G
Precocious puberty is termed as central (true) when
6 z2 v; _ f; H5 ^7 _" Q H- dit is caused by the premature activation of hypo-" G i" K, G2 m& s0 M1 z7 O. J, B" n
thalamic pituitary gonadal axis. CPP is more com-
/ c( d% @4 a2 @; H' L9 S: gmon in girls than in boys.1,3 Most boys with CPP
, e" ^" D2 Q' s- V3 Ymay have a central nervous system lesion that is- _: x; e& K, E2 ?7 z( }% a
responsible for the early activation of the hypothal-
) g: [% R2 o7 ?) z' E7 y( Gamic pituitary gonadal axis.1-3 Thus, greater empha-# u) U# F+ F2 h$ J- P& w0 J
sis has been given to neuroradiologic imaging in
( B6 F5 j7 s/ t5 M! qboys with precocious puberty. In addition to viril-
+ x+ R1 p$ w+ n \ization, the clinical hallmark of CPP is the symmet-
! l4 Q* v& ^2 n N+ Y: jrical testicular growth secondary to stimulation by
Z! }$ C& q6 ]# c2 pgonadotropins.1,3
0 r1 D7 O, z, c+ j% p: Q' B2 KGonadotropin-independent peripheral preco-
6 m, ~7 k% n( G! \2 p1 Ccious puberty in boys also results from inappropriate
2 @. f: m$ \; |androgenic stimulation from either endogenous or5 R) G. d& R' P- j1 u
exogenous sources, nonpituitary gonadotropin stim-
$ X* g7 a2 ^0 g2 hulation, and rare activating mutations.3 Virilizing9 i; ~% ?7 y' u! p3 z [( z9 r) ^
congenital adrenal hyperplasia producing excessive* Q: Y2 S8 _1 x1 S/ t( L
adrenal androgens is a common cause of precocious% ~' G7 u# K, Q6 a, i4 M
puberty in boys.3,4' {; R/ Y; Q$ W4 z' H8 d# a
The most common form of congenital adrenal
" T% e9 \ ]) T# L" H) ?9 S8 d8 |hyperplasia is the 21-hydroxylase enzyme deficiency.2 Z3 z0 ?0 Q& u6 h# o1 b6 {# h+ T
The 11-β hydroxylase deficiency may also result in
& a, ~( \5 p! e {; F; k/ kexcessive adrenal androgen production, and rarely,
2 \, B+ e8 f) `0 S# ^- z8 Wan adrenal tumor may also cause adrenal androgen
) ^ U y/ E1 \4 b7 x: Kexcess.1,3
$ _ e; E* b3 a1 E& Nat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
& Y$ s8 P; p& l" }/ b2 k542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
- S3 g% C1 E: Z6 ?8 Z9 s( Y1 N' y8 B, {A unique entity of male-limited gonadotropin-; Y" V p9 Y- V
independent precocious puberty, which is also known
# u5 t* v) J! c J! H( y4 ias testotoxicosis, may cause precocious puberty at a
$ E3 J" d6 b x, |very young age. The physical findings in these boys
+ y2 W. S7 [) i' u* L& C- pwith this disorder are full pubertal development,
, r1 h2 ]: g0 kincluding bilateral testicular growth, similar to boys5 G% [) W; f/ p$ S
with CPP. The gonadotropin levels in this disorder
2 ]7 y$ S7 A8 N, ^' n! V, p$ iare suppressed to prepubertal levels and do not show
* u% D7 |- `) ~+ d6 ?/ V, Opubertal response of gonadotropin after gonadotropin-6 r% `) y s: Y: e- p5 Z# v
releasing hormone stimulation. This is a sex-linked$ m# i R: A3 K. m+ g- i
autosomal dominant disorder that affects only9 ^( t: ~- S- T/ G7 J3 o+ Y
males; therefore, other male members of the family9 R" m; l' \. _& _, u: N2 M* N
may have similar precocious puberty.3
& `; q# V9 g( M( jIn our patient, physical examination was incon-# A) x# ~, S+ ^# y$ q9 v( B6 m* k
sistent with true precocious puberty since his testi-) f) y) t5 H5 }2 u% Z6 C. O& Y
cles were prepubertal in size. However, testotoxicosis, f3 {5 L$ J Y1 T
was in the differential diagnosis because his father- ?9 T! @- P! ?( f$ V
started puberty somewhat early, and occasionally,
8 N+ X7 z+ h' ]testicular enlargement is not that evident in the" o# c v+ Z7 I2 L% L
beginning of this process.1 In the absence of a neg-4 o) i0 ~' f0 f3 r7 I% d) j3 `
ative initial history of androgen exposure, our6 V( P! D5 G! S
biggest concern was virilizing adrenal hyperplasia,
$ N# A& C7 k: i* ?; P3 H( Ieither 21-hydroxylase deficiency or 11-β hydroxylase
: L. f" R; K! Q0 l* jdeficiency. Those diagnoses were excluded by find-5 _. _& [" |& V) K4 N5 ^
ing the normal level of adrenal steroids.' C6 E' C: p+ H8 W# B+ l
The diagnosis of exogenous androgens was strongly7 i- l! \( P1 n% {
suspected in a follow-up visit after 4 months because
) Y/ ?4 l3 B3 Y. e! w3 U4 {the physical examination revealed the complete disap-
/ V$ m/ Z' L# {2 Ipearance of pubic hair, normal growth velocity, and3 O: t2 f f8 c2 M, [- v+ A
decreased erections. The father admitted using a testos-5 N& J7 y( V% J6 ^
terone gel, which he concealed at first visit. He was) ?4 B! X8 j% i5 L
using it rather frequently, twice a day. The Physicians’% y! t, U0 T1 ~' t
Desk Reference, or package insert of this product, gel or
9 x6 }9 k4 Z' D$ d% Q! w* J1 x' K' @cream, cautions about dermal testosterone transfer to" A2 S9 t1 `$ a; `
unprotected females through direct skin exposure.
- F" L0 G* ?# ]$ x9 T. q4 K2 o0 b3 OSerum testosterone level was found to be 2 times the3 w% s6 D* I" y( v
baseline value in those females who were exposed to( {4 L4 h: U. j% O5 b& Z% p
even 15 minutes of direct skin contact with their male4 H$ j# J# t3 }1 k
partners.6 However, when a shirt covered the applica-- A. d4 g8 r1 m* I
tion site, this testosterone transfer was prevented.2 y. T: [- ^+ ~; H9 o3 W" Z
Our patient’s testosterone level was 60 ng/mL,; Y) N% e" S- u/ I7 ]1 O7 @1 z
which was clearly high. Some studies suggest that: { D' H9 T% x
dermal conversion of testosterone to dihydrotestos-5 f0 F; u3 K6 W, }4 K8 A
terone, which is a more potent metabolite, is more
9 M. G4 [4 ]( Aactive in young children exposed to testosterone& ~- z8 C4 B: x+ Y" d A
exogenously7; however, we did not measure a dihy-
+ l8 }/ ~9 K- e* g: L/ Rdrotestosterone level in our patient. In addition to
" @7 w0 h: n3 s: p2 g1 ?$ s& avirilization, exposure to exogenous testosterone in' Q( y8 r) V, D, H* o2 g
children results in an increase in growth velocity and! _8 u5 n- `1 f) Y& |+ g: m
advanced bone age, as seen in our patient.# @! z* |( F/ G8 `, z3 I6 `
The long-term effect of androgen exposure during1 `6 W6 [& C+ ~+ t& r f
early childhood on pubertal development and final$ t9 S* A# v2 E" P. g" k: U
adult height are not fully known and always remain8 y( W) o% R; n+ }- ]
a concern. Children treated with short-term testos-
! B9 B0 J1 {0 Q3 `terone injection or topical androgen may exhibit some
9 d5 S, w! b0 \5 U' kacceleration of the skeletal maturation; however, after% P. y/ P& Z7 x
cessation of treatment, the rate of bone maturation; I" D0 O$ g: o+ ]& i+ Y, i
decelerates and gradually returns to normal.8,9 @* A- }. X7 z4 P
There are conflicting reports and controversy: @! m( @' d( @% C. T, ?$ O: N
over the effect of early androgen exposure on adult- q8 z: p. I! H% d$ y
penile length.10,11 Some reports suggest subnormal1 |- a7 k; t$ X: d+ t4 }5 T* s
adult penile length, apparently because of downreg-
/ `7 F B7 @3 Dulation of androgen receptor number.10,12 However,9 N* }& r7 l( P! {$ A1 A0 j
Sutherland et al13 did not find a correlation between0 K* l0 ~7 X) O4 u3 w
childhood testosterone exposure and reduced adult
7 m6 N! Q4 D# Z! Q3 Apenile length in clinical studies.
U; n- s4 p/ ]5 ~) GNonetheless, we do not believe our patient is
' w' `! z9 U% a2 y6 j$ }- jgoing to experience any of the untoward effects from
) m- H+ N+ J. y$ r) U) c9 [/ F0 ftestosterone exposure as mentioned earlier because
6 s, a" R; S& P' C3 |; ^- I0 tthe exposure was not for a prolonged period of time.- @2 o6 B1 f0 S, B- I
Although the bone age was advanced at the time of
9 N+ [4 n6 f9 { {0 z: s% ndiagnosis, the child had a normal growth velocity at* V) e2 s6 [1 s! {7 q
the follow-up visit. It is hoped that his final adult
1 q$ e# o; y" Y% u& n0 Zheight will not be affected.
+ @# V& _# k: J! |Although rarely reported, the widespread avail-
9 N; E, V; z3 T: y! Gability of androgen products in our society may
: f- G3 f' D* sindeed cause more virilization in male or female4 { B. S! Z' X6 g6 F$ @
children than one would realize. Exposure to andro-0 W9 N6 M& P' ?
gen products must be considered and specific ques-0 d2 t; Y( {% l8 c
tioning about the use of a testosterone product or
6 v% O a( i2 H+ |gel should be asked of the family members during% {* p$ X/ r# b W3 N0 s. \
the evaluation of any children who present with vir-- }' F+ x! [# f3 I
ilization or peripheral precocious puberty. The diag-
3 a3 ]) Z9 z* Unosis can be established by just a few tests and by
; H6 w) M! w( t. T) i7 p Pappropriate history. The inability to obtain such a& l6 S! b$ Q; y7 a8 U$ J
history, or failure to ask the specific questions, may
1 i: s5 |8 |6 C) V8 Q" Dresult in extensive, unnecessary, and expensive# w0 V1 ^9 A, Y6 Q( u
investigation. The primary care physician should be+ X! f9 v+ r1 d, t% U: [1 ]
aware of this fact, because most of these children0 F2 j, ^$ Y5 K- A2 @1 @
may initially present in their practice. The Physicians’$ q( o2 b% Y, O& V
Desk Reference and package insert should also put a
$ d: G: C$ t% I* S+ W/ }+ iwarning about the virilizing effect on a male or0 I; T3 F, d" |! J" |; C
female child who might come in contact with some-
2 N8 K" I1 L6 i8 R; H& Z2 T Bone using any of these products.
$ I+ K8 b5 h. i1 }References
) c( k, z5 r4 @ H2 m( Y5 H1. Styne DM. The testes: disorder of sexual differentiation
; ]* E" m& a; b# K u) Band puberty in the male. In: Sperling MA, ed. Pediatric, l, z* m+ A5 r+ G
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
$ U$ H6 R- j0 _% c2002: 565-628.3 A: r, ]! O- U5 }8 V
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious" Z2 Q4 y: H. n& h9 s; f
puberty in children with tumours of the suprasellar pineal |
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