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Sexual Precocity in a 16-Month-Old# M6 J) Y- Z: {9 \
Boy Induced by Indirect Topical
6 q: Y& S% `; u _* }Exposure to Testosterone% `9 L/ k" R6 F; y. E
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
0 V, c* l3 W( z5 K7 X4 zand Kenneth R. Rettig, MD1
3 H6 g0 M% u2 E& d8 x, HClinical Pediatrics0 ?& ^! B3 g4 Q- h0 t0 l, ?6 i
Volume 46 Number 6( {6 J% o- ]/ U' z4 q P( k5 f
July 2007 540-543
) |( K& k1 W1 \4 q8 h) P' Z© 2007 Sage Publications0 r' D* \5 S4 C- @" ~3 @
10.1177/0009922806296651
) Z% ~" Y2 S% R" l' s1 Q+ ]http://clp.sagepub.com
1 c, V6 b3 _9 C6 O- Y% l) qhosted at- e+ ~. G9 ^, @
http://online.sagepub.com# c/ g' b3 d, O4 _
Precocious puberty in boys, central or peripheral,2 A) p5 ?' v, T$ h0 \
is a significant concern for physicians. Central; c8 H' ]2 Y3 P6 v- Y0 b; h9 Y' l
precocious puberty (CPP), which is mediated9 n# G; j; m- z" g# m
through the hypothalamic pituitary gonadal axis, has
3 u9 G% }: Q! \* V1 I: Aa higher incidence of organic central nervous system
, C* S. H! g; k8 Clesions in boys.1,2 Virilization in boys, as manifested. C- y1 S% l5 O" U. w
by enlargement of the penis, development of pubic
7 S2 ?4 {. {1 S8 C% Zhair, and facial acne without enlargement of testi-
/ Q( R; d, e v" a) }6 g, vcles, suggests peripheral or pseudopuberty.1-3 We
/ H* T3 }3 m# w1 X9 M9 n' k9 i% vreport a 16-month-old boy who presented with the
: l" p- Q- ?- d3 m# |4 O: fenlargement of the phallus and pubic hair develop-. B( I4 @1 `% F! s9 \; V( D
ment without testicular enlargement, which was due( Q3 B- S" u/ ]! {% d
to the unintentional exposure to androgen gel used by
" H0 B" M4 u) q! e7 D$ R: R9 Cthe father. The family initially concealed this infor-
+ g1 ]5 U5 ]! l4 M6 I. Nmation, resulting in an extensive work-up for this+ ^2 _' G9 t" S+ }" [
child. Given the widespread and easy availability of
. c; f* C: N: A+ A( Btestosterone gel and cream, we believe this is proba-
1 N2 [0 J9 g& Y, Lbly more common than the rare case report in the9 L7 ~4 r- ?3 V7 f! Z
literature.4! L; P6 t& N+ n- ~2 E% a
Patient Report
& k- U- p, Z {* c: P8 |8 xA 16-month-old white child was referred to the
; y7 [4 }4 z0 o5 f4 L sendocrine clinic by his pediatrician with the concern
/ C- Z! T' `" D6 K$ qof early sexual development. His mother noticed
{6 x1 [, M# l4 h0 ^* w( ~5 Nlight colored pubic hair development when he was! D& H( J+ {5 }
From the 1Division of Pediatric Endocrinology, 2University of0 y' [ J! R6 M/ c
South Alabama Medical Center, Mobile, Alabama.
: E. F/ r; R$ U8 gAddress correspondence to: Samar K. Bhowmick, MD, FACE,
7 ?: {$ b# k v7 _0 _Professor of Pediatrics, University of South Alabama, College of* s6 @' }: @: W5 k4 Y
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
, x7 _+ t$ l$ `" ]+ _e-mail: [email protected].
+ W. A$ X9 D5 Oabout 6 to 7 months old, which progressively became
" L$ p, v3 D8 \) E0 t1 B) d+ P! s; ydarker. She was also concerned about the enlarge-; p Z* X; r" k; y7 x( y7 x
ment of his penis and frequent erections. The child
/ h# R2 o2 g# o) F- \( M' A; `was the product of a full-term normal delivery, with J- r3 V7 w" s
a birth weight of 7 lb 14 oz, and birth length of5 L3 j a) T2 |2 r
20 inches. He was breast-fed throughout the first year) E6 E, i9 O0 s" f! B
of life and was still receiving breast milk along with
) X0 Z/ D w! p3 a2 q0 fsolid food. He had no hospitalizations or surgery,, q0 y' t" M6 l9 ]- g
and his psychosocial and psychomotor development
& M3 p; P& @4 B: ?, s Pwas age appropriate.5 M7 G7 S% R' B
The family history was remarkable for the father,: y2 a/ P7 @4 r
who was diagnosed with hypothyroidism at age 16,0 s* U7 B" ^+ \6 Q( \; ]
which was treated with thyroxine. The father’s
$ P- Q/ F7 l1 z8 j: S6 y1 g1 K. ^( kheight was 6 feet, and he went through a somewhat
9 \& N- a! x0 p C( gearly puberty and had stopped growing by age 14.
* B) c8 ]* \8 b* w6 o8 F- pThe father denied taking any other medication. The+ x% [; P' o4 A
child’s mother was in good health. Her menarche2 _' C1 T' i: M1 f: S7 K) l0 C/ t
was at 11 years of age, and her height was at 5 feet
& i) @ |7 q: V4 n# R5 inches. There was no other family history of pre-# O# U" I3 U6 x8 {: A, f
cocious sexual development in the first-degree rela-
8 H: Z Q4 Z# o1 `tives. There were no siblings.- ~* m* h; x& c' E% t, R
Physical Examination
; I7 V( f7 K- I. }8 b4 J; P5 |The physical examination revealed a very active,2 @$ W) r$ u5 w! C3 X+ r- p+ p
playful, and healthy boy. The vital signs documented% d6 Q1 w" h) ^& R2 Z! I5 ?9 Y+ J: l
a blood pressure of 85/50 mm Hg, his length was% J9 P1 U2 q. b, q1 L
90 cm (>97th percentile), and his weight was 14.4 kg
$ f, O# B! X1 m- q; ~; w(also >97th percentile). The observed yearly growth9 n3 X0 Z ~8 j9 \3 V0 |/ J% t* d1 a
velocity was 30 cm (12 inches). The examination of1 s0 V/ a9 _/ J4 m/ `4 h: S1 _8 X
the neck revealed no thyroid enlargement.
. s5 P) l2 L# aThe genitourinary examination was remarkable for [! V0 W6 q, l) G/ _
enlargement of the penis, with a stretched length of3 _6 G& c% `5 Z. k) |' G
8 cm and a width of 2 cm. The glans penis was very well
: x1 j" L% u$ m) c& b$ Edeveloped. The pubic hair was Tanner II, mostly around: `) C0 A- o* |9 n7 O/ z7 ]
540
9 ?* G9 A" o" w% @# { O$ bat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
0 ~$ ^# M; ~ o& M, {5 p e" Tthe base of the phallus and was dark and curled. The7 @% B$ x z2 K2 w/ n8 D( q
testicular volume was prepubertal at 2 mL each.4 W4 D+ _$ g7 L" {5 X k, Q P6 Z' |
The skin was moist and smooth and somewhat8 Z% L1 n' r( C$ p3 b
oily. No axillary hair was noted. There were no$ Y. y! I) R/ H4 M$ X! y! p
abnormal skin pigmentations or café-au-lait spots.
* ?, ~( c6 H2 ]( ANeurologic evaluation showed deep tendon reflex 2+
. n8 y" R+ v4 U$ g# ?bilateral and symmetrical. There was no suggestion) z6 p" L5 K4 F
of papilledema. W- a. c y, b
Laboratory Evaluation O" n, R) A/ M* L o/ d
The bone age was consistent with 28 months by
/ L9 }& }9 e: J; m9 Vusing the standard of Greulich and Pyle at a chrono-: |5 V- ~6 S+ t$ X7 Y, @, a- Y4 n
logic age of 16 months (advanced).5 Chromosomal9 [/ e6 z0 V9 D' G* g- `/ G+ ?2 k
karyotype was 46XY. The thyroid function test% d3 c5 |3 @1 d$ \7 \ ~
showed a free T4 of 1.69 ng/dL, and thyroid stimu-7 @6 C X8 L. ~# g5 ]' {
lating hormone level was 1.3 µIU/mL (both normal).1 I7 G2 J5 C8 y2 K' K# D$ S
The concentrations of serum electrolytes, blood! s1 \5 t6 n6 ~6 u4 x
urea nitrogen, creatinine, and calcium all were
; x" m/ \8 v4 i+ W. ]/ [+ {+ Mwithin normal range for his age. The concentration7 s4 O+ M0 ~3 G+ H
of serum 17-hydroxyprogesterone was 16 ng/dL
. q# n$ I( k' m) Q(normal, 3 to 90 ng/dL), androstenedione was 20 z/ ^& `- Q4 H0 a0 x2 l
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-9 f" G/ O: u# Z) }! o+ O1 I
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
) \: O* ^8 G' \0 e/ k: P$ o) mdesoxycorticosterone was 4.3 ng/dL (normal, 7 to) A: e x# R5 G* d% L
49ng/dL), 11-desoxycortisol (specific compound S)! ^# R& P+ `! Q& L" z7 Q$ Y& x7 B6 e
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-5 o8 h6 Z! `& g+ x' r' A7 |
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total. {: d* z, N1 E. J) l! R W/ u9 ~# t
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),+ A, z, v( \/ p4 ^, l
and β-human chorionic gonadotropin was less than7 Y; M3 L C) W. p# _
5 mIU/mL (normal <5 mIU/mL). Serum follicular5 e/ U& H6 {% t# [- i( M' P
stimulating hormone and leuteinizing hormone7 u" z1 ~- `$ J; G9 e3 {
concentrations were less than 0.05 mIU/mL
+ n: {% {# c+ E" t/ X(prepubertal).
0 O- Z5 d1 S$ DThe parents were notified about the laboratory3 F6 h! O+ `9 k) J% i
results and were informed that all of the tests were
1 \8 H8 e G' z, m P; r {$ i8 {normal except the testosterone level was high. The
2 }# }9 _) x( V, t! kfollow-up visit was arranged within a few weeks to' Z& _# ~. j3 @6 r" S9 i$ T
obtain testicular and abdominal sonograms; how-7 ~' z0 t2 ]( w, u# ^3 g0 _! o
ever, the family did not return for 4 months.% U" j' L; Y$ W; T3 K
Physical examination at this time revealed that the) z2 E9 u5 j0 b& W9 ?. u2 K9 V
child had grown 2.5 cm in 4 months and had gained
/ B: {9 }2 g x3 e7 b( T% ?( e8 K2 A2 kg of weight. Physical examination remained
r: ?; g! A6 I7 dunchanged. Surprisingly, the pubic hair almost com-
( L* q/ p: z0 Q3 }pletely disappeared except for a few vellous hairs at0 r5 b0 y4 V/ \: S
the base of the phallus. Testicular volume was still 2
8 U F8 ~" r+ K$ qmL, and the size of the penis remained unchanged.) I0 \# U' M7 v) u
The mother also said that the boy was no longer hav-
- y1 {, T+ J jing frequent erections.! O0 @) S% S' W) \
Both parents were again questioned about use of
% \) C. P f* h ^' ^any ointment/creams that they may have applied to
( W( L/ d4 h& athe child’s skin. This time the father admitted the
. o" a7 ?: r. t5 Y1 C( J& ?Topical Testosterone Exposure / Bhowmick et al 541
; O: X" x/ q! Quse of testosterone gel twice daily that he was apply-
9 s/ W. z( b7 Ting over his own shoulders, chest, and back area for2 ^# T7 U' o* d! K- L3 D8 S
a year. The father also revealed he was embarrassed
; A/ g4 |9 X- h; D' V2 xto disclose that he was using a testosterone gel pre-
/ K# S9 v8 ~: v9 {. q7 Mscribed by his family physician for decreased libido
- g% Y7 ?5 I# O3 r! ^ Csecondary to depression.
" [6 A$ b8 }' Q: j! l1 I2 J# T7 {The child slept in the same bed with parents.
4 r5 H1 ?& g5 k; K6 _The father would hug the baby and hold him on his
# ? F) U( \( P8 B7 Ychest for a considerable period of time, causing sig-( R% @5 F1 v0 p7 M9 a( L" `5 U- w% q* P
nificant bare skin contact between baby and father.2 T- H2 {+ [* \. [2 d
The father also admitted that after the phone call,
M6 v, U9 f E8 f& U; {6 R/ t8 \when he learned the testosterone level in the baby
% y1 u! b$ F4 x$ E. Pwas high, he then read the product information
W1 j _* S& F% T5 L' X6 apacket and concluded that it was most likely the rea-
8 b( }5 g. _; a# ` ?son for the child’s virilization. At that time, they
7 M4 K4 x- E6 i0 udecided to put the baby in a separate bed, and the
- \1 Q7 `# m2 d- a8 E' C% qfather was not hugging him with bare skin and had, s L9 K1 F' k. z5 ?4 }7 G
been using protective clothing. A repeat testosterone2 a- L! @* x6 I, {6 R# T
test was ordered, but the family did not go to the) L" F* ]! \. Q, g4 [5 R
laboratory to obtain the test.. E+ B6 m& Q+ U( m
Discussion; P0 u8 p* c7 W8 m7 K
Precocious puberty in boys is defined as secondary1 _6 p: ^* s) I1 ?, h
sexual development before 9 years of age.1,45 j4 X6 Z! Y/ a4 z1 E) [0 f9 L
Precocious puberty is termed as central (true) when- B% h1 ~/ v7 C9 i! q$ f/ [' S
it is caused by the premature activation of hypo-" K( ?9 c3 x' b% E7 t
thalamic pituitary gonadal axis. CPP is more com-
8 d3 K7 d/ E G6 bmon in girls than in boys.1,3 Most boys with CPP
, E- S) r- q1 R0 Q! A% Lmay have a central nervous system lesion that is# |0 Y5 a) D# @7 o( W# g+ n& [
responsible for the early activation of the hypothal-
" `. @: {* _% g+ uamic pituitary gonadal axis.1-3 Thus, greater empha-
: P9 R' x5 c5 Rsis has been given to neuroradiologic imaging in
5 ?! W4 T t1 Y7 B6 t( Lboys with precocious puberty. In addition to viril-" Q" s, l- t# s6 W' J: O* Q) A4 V
ization, the clinical hallmark of CPP is the symmet-
) t4 K4 B3 ^; x4 N& t3 p) }- Drical testicular growth secondary to stimulation by: y5 D) e* c* h+ L
gonadotropins.1,3* g3 I( v4 _4 ]
Gonadotropin-independent peripheral preco-7 a( ~; n6 X; [& b( k( p# b
cious puberty in boys also results from inappropriate; I4 i% m. V8 s& j: i. ~- T3 O8 {
androgenic stimulation from either endogenous or% G* x( J+ C9 y2 u! Q% q, M: o/ w
exogenous sources, nonpituitary gonadotropin stim-! _# y( z6 K( J0 D
ulation, and rare activating mutations.3 Virilizing, ]+ N' W6 S# p$ V. m0 e( g
congenital adrenal hyperplasia producing excessive! x$ P" c9 ~# q
adrenal androgens is a common cause of precocious
; z( s' Q/ X, y, E+ Ipuberty in boys.3,4( ]# \# g) j% V, G6 M
The most common form of congenital adrenal
* W! s. L% i0 K3 x: Rhyperplasia is the 21-hydroxylase enzyme deficiency.
$ C! \- N2 I! V9 eThe 11-β hydroxylase deficiency may also result in4 [, y9 z% b; A' l% f; r
excessive adrenal androgen production, and rarely,
0 f8 |, D4 @& jan adrenal tumor may also cause adrenal androgen
) W- w( ?4 F8 ~9 Z) t6 O! lexcess.1,3
+ g6 ]1 H2 C, Z" F; C+ D) c2 E- Lat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
# ~) E: F2 X2 e: m542 Clinical Pediatrics / Vol. 46, No. 6, July 2007( C* I' Y0 U' K
A unique entity of male-limited gonadotropin-* i1 @1 z0 Y' g1 k* P& ~
independent precocious puberty, which is also known
* _! N4 D n0 r7 G& m! D; c4 n2 kas testotoxicosis, may cause precocious puberty at a9 n3 k# o6 X5 I
very young age. The physical findings in these boys6 t/ y8 X( F2 j
with this disorder are full pubertal development,
; B: R4 {# D3 q" N2 Uincluding bilateral testicular growth, similar to boys
* h, Q+ }( w4 _with CPP. The gonadotropin levels in this disorder, P* A5 R4 {. N2 Y* L! c e
are suppressed to prepubertal levels and do not show
1 k- {$ B$ F& ~# H& P/ @! W$ o3 dpubertal response of gonadotropin after gonadotropin-
& H9 N6 w3 j4 h/ o& s7 V- T: {releasing hormone stimulation. This is a sex-linked
% V* P9 \6 X* Q' h% W+ dautosomal dominant disorder that affects only
. P% A% C& x3 _7 \ n' T* Omales; therefore, other male members of the family/ e% _ D2 ], ]; Y
may have similar precocious puberty.3* p; T5 k4 W3 \+ I
In our patient, physical examination was incon-9 G5 W3 d" r# k# x6 F6 p2 w
sistent with true precocious puberty since his testi-
" n" A7 x3 G$ e" @- Tcles were prepubertal in size. However, testotoxicosis
1 _" V# K( p5 ]was in the differential diagnosis because his father
J, k/ X% G, d+ u$ h8 \8 O. S- astarted puberty somewhat early, and occasionally,
* j' Y3 M: e, k/ O; Ztesticular enlargement is not that evident in the2 c3 V8 ~9 c9 E
beginning of this process.1 In the absence of a neg-& T! @" L9 Y* R: m1 d2 x$ Z
ative initial history of androgen exposure, our
4 K" ?% u5 }, Y; {& }1 G$ C& hbiggest concern was virilizing adrenal hyperplasia,/ J* n4 q$ p: U4 d& f `( h* p
either 21-hydroxylase deficiency or 11-β hydroxylase
: o4 V9 T6 X1 S+ k' [deficiency. Those diagnoses were excluded by find-
, q3 F5 W" D; l* G; a% Jing the normal level of adrenal steroids.9 B5 s' _" Z& f9 Z1 A1 O2 l0 A1 _& U; \
The diagnosis of exogenous androgens was strongly1 |3 j9 R2 |) F }: C0 L
suspected in a follow-up visit after 4 months because
" M0 @1 Z+ i, B9 Jthe physical examination revealed the complete disap-
0 ^0 m4 F' p( xpearance of pubic hair, normal growth velocity, and
7 u. u! |$ F+ B( Ldecreased erections. The father admitted using a testos-
( Z& {) ~% u# t$ ?7 ~: e5 {terone gel, which he concealed at first visit. He was
, W4 G3 |% G9 e% k* p3 W- {7 `using it rather frequently, twice a day. The Physicians’: L7 [! u. M; r5 E; C
Desk Reference, or package insert of this product, gel or
( Z M' Z. ^; ~5 A6 a! U3 E$ Qcream, cautions about dermal testosterone transfer to
& X, U5 i& n0 c# `# T3 J) L/ vunprotected females through direct skin exposure.! a! ]. t* K. e8 b/ ]. K/ l( Y1 O
Serum testosterone level was found to be 2 times the
. i: P# M* O' G$ I, sbaseline value in those females who were exposed to
' u% N1 b' e; keven 15 minutes of direct skin contact with their male
5 b7 M4 W* Y m3 Y: S; s4 K: ~7 {partners.6 However, when a shirt covered the applica-
8 ?0 [6 G# y# Htion site, this testosterone transfer was prevented.
; h$ F, q- F( c- F5 s% j0 P, c i( n, [Our patient’s testosterone level was 60 ng/mL,0 U, s. d( V7 z
which was clearly high. Some studies suggest that5 T% i" b" T& g6 e4 B* w9 A) Z
dermal conversion of testosterone to dihydrotestos-
' Z* |+ [0 C1 l" m2 Q `; p. Rterone, which is a more potent metabolite, is more
7 A3 s1 i" d2 }) M& ~( Kactive in young children exposed to testosterone3 L9 C, g, U/ A! l$ a
exogenously7; however, we did not measure a dihy-
- t& j; J W/ b" R# ndrotestosterone level in our patient. In addition to
# E, Y0 T5 h @$ Z* ~" dvirilization, exposure to exogenous testosterone in
# P7 X' K# K& h$ gchildren results in an increase in growth velocity and9 w+ q8 P$ L% P' a/ K- T
advanced bone age, as seen in our patient.
9 Z/ F+ m7 s( @( v( u: f7 S+ mThe long-term effect of androgen exposure during6 D, Q$ z7 @. A1 L$ Z( B
early childhood on pubertal development and final- Y2 ^0 f3 t7 C" E1 @) J! @ h
adult height are not fully known and always remain8 b( C4 m+ |) x9 O" W9 T' V) a
a concern. Children treated with short-term testos-
( }6 M0 o- b7 ~- {2 S9 \2 _terone injection or topical androgen may exhibit some( _6 P) d Z# y: [+ i( U
acceleration of the skeletal maturation; however, after9 ]4 f, ~) c# t9 S6 N
cessation of treatment, the rate of bone maturation
& i) T! b m2 b8 W5 Y+ Vdecelerates and gradually returns to normal.8,9: Z5 D& {: k! l, T- ?3 X8 Y
There are conflicting reports and controversy
# Y- M% D" ~- z; f( I+ c5 Kover the effect of early androgen exposure on adult
' D% `0 `5 s9 O) c6 Vpenile length.10,11 Some reports suggest subnormal
* K2 b; m* ]% g. @) _$ M wadult penile length, apparently because of downreg-3 z; d/ K$ P. t! s& E2 t
ulation of androgen receptor number.10,12 However,$ g" V8 f! B; \9 Q( U" W" }: f
Sutherland et al13 did not find a correlation between
; {" q/ ?+ u- a. n/ q achildhood testosterone exposure and reduced adult
- m( O5 V3 Y0 ~penile length in clinical studies.( ^( K& u- Z6 v3 P. N) Q
Nonetheless, we do not believe our patient is. [% q$ J ?1 N8 I" @. ]
going to experience any of the untoward effects from( z; y6 x; c w! A2 `$ u4 N* H
testosterone exposure as mentioned earlier because; X0 P1 b2 L* N: |8 Z5 |# R3 p5 z
the exposure was not for a prolonged period of time.- E& t* R: ~6 j" ]3 k
Although the bone age was advanced at the time of+ i9 m! a; l4 A
diagnosis, the child had a normal growth velocity at
9 X2 \8 C8 c/ V1 {( ^4 }3 {( O9 mthe follow-up visit. It is hoped that his final adult* t" ?! V. D! A% o
height will not be affected.
s2 s' w- f; U2 j; k, y6 QAlthough rarely reported, the widespread avail-+ z/ i$ a3 _( j! d
ability of androgen products in our society may
5 n; o. ^2 w( K6 {5 P5 {indeed cause more virilization in male or female
; \/ c5 U2 N( Qchildren than one would realize. Exposure to andro-# b3 k4 h3 F. j
gen products must be considered and specific ques-
' c+ x$ e1 @' A/ h' ?2 ? {tioning about the use of a testosterone product or0 c" }" ~6 h T% x/ z/ j+ y5 ]
gel should be asked of the family members during1 ]; u: l: `$ [4 K! I, P- s7 Z
the evaluation of any children who present with vir-! }8 }9 m* q0 G F; \
ilization or peripheral precocious puberty. The diag-: a$ p5 x% w! ]2 m+ }5 \1 }
nosis can be established by just a few tests and by
) E+ L( E9 M5 mappropriate history. The inability to obtain such a, j1 @) C$ \1 f; q/ n- j
history, or failure to ask the specific questions, may6 H+ M9 ]# c: q* z: o3 j
result in extensive, unnecessary, and expensive
! ]9 E! V% M$ Finvestigation. The primary care physician should be
! B" F, y! Q7 |; x I0 caware of this fact, because most of these children+ I& Z' p) l; ~" X' f
may initially present in their practice. The Physicians’# X! E( E) b* W. R3 K8 m
Desk Reference and package insert should also put a
E- U* M& R- Y- \) s3 T& Pwarning about the virilizing effect on a male or
& E: K" A5 ^( x# Z/ H- H" j' Mfemale child who might come in contact with some-
% [$ y/ Y- y- u) x p1 N( f) J& Vone using any of these products.
9 `# U, D3 G3 x( z8 | p. p$ kReferences( z/ j3 O+ l6 q3 F
1. Styne DM. The testes: disorder of sexual differentiation
4 ^2 X# z( ~1 d, [9 l2 }and puberty in the male. In: Sperling MA, ed. Pediatric2 J$ x' O) g% `( r1 K* F- F
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;! w# G! v+ Q8 K5 r
2002: 565-628.4 b) c6 Y' v6 \, W+ c
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious% N- f5 y# T9 }+ Z- H
puberty in children with tumours of the suprasellar pineal |
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