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Sexual Precocity in a 16-Month-Old9 N, M+ X9 E |3 K! e' n
Boy Induced by Indirect Topical+ _$ V2 I) O3 ~/ J, D
Exposure to Testosterone( X* y# ?" h& U* P% L ^% q, Y* T) ?
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2* ~0 l( M+ Z. P4 W6 n9 N9 j
and Kenneth R. Rettig, MD1
0 u! m8 T$ E) V$ }Clinical Pediatrics
% e) P* s$ C" A9 ~Volume 46 Number 6
: e+ ~9 H" @5 K5 A- z0 U4 {July 2007 540-543
! j! H6 T6 [$ m3 h, T© 2007 Sage Publications
9 `9 x/ g5 g/ e10.1177/0009922806296651! R' ^' Q A# \( E- d5 r, T
http://clp.sagepub.com
' I p/ \& B, mhosted at
+ O8 D- w3 B3 D Phttp://online.sagepub.com
( e' k) s# n& U& `. wPrecocious puberty in boys, central or peripheral,
" ^/ l6 _/ W! v. J |% k/ cis a significant concern for physicians. Central6 p5 g) G7 ?. l5 K3 ]+ X# {
precocious puberty (CPP), which is mediated
* y6 u4 V/ J/ M6 k5 Nthrough the hypothalamic pituitary gonadal axis, has$ k2 k0 n0 m9 E
a higher incidence of organic central nervous system
; ?5 Z( u; r, @) ], Vlesions in boys.1,2 Virilization in boys, as manifested8 R e9 g3 s5 U
by enlargement of the penis, development of pubic2 j3 W; g+ U+ E( f
hair, and facial acne without enlargement of testi-
; n1 l. s. x& w/ |/ U, v ]1 acles, suggests peripheral or pseudopuberty.1-3 We* b/ y6 f: n# E$ _! a5 E3 z/ E
report a 16-month-old boy who presented with the% u) ?1 s" ~ o& G9 w
enlargement of the phallus and pubic hair develop-
6 U o9 s# y5 Y6 I4 u) m" Yment without testicular enlargement, which was due
# m" O" @8 r) u5 wto the unintentional exposure to androgen gel used by
9 h8 I1 o0 z ?the father. The family initially concealed this infor-
1 x1 V1 k& w- `) ]- Wmation, resulting in an extensive work-up for this
) Y/ z- H7 K2 ?( t* k* [' z* ~# wchild. Given the widespread and easy availability of5 I5 _7 x. J# _/ [/ K3 l
testosterone gel and cream, we believe this is proba-
: E" j0 S3 S5 O1 l% E" Wbly more common than the rare case report in the
# a& H& |7 B3 @literature.4+ A; g: o& b5 O1 G- O
Patient Report
6 D( y3 i9 N m- x* `. o& J+ jA 16-month-old white child was referred to the
* X2 h8 V! J) m) tendocrine clinic by his pediatrician with the concern, A& d" D% d/ x6 o
of early sexual development. His mother noticed
, v5 P6 `. P5 `1 Q+ Z) J3 klight colored pubic hair development when he was
* R, J# v! j, h* q2 RFrom the 1Division of Pediatric Endocrinology, 2University of; d- F. q* [5 d
South Alabama Medical Center, Mobile, Alabama.' E/ I- |; H9 l8 j, Z
Address correspondence to: Samar K. Bhowmick, MD, FACE,1 r: [2 L P$ ~# M/ o5 X6 l
Professor of Pediatrics, University of South Alabama, College of. b( h: W x ?- b$ t
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
) E4 [) j( n& C3 i1 a, xe-mail: [email protected].
- K9 R' }% N% \* ^# a% m7 pabout 6 to 7 months old, which progressively became& c- ~ [4 u ^6 l
darker. She was also concerned about the enlarge-
1 Q, j+ `* T, W* x4 @ment of his penis and frequent erections. The child7 Q k e# J" v; E% L! }
was the product of a full-term normal delivery, with
2 L. ]3 g# W# h3 u ^) [& r' `a birth weight of 7 lb 14 oz, and birth length of( z0 q: {: H; D5 ~' U. c, z
20 inches. He was breast-fed throughout the first year
: J2 G/ }; F2 W. k- F4 n* k" U+ Uof life and was still receiving breast milk along with
5 t& x: z% K# Isolid food. He had no hospitalizations or surgery,
! M. J% ^, f6 K n1 T3 {and his psychosocial and psychomotor development1 P3 e2 k/ y' j2 x- N% t" w& g
was age appropriate.
^' J H# z( o9 L5 n% DThe family history was remarkable for the father,+ o$ O# q0 [6 w: H' _
who was diagnosed with hypothyroidism at age 16,
; C% ^3 k$ I' S3 Y- lwhich was treated with thyroxine. The father’s& m {$ {: \# u2 U
height was 6 feet, and he went through a somewhat
/ Z4 d: j1 O! E5 N8 k8 T1 W) [1 cearly puberty and had stopped growing by age 14.
% I- \0 n m/ K& e) oThe father denied taking any other medication. The7 j; Q. R1 C, y. G. i/ _4 q/ M
child’s mother was in good health. Her menarche" }# Z2 P: ~) J) G9 G I# K* ~- c' d
was at 11 years of age, and her height was at 5 feet
4 m! u# s+ l( ?" j0 `+ A0 ~$ A5 inches. There was no other family history of pre-
9 n; Y+ x2 _ S7 V4 r3 R" ^+ acocious sexual development in the first-degree rela-
$ |0 j* g) @' H" A! ?1 Stives. There were no siblings.8 Y7 c0 x3 T4 s7 b" Z E% ^' Z" n
Physical Examination
! f1 \! c) n T( fThe physical examination revealed a very active,
2 _- U7 R! Z4 L; B/ K! K. `) |# Mplayful, and healthy boy. The vital signs documented
: k$ P. H: _2 C: r3 Da blood pressure of 85/50 mm Hg, his length was7 {* y1 z7 R7 \' O, Q) B
90 cm (>97th percentile), and his weight was 14.4 kg4 `$ X- _ `: X/ N9 x9 C# n- m
(also >97th percentile). The observed yearly growth
0 b5 h6 y* ]1 u. h* \3 C2 ]velocity was 30 cm (12 inches). The examination of. E \7 ?; a! U+ w
the neck revealed no thyroid enlargement.
9 y7 Q4 s) e$ e- B7 C GThe genitourinary examination was remarkable for
8 p- }" ^" F3 |! ?$ Y7 i/ Zenlargement of the penis, with a stretched length of
6 o. k p4 Y$ E5 C l$ v' r3 { e8 cm and a width of 2 cm. The glans penis was very well
6 N5 w9 t6 s& ~' w kdeveloped. The pubic hair was Tanner II, mostly around
' v0 F) _- H O4 i9 P& v( \540
: q6 u6 q& f: Z7 p% j4 ]6 Mat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
& \5 [8 m$ M2 o, N9 l. kthe base of the phallus and was dark and curled. The' L. o6 m1 n/ Y9 g- A" S7 k b4 A: E
testicular volume was prepubertal at 2 mL each.
, h" a* _( g8 `& r4 N( A2 H. ^The skin was moist and smooth and somewhat/ V) q0 j6 t6 E* Y
oily. No axillary hair was noted. There were no& [+ }4 R9 R) j8 [- E3 n
abnormal skin pigmentations or café-au-lait spots.- R2 Y# P" A% Q5 i# V0 ~
Neurologic evaluation showed deep tendon reflex 2+
; P; [9 E9 S/ v! e; Q! ]8 L. ebilateral and symmetrical. There was no suggestion
0 q- Q1 @* @" b# n; f. dof papilledema.
, m1 O9 ?! K% pLaboratory Evaluation# u/ T1 x4 u+ v3 H4 }% F# c
The bone age was consistent with 28 months by
: c$ S8 G6 P2 ?/ e. p+ ]using the standard of Greulich and Pyle at a chrono-3 J! Z" k) J, w6 ]9 G- x
logic age of 16 months (advanced).5 Chromosomal
0 R% I$ N( O& X5 N: I! Rkaryotype was 46XY. The thyroid function test. i" C L, d1 A& I
showed a free T4 of 1.69 ng/dL, and thyroid stimu-( x q; q4 N. f9 Z# l+ f; n
lating hormone level was 1.3 µIU/mL (both normal).7 e) L b8 g8 s! v3 @- ~2 n( V
The concentrations of serum electrolytes, blood
7 ?0 ]) {( u% e/ Hurea nitrogen, creatinine, and calcium all were" h% d+ _, b9 w" B; b
within normal range for his age. The concentration
9 t9 J% O6 N* C3 ]/ ]* a% X7 @' cof serum 17-hydroxyprogesterone was 16 ng/dL
$ y$ H) G1 r' Q1 d: C(normal, 3 to 90 ng/dL), androstenedione was 20) w: ?# U) N9 J5 a
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-2 p+ d+ D. A7 |; s6 q+ f
terone was 38 ng/dL (normal, 50 to 760 ng/dL),- O; n4 d* w# v2 |
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
' P5 L* J: H. X% x2 v0 I/ w49ng/dL), 11-desoxycortisol (specific compound S)
) F& E( i3 Z& _$ p, ^% Twas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
% s* Y& ^6 B4 v0 Atisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total' K( X* Y d3 f- U K' c" p" |
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),/ d1 Y) d5 Z6 h) v' r
and β-human chorionic gonadotropin was less than, I7 N5 a1 G$ N9 R+ _
5 mIU/mL (normal <5 mIU/mL). Serum follicular
( T ]% c+ ^& A, Y# B' g8 Y, _stimulating hormone and leuteinizing hormone# a8 z4 F" S8 ?
concentrations were less than 0.05 mIU/mL0 s. z8 h6 w5 ~6 t) i2 E
(prepubertal).% v0 B: Z) u, O0 U6 A
The parents were notified about the laboratory
3 u! h, ]1 k9 {' C) Gresults and were informed that all of the tests were N0 c {1 D/ X B% `$ F" Z1 S- d
normal except the testosterone level was high. The
+ b: P# u. s' e/ \& S8 Ufollow-up visit was arranged within a few weeks to. }% A9 [: F9 N1 D2 {, `
obtain testicular and abdominal sonograms; how-/ b) V' d5 ]) k% O# i$ B
ever, the family did not return for 4 months.
* q( D' J! l) z) I. K- yPhysical examination at this time revealed that the9 q5 P& v, s: D. s' I
child had grown 2.5 cm in 4 months and had gained6 r: @6 A7 d3 i: D( b2 y
2 kg of weight. Physical examination remained
6 `8 V6 i9 v# q7 S: {! t: D. Runchanged. Surprisingly, the pubic hair almost com-: p* C8 W* o, ~) @( r
pletely disappeared except for a few vellous hairs at) G& V9 Z8 b9 V1 k2 `' S
the base of the phallus. Testicular volume was still 29 ~: q( k3 w. r8 B2 S, Y
mL, and the size of the penis remained unchanged.! k+ S$ k$ h. L/ n
The mother also said that the boy was no longer hav-: V& ^0 w' e) r1 E
ing frequent erections.
4 U1 S( W4 u. U& O$ n$ V" uBoth parents were again questioned about use of
$ l0 g x d7 y* ^' g: C* @any ointment/creams that they may have applied to
% o6 m2 T& I | Hthe child’s skin. This time the father admitted the
, P, e9 |5 N& VTopical Testosterone Exposure / Bhowmick et al 5410 K7 `7 n4 O! l' U7 k
use of testosterone gel twice daily that he was apply-
% O2 l, A" V) y) r6 `4 M1 z4 r( G2 Ring over his own shoulders, chest, and back area for- A$ D. ^+ o! P5 P
a year. The father also revealed he was embarrassed8 F8 ~; u6 }/ ?. f8 Y: `: P
to disclose that he was using a testosterone gel pre-
. @; x1 |% X9 e4 z0 X4 y) O. `scribed by his family physician for decreased libido
$ Z0 d0 u$ P* R0 m% Q6 n6 Ksecondary to depression.; G/ ?# K8 M0 w
The child slept in the same bed with parents.
+ a3 j9 ?; q& g) ^1 x: PThe father would hug the baby and hold him on his
8 N) W F$ S& ichest for a considerable period of time, causing sig-3 ?; |9 z. q& X
nificant bare skin contact between baby and father.
9 n: Z) k! V7 R' N3 b2 w5 OThe father also admitted that after the phone call,
5 _' k* Y/ E1 X! @7 rwhen he learned the testosterone level in the baby# A _3 k3 C5 n) I. c* ], X. Y
was high, he then read the product information' Y9 j6 q0 `4 A
packet and concluded that it was most likely the rea-! k4 M8 b0 ]5 z T' R, I: P8 U
son for the child’s virilization. At that time, they
- o0 v7 D1 @* Fdecided to put the baby in a separate bed, and the! P" g1 A3 K: T- y, `! s
father was not hugging him with bare skin and had
! E8 k) J6 P/ O2 H" u" d" y* `3 P. O0 ebeen using protective clothing. A repeat testosterone
+ x3 o ^5 H7 V5 M9 Otest was ordered, but the family did not go to the
, A0 r1 K3 R7 k% a* Slaboratory to obtain the test.6 D0 I1 `8 |: h0 @0 {
Discussion$ K* h# }& W4 }4 T% y: E$ W$ `8 D
Precocious puberty in boys is defined as secondary
5 w& Y1 I, |. X5 s5 ~4 W0 i2 {9 rsexual development before 9 years of age.1,4
& l( V* F. {3 S" \Precocious puberty is termed as central (true) when2 v) l0 j/ } ^; F# ^, g1 s
it is caused by the premature activation of hypo-% k8 S% V6 {4 |
thalamic pituitary gonadal axis. CPP is more com-! P- |- Y0 ?3 h9 F' y3 D7 Y' c
mon in girls than in boys.1,3 Most boys with CPP% u: w/ \2 b }8 ~* q# k- F6 ]( m) k/ D
may have a central nervous system lesion that is
2 @0 `: Q/ g, m2 }0 q+ F. sresponsible for the early activation of the hypothal-, z$ G- a" z! Q8 Z/ V( \
amic pituitary gonadal axis.1-3 Thus, greater empha-# O( Y( }0 b) z3 z! m
sis has been given to neuroradiologic imaging in, S6 {0 `' I2 s* m4 h, ^
boys with precocious puberty. In addition to viril-6 b( ?2 v4 T2 Q' K/ F4 d
ization, the clinical hallmark of CPP is the symmet-" ^: u1 |# Q( C
rical testicular growth secondary to stimulation by+ r8 A' b0 x7 D7 ]2 z
gonadotropins.1,3
' U6 p7 H8 q8 `: [( Y# q6 AGonadotropin-independent peripheral preco-
+ a U4 ?- `& A/ Q7 o: jcious puberty in boys also results from inappropriate
/ r3 p+ ^" q$ H6 {3 _9 Yandrogenic stimulation from either endogenous or
, W; U2 {7 i$ R$ f2 Z& H P+ }$ S+ Y6 cexogenous sources, nonpituitary gonadotropin stim-
* e( R- b- g) V4 f- Pulation, and rare activating mutations.3 Virilizing3 G. [; P4 T5 \# f. }
congenital adrenal hyperplasia producing excessive6 E$ S3 y h2 I) z( S7 Q% K
adrenal androgens is a common cause of precocious0 a* m- l; Q* J4 P3 D, b
puberty in boys.3,4/ J5 D0 w& X' p( r8 P7 {/ I
The most common form of congenital adrenal
& ?1 W% ~# B1 w3 H3 u2 Xhyperplasia is the 21-hydroxylase enzyme deficiency.7 `* }" S- l+ j2 F' O
The 11-β hydroxylase deficiency may also result in
% \4 a6 G; J0 g. o/ Z9 B( K. ?) w+ mexcessive adrenal androgen production, and rarely,
# E7 g A: Y. x, h+ b8 ^an adrenal tumor may also cause adrenal androgen6 \' Q! B1 Q1 Y
excess.1,3
$ N& j& I. s* iat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from' z! d/ G4 @9 b {
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007$ \/ f' G0 Q* O5 C2 a6 Q. ^
A unique entity of male-limited gonadotropin-
, z+ a0 L: @) b+ m* Bindependent precocious puberty, which is also known
9 V2 [5 z- A, O- o. Sas testotoxicosis, may cause precocious puberty at a" ]: c; Y) M& |% v9 n5 q
very young age. The physical findings in these boys7 v, Z% A% W/ H9 G ]8 J) w
with this disorder are full pubertal development,
$ K% O7 g U; C- V9 U. Y; R/ uincluding bilateral testicular growth, similar to boys8 h& A6 E6 u. Q2 D7 c) ~" A8 _; k2 T
with CPP. The gonadotropin levels in this disorder* |1 m1 B9 \* G" H
are suppressed to prepubertal levels and do not show
% O* M+ i \3 e+ P/ y+ Jpubertal response of gonadotropin after gonadotropin-
* A; i( ]+ s6 G5 H' z- Nreleasing hormone stimulation. This is a sex-linked
7 D8 J1 w8 V* t7 Wautosomal dominant disorder that affects only) V( |! w9 J/ I' G+ v
males; therefore, other male members of the family
2 e# [7 G7 B4 ~' @* o( xmay have similar precocious puberty.3
! _+ V0 F2 V: S% H: zIn our patient, physical examination was incon-8 B5 ]+ f6 v5 e. {) B- c* L* r
sistent with true precocious puberty since his testi-
' }3 @) I" F& Pcles were prepubertal in size. However, testotoxicosis7 S+ G! c. J: m( Y
was in the differential diagnosis because his father5 J7 _7 u0 m/ X9 x2 A# h+ t/ F
started puberty somewhat early, and occasionally,
6 ~9 E: C2 g0 Ttesticular enlargement is not that evident in the
% V( R, b0 N5 b: w0 V& Z7 Ybeginning of this process.1 In the absence of a neg-( m1 C! G. [5 }& J
ative initial history of androgen exposure, our
& n8 ^5 F( k/ q/ Y7 V& Dbiggest concern was virilizing adrenal hyperplasia,1 e3 {& U: v. J: f' }/ o, |! J: `
either 21-hydroxylase deficiency or 11-β hydroxylase
E. m0 E7 Z" G7 F7 x( R) t. Pdeficiency. Those diagnoses were excluded by find-3 q8 }. e- L8 T/ x( M
ing the normal level of adrenal steroids.
: f/ b' y' E, mThe diagnosis of exogenous androgens was strongly g+ T' p; O9 v7 g
suspected in a follow-up visit after 4 months because3 Z* B S, `. Y3 s/ p
the physical examination revealed the complete disap-
# G& B# q' {, {pearance of pubic hair, normal growth velocity, and6 ~1 q% s) ]. D: u/ ?; H4 v- M: ~( q2 v
decreased erections. The father admitted using a testos- G$ D1 [0 v' F p0 n
terone gel, which he concealed at first visit. He was* T: ~* c/ j. m7 Y, ]
using it rather frequently, twice a day. The Physicians’
; s" g" M" O7 P0 ^$ @Desk Reference, or package insert of this product, gel or
) ~8 s2 b; q! U2 acream, cautions about dermal testosterone transfer to. A7 j' H6 ~& W4 J8 X; `
unprotected females through direct skin exposure.
6 f( Z3 k: v/ C7 c1 T% zSerum testosterone level was found to be 2 times the6 g& K) f1 ~ U
baseline value in those females who were exposed to
. e, j$ S7 s3 J: p8 t' beven 15 minutes of direct skin contact with their male+ f! |0 |% }: V( V) q y6 j! a
partners.6 However, when a shirt covered the applica-
5 i, A, u. n7 x6 y0 c% w$ `( Dtion site, this testosterone transfer was prevented.
, _$ U, b* L- e; p9 f9 p! r7 zOur patient’s testosterone level was 60 ng/mL,/ b" U; Y/ w1 X- `4 t0 A4 A
which was clearly high. Some studies suggest that
4 W; @, Q5 ~2 [( kdermal conversion of testosterone to dihydrotestos-( j) J0 w$ Q8 \" \3 @$ Q
terone, which is a more potent metabolite, is more
" D8 \5 l; B; J, F; R. Mactive in young children exposed to testosterone
5 {' o# [! b) H* \3 z6 n' ?exogenously7; however, we did not measure a dihy-
5 [ C9 `* C- r# Ldrotestosterone level in our patient. In addition to
) z; r5 }- X) J* _( c& @virilization, exposure to exogenous testosterone in# ~4 D$ Z. C. _' L* a) r8 x4 ]
children results in an increase in growth velocity and
5 S; x, A+ T3 j- P9 A7 iadvanced bone age, as seen in our patient.
9 i9 C3 Y. ~4 C. e( oThe long-term effect of androgen exposure during
$ K$ b5 ~. {4 j& k2 Y/ hearly childhood on pubertal development and final
* ~: k" d5 R; k5 R5 r# Radult height are not fully known and always remain
( z8 k/ e: r' d) A+ ia concern. Children treated with short-term testos-
* r1 B. X' P7 W3 } d4 Q- nterone injection or topical androgen may exhibit some
0 G; f8 Q2 m f3 d1 Facceleration of the skeletal maturation; however, after% A- h7 [" Y5 w5 M
cessation of treatment, the rate of bone maturation* X- h8 M& y$ V( d6 F* A# e
decelerates and gradually returns to normal.8,9 ]2 I( R7 B& G6 h8 y
There are conflicting reports and controversy
+ g: [. H5 i1 Oover the effect of early androgen exposure on adult
9 Q% E3 H# k2 [! }. U+ { Fpenile length.10,11 Some reports suggest subnormal# Z1 _2 N. `& i5 V8 B* Z1 k' r. J
adult penile length, apparently because of downreg-6 r! Y9 I4 \$ h) M9 E3 y5 S
ulation of androgen receptor number.10,12 However,
/ F% t6 J9 A, d2 \: W) `7 FSutherland et al13 did not find a correlation between
7 t6 S) K2 n* \( L* ?8 tchildhood testosterone exposure and reduced adult
5 p0 l: e4 u1 i/ h5 k' wpenile length in clinical studies.0 O# l; C- h* D
Nonetheless, we do not believe our patient is
* V. ?( s: t* Dgoing to experience any of the untoward effects from/ ], [2 e1 e& A! a) y( S, `
testosterone exposure as mentioned earlier because, \4 d6 q' x5 N8 P# `, Q
the exposure was not for a prolonged period of time./ F" b9 B( L; O: O- [
Although the bone age was advanced at the time of
# k. W+ P- p. q: [; j& Adiagnosis, the child had a normal growth velocity at! D/ J9 x3 [) I2 _3 K
the follow-up visit. It is hoped that his final adult' V3 I; Y, K& U, r" p5 A [! n
height will not be affected.; @3 J1 d, v$ @, S; e: g9 s
Although rarely reported, the widespread avail-
8 R. m' B4 P4 c; m/ W0 l) lability of androgen products in our society may
' B* c" Q5 v, y0 U( C" u# lindeed cause more virilization in male or female
- G p# A/ u: r/ }( x! }* A! fchildren than one would realize. Exposure to andro-1 \- X# ]7 m; k2 F
gen products must be considered and specific ques-2 m3 T5 R/ C* e! \( @" A4 e
tioning about the use of a testosterone product or
2 g: r# Z; r" [1 K) Ggel should be asked of the family members during+ A7 L: v7 p+ |9 B; X
the evaluation of any children who present with vir-0 C8 m& D0 [. U2 v% q
ilization or peripheral precocious puberty. The diag-/ J" T- G( Z1 v6 w! F7 Q5 P
nosis can be established by just a few tests and by* C+ O" ]" r5 V, _
appropriate history. The inability to obtain such a
5 B4 S# a5 s: {. ^: {. J6 H/ Y Yhistory, or failure to ask the specific questions, may4 G% k# s7 d* P4 h* t2 Q! o
result in extensive, unnecessary, and expensive3 A0 a J ^# d3 I8 ], W A) v, k: _
investigation. The primary care physician should be
2 Y- d' N* P$ n. Iaware of this fact, because most of these children- _& X% t+ G$ A& G+ v* }3 [
may initially present in their practice. The Physicians’
; d8 h0 r" ^9 o$ l" T% xDesk Reference and package insert should also put a9 o) ^$ x; r3 y5 ], X* j/ R
warning about the virilizing effect on a male or
$ o0 V, O- D; R( y* L, Dfemale child who might come in contact with some-8 h( W9 x8 d( G6 C7 a! W1 e7 g
one using any of these products.4 l+ x1 t: w$ k1 b
References4 X1 y& F# ?4 P7 B. k
1. Styne DM. The testes: disorder of sexual differentiation% x2 Q8 f* q9 K ?( j' C8 L
and puberty in the male. In: Sperling MA, ed. Pediatric9 p+ [3 ]0 Z2 `9 X2 v+ @# u
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
3 _6 B# n5 x- L* [2002: 565-628.6 w# H6 k* y, Q, X$ e: o
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
, |) [! c: f6 P! apuberty in children with tumours of the suprasellar pineal |
|