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Sexual Precocity in a 16-Month-Old
% R3 F R3 {* _4 f; _Boy Induced by Indirect Topical" x8 R" J3 ?& I" L e
Exposure to Testosterone. ]# [* |. Q4 T, V$ ^
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
" X' [( L4 F) p1 ]' v4 h6 q; `and Kenneth R. Rettig, MD1' t0 z) R6 c, I9 p( o7 q
Clinical Pediatrics
/ \8 b% ]; E8 e2 }Volume 46 Number 6* R6 U3 r- g) V: s
July 2007 540-543# Q/ W9 O! c; d! p: P0 x/ S V& t8 T
© 2007 Sage Publications
: j% H2 V G3 @5 S10.1177/0009922806296651
& P3 p$ Q+ e+ r$ I- K0 T5 f6 A, {: J' u Hhttp://clp.sagepub.com
7 T* |, }2 ]4 \) m% f+ q* I* C3 ]hosted at( s8 W/ w- b6 W# r! u
http://online.sagepub.com
6 q" m# p8 k2 m' D9 I6 O/ r& V! zPrecocious puberty in boys, central or peripheral,$ ~; ]' c& N x
is a significant concern for physicians. Central- d$ U6 e2 B4 N% f4 Z4 w: ?9 e
precocious puberty (CPP), which is mediated% R' n2 u$ Q; D! ~' A
through the hypothalamic pituitary gonadal axis, has0 p! g( Q5 S1 g6 G& z1 `+ N
a higher incidence of organic central nervous system8 D6 w1 v6 i0 V3 J" ~9 Z
lesions in boys.1,2 Virilization in boys, as manifested
4 Q( v2 U* f, k8 ^by enlargement of the penis, development of pubic
5 g( f: X! c& G# ^8 P1 `hair, and facial acne without enlargement of testi-
* y. T" X! t) f( Scles, suggests peripheral or pseudopuberty.1-3 We
- k. }+ ]0 _9 p6 i& v5 F {1 Lreport a 16-month-old boy who presented with the
0 B! L) ~, m1 Q& L: b7 q8 Z) @enlargement of the phallus and pubic hair develop-
{. \5 g& w% T3 ` a' D: D9 Lment without testicular enlargement, which was due3 ?6 f3 e* h! R; |# A; z% d
to the unintentional exposure to androgen gel used by
A0 y% p: C: h5 l$ }- xthe father. The family initially concealed this infor-
8 w4 g; ?7 S7 d8 N# h7 R+ I0 ~( c; T9 Lmation, resulting in an extensive work-up for this
* x; Y" b* A% B0 B. n9 Dchild. Given the widespread and easy availability of5 B4 }% N4 C. ]8 q- U) @
testosterone gel and cream, we believe this is proba-9 i+ ?' d: `3 g) \% E% d2 h
bly more common than the rare case report in the* e* |5 R" o7 O
literature.43 w; q8 H' t1 S+ P( N
Patient Report
% v* H. _- e; e) A, ^; }/ ^A 16-month-old white child was referred to the
' P& Y. r# ]! U. x4 dendocrine clinic by his pediatrician with the concern" H3 O1 n3 Q2 ^1 W! q: x
of early sexual development. His mother noticed
- t. B s1 B# glight colored pubic hair development when he was
. p+ W& F+ x2 v* D/ a$ gFrom the 1Division of Pediatric Endocrinology, 2University of
. ]& y( a0 E! c+ L) KSouth Alabama Medical Center, Mobile, Alabama., }! m7 O5 e" p1 D1 R; b/ M
Address correspondence to: Samar K. Bhowmick, MD, FACE,
- W: F: g. ?# p3 V# q0 mProfessor of Pediatrics, University of South Alabama, College of
F$ M5 g/ z. {; RMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;3 W) f1 s" H! ]
e-mail: [email protected].
. D% H, O2 v1 ?) O; A) h# L7 Yabout 6 to 7 months old, which progressively became
7 d+ q6 g1 I0 m# a) ?9 @darker. She was also concerned about the enlarge-
; j, t7 p0 P! {- x7 s3 ]ment of his penis and frequent erections. The child
7 U6 k& H2 ?+ N) [; d+ t2 Kwas the product of a full-term normal delivery, with
+ d2 i& x$ k# w, Q' a6 ?a birth weight of 7 lb 14 oz, and birth length of
( ]/ h% g: i0 G& b; m+ `% R! y20 inches. He was breast-fed throughout the first year
" }2 ?& q, }7 y0 S4 d, a0 c1 @of life and was still receiving breast milk along with
: b* T ~" \$ [4 d; M7 J0 @ O! rsolid food. He had no hospitalizations or surgery,
: k3 u4 ]$ }3 g9 A+ h5 a" B3 d- Nand his psychosocial and psychomotor development# d5 T5 | d* x9 I
was age appropriate.9 y- c+ h! U. f) f, o
The family history was remarkable for the father,: @- b' Z9 F4 D' d8 F
who was diagnosed with hypothyroidism at age 16,
: R3 O" I. C% n' v4 Dwhich was treated with thyroxine. The father’s7 d" b% z' h+ S) J" V1 k5 O4 h& Y
height was 6 feet, and he went through a somewhat
. i" ?/ H- y& ]6 E* bearly puberty and had stopped growing by age 14.; R) X0 u. W* M0 o" p3 H
The father denied taking any other medication. The0 R( W2 a* b, a
child’s mother was in good health. Her menarche& |$ c- w, W0 E# {/ H
was at 11 years of age, and her height was at 5 feet, \$ u2 J+ c# I0 b; a. d( m
5 inches. There was no other family history of pre-, }" N( q: }. ^8 H) N
cocious sexual development in the first-degree rela-0 k1 O/ E( n n v( |5 E4 g
tives. There were no siblings.' K$ S3 e9 C# ~0 Y4 `6 c! i4 b
Physical Examination( L3 B V; x9 O, W
The physical examination revealed a very active,5 p1 ?$ D) j2 G, p' N
playful, and healthy boy. The vital signs documented
" Q$ ^3 |: k) X5 b, Ia blood pressure of 85/50 mm Hg, his length was) u y) N% x) Y5 |# A. H
90 cm (>97th percentile), and his weight was 14.4 kg7 M8 M: N. p2 F3 p
(also >97th percentile). The observed yearly growth
- q5 }. W) x9 y2 J2 uvelocity was 30 cm (12 inches). The examination of
0 z- F. ?# Z% r, c7 S" Sthe neck revealed no thyroid enlargement.
- K; e' i/ ~6 ?+ b( mThe genitourinary examination was remarkable for
+ N- B2 U' [3 k* F# M) ?4 E( wenlargement of the penis, with a stretched length of" {; Y1 u) B& r! L* l* h
8 cm and a width of 2 cm. The glans penis was very well
$ [ ^) x& g" I8 M# Y* |developed. The pubic hair was Tanner II, mostly around
4 {, ^* G% p# H, g0 m540
$ ]; j3 ^3 e# B5 U0 b5 aat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
9 j/ [+ ~( |, V% S6 f: xthe base of the phallus and was dark and curled. The
/ c0 y6 r+ W# `8 K ]testicular volume was prepubertal at 2 mL each.
# d! ` f; r) K. j- wThe skin was moist and smooth and somewhat- ~8 z7 x" V( K! q. Y+ g3 F5 A7 o
oily. No axillary hair was noted. There were no2 r: P1 E5 T# O1 |2 s% F) @
abnormal skin pigmentations or café-au-lait spots.' V0 x- n- l7 ?: a
Neurologic evaluation showed deep tendon reflex 2+
* q# d, S/ j/ l* ]7 g% {0 Nbilateral and symmetrical. There was no suggestion
- p; {1 E2 a$ g+ Jof papilledema.
; D, _6 M# x( C! g2 l8 xLaboratory Evaluation; w4 u3 U: m& R
The bone age was consistent with 28 months by
: v, d- H6 I8 F* Y$ D9 u5 Gusing the standard of Greulich and Pyle at a chrono-) n9 e$ g; X6 M% o; w/ y
logic age of 16 months (advanced).5 Chromosomal* W, Z% W& o/ v0 o( Q7 q
karyotype was 46XY. The thyroid function test
. B4 z0 r3 X$ B) g7 |3 _showed a free T4 of 1.69 ng/dL, and thyroid stimu-
5 w+ m. w% S& c9 `+ X+ Nlating hormone level was 1.3 µIU/mL (both normal).
0 }) z' J- F* z8 j- W+ _) b; vThe concentrations of serum electrolytes, blood8 ]( j$ d4 Q2 | j9 f
urea nitrogen, creatinine, and calcium all were
$ u4 {# L" M* D- p, h/ v1 jwithin normal range for his age. The concentration7 r+ s+ J' U$ q$ o+ v% {
of serum 17-hydroxyprogesterone was 16 ng/dL& e7 s/ c0 T# e& b( l
(normal, 3 to 90 ng/dL), androstenedione was 20% t6 ^( M( R9 R% q
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-7 B( W K+ @9 E3 ?0 t
terone was 38 ng/dL (normal, 50 to 760 ng/dL),) h9 W7 u. a8 b. o
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
0 R% W+ K* f7 Y; U7 Y9 U49ng/dL), 11-desoxycortisol (specific compound S)
0 F+ n% t3 f( z# z+ d. v6 M; ywas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
5 ]3 {6 y8 s( M) u; u7 ~& ^tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total# m2 X+ f& f4 m2 |
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),. ]- f( I1 Y# s# Y
and β-human chorionic gonadotropin was less than7 Q S$ j" B P! O, N
5 mIU/mL (normal <5 mIU/mL). Serum follicular
0 j8 L0 v7 J5 x2 t3 |3 v! ?+ `stimulating hormone and leuteinizing hormone" N" B0 T- N5 C3 L; I9 U% P
concentrations were less than 0.05 mIU/mL
7 x( H/ }. p+ z" e! ](prepubertal).
% O7 G4 M! B% @8 l6 AThe parents were notified about the laboratory2 P; \4 Q( }( T: s3 [6 @3 w
results and were informed that all of the tests were7 `+ K' S6 {' \' ~' M5 O8 }
normal except the testosterone level was high. The
, x& ?; Z0 B9 y$ v/ x7 E6 x! ofollow-up visit was arranged within a few weeks to2 M/ A# _- I V6 p
obtain testicular and abdominal sonograms; how-7 D4 e7 [/ `/ H K1 M2 h
ever, the family did not return for 4 months." W( l% R4 E# A7 ^9 O) H
Physical examination at this time revealed that the) d7 f$ Q$ t8 q6 a3 S, B) a2 ~
child had grown 2.5 cm in 4 months and had gained+ y* m+ w: o N i C
2 kg of weight. Physical examination remained9 w& _7 q+ X. |" r
unchanged. Surprisingly, the pubic hair almost com- e( n9 k" E, I. J. S7 X4 z0 @
pletely disappeared except for a few vellous hairs at8 U: Q i) c! f! \# w4 a6 S
the base of the phallus. Testicular volume was still 2
& k+ N; B) v2 c4 W) h9 [mL, and the size of the penis remained unchanged.
+ r% S) n+ v( U0 zThe mother also said that the boy was no longer hav-4 O( y& `9 ]6 w/ P+ T5 r$ s
ing frequent erections.& x5 W+ z# ]! a4 G4 z
Both parents were again questioned about use of7 f5 d" M0 H5 n$ p: |
any ointment/creams that they may have applied to
1 h* [5 f- u0 i \* _the child’s skin. This time the father admitted the
- Q8 ~4 h0 X+ t8 |Topical Testosterone Exposure / Bhowmick et al 5414 T' E4 T' g7 R/ i; ~
use of testosterone gel twice daily that he was apply-
e$ P& b2 U" a$ Iing over his own shoulders, chest, and back area for. }: r- P- @' ^) u9 Q+ o' b
a year. The father also revealed he was embarrassed
) j1 S W/ M) A, m6 \9 Q' i9 D8 ` Nto disclose that he was using a testosterone gel pre-
6 f0 F1 \7 c8 K; j, M( gscribed by his family physician for decreased libido" ^% q' f' ]; v2 [
secondary to depression.
+ D- J- d4 k j% B# xThe child slept in the same bed with parents.! [3 w# A5 P6 z+ N+ k( U6 \
The father would hug the baby and hold him on his
6 W! T8 w0 s1 vchest for a considerable period of time, causing sig-
& w* h4 G, Q5 F: p% A) P# X bnificant bare skin contact between baby and father.
2 I1 p! m' F' R' I$ e$ [' ]The father also admitted that after the phone call,
) q7 O: ]) Q& ^when he learned the testosterone level in the baby
$ H$ w& ?# `+ [3 r4 P+ s0 uwas high, he then read the product information
4 L- K- H- t* c+ D# `packet and concluded that it was most likely the rea-, a( j( v3 y% P1 A: u8 h
son for the child’s virilization. At that time, they7 F! Z4 z- l( q: e( |; a/ S3 f
decided to put the baby in a separate bed, and the
- O2 N; |, Z O; X: lfather was not hugging him with bare skin and had3 C7 O7 k' E5 v I U; d! v
been using protective clothing. A repeat testosterone
6 X9 Z+ S0 |; g1 Ptest was ordered, but the family did not go to the
/ i% W' u# d Llaboratory to obtain the test.5 P$ c% r! [2 v% D: c; B* |5 s7 _7 M
Discussion
& k$ Z+ s' I6 `Precocious puberty in boys is defined as secondary
" |1 C9 Y# M6 G3 ?; ^" xsexual development before 9 years of age.1,4' t2 A# m; V4 ^2 @
Precocious puberty is termed as central (true) when+ w! t* V2 l g( [$ |
it is caused by the premature activation of hypo-
3 F4 h: U c1 v1 }9 A: tthalamic pituitary gonadal axis. CPP is more com-
+ z9 `* H7 l$ @$ J/ R9 z! w4 I$ wmon in girls than in boys.1,3 Most boys with CPP
9 V3 [7 B- q* _6 c# zmay have a central nervous system lesion that is
4 F+ c' k ?" iresponsible for the early activation of the hypothal-/ }" J. J+ @$ R6 L6 H" j4 G
amic pituitary gonadal axis.1-3 Thus, greater empha-- G- `( o# u3 |$ u; v' y( o
sis has been given to neuroradiologic imaging in
& J. H( h1 N) s2 y1 r0 {2 bboys with precocious puberty. In addition to viril-4 R- h; ~9 G" J1 W" s0 k* J
ization, the clinical hallmark of CPP is the symmet-
- Y/ H) q3 o0 z4 q' drical testicular growth secondary to stimulation by
/ Y: H, {& U4 [* D/ ngonadotropins.1,3
1 E2 A5 ^2 d9 k6 G {% KGonadotropin-independent peripheral preco-
" W% p: @7 Q+ @3 [& N3 Pcious puberty in boys also results from inappropriate
6 o- L* v( g+ N( Z3 [* Vandrogenic stimulation from either endogenous or
8 z2 p5 Z/ P1 y6 W& ?$ ]2 Nexogenous sources, nonpituitary gonadotropin stim-
9 G& F$ D7 |4 a: Z* yulation, and rare activating mutations.3 Virilizing
' F. ^. l3 T$ ccongenital adrenal hyperplasia producing excessive, f6 w8 B: o) S g9 Q
adrenal androgens is a common cause of precocious) b/ B: a# G- N, D$ s9 J
puberty in boys.3,4
9 y8 o- \; N7 t( S" W) X% kThe most common form of congenital adrenal
* S: W2 H$ ]- n% \: U# H) ]" @1 ]: Khyperplasia is the 21-hydroxylase enzyme deficiency.4 [5 o" [: f5 h/ e. b/ n: g
The 11-β hydroxylase deficiency may also result in
0 U, `" l, ?0 H0 S8 ^) ~. E3 Jexcessive adrenal androgen production, and rarely,
- g4 T* v; A% ~2 `an adrenal tumor may also cause adrenal androgen ?5 k0 b/ [! Z) h1 `
excess.1,3
' _1 e/ S7 T# W! x; w! Cat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from1 a6 l2 V6 S2 U* X
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
$ P4 H9 i, ~6 s6 _3 y6 cA unique entity of male-limited gonadotropin-( D3 {; u# P! O# ]# i
independent precocious puberty, which is also known
7 e1 f4 \4 U- B. t- Tas testotoxicosis, may cause precocious puberty at a
- x3 s6 m! B, v% b4 fvery young age. The physical findings in these boys
' R' P7 k% \# x5 b G1 R |with this disorder are full pubertal development,
# Z3 v/ ]8 r) U6 O4 vincluding bilateral testicular growth, similar to boys; c- L$ v" I% ]; l6 |; I. v; w
with CPP. The gonadotropin levels in this disorder# l5 K7 L. b8 A$ x! u, g0 v4 S' {
are suppressed to prepubertal levels and do not show
7 P6 E2 M' B( g0 Y, |pubertal response of gonadotropin after gonadotropin-4 y6 a3 |# o4 x
releasing hormone stimulation. This is a sex-linked# T# Y: c$ s" B% K* ^ M
autosomal dominant disorder that affects only( Q6 U. r9 t. }& F! d: Z* T% F
males; therefore, other male members of the family
. y* O* G/ ^1 u1 q8 U0 K, umay have similar precocious puberty.3
1 O* ~4 N- X o. ^: P: \. F& tIn our patient, physical examination was incon-; p; S' [% G5 b U, A/ Y
sistent with true precocious puberty since his testi-3 @' ^7 s& S: e9 @2 Z- c5 @
cles were prepubertal in size. However, testotoxicosis
9 b& i d( h) v; Q9 }) n! `) Ywas in the differential diagnosis because his father6 V u5 y8 ]3 }! Y) f a
started puberty somewhat early, and occasionally,9 |# U2 J; y/ E
testicular enlargement is not that evident in the; c( W" E# p4 Q# Z
beginning of this process.1 In the absence of a neg-' W3 V2 {# Z7 H" V7 ?' B/ ]
ative initial history of androgen exposure, our
! c. `" f, v0 K; m# p7 `biggest concern was virilizing adrenal hyperplasia,
1 p/ }9 A& S) Y2 q. Peither 21-hydroxylase deficiency or 11-β hydroxylase& f: Y- x3 c \# M) X$ K
deficiency. Those diagnoses were excluded by find-
7 U& ]* O( i2 ]# G# G# z7 Jing the normal level of adrenal steroids.
+ d6 T2 O9 y! D7 j1 mThe diagnosis of exogenous androgens was strongly
( p( ~8 Q! a/ q4 h# qsuspected in a follow-up visit after 4 months because
+ D: G. c1 t, x+ K1 V7 j: Uthe physical examination revealed the complete disap-
% H/ o( X" }9 t/ Zpearance of pubic hair, normal growth velocity, and
1 g* t0 {+ O' i/ q, Ldecreased erections. The father admitted using a testos-1 K0 U6 J& K8 A3 P! k, v3 o
terone gel, which he concealed at first visit. He was
7 f G- t) a0 U. j! w5 V6 Gusing it rather frequently, twice a day. The Physicians’
- J1 q$ G' l) q9 N' L. J2 dDesk Reference, or package insert of this product, gel or
( _, H- \, o4 H4 E+ R4 bcream, cautions about dermal testosterone transfer to0 [/ K8 {3 Y8 ?1 X+ E
unprotected females through direct skin exposure.' S7 [# S8 M% x
Serum testosterone level was found to be 2 times the* p: O' F3 _" w, ^
baseline value in those females who were exposed to
! `! ?! d, z3 {- O6 g3 ?- ]even 15 minutes of direct skin contact with their male
0 z$ k1 J4 G4 f; l. }partners.6 However, when a shirt covered the applica-' c3 b+ @) @1 q
tion site, this testosterone transfer was prevented.* L" I+ w* o: l8 C( l' ~" j+ o* j
Our patient’s testosterone level was 60 ng/mL,
, n9 h% x% r4 zwhich was clearly high. Some studies suggest that
6 f& w4 B( {8 n! k6 o, b2 V8 Wdermal conversion of testosterone to dihydrotestos-, U; e1 e$ p$ @
terone, which is a more potent metabolite, is more
8 K0 A' w4 A: x5 a: Aactive in young children exposed to testosterone
2 V) o( S2 W7 d0 B- J4 E% @$ jexogenously7; however, we did not measure a dihy- o3 W. @# e( i8 T
drotestosterone level in our patient. In addition to, t3 w7 n3 w! p5 a9 I) b
virilization, exposure to exogenous testosterone in
! K4 S8 B8 D ychildren results in an increase in growth velocity and/ W2 p" u* d! L* s. `% z* b. o
advanced bone age, as seen in our patient.
6 h: L3 S7 U0 S4 i8 VThe long-term effect of androgen exposure during3 e0 ?6 R+ W \* x0 y0 T* @
early childhood on pubertal development and final i/ m" S. _8 @9 L9 ^% Z# J: c7 X7 Z( F
adult height are not fully known and always remain
& D ?9 J2 N8 u |! b6 v5 ^a concern. Children treated with short-term testos-
; l8 g" S; o" N& l! zterone injection or topical androgen may exhibit some
$ t' G* y! ~4 @! qacceleration of the skeletal maturation; however, after5 M: n! `: l" I ?* l
cessation of treatment, the rate of bone maturation+ b6 v w$ J* F, M" j* l8 r
decelerates and gradually returns to normal.8,9
* c3 U; N. x, `$ f- ZThere are conflicting reports and controversy" i0 ?* `2 \5 R4 h: A% r
over the effect of early androgen exposure on adult
, n. E- D3 o( M$ i, j' B" epenile length.10,11 Some reports suggest subnormal: i9 O P' M. f# Y2 S2 V1 e4 i* l
adult penile length, apparently because of downreg-
2 V- x# o D& ?. {! t: g1 ?ulation of androgen receptor number.10,12 However,
# }* Q u" Y- l$ z2 t5 R4 R0 g! H7 ?4 [Sutherland et al13 did not find a correlation between
* `* f7 t$ E5 I$ Y, G& [childhood testosterone exposure and reduced adult
: D* u6 Y, m6 e+ y5 o5 Vpenile length in clinical studies.
% |- g' C. j9 \1 ?: `Nonetheless, we do not believe our patient is* D( v% L% [$ y. T% y0 ~$ m
going to experience any of the untoward effects from; s' u' P7 V* H7 H9 u8 j7 o9 @
testosterone exposure as mentioned earlier because
; x/ P0 V0 h! v! J6 G0 m0 P9 L3 U6 bthe exposure was not for a prolonged period of time.0 }7 l; _/ g ]! K: C
Although the bone age was advanced at the time of5 k" x _6 K7 k A) j
diagnosis, the child had a normal growth velocity at
) o3 D2 |0 ~( O1 `' Cthe follow-up visit. It is hoped that his final adult
; O% T3 ~( r+ u0 oheight will not be affected.1 ?9 Q1 U e1 L: o& x
Although rarely reported, the widespread avail-/ m/ O: H/ P9 j
ability of androgen products in our society may; K( p k) J3 k3 m# d+ E! D" o
indeed cause more virilization in male or female2 k. O- T. m' ^& M
children than one would realize. Exposure to andro- ~0 @9 g* E& y9 R" }" {! d
gen products must be considered and specific ques-
. u$ M" B8 f7 ?# A" x' @5 C0 X) [tioning about the use of a testosterone product or
: y9 C$ ~4 {8 t) s$ w, Fgel should be asked of the family members during
0 _+ h* F4 b+ {! P9 F" ~7 jthe evaluation of any children who present with vir-
9 |2 G% v( A6 K( Lilization or peripheral precocious puberty. The diag-
0 Q, c/ K1 r0 @/ F( H4 p7 jnosis can be established by just a few tests and by
( j( F- z( w1 U- ~: kappropriate history. The inability to obtain such a+ P8 w5 u5 V9 u6 F9 W$ |. j: e
history, or failure to ask the specific questions, may
# u2 c; q9 D F7 Z! R/ W6 q* ~3 m6 m: ~result in extensive, unnecessary, and expensive
* m6 Y1 U" j1 V( g' uinvestigation. The primary care physician should be
! z; ?; a' A( i& |' J( Yaware of this fact, because most of these children/ j3 T3 E+ O( `; O( D
may initially present in their practice. The Physicians’
, U& I# [- P- R% }! r# K, M; {$ RDesk Reference and package insert should also put a# Z" X1 h E, Q0 Y" ^7 \+ S
warning about the virilizing effect on a male or* t5 d3 g7 I0 l* h: G
female child who might come in contact with some-) j) {( g8 v, \% S% o7 z
one using any of these products.9 C1 g6 l& S+ C6 b/ N. e1 T
References
8 F- t+ o6 h. b4 M8 b1. Styne DM. The testes: disorder of sexual differentiation
% g3 T- U. I0 b8 Y) ]and puberty in the male. In: Sperling MA, ed. Pediatric
" S1 J- G1 V' |$ q" wEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
" B) L2 o4 I1 P/ Q: U2002: 565-628.1 A1 _, T% ^( p: P4 G
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious* X6 E" R) E9 L; Z' R4 S% I
puberty in children with tumours of the suprasellar pineal |
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