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Sexual Precocity in a 16-Month-Old: Q; L4 l* k2 @% R' |0 t4 P
Boy Induced by Indirect Topical" j/ P) t3 ?% F9 F+ D
Exposure to Testosterone
! `' ?3 `6 ]( R7 i# R, RSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2( _* n/ D) R9 ]+ J
and Kenneth R. Rettig, MD14 |( P$ ^) _2 c3 a0 |5 X
Clinical Pediatrics& y9 a9 _6 ]! W" c+ ^' O
Volume 46 Number 6
4 R- ?) |1 [+ OJuly 2007 540-543
# G0 u7 L" K$ i7 e0 u* v© 2007 Sage Publications9 D) k$ M/ ~- U' |2 K9 f" q
10.1177/0009922806296651
$ x8 e0 |+ x g: W: q: B% Ihttp://clp.sagepub.com$ b. S( E0 m! c) K
hosted at
! U" l3 ]4 m- }4 j( b# y+ [) Bhttp://online.sagepub.com6 o/ O. w! `# S
Precocious puberty in boys, central or peripheral,
. o6 C+ k. }& {. y; X1 |# fis a significant concern for physicians. Central( r8 C4 e% G0 T9 w9 J
precocious puberty (CPP), which is mediated
/ t2 O! E/ \3 w9 Q& q5 wthrough the hypothalamic pituitary gonadal axis, has" m! _& Y% O/ m' V
a higher incidence of organic central nervous system! |. `. S. w5 {) v1 D$ G
lesions in boys.1,2 Virilization in boys, as manifested
1 M1 D# e1 w" \+ f) x% w. Sby enlargement of the penis, development of pubic
! W( L2 N2 b' U5 x- z8 ~- X3 Ehair, and facial acne without enlargement of testi-1 Q, x5 T* D4 H6 c% `) ~4 F
cles, suggests peripheral or pseudopuberty.1-3 We
# y) f* m* M$ r& J1 G5 Kreport a 16-month-old boy who presented with the! X5 A+ y- A% e1 b5 Q
enlargement of the phallus and pubic hair develop-
& s* V$ Z" M9 D! V0 u5 V" qment without testicular enlargement, which was due
* H a. U- X; q! M2 Z6 pto the unintentional exposure to androgen gel used by
7 K; g* D8 d- A/ j7 ?the father. The family initially concealed this infor-+ x9 L/ I ^7 A% S5 ~7 h$ p$ L. y
mation, resulting in an extensive work-up for this
! B: x7 T. H: J. Echild. Given the widespread and easy availability of
% e* b0 C6 ~" X$ B: T" Y& Itestosterone gel and cream, we believe this is proba-1 I" T/ z& o5 y7 [- ^
bly more common than the rare case report in the3 M. y% d# | [* P5 s4 [
literature.4
$ g; Z5 W, @- V- B9 NPatient Report7 m7 X% O. g# e' Q! W0 G
A 16-month-old white child was referred to the- T! b6 I9 Z% `0 d6 Q9 Q
endocrine clinic by his pediatrician with the concern P9 o" v6 g- T6 `
of early sexual development. His mother noticed/ J: u; |, h8 o T2 [
light colored pubic hair development when he was2 o9 E: G$ e6 s5 F
From the 1Division of Pediatric Endocrinology, 2University of+ H- h" m: ?" T* Y4 L) e# C8 H
South Alabama Medical Center, Mobile, Alabama.2 ]( \+ Y0 g- G! F; k
Address correspondence to: Samar K. Bhowmick, MD, FACE,9 W8 \3 U8 ]$ i( D; Z% q8 `% X
Professor of Pediatrics, University of South Alabama, College of
1 P: x# @9 z2 E0 rMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;- O$ e$ i- y% h; @* p8 S; i: k2 ^
e-mail: [email protected].
/ _* l" a, C. g- t4 yabout 6 to 7 months old, which progressively became- y7 \+ w- ^0 j4 t7 q9 _8 t
darker. She was also concerned about the enlarge-
8 d" ~+ t- p$ i4 f) a# dment of his penis and frequent erections. The child( f* f- D0 r1 V8 {) B3 D
was the product of a full-term normal delivery, with8 r- h5 F+ x0 d8 i6 Q
a birth weight of 7 lb 14 oz, and birth length of
* |) E) e0 z$ I" t, y20 inches. He was breast-fed throughout the first year
- `2 }9 h' o! a/ F" hof life and was still receiving breast milk along with2 l i% t* ]1 P
solid food. He had no hospitalizations or surgery,+ `' K# w' Q/ ]) j! \
and his psychosocial and psychomotor development; _( n3 T$ A7 A
was age appropriate.( _, }' x0 B: o9 ~
The family history was remarkable for the father,
- P* D+ M2 ~8 S; ]. V4 b9 ]5 A6 @1 Dwho was diagnosed with hypothyroidism at age 16,
" ?. W& _/ ]. \8 x$ _, pwhich was treated with thyroxine. The father’s3 t7 o- n2 p& X
height was 6 feet, and he went through a somewhat
% _- G. z6 f/ S2 d4 s0 R5 `3 S# \early puberty and had stopped growing by age 14. t9 r( c' [# f& a3 i+ S* z |, t
The father denied taking any other medication. The
) m' q/ r+ k3 Qchild’s mother was in good health. Her menarche& Z& U$ T* j; Q, m/ |1 X8 e
was at 11 years of age, and her height was at 5 feet7 G" f4 R& `8 B }0 X) L! d* _- S
5 inches. There was no other family history of pre-) u7 j$ r# K2 r. F8 y" P
cocious sexual development in the first-degree rela-
/ q& ^+ ?) O5 v. E) k2 x# rtives. There were no siblings.0 r: r% p- r2 ?$ A1 ]+ z5 v! @
Physical Examination( q" x% c( i+ J4 l' _$ P4 r5 G
The physical examination revealed a very active,! h2 u5 c. ^# Q
playful, and healthy boy. The vital signs documented
; h5 n) S2 Z/ ]7 L6 {7 B5 sa blood pressure of 85/50 mm Hg, his length was
0 J# t; l9 H" o90 cm (>97th percentile), and his weight was 14.4 kg
2 t% l4 [) I- t% c: J& G, P$ ^(also >97th percentile). The observed yearly growth$ G1 [+ \( e' U. \$ u) y5 Y' a- g# l" T
velocity was 30 cm (12 inches). The examination of
* }0 B7 `# r1 S# |% l3 c* Bthe neck revealed no thyroid enlargement.
' \9 H! H& e# S% HThe genitourinary examination was remarkable for9 J4 s0 _5 n# j$ H, U( i4 e
enlargement of the penis, with a stretched length of W+ K# ]3 Q7 @- Z, C
8 cm and a width of 2 cm. The glans penis was very well
8 T- S8 u# Y7 x% N: C1 [' `developed. The pubic hair was Tanner II, mostly around M8 {. W3 I' Q9 C) Z% b
540
, b3 V- {/ W' i4 |- ~9 Iat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from- e* e7 \ _' W/ S0 Z' p
the base of the phallus and was dark and curled. The
" d' V; b: T! r7 h% l8 xtesticular volume was prepubertal at 2 mL each.* \* _% {6 t1 N8 P. m \, v
The skin was moist and smooth and somewhat8 T B( a9 G k( j8 g5 K+ G: @
oily. No axillary hair was noted. There were no
5 ^7 R& ]6 M9 z2 ^9 I4 Eabnormal skin pigmentations or café-au-lait spots.& `! [+ A4 y3 i& o5 j/ b- h
Neurologic evaluation showed deep tendon reflex 2+/ t+ n" e: a' T& s) y; a% q
bilateral and symmetrical. There was no suggestion
l6 l3 R" p; @) Nof papilledema.
- f6 U- m/ ]8 n9 r4 |$ b( BLaboratory Evaluation3 _1 C) a" n+ V. {
The bone age was consistent with 28 months by
* s1 Z7 Q9 |' D2 d* D7 S0 G8 busing the standard of Greulich and Pyle at a chrono-
/ l# C' g0 X7 h; i( b- dlogic age of 16 months (advanced).5 Chromosomal6 a& D S% C, P ~
karyotype was 46XY. The thyroid function test
$ L' r5 {9 L: nshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
6 u! b; U9 p/ n, j5 e- i; K/ jlating hormone level was 1.3 µIU/mL (both normal).7 R9 b* T8 J' w$ |5 z( l/ `
The concentrations of serum electrolytes, blood
5 D" z8 ?6 c% P4 V# e$ c; n p' m) qurea nitrogen, creatinine, and calcium all were
& x V: B' |0 {, Z4 Y1 F# pwithin normal range for his age. The concentration
2 l0 a5 a, h, X' f$ x; F# E4 ^+ g" J0 Jof serum 17-hydroxyprogesterone was 16 ng/dL
+ j7 {* E3 A0 w(normal, 3 to 90 ng/dL), androstenedione was 20
- q$ g" u+ O* ?8 [4 ]8 ^- @7 b& Bng/dL (normal, 18 to 80 ng/dL), dehydroepiandros- R& v7 P6 U* q4 H
terone was 38 ng/dL (normal, 50 to 760 ng/dL), Q% s9 T- S0 T' U" A- U
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
0 s6 {( }) \: g; I. E% n7 g49ng/dL), 11-desoxycortisol (specific compound S)4 P% ?1 y: C$ t) y; v% d4 D) r2 x
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
" p, l/ K# F9 H) [" ~: ptisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total8 i" C4 X' v3 N
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),( B4 }" D" h* j! {. g& Q: O& m
and β-human chorionic gonadotropin was less than' Q4 r6 b& C% ?$ z( X; [; @
5 mIU/mL (normal <5 mIU/mL). Serum follicular* {4 L+ B9 Z2 p+ t& `7 B7 S+ {) D
stimulating hormone and leuteinizing hormone
; J4 x# n8 [/ r2 F0 _4 Iconcentrations were less than 0.05 mIU/mL# y- X% n4 i: h7 L2 e! T' o3 W, g& G
(prepubertal).
3 ~; w/ y7 n2 ?: }* i8 ]. h% \The parents were notified about the laboratory
5 t8 L& x7 L8 z2 Y8 Oresults and were informed that all of the tests were
* p' e! U, Q, Q. O; ^$ E+ knormal except the testosterone level was high. The
6 g1 k5 X& O2 D, B/ ~, Ofollow-up visit was arranged within a few weeks to) M _, M9 ^& c3 i( `( D
obtain testicular and abdominal sonograms; how-
5 e; o" ^2 H9 b7 Dever, the family did not return for 4 months.
" z& x, O$ {/ R: j* _6 ^0 yPhysical examination at this time revealed that the
7 }0 F8 ~0 l. G6 X! W Hchild had grown 2.5 cm in 4 months and had gained
3 K" B8 m# |- c2 kg of weight. Physical examination remained9 D. p" S7 p/ K3 r8 b1 A2 m, S2 B
unchanged. Surprisingly, the pubic hair almost com-
, q2 z, a/ P) }* q4 Opletely disappeared except for a few vellous hairs at$ I" s; Q: c+ m" }
the base of the phallus. Testicular volume was still 2/ ^' J5 ^7 K9 h+ @5 g7 X
mL, and the size of the penis remained unchanged.
- i7 K9 `/ R6 u5 x9 m2 _; g8 TThe mother also said that the boy was no longer hav-
1 e. m* m5 [. _1 D. Ving frequent erections.0 n) g2 p9 m: T1 J: C0 J: l7 j! u5 V
Both parents were again questioned about use of3 {& s. e/ W' n) Y; j6 t1 q: R2 a5 D# P
any ointment/creams that they may have applied to
! m( V( ^- s$ d, L( A+ R) X2 ^6 l3 Wthe child’s skin. This time the father admitted the
5 x- ], ^3 ]: [Topical Testosterone Exposure / Bhowmick et al 541
$ s+ P6 t* A6 v! [0 ruse of testosterone gel twice daily that he was apply-7 J' Q, W4 |% T$ Y+ C5 N1 E3 V
ing over his own shoulders, chest, and back area for4 s1 m# A: ~$ u! T7 l
a year. The father also revealed he was embarrassed
( }; r8 p- B C" [to disclose that he was using a testosterone gel pre-
! ` l+ n6 z2 ?2 q: \+ }scribed by his family physician for decreased libido
" D) D/ V) [9 b- w/ {secondary to depression.
" R+ ^* m! y0 N( uThe child slept in the same bed with parents.4 @& y1 c1 E- Y
The father would hug the baby and hold him on his: y! b2 Z% J; q" h0 T- _, ]
chest for a considerable period of time, causing sig-
! I. l5 ^: U7 f- L/ E% hnificant bare skin contact between baby and father.' z( [7 R, k& v' \- a- s
The father also admitted that after the phone call,. y9 G$ p, [9 B" y4 l; g: M0 q, Q
when he learned the testosterone level in the baby8 u" s9 P+ L3 a% |; K- g j
was high, he then read the product information
" [9 V% ~' e8 b- B7 ]packet and concluded that it was most likely the rea-
# R" G, \1 S$ P7 I9 _son for the child’s virilization. At that time, they/ }* ^+ {( b+ c1 s" { x6 v
decided to put the baby in a separate bed, and the: V4 R2 r, |5 ?6 a" D, y9 F
father was not hugging him with bare skin and had
* Z" n9 [& \. }9 Hbeen using protective clothing. A repeat testosterone" K+ a4 [/ E! J& e
test was ordered, but the family did not go to the
8 H( t5 o) E8 Y f9 |; y% K( S2 slaboratory to obtain the test.
5 r. g) N; P2 v) i) @+ S" VDiscussion
, J. X/ p' l1 z3 F+ e7 v" `Precocious puberty in boys is defined as secondary
1 i) f$ W5 ]- U' S6 M# Psexual development before 9 years of age.1,4& J U7 H* c- q' b0 L
Precocious puberty is termed as central (true) when) Y0 H ]7 }9 B
it is caused by the premature activation of hypo-
7 M/ E5 E# R# I1 x2 R: c. Cthalamic pituitary gonadal axis. CPP is more com-
9 R+ B# D0 Z% b5 cmon in girls than in boys.1,3 Most boys with CPP/ i( W+ Z8 d C: y! L i
may have a central nervous system lesion that is
* t6 Y7 v7 m3 a7 }7 Bresponsible for the early activation of the hypothal-! G9 u7 q) ^5 G/ g! y7 X3 t
amic pituitary gonadal axis.1-3 Thus, greater empha-
8 F! u s& ]$ O; osis has been given to neuroradiologic imaging in: C+ a, c: X3 O& B$ g
boys with precocious puberty. In addition to viril-7 h" H& i- Z6 R8 ~
ization, the clinical hallmark of CPP is the symmet-
0 X' Y, F1 ^4 frical testicular growth secondary to stimulation by
, ], N8 a4 d: l- } Y" t7 @$ L! Bgonadotropins.1,3
% r. o, e/ I$ H, O* BGonadotropin-independent peripheral preco-7 M' H5 Y/ I5 O5 b
cious puberty in boys also results from inappropriate
- ?2 b ~, [- j5 xandrogenic stimulation from either endogenous or5 L- f9 D7 B6 z0 A2 {, c
exogenous sources, nonpituitary gonadotropin stim-
" ~) j0 |) |1 O" Xulation, and rare activating mutations.3 Virilizing
# e+ x: d9 S, v0 lcongenital adrenal hyperplasia producing excessive" f j: N; C2 \9 p5 z4 i
adrenal androgens is a common cause of precocious
: _7 L# p' K% n. x% g) o( u; D! A% tpuberty in boys.3,4
7 Z* `6 b5 Z0 U) b/ h2 bThe most common form of congenital adrenal
3 x; h# G Q5 m, o' f- v# Bhyperplasia is the 21-hydroxylase enzyme deficiency.
' n4 i* f. V2 y) ~! xThe 11-β hydroxylase deficiency may also result in V% U" Z2 R3 [; }' R' Z0 S9 ^4 e, R5 h
excessive adrenal androgen production, and rarely,
7 j) p# D. h( w, o b& I, Kan adrenal tumor may also cause adrenal androgen
7 p; \& E% y" r( P, `# ?excess.1,3: E% a% B u# K% p- R* b
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from) }% G, O9 [" E" _' B5 s
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
9 Z. ?' p6 H( t o, |A unique entity of male-limited gonadotropin-
$ d9 M; g- \* K3 ~- q- U+ \independent precocious puberty, which is also known
% A, {$ @) k- I$ A4 X" eas testotoxicosis, may cause precocious puberty at a0 _, X4 i, F9 J; @, Q- H
very young age. The physical findings in these boys: a& a" y3 I! T' c' [7 e* f
with this disorder are full pubertal development,$ Q! c6 S2 A& D5 @% o
including bilateral testicular growth, similar to boys& d5 x8 P' r$ T3 |5 y- @
with CPP. The gonadotropin levels in this disorder- R k T; | ~
are suppressed to prepubertal levels and do not show
& w$ s( U1 r/ h# Z" Apubertal response of gonadotropin after gonadotropin-( d7 z. r8 c |, ^9 y8 t: e2 o
releasing hormone stimulation. This is a sex-linked* R% \# A/ C/ J( }* A" ~
autosomal dominant disorder that affects only
4 O! Y0 L0 F9 K6 {" dmales; therefore, other male members of the family
- T8 r, f4 m7 u& hmay have similar precocious puberty.3
2 f& p. U, O$ F- o+ s/ `In our patient, physical examination was incon-
: t' Y! W" N$ Z+ Q' ?: xsistent with true precocious puberty since his testi-
& ^6 f) c9 d# k+ {- `. R8 q( Lcles were prepubertal in size. However, testotoxicosis
e$ }7 D8 `! Q6 g5 Qwas in the differential diagnosis because his father5 v1 x+ c* J3 y0 r" I
started puberty somewhat early, and occasionally,
8 [; U Y4 D2 f- {) t, Gtesticular enlargement is not that evident in the
9 l: c2 q" A8 r7 l3 h: u0 K- Sbeginning of this process.1 In the absence of a neg-
2 `0 c# Y# z9 Cative initial history of androgen exposure, our+ |+ ]7 y, G' m! E, c: k: U
biggest concern was virilizing adrenal hyperplasia,8 M7 U! j+ q0 k* f7 a1 X+ N
either 21-hydroxylase deficiency or 11-β hydroxylase
, i% G3 o- J7 q7 @* sdeficiency. Those diagnoses were excluded by find-
( e, t/ I( F p$ g$ ding the normal level of adrenal steroids.! B7 p) V; h+ U2 [) D: f y
The diagnosis of exogenous androgens was strongly
2 `! U; H( x* \suspected in a follow-up visit after 4 months because( o: K: E x) b/ G0 K, J
the physical examination revealed the complete disap-; P* R. @! r* ?8 R, m9 {
pearance of pubic hair, normal growth velocity, and
5 S' t3 ^6 w+ n4 Y* [2 m5 E* ^decreased erections. The father admitted using a testos-
, _# e8 M/ t( ]- Y; kterone gel, which he concealed at first visit. He was
8 A- h0 ]. t% ~; r1 V9 D8 ^using it rather frequently, twice a day. The Physicians’1 L% [6 ]5 q* \5 k& A" m
Desk Reference, or package insert of this product, gel or3 e# y6 z' T, s/ T$ w6 a0 |& z# Y
cream, cautions about dermal testosterone transfer to" W2 x/ i+ ]8 Z5 n D! E) c! c* n
unprotected females through direct skin exposure.& r; z: d) d0 O% `% q3 M
Serum testosterone level was found to be 2 times the
& O5 B; c# ?0 f& k# F% W9 k! _% Abaseline value in those females who were exposed to
+ C6 c: M ]' W/ B7 c+ [6 Reven 15 minutes of direct skin contact with their male8 b3 p1 S0 I1 a$ |# r! k
partners.6 However, when a shirt covered the applica-5 u' q3 S& c* T# r5 P& y
tion site, this testosterone transfer was prevented.+ v& } Z8 G# H1 n9 _7 b, Q: {
Our patient’s testosterone level was 60 ng/mL,
b6 l# S! L3 Z1 T5 X, w F1 Z' dwhich was clearly high. Some studies suggest that
9 t8 Q6 q5 ^8 v6 a! m9 _dermal conversion of testosterone to dihydrotestos-
; A1 R( i+ q2 P& s qterone, which is a more potent metabolite, is more9 s8 e1 D/ a$ Q* y# |( u& e/ O
active in young children exposed to testosterone$ A- h4 b6 h7 O/ n' s
exogenously7; however, we did not measure a dihy-
- h1 w) p3 j4 [ v7 n3 E7 ^drotestosterone level in our patient. In addition to2 e0 }- K# Y# ?
virilization, exposure to exogenous testosterone in
, i* I/ Z- @9 [. C) ~4 h8 ?0 ~children results in an increase in growth velocity and
7 x) h w( e. S4 |* j- G+ |advanced bone age, as seen in our patient.
, L: o. e4 _4 _The long-term effect of androgen exposure during
1 b9 g( {9 k7 J8 j% J2 z# P0 i1 yearly childhood on pubertal development and final3 Z* G0 U, ]5 ^, t& Y' A% E
adult height are not fully known and always remain4 {0 U/ s7 _! D+ J; n0 U( O
a concern. Children treated with short-term testos-+ W$ Y( k+ i C; S2 x5 ^
terone injection or topical androgen may exhibit some
9 C! t' M8 I+ v- ?, H* }+ Q' Zacceleration of the skeletal maturation; however, after
2 q* [- c" d; w. d @. Pcessation of treatment, the rate of bone maturation( N8 I& l" Z/ Y& D% Z
decelerates and gradually returns to normal.8,9
X' V' I7 q7 e0 B6 P2 ?There are conflicting reports and controversy
" o5 ^" P* b3 K& a( l' ^over the effect of early androgen exposure on adult+ j" Q& E. N5 @. h
penile length.10,11 Some reports suggest subnormal
& u+ z8 ?) ]: n" M Jadult penile length, apparently because of downreg-& Z' s, Z0 Z7 j* x& N1 s
ulation of androgen receptor number.10,12 However,4 i$ B3 ]" `+ d
Sutherland et al13 did not find a correlation between
, Q$ K. N& C! Q7 gchildhood testosterone exposure and reduced adult
1 D# E: {1 y6 U4 C8 ?/ Cpenile length in clinical studies.7 o' W! q8 S3 l4 I' E2 q
Nonetheless, we do not believe our patient is
2 G( R! q% j( j; q- d$ Q {going to experience any of the untoward effects from
% t. a7 D* n. g6 I" btestosterone exposure as mentioned earlier because
, ], Z3 k! U8 N; athe exposure was not for a prolonged period of time., o4 v* S+ ]5 B* K) \
Although the bone age was advanced at the time of
( _- i6 E8 J# M; `diagnosis, the child had a normal growth velocity at. J3 Q& | A: Z" D
the follow-up visit. It is hoped that his final adult- P# h; B$ l. O0 m/ u4 i
height will not be affected.
. @' _) P3 b6 x6 f* GAlthough rarely reported, the widespread avail-
+ s T0 _% v3 Y F3 }ability of androgen products in our society may- q4 Z$ |8 C. I, ]
indeed cause more virilization in male or female, U$ c7 o7 [7 D% C
children than one would realize. Exposure to andro-
$ w& J/ d- J7 S4 }* y% ogen products must be considered and specific ques-
' y; _* y8 ~# u! t% utioning about the use of a testosterone product or
* z5 e5 x) L" t( ]4 p5 `gel should be asked of the family members during
0 _: D. F- [0 i% H9 r3 H% T( Zthe evaluation of any children who present with vir-
8 D# l% y3 i' X! [ilization or peripheral precocious puberty. The diag-
" `; |5 Q' S) j5 ]* y pnosis can be established by just a few tests and by, s I/ T6 R: t8 s* ?
appropriate history. The inability to obtain such a
+ Z& X2 L! X4 E5 b/ ~9 yhistory, or failure to ask the specific questions, may1 s/ y b4 {# q8 z' {
result in extensive, unnecessary, and expensive
4 U6 ~; j: {& b. f/ finvestigation. The primary care physician should be
' v" E8 _9 I. K* Taware of this fact, because most of these children
& }/ p3 a% o; a* |5 k: jmay initially present in their practice. The Physicians’! b5 B. N4 L5 v9 {
Desk Reference and package insert should also put a
) L# T' d2 m% x! y) }. j7 D [1 |warning about the virilizing effect on a male or; \2 ~0 i0 A6 j7 S- q/ ^' S+ J6 h
female child who might come in contact with some-
5 _/ _6 H8 j1 V& r; {one using any of these products.
8 o' @0 k& t+ X& _References, W( K/ ` s5 F+ z: o& z
1. Styne DM. The testes: disorder of sexual differentiation
6 C) w1 }6 E3 U rand puberty in the male. In: Sperling MA, ed. Pediatric9 y! Z# r/ z+ w% C/ Z* i3 N
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;, U2 Z7 }0 ]: K3 g$ t3 y
2002: 565-628.# P( J8 n% q! D' D
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
! k+ x$ o. L" l- dpuberty in children with tumours of the suprasellar pineal |
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