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Sexual Precocity in a 16-Month-Old
. B# _4 s5 E3 I5 ?$ vBoy Induced by Indirect Topical
8 ~1 R& _2 b' w" ]2 m$ r# B& }, tExposure to Testosterone- ?+ L: {- m! }
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,26 f' b# P) b }0 ^8 {& Y1 }# @7 V
and Kenneth R. Rettig, MD1
: A" c9 f0 ]% f% ?- ?Clinical Pediatrics
6 U# x' j0 k1 w/ n. V$ ?Volume 46 Number 6# K! ?' y c# N4 K3 x6 L
July 2007 540-543
1 o i9 l0 Q! u8 G© 2007 Sage Publications
) S" e4 j) W+ x( }: y H; o10.1177/0009922806296651
) f |! l7 ~) x8 Rhttp://clp.sagepub.com
5 n& Q4 u* f$ ?: w) ?hosted at
2 e8 H4 d" f* H; n- S" [& o; U& xhttp://online.sagepub.com. |: c- | {' j( O& I
Precocious puberty in boys, central or peripheral,
% z. ]8 ~# O; b8 z: O9 O! z$ [is a significant concern for physicians. Central* D5 v0 W" N* T( I- b i1 v& F
precocious puberty (CPP), which is mediated9 O- E: R/ [ q* Q1 L
through the hypothalamic pituitary gonadal axis, has1 S9 u$ e! i3 _0 d' u9 ^" B5 |
a higher incidence of organic central nervous system
9 M0 ]+ J) _- E* W/ Alesions in boys.1,2 Virilization in boys, as manifested
( B c+ p) |) d2 @0 dby enlargement of the penis, development of pubic
4 q% Q4 r o* ], qhair, and facial acne without enlargement of testi-; x; u' a* W3 _4 D
cles, suggests peripheral or pseudopuberty.1-3 We E, g+ o2 r2 P3 p: m1 d
report a 16-month-old boy who presented with the. k: s0 V0 E1 s" `
enlargement of the phallus and pubic hair develop-: U; M" W: H3 e, _/ ]3 S
ment without testicular enlargement, which was due
: ~! p3 p, S9 P5 v! m; uto the unintentional exposure to androgen gel used by
& z' o9 U6 M7 b/ v$ x. j8 Dthe father. The family initially concealed this infor-/ x# l- [+ J9 t9 T
mation, resulting in an extensive work-up for this
3 O; j2 h0 T0 Z$ I" hchild. Given the widespread and easy availability of& X1 A F- n J6 f( e4 O; R" d
testosterone gel and cream, we believe this is proba-" @1 J7 `7 k# n. {% i3 x
bly more common than the rare case report in the
, Q+ F6 \% H. r; \- M _literature.4
' g/ X6 b. D' R/ q9 y1 f |Patient Report. @9 ^3 x) h* D6 F$ @9 J' g6 l* W
A 16-month-old white child was referred to the
) s; O2 o! h# cendocrine clinic by his pediatrician with the concern# Z1 |# m$ G6 \* J
of early sexual development. His mother noticed
# i2 m0 h6 F2 Elight colored pubic hair development when he was
1 t4 k! Y* G8 E; J( r+ qFrom the 1Division of Pediatric Endocrinology, 2University of
0 t% r4 R# i1 G/ z- ^% B! }9 pSouth Alabama Medical Center, Mobile, Alabama.
! g4 ?! T6 `+ ?5 t; U- [) uAddress correspondence to: Samar K. Bhowmick, MD, FACE,0 R3 j& z, Y. |$ a
Professor of Pediatrics, University of South Alabama, College of
9 ~; a3 T+ b7 K0 W; fMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
/ J9 ?6 ~* A/ i a$ J5 _' v9 ue-mail: [email protected].
0 n: l) Y3 O, T# a5 zabout 6 to 7 months old, which progressively became0 t' O* {! H$ X1 ~
darker. She was also concerned about the enlarge-
+ L6 @5 h, {: @. @3 e8 n6 }ment of his penis and frequent erections. The child
! V; U! x0 J! U9 U( f! cwas the product of a full-term normal delivery, with2 _) J# l' g0 d4 B: I' ]4 z
a birth weight of 7 lb 14 oz, and birth length of
5 c8 k- L) m: q8 E# m. y20 inches. He was breast-fed throughout the first year
) x6 A2 Q1 b6 N7 f6 j, p6 _8 b4 zof life and was still receiving breast milk along with# E; ^2 ~! K5 W2 S8 c9 w5 b3 l# I
solid food. He had no hospitalizations or surgery,
. t. S8 z" B& x9 y4 d- G; }/ Hand his psychosocial and psychomotor development
; W8 P6 l5 ?: L% G5 Z: Nwas age appropriate.. v/ L3 h- c4 B* C, |
The family history was remarkable for the father,
u$ h. f& W$ E" y$ ?( Dwho was diagnosed with hypothyroidism at age 16,7 m6 X4 ?4 b6 N$ L. ~' z- d5 R% H9 Y2 \
which was treated with thyroxine. The father’s8 \ U9 j; ]" k) c+ y- }4 h- v) z
height was 6 feet, and he went through a somewhat- J* L) K- D8 y9 C, F+ w! s- Q
early puberty and had stopped growing by age 14.) @- j$ W$ D' m0 A0 U
The father denied taking any other medication. The3 T6 H9 {6 Y& t, T) G' p
child’s mother was in good health. Her menarche
3 d/ w) ]: }( Cwas at 11 years of age, and her height was at 5 feet+ t% o8 ]9 m$ b/ A' q
5 inches. There was no other family history of pre-
- @7 }0 O& o% H3 \% r9 T8 @cocious sexual development in the first-degree rela- Q0 f* K# I% V4 `. _+ h* d
tives. There were no siblings.- V/ j( @8 X$ I+ D# h3 L
Physical Examination
7 Q8 w; r: R5 sThe physical examination revealed a very active,
" p2 }+ k: k( ~: Q" v5 @. s5 K$ Z" Kplayful, and healthy boy. The vital signs documented+ |# R, ?2 J7 m& t5 o
a blood pressure of 85/50 mm Hg, his length was
( O" W2 M/ |5 c( l6 b' C90 cm (>97th percentile), and his weight was 14.4 kg' F2 r* F( \* u8 _( C, }" s8 Y6 s
(also >97th percentile). The observed yearly growth* w( c9 t- S9 K2 J: p# A
velocity was 30 cm (12 inches). The examination of
7 n- u U: f( B$ _2 i- B- ~/ Dthe neck revealed no thyroid enlargement./ w1 m" j: I3 ?0 p" o" U/ x
The genitourinary examination was remarkable for: A. F; H4 ]0 x4 g0 i7 j6 G/ `
enlargement of the penis, with a stretched length of
% o2 ]1 l# y4 A* @; l8 cm and a width of 2 cm. The glans penis was very well4 i3 C/ Y( X; W( J+ w8 T
developed. The pubic hair was Tanner II, mostly around
7 i0 G9 C+ R# l! X& Y5401 O5 G( p7 d, q6 ~" w
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from7 y; m3 E/ ~: z% q: D% @, @
the base of the phallus and was dark and curled. The6 d4 J% i5 O) ?' J3 V& P! I
testicular volume was prepubertal at 2 mL each.! Q$ e' `! i$ ?! S9 J
The skin was moist and smooth and somewhat N$ t# z$ o4 D9 T% P) x
oily. No axillary hair was noted. There were no
- ^& S7 R/ x: i% s/ Habnormal skin pigmentations or café-au-lait spots.
1 B8 t- w/ w+ a2 dNeurologic evaluation showed deep tendon reflex 2+' Y! h: t9 |6 q' J0 S1 I. m
bilateral and symmetrical. There was no suggestion8 \! U2 y, k; p3 U5 t
of papilledema.
2 Q1 {/ v" z% }2 jLaboratory Evaluation6 t2 `( [( h! `" Y" t
The bone age was consistent with 28 months by
0 a% x# s) a( P; c5 j$ [using the standard of Greulich and Pyle at a chrono-# {3 L' v1 ?: N/ ^4 W
logic age of 16 months (advanced).5 Chromosomal
/ D# U3 t. w) H! ^karyotype was 46XY. The thyroid function test
* ]5 N2 f( d5 c# K5 @) Cshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
+ W s' `$ i6 p7 b5 G, y! f* ?' Rlating hormone level was 1.3 µIU/mL (both normal)." v# m4 O& z9 [
The concentrations of serum electrolytes, blood! O5 p' C& t! l/ L O
urea nitrogen, creatinine, and calcium all were
: _ T" B8 c0 V8 ^/ vwithin normal range for his age. The concentration
( A# N/ b0 P! u. f/ ?of serum 17-hydroxyprogesterone was 16 ng/dL
5 I2 U6 m; g2 H7 V" I3 `- n2 D8 B(normal, 3 to 90 ng/dL), androstenedione was 206 ]3 {) K# s# W9 K+ N/ H8 _- `
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-( e9 O6 ^0 d0 }* v
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
: l! {9 }4 c7 ^9 a5 w% b+ adesoxycorticosterone was 4.3 ng/dL (normal, 7 to* x$ j/ E' f) K
49ng/dL), 11-desoxycortisol (specific compound S)
: V# g$ V: N0 \( f. ewas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
- g4 }7 T; O: Btisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
6 e1 d9 c" l7 A0 ^; n5 S( etestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
; m8 z( f6 w' Z) a5 Y3 q& j, Kand β-human chorionic gonadotropin was less than- V% S; T5 A% n
5 mIU/mL (normal <5 mIU/mL). Serum follicular( ~# E, X) \* t& q( ?; q
stimulating hormone and leuteinizing hormone
% _: [5 S3 a3 F0 q$ e7 {$ r7 iconcentrations were less than 0.05 mIU/mL
! n, r! L/ j6 x6 V; V* R7 ?(prepubertal).' t( J. x+ l* T: ^: M
The parents were notified about the laboratory
& ^* w. Q8 [! S1 { wresults and were informed that all of the tests were' Y- S4 c, c( s' T4 @3 E
normal except the testosterone level was high. The
- f8 c3 J* x& s. T7 P7 @follow-up visit was arranged within a few weeks to
7 Y8 G+ U. C* o% I9 P3 l7 n* Robtain testicular and abdominal sonograms; how-
5 x5 W0 f/ @: m7 Dever, the family did not return for 4 months.* O6 ?$ ]: B6 x: u* r
Physical examination at this time revealed that the9 ~; ]9 J- Q: o1 p: E3 V/ T Y
child had grown 2.5 cm in 4 months and had gained7 h8 h0 v; c, C4 y+ ?. u
2 kg of weight. Physical examination remained
, s. q+ ?7 D2 ~8 p* b) S0 c' yunchanged. Surprisingly, the pubic hair almost com-5 b# u, X& x2 m! |; O
pletely disappeared except for a few vellous hairs at5 W2 n( r# c" o) o; g
the base of the phallus. Testicular volume was still 2
" g4 t$ i2 v4 J5 i- KmL, and the size of the penis remained unchanged.
6 v% H, M) S% S( qThe mother also said that the boy was no longer hav-
+ V# P8 W* k+ Xing frequent erections.
) p5 [) ^5 P% d8 SBoth parents were again questioned about use of
" Y* z, R8 p) t- ?5 j. @% tany ointment/creams that they may have applied to
! P* S& T1 W0 a8 h( t! q( ^3 athe child’s skin. This time the father admitted the
+ n) n/ R7 R' {6 o4 MTopical Testosterone Exposure / Bhowmick et al 541- ~5 k( J, o1 ~& Q, G
use of testosterone gel twice daily that he was apply-
" _! Y# O' b! u) ^ ging over his own shoulders, chest, and back area for. z; E4 [% Q Z7 j& Z, Z
a year. The father also revealed he was embarrassed5 @/ t( T* @- [
to disclose that he was using a testosterone gel pre-0 w8 b1 z, }1 ~0 w$ `5 h
scribed by his family physician for decreased libido9 F+ g, o9 E# z8 N# L
secondary to depression.
$ m. i4 r, D1 W0 {1 hThe child slept in the same bed with parents.% B1 x5 U! C- l' B8 z3 E
The father would hug the baby and hold him on his
2 f, n& i( K1 c4 Xchest for a considerable period of time, causing sig-
# f9 H2 w9 x. E. I4 m8 ^3 Vnificant bare skin contact between baby and father.
. ?- o* n, E V* [- S. VThe father also admitted that after the phone call,
& x' j/ w F7 Nwhen he learned the testosterone level in the baby
8 ]6 U# s. y# H* O w6 Xwas high, he then read the product information3 O" `" T, {$ V6 G2 n& o
packet and concluded that it was most likely the rea-3 F9 X. |* |1 w" A# E1 [ y, V
son for the child’s virilization. At that time, they8 r" [% S* h6 c9 N! F
decided to put the baby in a separate bed, and the
* g- T& a( b% b9 s' m( c+ \/ Gfather was not hugging him with bare skin and had2 i- h5 l7 h: i* a+ p* {
been using protective clothing. A repeat testosterone0 e8 s4 S; l/ z2 Y) H
test was ordered, but the family did not go to the
1 j8 F( V5 y7 O2 ?1 I8 Jlaboratory to obtain the test.
+ ?$ Y! ?/ Z7 u0 i o: C& ?Discussion3 O8 D$ l7 g. h5 x- X
Precocious puberty in boys is defined as secondary
1 z, q" s: i- F$ Hsexual development before 9 years of age.1,4
. Y; u( o x- z: g+ v& m" XPrecocious puberty is termed as central (true) when6 V# ^; p7 G8 Z3 A/ D6 j- H( Y6 U
it is caused by the premature activation of hypo-; a6 D8 Z/ |: V, F( E
thalamic pituitary gonadal axis. CPP is more com-9 q; B- ]% [& m) e. ^9 A
mon in girls than in boys.1,3 Most boys with CPP
8 ~: m& Z* I# m( L1 c7 z E/ o$ mmay have a central nervous system lesion that is
( v. R/ q2 z1 U9 c$ i5 q, l8 zresponsible for the early activation of the hypothal-
8 o/ P T; r1 Y, d. o4 Samic pituitary gonadal axis.1-3 Thus, greater empha-
0 \/ g; \2 s, }$ I3 }+ Gsis has been given to neuroradiologic imaging in# k& g! s" S! z
boys with precocious puberty. In addition to viril-/ a3 {- p5 ?8 a6 Q8 h
ization, the clinical hallmark of CPP is the symmet-* w3 N+ \$ @6 s: \! K8 Y
rical testicular growth secondary to stimulation by; K4 ?( u& T0 \* O6 b k- @8 G
gonadotropins.1,3
& k; [/ c- z7 {$ C4 g, rGonadotropin-independent peripheral preco-- C, O: d% _$ z
cious puberty in boys also results from inappropriate
' Z) x+ E: k' Pandrogenic stimulation from either endogenous or
- ]7 ^7 Z% {* jexogenous sources, nonpituitary gonadotropin stim-
# U# ?1 n: C" Q: mulation, and rare activating mutations.3 Virilizing: k1 M9 r' H: K9 P9 s% Y$ q
congenital adrenal hyperplasia producing excessive/ c& n" T/ | U' K3 [: U
adrenal androgens is a common cause of precocious
# v9 _ g8 K8 f# Q3 Vpuberty in boys.3,4
/ z2 ]( o0 M: A4 D" u6 M: @' _ hThe most common form of congenital adrenal
1 J" H1 p2 c0 J9 g+ [& bhyperplasia is the 21-hydroxylase enzyme deficiency.5 X2 t- `/ ]& I& }2 l! h- ?# L6 E: d
The 11-β hydroxylase deficiency may also result in+ Q' l5 c. W" M% r3 v& d
excessive adrenal androgen production, and rarely,
`& ~/ b6 x9 q* I! t7 e7 kan adrenal tumor may also cause adrenal androgen
$ M8 j" j4 @" C% i. bexcess.1,3$ e- B- p+ ^) [8 U9 f
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from% t0 f) z! E, F( y
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007' J) G# S/ l) Q9 u) ~
A unique entity of male-limited gonadotropin-' y Q# ~5 @% ?& Q; Q
independent precocious puberty, which is also known
+ ^# F6 H7 `1 T5 Y9 E6 ras testotoxicosis, may cause precocious puberty at a3 e$ q p" A) N4 u2 i% H
very young age. The physical findings in these boys
/ X8 [" c6 \" P$ m3 h. Ewith this disorder are full pubertal development,
0 F$ u& n& ?4 S3 W& p2 kincluding bilateral testicular growth, similar to boys
* q2 w& c$ [ G+ q+ A# y; hwith CPP. The gonadotropin levels in this disorder
2 Y7 ^8 c! Y8 N, Z1 v9 p2 K+ p: v8 xare suppressed to prepubertal levels and do not show: n- e* N0 Q9 b
pubertal response of gonadotropin after gonadotropin-$ i0 ]: D+ G4 i5 v: A
releasing hormone stimulation. This is a sex-linked
8 W+ K0 l9 ? O! o# J4 K' ?8 Z" [autosomal dominant disorder that affects only
. m2 l6 z9 h. m1 K Y4 N% W( omales; therefore, other male members of the family
$ [- @3 H8 Q/ z' x5 H. C) cmay have similar precocious puberty.3* X, t4 W' Z9 S) ?1 Z# v; I
In our patient, physical examination was incon-
. i& x( {/ u7 `% zsistent with true precocious puberty since his testi-
$ f" u% v* ?1 \2 {cles were prepubertal in size. However, testotoxicosis
2 ~6 f/ S( ~, F$ R3 F% gwas in the differential diagnosis because his father3 c3 A+ _/ D' m, R8 Y( q) e" a
started puberty somewhat early, and occasionally,
5 h6 l) |) s, o2 q( O) mtesticular enlargement is not that evident in the& r* P h9 ~& B
beginning of this process.1 In the absence of a neg-/ ]8 m9 S$ L; D* o/ Z/ S6 }
ative initial history of androgen exposure, our
! K$ L9 i9 j, [. O) F, H0 gbiggest concern was virilizing adrenal hyperplasia,
) \% L; j. G& @9 _either 21-hydroxylase deficiency or 11-β hydroxylase c' {, d2 A' e1 @' k, |
deficiency. Those diagnoses were excluded by find-$ r! H5 F- n/ }
ing the normal level of adrenal steroids.
$ l, j" }& |" R/ B5 c7 aThe diagnosis of exogenous androgens was strongly I1 N/ n4 F$ ~9 K% w* P' D7 K
suspected in a follow-up visit after 4 months because
1 k# R, x- ?& m( b$ ythe physical examination revealed the complete disap-
) A8 p# o" h& b8 Y; P, T- W3 l/ r" gpearance of pubic hair, normal growth velocity, and, _ x1 n) J% @$ q0 ]* c
decreased erections. The father admitted using a testos-
2 z8 K- H5 C9 r1 aterone gel, which he concealed at first visit. He was; o; M; U' T# `, W+ a8 U
using it rather frequently, twice a day. The Physicians’ b' n; y! P r, i
Desk Reference, or package insert of this product, gel or
( c! R6 F4 o5 i h3 h& Y; `cream, cautions about dermal testosterone transfer to+ ^) \0 v& K' w
unprotected females through direct skin exposure.
4 Z( j# l( `6 U8 v3 `6 \Serum testosterone level was found to be 2 times the/ w9 M6 y6 H! Y3 d8 e: R) {
baseline value in those females who were exposed to2 U4 H6 Q6 {. c
even 15 minutes of direct skin contact with their male
% k# p; t4 W" Spartners.6 However, when a shirt covered the applica-
& P5 r- G; `/ R$ @9 W4 ition site, this testosterone transfer was prevented.
; B1 `9 v! k: vOur patient’s testosterone level was 60 ng/mL,& e% d( \5 i2 N2 z# m6 c% i1 W; C
which was clearly high. Some studies suggest that
# @8 X6 Q) Q( o8 `8 }8 ?3 Cdermal conversion of testosterone to dihydrotestos-5 [8 j8 K/ `$ w- J
terone, which is a more potent metabolite, is more. N' i' m1 ]1 a% U! t# U( a: `
active in young children exposed to testosterone9 l! x# H; v! T; u! |
exogenously7; however, we did not measure a dihy-
" e/ _2 q/ ^" D: {& c. b# v. @6 Fdrotestosterone level in our patient. In addition to ~9 L/ N& `( o/ w" u
virilization, exposure to exogenous testosterone in0 A' m; M) A( D2 x0 }. z
children results in an increase in growth velocity and7 U$ I: w: E# q- t2 `2 Y q
advanced bone age, as seen in our patient.. S* v! A6 C/ g+ H
The long-term effect of androgen exposure during
% j- ^0 J- c/ I' X. dearly childhood on pubertal development and final
. w1 f( U2 m* |! Q0 Z/ O! sadult height are not fully known and always remain1 T8 Z3 L( y, m/ N3 L' w
a concern. Children treated with short-term testos-
9 z* F' Q$ k, o/ D# kterone injection or topical androgen may exhibit some
: K) C: v, [9 R* g0 ]acceleration of the skeletal maturation; however, after ]7 e7 }, K0 d* H c) p
cessation of treatment, the rate of bone maturation
6 A& q( [2 d) X4 B6 M+ M6 ldecelerates and gradually returns to normal.8,97 m6 J% j9 `4 e4 {
There are conflicting reports and controversy4 [% j) N: W6 y" H
over the effect of early androgen exposure on adult" b9 H6 }4 _7 v7 B6 A7 m1 E) \
penile length.10,11 Some reports suggest subnormal
- I/ M1 y0 G! F, ^2 uadult penile length, apparently because of downreg-. Y9 \# j. N8 J& H6 M
ulation of androgen receptor number.10,12 However,5 E3 i6 E0 H" @# P `
Sutherland et al13 did not find a correlation between. I' Q g* M* a( [+ ]: M$ x
childhood testosterone exposure and reduced adult9 N! M8 t7 h/ H+ B5 @
penile length in clinical studies.; e$ b6 h" v, a5 ^2 u1 v K% A% _
Nonetheless, we do not believe our patient is
8 w7 q1 B5 d- s- Jgoing to experience any of the untoward effects from
# D* \7 v {8 z/ j8 Dtestosterone exposure as mentioned earlier because
- O% E) ?3 w) V# e4 Q1 t. rthe exposure was not for a prolonged period of time.& c9 Z1 b" o2 g8 V% | e
Although the bone age was advanced at the time of3 r8 B' ?' {9 S% Y
diagnosis, the child had a normal growth velocity at& {& X, j6 D* [' o& B
the follow-up visit. It is hoped that his final adult$ `# E6 d# @6 p; x* L* S
height will not be affected.# T0 h' O- c% R$ F+ i+ @* @: T
Although rarely reported, the widespread avail-
$ n7 P( I0 z* K, sability of androgen products in our society may
4 g; o/ f. [# i3 n2 _indeed cause more virilization in male or female
) G; ?8 c+ V* M9 a1 Zchildren than one would realize. Exposure to andro-; {/ k/ ^: i l% p3 P6 b* S+ S
gen products must be considered and specific ques-
4 g" `& C. h' ktioning about the use of a testosterone product or
/ }9 s* b: _- p) d! b7 P8 I! sgel should be asked of the family members during8 Q2 Z& ?+ X9 B( I* l* w' |: C
the evaluation of any children who present with vir-& Q/ J1 L9 B, ]6 o/ b& J
ilization or peripheral precocious puberty. The diag-
/ O: R! X& F& R2 x: rnosis can be established by just a few tests and by
% |3 b, j) T; d6 S% Lappropriate history. The inability to obtain such a
% |# x$ o5 {$ Chistory, or failure to ask the specific questions, may+ ?( M" V. B$ K; _! Z* ?* h
result in extensive, unnecessary, and expensive1 Q1 J M4 p9 \% I! }2 b3 t# s8 \9 P2 V
investigation. The primary care physician should be9 P) w9 i8 p# S, P( N$ Y
aware of this fact, because most of these children
& s: x. G4 {( P4 O7 i! G5 _may initially present in their practice. The Physicians’* o. Z& D, p6 B2 E, J+ n* F* D% i
Desk Reference and package insert should also put a) C2 I2 i+ x* A8 M* G0 x) v
warning about the virilizing effect on a male or
) c6 x) f$ o( A2 T" W( P6 K$ bfemale child who might come in contact with some-8 v, ^& m; i& V% _8 k/ |& k
one using any of these products.3 m' a" |4 u5 E0 F( V: T, q S
References- A" {4 p0 F5 P8 h% p' P. v
1. Styne DM. The testes: disorder of sexual differentiation3 w# z! I' ?7 Z
and puberty in the male. In: Sperling MA, ed. Pediatric& Y0 ~1 W7 m9 Z( ]2 Z' v
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
0 G3 F c% w5 u$ B o5 Z2002: 565-628.
( n2 \! u5 f8 [2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious6 b! Y$ X7 u1 `0 E+ ^# k: ?
puberty in children with tumours of the suprasellar pineal |
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