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Sexual Precocity in a 16-Month-Old) i# d0 K. x! A& O2 R, L5 w
Boy Induced by Indirect Topical
3 w5 Z* L' W/ W2 K- Z& O f: n$ U* kExposure to Testosterone
" J) M# b: V5 `1 RSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2% O O- {5 e1 d/ E
and Kenneth R. Rettig, MD1$ ]; A* o( n4 ]# C' X5 s
Clinical Pediatrics: I8 _# U1 P* Y7 B/ {6 {
Volume 46 Number 6
7 B7 u9 z8 M, [, D7 }! ~/ QJuly 2007 540-543
6 h% g6 H* h$ v% @* [© 2007 Sage Publications8 r/ l2 O2 s+ E
10.1177/0009922806296651
2 y, e/ A- B, d9 _) t( zhttp://clp.sagepub.com2 O8 C7 h' j' Q/ `
hosted at
* k: K" e$ ]) Y5 O I7 Phttp://online.sagepub.com
- B8 q; r( W/ p% s6 V) c0 D* B5 ]Precocious puberty in boys, central or peripheral,
" `! p' T# O6 [is a significant concern for physicians. Central$ _6 |1 u) C" {
precocious puberty (CPP), which is mediated' X* t/ L# T0 {: |! B0 f
through the hypothalamic pituitary gonadal axis, has
4 w M1 y+ Z' J. La higher incidence of organic central nervous system* V6 a- K5 Q) Z7 P O T/ w9 l
lesions in boys.1,2 Virilization in boys, as manifested
m3 r g7 e8 ]. z# |6 o5 t2 R6 Fby enlargement of the penis, development of pubic! e5 M' Y* N, U3 t N0 L
hair, and facial acne without enlargement of testi-$ E' A+ H/ l& l# S! B! l
cles, suggests peripheral or pseudopuberty.1-3 We
& e% G$ f0 c& S9 u% H8 |/ u/ ~report a 16-month-old boy who presented with the& [5 o" F; X b% w& v. Q
enlargement of the phallus and pubic hair develop-. n' N+ d3 ]: h+ |* R7 i
ment without testicular enlargement, which was due
" l2 s/ r, F$ V2 V3 ~to the unintentional exposure to androgen gel used by* F# `" y4 Q" X8 @ F5 x
the father. The family initially concealed this infor-
+ B1 K$ r# z T: p, kmation, resulting in an extensive work-up for this
4 L2 N5 U; M2 _+ zchild. Given the widespread and easy availability of- Y1 ?3 n! D! r8 o, S7 o2 `9 X) \
testosterone gel and cream, we believe this is proba-: G7 `8 j5 c- V t5 u* z
bly more common than the rare case report in the
" M# K6 R4 f4 mliterature.4- Q. Q# Z" Z$ E v, F3 _' I) G
Patient Report
! X$ D1 \- h" |+ L3 Q' \3 M5 TA 16-month-old white child was referred to the
8 w' }+ V, [' T# g* hendocrine clinic by his pediatrician with the concern
H3 W! q0 q) a+ s9 w# iof early sexual development. His mother noticed1 Z: D) {1 V% {% ^6 ?
light colored pubic hair development when he was7 K ~9 l" }% U
From the 1Division of Pediatric Endocrinology, 2University of9 X& B5 R% c9 p& W, j
South Alabama Medical Center, Mobile, Alabama.% _( I. N* g! @, e$ H7 g) ^
Address correspondence to: Samar K. Bhowmick, MD, FACE,
7 H, h& s% X, d0 Z2 x7 R9 lProfessor of Pediatrics, University of South Alabama, College of
7 U. t) I! U. I+ {" o4 ]1 Q) }7 AMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
- V4 ^; a# I$ L3 be-mail: [email protected].1 G r0 U% q! K6 i7 N/ r0 u
about 6 to 7 months old, which progressively became
; }5 G6 W: j. N6 }darker. She was also concerned about the enlarge-% c9 ~6 O. V4 A' {4 p
ment of his penis and frequent erections. The child' ]% x8 c' @' H& C5 r7 i3 u- }8 H! f
was the product of a full-term normal delivery, with' B4 N5 {' c1 x& p- i& M2 Q3 u
a birth weight of 7 lb 14 oz, and birth length of2 o) k* U8 [ {9 Z6 c( Z6 u* }
20 inches. He was breast-fed throughout the first year
8 H" j: Q9 s7 r+ Mof life and was still receiving breast milk along with
& w; o# g3 q* bsolid food. He had no hospitalizations or surgery,* s8 b: o2 m; C5 f
and his psychosocial and psychomotor development/ J0 E5 f) M7 a- ?9 [, |" ]; b- U
was age appropriate.
# I" x9 O3 l/ j# B/ h# X$ dThe family history was remarkable for the father,& v% e" q9 l" K& L' ~4 e
who was diagnosed with hypothyroidism at age 16,6 E- w% H0 ?( L% d$ w
which was treated with thyroxine. The father’s3 }- P, E$ X' o7 x
height was 6 feet, and he went through a somewhat8 W1 U% w0 H. _: {; h- @
early puberty and had stopped growing by age 14.: k& W1 Q& n" N. S
The father denied taking any other medication. The N' |% {' B- x" @, D
child’s mother was in good health. Her menarche, w& b% W! u! D6 g2 p, Y: ^
was at 11 years of age, and her height was at 5 feet# r4 D: I- l6 M& U6 [0 R6 r
5 inches. There was no other family history of pre-
8 C; y+ i& Y2 `- @7 ]& vcocious sexual development in the first-degree rela-% U" G: `2 ~8 c; V! A0 k( G
tives. There were no siblings.) J6 f6 N& ]8 I: R
Physical Examination
+ I$ R5 t; q3 r) ]/ F. G* i7 MThe physical examination revealed a very active,! x+ [4 U1 e, d! @
playful, and healthy boy. The vital signs documented8 s, B4 P. P$ [- l+ `
a blood pressure of 85/50 mm Hg, his length was5 v; U5 }6 G0 c$ ~# K
90 cm (>97th percentile), and his weight was 14.4 kg
9 R3 b3 V6 P& y# c(also >97th percentile). The observed yearly growth
3 ]( N4 C' G* O( P ~9 ?velocity was 30 cm (12 inches). The examination of
+ @! l* j" V% h( Z+ zthe neck revealed no thyroid enlargement.
3 p& _/ k3 r5 Q* r* I8 p2 V( N5 FThe genitourinary examination was remarkable for# }8 K6 O( x: y% Y& M C# N
enlargement of the penis, with a stretched length of% S4 a! m& ^" H! g# t4 q+ ^7 d
8 cm and a width of 2 cm. The glans penis was very well [- u M2 \' q2 ?6 Y# Z; y h
developed. The pubic hair was Tanner II, mostly around
6 m5 I& W8 j! P! P( l540
$ ]/ U9 J# F# d( O3 K1 Tat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
& T) |4 e- x4 s6 }0 G/ Dthe base of the phallus and was dark and curled. The) m3 Q3 g5 h: M" E* L" s/ X: K; J
testicular volume was prepubertal at 2 mL each.
) G2 u- c2 t& e0 m. |1 S5 kThe skin was moist and smooth and somewhat1 i9 F" P7 }+ ^$ `2 P& @
oily. No axillary hair was noted. There were no9 ^. |8 a1 L* q, S/ L0 l9 v' f) E. O
abnormal skin pigmentations or café-au-lait spots.: u4 b4 }+ c$ W5 h
Neurologic evaluation showed deep tendon reflex 2+4 b! X/ p3 D' u
bilateral and symmetrical. There was no suggestion7 Y7 Q+ _# d4 ~0 ]! {: e3 p
of papilledema.; g/ S" N: _7 _5 ^! g, f
Laboratory Evaluation# W5 @. b; W- @1 Y+ J; v2 \7 t% a
The bone age was consistent with 28 months by T7 x/ @* m, K, _6 S0 C' m
using the standard of Greulich and Pyle at a chrono-! k- _- Q4 g; v
logic age of 16 months (advanced).5 Chromosomal
+ O+ {- u5 q& A, m# \" |( Xkaryotype was 46XY. The thyroid function test5 s) g# n& I5 m( O, K
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
% J9 j% N, k. S8 T4 q9 D- dlating hormone level was 1.3 µIU/mL (both normal).0 Q ^, ]6 w+ Y; r
The concentrations of serum electrolytes, blood9 l: m5 Z+ T2 `8 y: x! @" ~5 d$ X
urea nitrogen, creatinine, and calcium all were8 R) |" a( `- T. I
within normal range for his age. The concentration) z. A2 u$ A5 U6 L# ^
of serum 17-hydroxyprogesterone was 16 ng/dL5 P) M! D( _* B! v2 u. V% w
(normal, 3 to 90 ng/dL), androstenedione was 20
$ B3 ]- X- S% }' m; ?# @ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-% T# @% ~' z. `( m" H5 i( v
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
. J- `. M! b9 k9 P& zdesoxycorticosterone was 4.3 ng/dL (normal, 7 to) b% c: M0 d) a# F, m; q
49ng/dL), 11-desoxycortisol (specific compound S)
; q3 z# {0 l. y9 Twas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
( f3 d, g8 _1 Y! D- _tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total4 F( m, e6 O) r' T, F; D5 i+ ^1 u% ~
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),- R' T8 {2 Y' `( U" J* A# G" [$ V
and β-human chorionic gonadotropin was less than
( J6 w1 i, U$ c; `) t0 m( \5 mIU/mL (normal <5 mIU/mL). Serum follicular( n& ^/ {/ V, z% W
stimulating hormone and leuteinizing hormone
* r, T* T( m- _concentrations were less than 0.05 mIU/mL) G9 z. Y% A6 A( U% |7 G( H- e F1 s
(prepubertal).
- Q3 Q5 [' v! ]( O; \The parents were notified about the laboratory
1 U4 E" c. I, y8 X2 kresults and were informed that all of the tests were+ M( R! w7 W; s" c0 `/ s3 Q
normal except the testosterone level was high. The
4 f/ ?" u; Q: U* ~8 Nfollow-up visit was arranged within a few weeks to9 n [( M6 h/ d, w6 q2 s
obtain testicular and abdominal sonograms; how-
8 C# R/ J5 s m( {& d/ |" oever, the family did not return for 4 months.
% H; p$ Q4 H6 I9 c& a" QPhysical examination at this time revealed that the
5 T E0 {. F6 {' G8 }$ a$ ~child had grown 2.5 cm in 4 months and had gained
7 ^% e+ S5 F1 _2 kg of weight. Physical examination remained
( {: S! F5 i1 H8 Zunchanged. Surprisingly, the pubic hair almost com-
% J) J) T+ v9 T4 I" T& w9 _pletely disappeared except for a few vellous hairs at5 G# z0 b2 R" a4 w6 q
the base of the phallus. Testicular volume was still 2
! j1 m# \7 p) J5 o( imL, and the size of the penis remained unchanged. Z- O2 [! i6 n, P9 d9 X7 V
The mother also said that the boy was no longer hav-$ \" _ n5 ~7 U. t& ]
ing frequent erections.
& ?: U" g( n5 P- PBoth parents were again questioned about use of4 z0 E3 j1 _! r
any ointment/creams that they may have applied to+ d3 S6 g; q8 |% V+ }" p- _9 t+ }; K
the child’s skin. This time the father admitted the/ x2 c, r$ Q& t# r4 X8 E$ H
Topical Testosterone Exposure / Bhowmick et al 541
: P( @* @5 c. p S. b7 duse of testosterone gel twice daily that he was apply-- |. Z: Q9 D+ F2 @
ing over his own shoulders, chest, and back area for) n8 b& R. l' G; t1 s, b
a year. The father also revealed he was embarrassed
/ a( ?* J, H1 C: Pto disclose that he was using a testosterone gel pre-
" w/ G$ }8 s. ^scribed by his family physician for decreased libido
9 A6 r u4 [% l" i9 fsecondary to depression.
+ Z4 g: J7 H2 R* M! G, V; W4 `The child slept in the same bed with parents.
0 Y! {" Z; \+ j' MThe father would hug the baby and hold him on his- ~0 A$ _, E! Y" f
chest for a considerable period of time, causing sig-$ Q0 \8 a) X( h
nificant bare skin contact between baby and father.) |; K/ y {) ]( z9 a; {: p
The father also admitted that after the phone call,
5 ^8 }3 g" P" Y' i4 p! l1 ~% X* Owhen he learned the testosterone level in the baby
+ T b! k6 v. X; @% g8 [: pwas high, he then read the product information$ P) K: ?4 r1 r
packet and concluded that it was most likely the rea-) ]: ?6 }- {) l9 j3 x% _3 N
son for the child’s virilization. At that time, they
" j. r; b5 z: y6 }. R- u- z$ d% Edecided to put the baby in a separate bed, and the
: x$ a3 O' l; A5 `8 }* h7 z! u# Rfather was not hugging him with bare skin and had
9 n3 `+ x4 @( b3 {+ Abeen using protective clothing. A repeat testosterone5 J0 ?6 p7 [, `* E) e$ P/ e
test was ordered, but the family did not go to the; M3 S& P; @, { t* H |
laboratory to obtain the test.
z7 Y* u5 X" n8 C( `- yDiscussion
: F; g# \* O* [ N: KPrecocious puberty in boys is defined as secondary
. R; C8 ]! W! t% u I5 {sexual development before 9 years of age.1,4
5 ^- E( n2 @1 p) C/ aPrecocious puberty is termed as central (true) when; C: [( \. Z& X8 b. P0 M
it is caused by the premature activation of hypo-
l6 B( \: w# {- v1 |( N9 F$ d5 Tthalamic pituitary gonadal axis. CPP is more com-
0 I; I0 d# g; S+ _6 i# O. [' rmon in girls than in boys.1,3 Most boys with CPP
3 A0 r) N4 N: k% E1 cmay have a central nervous system lesion that is ]( O8 W; s _" Q8 q9 X/ ^" t
responsible for the early activation of the hypothal-, i; W5 r7 U/ }& n+ D! H
amic pituitary gonadal axis.1-3 Thus, greater empha-
) P( s4 e! N& j* ^$ esis has been given to neuroradiologic imaging in
, w1 M4 `' }- P. Wboys with precocious puberty. In addition to viril-3 |, G- e7 f, a6 o* e' F, \; C& [' p
ization, the clinical hallmark of CPP is the symmet-
. C: r* K6 {! ~5 Yrical testicular growth secondary to stimulation by
k* R2 E- L7 H% Ygonadotropins.1,39 z1 n6 {" g Q2 r. B$ i& Z1 P
Gonadotropin-independent peripheral preco-
' {% x3 _6 X. m. M" t1 M: Z$ `cious puberty in boys also results from inappropriate8 o2 p! \7 @/ n J5 U# o4 z9 l
androgenic stimulation from either endogenous or1 J; |. j& P* O0 Z. C, h1 L
exogenous sources, nonpituitary gonadotropin stim-
/ D. R& _2 y( |ulation, and rare activating mutations.3 Virilizing
1 ]6 j0 H+ m% j2 bcongenital adrenal hyperplasia producing excessive, Z3 I0 q# c) _( ` |
adrenal androgens is a common cause of precocious
: T4 o- ~( R/ w# K0 Lpuberty in boys.3,48 E% s3 N5 ^' D
The most common form of congenital adrenal8 q6 S% S, e" a ~7 c
hyperplasia is the 21-hydroxylase enzyme deficiency.' C! d) T* w: Q$ X' J, ~6 x
The 11-β hydroxylase deficiency may also result in/ e4 ]6 b R9 ^1 ^* n3 J9 O
excessive adrenal androgen production, and rarely,; c% H. @1 @. ~) ]
an adrenal tumor may also cause adrenal androgen
) D7 c& |9 w: V5 W2 o3 S# aexcess.1,3
; k+ M) Q1 d6 m3 c) ?( Iat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
! g W4 h0 q- g$ x( h542 Clinical Pediatrics / Vol. 46, No. 6, July 2007( S+ T7 p$ b8 s9 e5 O
A unique entity of male-limited gonadotropin-; B( j/ N/ d5 T8 L
independent precocious puberty, which is also known9 a5 w' K4 P& [+ ?1 G
as testotoxicosis, may cause precocious puberty at a
5 b0 R* b0 ?% B+ o! O/ ^6 avery young age. The physical findings in these boys
: J J! W0 y* Z0 U8 r4 }9 rwith this disorder are full pubertal development,# B3 z2 J- O+ _
including bilateral testicular growth, similar to boys
) U* v7 D7 E3 v( T swith CPP. The gonadotropin levels in this disorder5 q: s" Y& b3 S( B7 [# b
are suppressed to prepubertal levels and do not show- b$ y! o+ x' C5 b( a
pubertal response of gonadotropin after gonadotropin-
9 k$ m; @! A3 s# i. O0 `releasing hormone stimulation. This is a sex-linked P7 m7 |( G: w1 G. w4 r4 e
autosomal dominant disorder that affects only4 f! U' C/ k7 h: g% y$ I6 P2 B$ c
males; therefore, other male members of the family
$ ?3 U9 G ?6 r5 K5 _may have similar precocious puberty.3* I& b& G$ P: R! R9 o9 n2 x. O
In our patient, physical examination was incon-
9 J; q: f5 q/ O! Nsistent with true precocious puberty since his testi-
1 S6 m$ }7 o% ~8 y6 a. o" j) }7 _cles were prepubertal in size. However, testotoxicosis
9 T& J: V3 G {3 s+ Mwas in the differential diagnosis because his father9 S, A1 n3 W8 r ?- l; Z
started puberty somewhat early, and occasionally,
$ X$ W, {3 Y$ d4 ctesticular enlargement is not that evident in the& ^3 j6 f( X1 c' r1 M& }
beginning of this process.1 In the absence of a neg-
9 b1 _: D0 v. k" vative initial history of androgen exposure, our
. {* `0 o. O0 ~, o& M" t+ [6 Ubiggest concern was virilizing adrenal hyperplasia,
2 P! W B, m5 V `0 feither 21-hydroxylase deficiency or 11-β hydroxylase
- n' P9 M4 z2 [( l% K% adeficiency. Those diagnoses were excluded by find-+ l8 e) K- ^- [2 n( z5 K, M6 O
ing the normal level of adrenal steroids.
0 F [8 x0 x# w4 Y" Y7 p: m6 `The diagnosis of exogenous androgens was strongly
3 L5 l+ P9 f2 S$ ?& c9 @suspected in a follow-up visit after 4 months because
5 n- H4 G: K h3 Nthe physical examination revealed the complete disap-# k% R2 @, q5 s# O
pearance of pubic hair, normal growth velocity, and
! ~) e; B# l6 y" W, j M$ odecreased erections. The father admitted using a testos-
4 Q* {4 K3 |$ k) ^+ o7 qterone gel, which he concealed at first visit. He was+ M) J6 i- H$ v! n! p6 w( {
using it rather frequently, twice a day. The Physicians’; A: J \, V" P
Desk Reference, or package insert of this product, gel or3 a) Q* b% T# c6 }( _: {
cream, cautions about dermal testosterone transfer to4 x* _( m9 _# J8 W# v% i
unprotected females through direct skin exposure.
/ p1 u n2 E5 v3 C8 b; L& I8 pSerum testosterone level was found to be 2 times the: c& [) ]$ r* c6 _( A
baseline value in those females who were exposed to# W( F. K* d- b% Q
even 15 minutes of direct skin contact with their male
" k9 }% k5 C+ `1 x/ rpartners.6 However, when a shirt covered the applica-
$ a( ]9 M% W: e2 q5 }/ Etion site, this testosterone transfer was prevented.
8 d8 l' g. ~4 O# ?% YOur patient’s testosterone level was 60 ng/mL,
$ j" T3 b0 b9 P; i! t! Hwhich was clearly high. Some studies suggest that
7 A- B& @5 G$ S1 Cdermal conversion of testosterone to dihydrotestos-" T4 q0 y, N& W2 S5 ]* v9 N0 x! G1 }% }
terone, which is a more potent metabolite, is more
( t4 q3 \8 G+ p% [/ `' G3 yactive in young children exposed to testosterone$ {9 u- S$ k( a: w# N
exogenously7; however, we did not measure a dihy-
3 e* I k+ B t* `- y0 {7 pdrotestosterone level in our patient. In addition to* {' V' H; ^2 y% i! l6 ?$ _
virilization, exposure to exogenous testosterone in
+ C5 O. A8 r! achildren results in an increase in growth velocity and
O; m! I, l3 ]: e, Badvanced bone age, as seen in our patient.' Y Z8 ^) \" o+ {3 c- Q
The long-term effect of androgen exposure during
9 f7 m# o* `2 F- cearly childhood on pubertal development and final9 w% d N+ Z! r" C5 n1 ^7 \6 b
adult height are not fully known and always remain, W+ ?+ S4 u* v: P
a concern. Children treated with short-term testos-. w( B7 f' r4 ` L% u( M' x9 `! K7 V6 A7 T
terone injection or topical androgen may exhibit some
9 w! B4 C5 T' T8 bacceleration of the skeletal maturation; however, after
/ l1 r5 ~, `* s: Ycessation of treatment, the rate of bone maturation
. \0 f( _3 s1 u" \2 q& J$ ydecelerates and gradually returns to normal.8,90 B6 z% E- Y/ C$ e0 f, d
There are conflicting reports and controversy
/ Y; v4 h- J h$ v1 Bover the effect of early androgen exposure on adult
$ J, N) y9 w1 F: I$ Ipenile length.10,11 Some reports suggest subnormal
6 R+ Z4 D5 U- F& ?9 z! zadult penile length, apparently because of downreg-) r+ W7 p1 d2 V9 d. n
ulation of androgen receptor number.10,12 However,7 O5 o" i& z9 |: m& Q, L; Q; _: ~
Sutherland et al13 did not find a correlation between
2 u) y, D P0 s: s/ }# P9 m) tchildhood testosterone exposure and reduced adult7 W6 `& a; v- q; ]. Z I
penile length in clinical studies.( J# F1 I9 [8 G6 }7 l- @ k4 e
Nonetheless, we do not believe our patient is3 L5 ?( c2 R( G& ^3 `, _3 |
going to experience any of the untoward effects from6 f' y( _; B6 p# u, J
testosterone exposure as mentioned earlier because
- u& C( y* p2 b1 p$ A6 j7 y3 Ethe exposure was not for a prolonged period of time.
/ E/ y0 Q; N6 O9 DAlthough the bone age was advanced at the time of4 k6 ^/ x5 m: H7 r- y2 m
diagnosis, the child had a normal growth velocity at9 s- e+ k9 m( H& i- T+ C
the follow-up visit. It is hoped that his final adult( _3 ~0 L. Z8 l
height will not be affected.8 N& X) k h- e7 H
Although rarely reported, the widespread avail- X- F: r# A' ^& m& w# e
ability of androgen products in our society may
7 p3 {! `$ k' l% vindeed cause more virilization in male or female
2 x& [- @1 A/ G7 F$ A2 s. p2 Cchildren than one would realize. Exposure to andro-
9 q i8 _" q. s8 R) W! _. ogen products must be considered and specific ques-/ Y" Q# l3 ~; V
tioning about the use of a testosterone product or. Y) ^9 F, I- y* N2 d+ x+ G# [) I
gel should be asked of the family members during: ?! s& _" q; K8 [
the evaluation of any children who present with vir-
/ E$ s2 x0 j$ G4 t0 N, h& Tilization or peripheral precocious puberty. The diag-4 d- E; ]: z5 i2 E' O% \0 v+ ~
nosis can be established by just a few tests and by$ u3 L" c% I2 _3 z6 N. o. h
appropriate history. The inability to obtain such a e2 G& Z5 ^0 k& z) Y( @4 U- _! J: p
history, or failure to ask the specific questions, may7 _6 N; W2 H) { s
result in extensive, unnecessary, and expensive
) Y, o+ _) q P6 @) P* Winvestigation. The primary care physician should be
/ N3 k5 T' k1 E2 T" Eaware of this fact, because most of these children% v: P1 B1 X3 k5 v7 d2 N/ ?
may initially present in their practice. The Physicians’8 v& v, P, w9 @5 o0 A/ [5 R8 ^9 h
Desk Reference and package insert should also put a
! o n9 Y6 n6 r* s3 swarning about the virilizing effect on a male or
1 y0 ?$ ?: t0 ^female child who might come in contact with some-' T) N$ b+ b1 i3 k5 p8 G. _( ?
one using any of these products.2 O- n# V, m3 F; X
References
' t2 Y0 v* H/ P) c6 Y. l8 h1. Styne DM. The testes: disorder of sexual differentiation
; G# }: Z' x9 g% B. Qand puberty in the male. In: Sperling MA, ed. Pediatric
. h& F) I' b5 Z8 SEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
x3 u$ `# Z8 s2002: 565-628.
; W- m* ?! _) _) C; T2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
( F' a! O9 d* k# Z9 p% Fpuberty in children with tumours of the suprasellar pineal |
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