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Sexual Precocity in a 16-Month-Old
- Z) T. ]" V1 R) E8 d' i, kBoy Induced by Indirect Topical* S- o" d$ C: V- H7 v
Exposure to Testosterone
2 Z- [7 `3 h5 h( x. KSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2- g8 p D: b' E8 L+ t) f: K$ L
and Kenneth R. Rettig, MD1
6 a e. j. z, k7 HClinical Pediatrics3 l. C1 f, |' P
Volume 46 Number 69 [7 K/ ~& I T
July 2007 540-543
6 D+ w; V) T% G8 i0 p© 2007 Sage Publications; A/ V- i( s9 P" s+ }( ~0 M5 T
10.1177/0009922806296651
0 k! G1 U, _- ?" Mhttp://clp.sagepub.com
4 D5 M* z! K1 H( V! e. g1 lhosted at
3 v4 Z* p3 O; P' hhttp://online.sagepub.com1 H6 d: O- l, j
Precocious puberty in boys, central or peripheral,
# v% ^$ Y2 W/ x, r, }is a significant concern for physicians. Central
( n* L* r, ^& K4 f& Z' ]1 r: x3 vprecocious puberty (CPP), which is mediated0 t5 r( `5 K2 X6 ~$ j$ B
through the hypothalamic pituitary gonadal axis, has
" _- b1 ^ E" _7 y, pa higher incidence of organic central nervous system
0 R+ x3 h. T* n" M/ vlesions in boys.1,2 Virilization in boys, as manifested
, N/ }/ `9 G( N- M2 Sby enlargement of the penis, development of pubic
, N3 F; O! G. w& ^1 Z% x- khair, and facial acne without enlargement of testi-
1 Q7 `. {) }# L* C& Lcles, suggests peripheral or pseudopuberty.1-3 We L1 C u: i0 O1 f; d( H" F
report a 16-month-old boy who presented with the7 [5 J) {0 ~0 m5 w
enlargement of the phallus and pubic hair develop-
/ T7 k( i$ j2 g9 [5 U# \! @ment without testicular enlargement, which was due7 a0 e& Y( {8 P* a: x4 k2 i
to the unintentional exposure to androgen gel used by
3 { B$ M1 k- y0 k* F, i6 w) s( z% `the father. The family initially concealed this infor-
8 {' n' E7 o( A- @3 f$ Ymation, resulting in an extensive work-up for this! x: W( \. }4 y+ M2 X( v
child. Given the widespread and easy availability of
+ X9 d" }; K# I/ m* ttestosterone gel and cream, we believe this is proba-
0 e# _: B7 S( m# Gbly more common than the rare case report in the# G* w4 s) v& q1 O+ Y2 P
literature.42 D X9 v6 v# ~" H) ?8 o& d
Patient Report1 I6 k5 h! q1 k
A 16-month-old white child was referred to the# _% t1 |4 w$ Z' S
endocrine clinic by his pediatrician with the concern
7 u0 t: f/ a5 ?- I. Uof early sexual development. His mother noticed
7 M c( {9 Z! Dlight colored pubic hair development when he was
& l% Y2 t: P0 @5 U6 L, kFrom the 1Division of Pediatric Endocrinology, 2University of
- F; V, o4 t4 JSouth Alabama Medical Center, Mobile, Alabama.' C! Q) \- E& ~7 ?1 G6 T- ^, x
Address correspondence to: Samar K. Bhowmick, MD, FACE,
9 k, a% t% s5 K$ y% |& N2 s2 EProfessor of Pediatrics, University of South Alabama, College of. s: i, c' b7 l: }
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;' V. H; j+ y7 Z5 z: y
e-mail: [email protected].
* ^8 [4 r; w! `! I4 R! Xabout 6 to 7 months old, which progressively became
; R/ A, W, T. B9 f- S# Ydarker. She was also concerned about the enlarge-
% o; {' x1 H3 I) K& jment of his penis and frequent erections. The child
$ u8 Y2 V/ f" _3 k! {was the product of a full-term normal delivery, with
8 k( u* i- i% R' D6 f, T3 _, `% ta birth weight of 7 lb 14 oz, and birth length of1 u6 {6 h7 ]4 {/ c( p2 r
20 inches. He was breast-fed throughout the first year
, K* V1 Q# d E& Xof life and was still receiving breast milk along with) q" ~+ |3 m6 _- a8 c- c# Z" S. S
solid food. He had no hospitalizations or surgery,; T6 K: f- F+ w* u
and his psychosocial and psychomotor development# G( J3 W6 y! o& f$ [+ T% j
was age appropriate.1 ~: w$ H0 p% ~# n
The family history was remarkable for the father,3 f3 s ^1 G6 O( r# S
who was diagnosed with hypothyroidism at age 16,8 k% ~) @/ Q, b3 ]
which was treated with thyroxine. The father’s
: ~; f1 D, `2 O1 {height was 6 feet, and he went through a somewhat
, J& ], ]5 E: S6 L. x3 _; J! S/ E8 Aearly puberty and had stopped growing by age 14.
7 ?; e- h1 f- X( F; p# [, a& YThe father denied taking any other medication. The) p+ k- F5 m9 ]( A* `
child’s mother was in good health. Her menarche4 s4 L3 }6 y9 l( C' j
was at 11 years of age, and her height was at 5 feet
; _: q0 U5 y3 p$ B, h8 V5 inches. There was no other family history of pre-
8 _( O9 s: p1 L1 Q6 Ucocious sexual development in the first-degree rela-7 @1 ^/ P* ?( V6 j# u5 K- G5 y3 m
tives. There were no siblings.8 [- c- Q; C" H1 t+ w
Physical Examination! ~( S0 {% ] f0 |1 x
The physical examination revealed a very active,7 N6 g7 ^) C7 x B. r- Z/ R, z
playful, and healthy boy. The vital signs documented3 y4 B' |$ X. B' \8 V( {1 X) [0 j
a blood pressure of 85/50 mm Hg, his length was" u0 Z4 u9 C: w0 E( ]
90 cm (>97th percentile), and his weight was 14.4 kg4 i! q, u, c$ P `% x# z$ o1 B
(also >97th percentile). The observed yearly growth5 W) }0 T& D% ~+ s( s, `
velocity was 30 cm (12 inches). The examination of
" \6 f0 u- U1 B! xthe neck revealed no thyroid enlargement.4 v$ d& K1 d7 w: |" a, m5 u( c
The genitourinary examination was remarkable for
, A- Q5 Q1 m: x: ?; W, t, P% oenlargement of the penis, with a stretched length of
( `9 r G, A! I8 c! L" i4 N- D8 cm and a width of 2 cm. The glans penis was very well
1 i% Q$ l2 s; `& G! b: `developed. The pubic hair was Tanner II, mostly around
+ o* P6 R2 Z" k+ h% [540
9 c+ e5 p0 Q/ p: U# vat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
# \( L6 |5 m3 ^- D! P) Fthe base of the phallus and was dark and curled. The' p0 s: N' x* A, o$ i
testicular volume was prepubertal at 2 mL each.' U5 z7 b) v! q: @: ~
The skin was moist and smooth and somewhat
# {: X3 \4 b' A' G) w- }oily. No axillary hair was noted. There were no% E2 W; t5 T( m8 I# d. R. S1 U
abnormal skin pigmentations or café-au-lait spots.
$ z2 y' L* m# V4 ]1 }Neurologic evaluation showed deep tendon reflex 2+- {8 p: c% ^3 ?$ m
bilateral and symmetrical. There was no suggestion6 R, C1 U, m7 u$ D- n
of papilledema.
- J8 `/ q4 a: s) o; ]Laboratory Evaluation
3 g9 ?0 k7 ~& i" AThe bone age was consistent with 28 months by
+ N. l0 d3 h5 u7 Y a# z# G" G& w: P5 _using the standard of Greulich and Pyle at a chrono-
: T5 o; ?+ i9 dlogic age of 16 months (advanced).5 Chromosomal
+ x \! R! `+ M! l/ vkaryotype was 46XY. The thyroid function test* K; I$ \) A/ d, L9 @( }5 G
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
" Q% h8 \; {' l! X6 dlating hormone level was 1.3 µIU/mL (both normal).( k( h1 U, }9 X: }6 E7 E
The concentrations of serum electrolytes, blood U: l0 ~- |) d9 h% B
urea nitrogen, creatinine, and calcium all were
% S5 J5 n6 Y; h8 i0 twithin normal range for his age. The concentration
+ { F7 m* z, b+ Y G: |of serum 17-hydroxyprogesterone was 16 ng/dL
, f: W+ z- Z! x0 A8 {; X(normal, 3 to 90 ng/dL), androstenedione was 20
. i3 W1 }/ S2 T& Y( a' wng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
8 @' T. |: I5 p& y9 uterone was 38 ng/dL (normal, 50 to 760 ng/dL),
$ w' H2 o6 f! J) Edesoxycorticosterone was 4.3 ng/dL (normal, 7 to- l$ Z, d9 l6 A- ?, D9 g" f8 G; m
49ng/dL), 11-desoxycortisol (specific compound S)
, o' r9 z$ _+ }9 ^& Qwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-7 a C0 x7 `7 h, T) x9 H
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total' Z+ R7 l1 A h" d/ Z+ a# N8 v
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),: @: ^; e/ G8 W7 E4 l
and β-human chorionic gonadotropin was less than' E1 g1 S8 W! c# G1 Y' R
5 mIU/mL (normal <5 mIU/mL). Serum follicular; ^+ ?; k# C1 ^8 E+ K
stimulating hormone and leuteinizing hormone
4 z8 n' C+ B4 y5 E! o# u" vconcentrations were less than 0.05 mIU/mL( L& j) y, W5 i- X) W
(prepubertal).
% _* n: w/ t! o; r' t3 wThe parents were notified about the laboratory
# r9 E2 o5 C2 V: z) s$ t; K9 Uresults and were informed that all of the tests were8 o. ^: p; L. S: j
normal except the testosterone level was high. The) x! n3 H+ ^1 y- r& s+ P, K
follow-up visit was arranged within a few weeks to5 h1 [ P9 r4 G; J2 a( F7 u9 S
obtain testicular and abdominal sonograms; how-
" [9 q6 m( G+ l0 B% yever, the family did not return for 4 months.
) ^0 o) N+ ~$ @4 z7 SPhysical examination at this time revealed that the
2 ~4 C3 u2 v8 v: N9 gchild had grown 2.5 cm in 4 months and had gained
" i) P+ I/ S/ k9 Z# R2 kg of weight. Physical examination remained6 f) V* Y9 M1 m: o7 y8 l. X
unchanged. Surprisingly, the pubic hair almost com-
! Y5 m4 y9 ] O" F! ypletely disappeared except for a few vellous hairs at
' V4 y! G I4 f" b9 `6 ~; d1 Ithe base of the phallus. Testicular volume was still 2! }1 l' K% S% n. `* B9 _
mL, and the size of the penis remained unchanged.3 | t j2 C+ U4 F) z8 V3 W# Y
The mother also said that the boy was no longer hav-
6 p0 q' D2 Z8 Q3 j, A6 {. ^ing frequent erections.. @+ {9 n: R$ F4 I+ L; }
Both parents were again questioned about use of/ t! ~' g" B6 r' T0 z3 f0 X
any ointment/creams that they may have applied to
2 L" O' {- k2 r5 Q3 Rthe child’s skin. This time the father admitted the
: {: J# ?) K) l1 _& f+ ~Topical Testosterone Exposure / Bhowmick et al 541; f0 _/ ~) i" Z1 | p$ G* _
use of testosterone gel twice daily that he was apply-
$ i$ y {" \0 ^+ _6 u! X) W) ^! Hing over his own shoulders, chest, and back area for, B# ^& B' L) M# @1 T' g7 ~" a Y0 Q
a year. The father also revealed he was embarrassed, Z7 \7 s# C: c, V; J+ r$ \) {' G- a
to disclose that he was using a testosterone gel pre-
8 {7 F d. [8 b/ s! Wscribed by his family physician for decreased libido
. O" E1 O; c& f; K5 ksecondary to depression.$ [% X. a3 N6 {1 F
The child slept in the same bed with parents.3 P# C/ L) A5 `, ^; |
The father would hug the baby and hold him on his
3 a( s, x% Q2 C; M) jchest for a considerable period of time, causing sig-& U: V* {2 y$ L
nificant bare skin contact between baby and father.: U, w* J% {3 W/ a% k0 K, t
The father also admitted that after the phone call,6 T! Z6 m9 I8 u t7 z
when he learned the testosterone level in the baby
0 l, O4 S8 z; E lwas high, he then read the product information% n' s; V' c" c) l: T: R
packet and concluded that it was most likely the rea-
, _; c) \/ D4 u+ J( e/ G. oson for the child’s virilization. At that time, they) D9 l, ]+ A0 g, U
decided to put the baby in a separate bed, and the
1 M5 h% p$ A. n, k/ G/ R ffather was not hugging him with bare skin and had1 Z y3 q- L* L! G! a. K- f
been using protective clothing. A repeat testosterone
; _! p# W( w7 g7 X# Htest was ordered, but the family did not go to the
" ]" O( K7 g$ e) C) nlaboratory to obtain the test. k# L) l. h2 ? R; o7 q( w
Discussion- D* e9 H. F) x6 v: |
Precocious puberty in boys is defined as secondary1 U2 {- K4 B4 e! Q) x% `, b8 V
sexual development before 9 years of age.1,4
0 t. }- p1 D6 ?) y. ?) _Precocious puberty is termed as central (true) when6 E4 a0 g2 S0 p) f: G6 m
it is caused by the premature activation of hypo-
% m0 n( z5 Q6 o( Uthalamic pituitary gonadal axis. CPP is more com-
5 n% o+ R5 r- E3 l& ]7 i" hmon in girls than in boys.1,3 Most boys with CPP. h+ w) T ]+ l6 @ s9 v
may have a central nervous system lesion that is0 _# u- z& B7 T4 M- f
responsible for the early activation of the hypothal-
, Z* ~& K W: s) v/ Z! F8 qamic pituitary gonadal axis.1-3 Thus, greater empha-% `9 T7 ^1 I- a& ?! R L# b
sis has been given to neuroradiologic imaging in4 e, ~2 Y" [, ~! X2 N- q+ G
boys with precocious puberty. In addition to viril-# J% h( Z4 S# T8 [- \6 f# z
ization, the clinical hallmark of CPP is the symmet-# g! D8 s. U5 c2 Z: t
rical testicular growth secondary to stimulation by
}; L& f! R( h- _# v9 H# b* lgonadotropins.1,3) P: I8 z' y6 H$ t" a! t @
Gonadotropin-independent peripheral preco-
& s; ]) J2 I! j! K1 K# x% V6 Ecious puberty in boys also results from inappropriate
" J8 p9 B' M$ q/ D6 Q% k& ~& yandrogenic stimulation from either endogenous or
; N' G& }( [8 V, F. @. d/ w' {exogenous sources, nonpituitary gonadotropin stim-+ X: i; [2 X! F- i2 H: T
ulation, and rare activating mutations.3 Virilizing
: t- t( u; `4 Z4 g9 ?congenital adrenal hyperplasia producing excessive
) N- u* o8 h) S4 badrenal androgens is a common cause of precocious
: W5 w+ J4 V7 A3 d! ypuberty in boys.3,4" t3 o; q# H M \* Y, Q
The most common form of congenital adrenal2 B7 A. Z+ q; }+ ~. Z4 q" q
hyperplasia is the 21-hydroxylase enzyme deficiency.
$ X! u2 W; O6 }9 I( lThe 11-β hydroxylase deficiency may also result in- P4 A/ k7 Z3 Y' ^# D4 ~9 n
excessive adrenal androgen production, and rarely,/ p4 y- x6 c- M) x+ z" ?* C
an adrenal tumor may also cause adrenal androgen3 Z" {2 \" h5 r3 w1 O) l
excess.1,33 J7 }$ `- R% i c3 n+ L/ ?& z
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from- P2 J# ]7 f- T+ H
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007, c7 X0 X6 x; x, s; `2 X: ^- b: `
A unique entity of male-limited gonadotropin-
9 @# v$ a4 {5 Y" ~2 pindependent precocious puberty, which is also known
, y- d' D" p$ V& `% ^$ [) M/ Cas testotoxicosis, may cause precocious puberty at a6 ~- }5 p9 R7 q7 z; X
very young age. The physical findings in these boys
+ ^9 \5 j3 S( y, f" R; |/ Mwith this disorder are full pubertal development,
* p. x( k0 P% r, h* X, S) t2 Sincluding bilateral testicular growth, similar to boys& j3 n+ i& X& p) ?# n% q
with CPP. The gonadotropin levels in this disorder
$ h, A0 M- r2 D0 H C7 mare suppressed to prepubertal levels and do not show
5 M: j8 R1 k+ m" M2 h$ h6 c q( xpubertal response of gonadotropin after gonadotropin-0 u1 P& d) U$ g3 z9 @# l
releasing hormone stimulation. This is a sex-linked' k% M* i, r; H6 t6 ^
autosomal dominant disorder that affects only
0 m3 Q2 n1 ~# ~* N- D4 dmales; therefore, other male members of the family
! D2 P; {9 H$ m) P, [6 @may have similar precocious puberty.3% @; B. B" r A" w. W# [7 A9 C
In our patient, physical examination was incon-& V. h- d$ u0 B' D
sistent with true precocious puberty since his testi-& f! G& T; p; z W8 M6 y6 Q
cles were prepubertal in size. However, testotoxicosis% g% m8 C" [( }' P
was in the differential diagnosis because his father
& q* {7 E" L; r I" z5 ustarted puberty somewhat early, and occasionally,1 V5 u: e; ]( V
testicular enlargement is not that evident in the
, T7 R2 C% D" V% B4 Z/ Z+ l2 @( k1 E. ?beginning of this process.1 In the absence of a neg-
/ J G5 m' E- P: Iative initial history of androgen exposure, our4 W- R# M5 }- X+ s
biggest concern was virilizing adrenal hyperplasia,
1 [" a I/ } H' ]) xeither 21-hydroxylase deficiency or 11-β hydroxylase
) K: c0 |3 K+ r" n+ Jdeficiency. Those diagnoses were excluded by find-
& O' M8 x7 E7 b( \# {ing the normal level of adrenal steroids.
/ P, W+ T2 J$ R, ^) PThe diagnosis of exogenous androgens was strongly/ _6 @: @$ w, ^/ r) N! v5 K
suspected in a follow-up visit after 4 months because/ b' }8 g: X* l
the physical examination revealed the complete disap-
a" ~1 w6 K2 \pearance of pubic hair, normal growth velocity, and
, L# d# z9 a' h5 b- Hdecreased erections. The father admitted using a testos-
* o0 l4 ]1 E5 ~3 i+ E& x. h, g( kterone gel, which he concealed at first visit. He was$ f+ S8 m5 f5 h" J2 O9 U# O
using it rather frequently, twice a day. The Physicians’
( h, P/ l7 u" u. PDesk Reference, or package insert of this product, gel or4 I4 d0 Z6 e( Y% b7 O% X
cream, cautions about dermal testosterone transfer to# o. n! B5 s! |3 @1 f
unprotected females through direct skin exposure.
. [+ P9 v. J- ]2 g0 O, xSerum testosterone level was found to be 2 times the( X! b$ G5 V' E' t; Q
baseline value in those females who were exposed to
$ `8 V: _7 D9 beven 15 minutes of direct skin contact with their male
7 j" I) G4 g1 ^1 E% N- W5 Kpartners.6 However, when a shirt covered the applica-. [. O( u9 [0 ?% I: W5 Q
tion site, this testosterone transfer was prevented." o+ k# P* q6 r1 E6 P5 p
Our patient’s testosterone level was 60 ng/mL,# Q6 ?4 b2 s* x" }' \' U& y
which was clearly high. Some studies suggest that/ a7 D: }1 n5 `+ ^8 q: y7 h4 V! g
dermal conversion of testosterone to dihydrotestos-
2 Z3 U7 E; r$ @! Z/ Q9 {9 L/ I8 Uterone, which is a more potent metabolite, is more( N' i1 N( {. v1 ^7 a) @
active in young children exposed to testosterone
: d4 r- l# Z" c' v$ U, [2 P' P6 Nexogenously7; however, we did not measure a dihy-
' B% M1 T9 S) Q( I5 @9 Pdrotestosterone level in our patient. In addition to1 r9 A) X* ^3 N* Z; p0 w2 k6 i
virilization, exposure to exogenous testosterone in
2 ~ y' Z0 h0 ?* @$ F, r5 schildren results in an increase in growth velocity and
) k8 w; a1 T2 D \; badvanced bone age, as seen in our patient.
" F- ^( F. N' s, }: I, WThe long-term effect of androgen exposure during3 Y; j, G+ f6 ~: b, \+ m+ \. a
early childhood on pubertal development and final; J5 T: B5 t; R0 l! O; m: J
adult height are not fully known and always remain
, k4 b3 I U0 @* }, f9 M. x9 r/ ]a concern. Children treated with short-term testos-# k; F& V& G4 u
terone injection or topical androgen may exhibit some
+ F: u, ]4 n9 D0 W& |7 qacceleration of the skeletal maturation; however, after
) h) U; Q4 ^# ^1 J- P& G/ Dcessation of treatment, the rate of bone maturation" |5 A# D( m/ v7 @' t
decelerates and gradually returns to normal.8,9
: _6 H) G2 q3 B- q) `- qThere are conflicting reports and controversy
# F w/ j0 n: w: l( `% p" tover the effect of early androgen exposure on adult/ d* k- I$ p, F3 V& U! Z
penile length.10,11 Some reports suggest subnormal
7 H$ d+ L; n& R3 V9 Xadult penile length, apparently because of downreg-
* Y2 y+ N% {/ f/ H) k. qulation of androgen receptor number.10,12 However,
4 Q* ^ u! K) d4 ?Sutherland et al13 did not find a correlation between' u7 @ F" K/ p: s
childhood testosterone exposure and reduced adult: Y7 r! _/ t2 e, p! @! @/ E4 R
penile length in clinical studies.3 H c$ G! d9 \" P8 j
Nonetheless, we do not believe our patient is9 J) P% R2 V, h2 D2 n! C; v* T
going to experience any of the untoward effects from6 v" [: i# @+ a9 T F7 i! o7 [
testosterone exposure as mentioned earlier because
) a* O9 O- v& h( M, b) H6 athe exposure was not for a prolonged period of time.5 g8 `; U% m- R4 J4 m0 s0 |% X
Although the bone age was advanced at the time of7 `3 {4 F/ X6 ]: ~5 Z: ^/ ~
diagnosis, the child had a normal growth velocity at
) R# r6 A9 f$ j; Z- @& uthe follow-up visit. It is hoped that his final adult
$ x5 | r' A: a* e3 l8 Rheight will not be affected.
! G! ^$ i2 x, ?! ]' h9 FAlthough rarely reported, the widespread avail-0 {6 v2 G7 @( f I
ability of androgen products in our society may
" [8 d+ ~+ N& T5 M' Q6 P* N: d- findeed cause more virilization in male or female
$ k$ H) ]/ C& D' D) `children than one would realize. Exposure to andro-4 |1 ]: X, w9 |
gen products must be considered and specific ques-- ^' x& n5 v' u# M' P
tioning about the use of a testosterone product or
4 Q/ r9 G% I4 C2 mgel should be asked of the family members during) n- }" i! {5 ~) N2 S; R. h
the evaluation of any children who present with vir-
6 O$ i: d) E+ n/ w/ Q9 Z- Pilization or peripheral precocious puberty. The diag-
* z9 z8 N- A1 wnosis can be established by just a few tests and by# z' Z( y& @6 H, k6 s1 `$ w5 A
appropriate history. The inability to obtain such a
. K/ P; c! u; [7 uhistory, or failure to ask the specific questions, may
& i1 E! M; l1 E2 B$ Lresult in extensive, unnecessary, and expensive: a4 e6 E5 u# k
investigation. The primary care physician should be
+ d* O! B) X6 ^* a7 c5 Taware of this fact, because most of these children
; Z2 P- m4 Z% m$ G1 emay initially present in their practice. The Physicians’
7 C p* B0 w# Y0 M3 {" ADesk Reference and package insert should also put a' _$ o$ A( U% E* M
warning about the virilizing effect on a male or
4 i8 F) J+ n7 Qfemale child who might come in contact with some- N* d6 Q* X6 y6 ]$ y& b
one using any of these products.0 r, H4 u) H$ a
References
7 o9 G4 i) B p. t0 u1. Styne DM. The testes: disorder of sexual differentiation
3 p% `6 K( a3 E8 |& Z8 \& land puberty in the male. In: Sperling MA, ed. Pediatric
. O. y6 D& U8 z) L0 UEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
& f. y( J. Z' { f& c4 U2002: 565-628.
% t6 p7 a* q# O {& B) V% B2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious. r' h1 G2 m5 X# n! r( S
puberty in children with tumours of the suprasellar pineal |
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