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Sexual Precocity in a 16-Month-Old
2 C: s2 S4 n4 ~7 Y) ]7 qBoy Induced by Indirect Topical
) v3 [. h) ]1 a- f O7 F2 d, pExposure to Testosterone; U4 [3 s+ I3 C: i
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
p- H& g/ o w _) Pand Kenneth R. Rettig, MD1* Q) V9 i0 j) S7 U8 m# r
Clinical Pediatrics
. ]2 G, X$ D% |Volume 46 Number 6+ s3 }3 l$ ]& E
July 2007 540-543
. o! _% y+ H9 }! O9 |© 2007 Sage Publications) y5 o" ` T; ~- H3 V
10.1177/0009922806296651
' g) d, p$ [7 R) _' ~# lhttp://clp.sagepub.com
5 p! P5 i4 N$ M/ @: shosted at
" j' T( G9 A# u% O: E3 ehttp://online.sagepub.com
! |: i4 x' i8 rPrecocious puberty in boys, central or peripheral,& ]! E; Z. I$ f3 P$ p+ w1 m
is a significant concern for physicians. Central
# @" y) |1 _' ~" l& Dprecocious puberty (CPP), which is mediated
* Y5 S% I j+ q( e7 Mthrough the hypothalamic pituitary gonadal axis, has
$ A: j; {0 y( }0 r- d9 Y$ v; [a higher incidence of organic central nervous system6 { \+ K* t' ]- I* v
lesions in boys.1,2 Virilization in boys, as manifested
) o. Y7 |: S9 s% }" W. s' d4 Lby enlargement of the penis, development of pubic
) Q/ _9 W0 i$ ^( G1 U' c* Bhair, and facial acne without enlargement of testi-/ _; W. P+ |; A' f& m, J/ c0 R
cles, suggests peripheral or pseudopuberty.1-3 We# p9 d5 b$ K7 Q/ ?! c/ d/ u' X
report a 16-month-old boy who presented with the
- v; S; v0 ~5 c6 d( m/ Kenlargement of the phallus and pubic hair develop-+ d& G' |- g6 i% {$ w
ment without testicular enlargement, which was due
4 z9 f+ w Z$ ]+ k. G" c' tto the unintentional exposure to androgen gel used by+ D% f ^3 J% q" K `" r/ T
the father. The family initially concealed this infor-
; O; L& V, j; J% }3 i; F" U/ w4 fmation, resulting in an extensive work-up for this) N, o; v# Z$ Y/ ^; y9 K0 M
child. Given the widespread and easy availability of
9 g O* U( e! a% Ctestosterone gel and cream, we believe this is proba-
( X& K/ {2 W' V* G9 ?# D. Mbly more common than the rare case report in the
8 R, G7 b7 o; B: J+ wliterature.4( _3 j9 G9 P1 k- O3 _
Patient Report" S- D1 t" }0 Z2 v' l& Q
A 16-month-old white child was referred to the! i1 ^# ~: [/ y6 }
endocrine clinic by his pediatrician with the concern
, Y/ U1 A3 U$ d. P$ kof early sexual development. His mother noticed
4 J) y9 p1 u$ R4 Vlight colored pubic hair development when he was
! I! \+ r5 a8 A( _. a+ S3 A; H- n. ZFrom the 1Division of Pediatric Endocrinology, 2University of1 T# [ g2 G; J) w
South Alabama Medical Center, Mobile, Alabama.
1 h1 r% N$ n3 HAddress correspondence to: Samar K. Bhowmick, MD, FACE,
' ^+ {+ G$ @. x& {Professor of Pediatrics, University of South Alabama, College of. r- p8 K; e& a' H' M
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
. ~5 ]1 Z3 }. R$ c( W4 `* Ye-mail: [email protected].( [4 q+ J( G0 R+ p4 d# k- s
about 6 to 7 months old, which progressively became( z! H/ n! m) [& |& V
darker. She was also concerned about the enlarge-7 s& x* _7 j9 u0 @6 F! {
ment of his penis and frequent erections. The child& N) d- b3 U% s7 k- l
was the product of a full-term normal delivery, with
. q0 }; a! v+ E* x7 Ua birth weight of 7 lb 14 oz, and birth length of
, u* s4 M6 S6 O8 z3 T! m20 inches. He was breast-fed throughout the first year
! p- ^) X5 B9 }! x6 @) }of life and was still receiving breast milk along with
. N0 u8 j; t- }5 K7 e" Ksolid food. He had no hospitalizations or surgery,
" J3 D( ?' ]$ A6 d3 a7 G t& n6 q" \and his psychosocial and psychomotor development. q I9 ~& O' ^; |' U) H3 e0 ]
was age appropriate.
7 Q1 ]/ F4 g, h& D+ WThe family history was remarkable for the father,
% f" c' x; w' |' ]& M) e5 j, O: _who was diagnosed with hypothyroidism at age 16,
3 Z8 ~3 [1 b) h) t( ywhich was treated with thyroxine. The father’s# W6 {7 j& b, b+ }
height was 6 feet, and he went through a somewhat e& v+ g& S& ]
early puberty and had stopped growing by age 14.
. g# P8 n* y! d2 {( Z% wThe father denied taking any other medication. The/ G" e, G. J4 }) D% W8 [* V
child’s mother was in good health. Her menarche
: b- b: b" \& ~5 Z$ Z1 Hwas at 11 years of age, and her height was at 5 feet- N$ Y. b: c2 J4 U0 U8 [0 q# T
5 inches. There was no other family history of pre-
6 w# p5 {, P/ C0 L! M' f% S& ~cocious sexual development in the first-degree rela-$ I1 [$ P& H) a! d5 B
tives. There were no siblings.
9 O4 l5 `7 I# B- V) W/ L7 G OPhysical Examination# y5 Y6 q, g+ ]
The physical examination revealed a very active,
4 Z- r, j8 ^& a4 r4 t/ Pplayful, and healthy boy. The vital signs documented
, C4 u# P9 q) ]+ E# n+ V% xa blood pressure of 85/50 mm Hg, his length was
2 V4 ?5 J' ~* t) y) O' o; d' ~! i7 x90 cm (>97th percentile), and his weight was 14.4 kg- R. e0 X1 `2 I) ?0 t. e* Y1 L. V
(also >97th percentile). The observed yearly growth
E' i( z; E+ pvelocity was 30 cm (12 inches). The examination of
; |/ f* }5 @! _the neck revealed no thyroid enlargement.
8 _) i- o0 Q# f" k8 jThe genitourinary examination was remarkable for3 x% [. w! Q* b' Y
enlargement of the penis, with a stretched length of
- b$ o* W$ X* `4 a/ j8 cm and a width of 2 cm. The glans penis was very well- V6 @1 z+ I% o W6 D. G$ e
developed. The pubic hair was Tanner II, mostly around# P- B4 y9 ]" B0 s8 y) u
540* V# _$ Z5 J7 G0 J8 ~
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from0 }1 s4 {7 M& J5 j
the base of the phallus and was dark and curled. The
; T# X1 t$ C& N8 S/ z/ @testicular volume was prepubertal at 2 mL each.% f# e9 ^- B2 w4 C. q" g
The skin was moist and smooth and somewhat: J) L' s* I6 R6 G; H; w ^( C6 f
oily. No axillary hair was noted. There were no! b6 Z# {* o- m0 Y+ v# M& W3 q
abnormal skin pigmentations or café-au-lait spots.3 U' ^4 j7 Q, H6 ~. O
Neurologic evaluation showed deep tendon reflex 2+- `+ G6 q, E9 }+ R1 y# r8 s# {
bilateral and symmetrical. There was no suggestion" E6 e* r8 a! J
of papilledema.
. f. j& a, A sLaboratory Evaluation
9 f ]0 ^" v; iThe bone age was consistent with 28 months by
1 l4 Y, N; U2 Q. [7 h% susing the standard of Greulich and Pyle at a chrono-
% D' b M/ O3 |4 L( l2 Ulogic age of 16 months (advanced).5 Chromosomal7 g: T8 i3 P5 q
karyotype was 46XY. The thyroid function test* A: J \3 ]+ q# Z1 S
showed a free T4 of 1.69 ng/dL, and thyroid stimu-$ C B% S2 _) I0 ?* W( n
lating hormone level was 1.3 µIU/mL (both normal).
7 F1 u2 `2 }, e; Y+ ~3 V; `" yThe concentrations of serum electrolytes, blood
( e4 c" g- F( H0 k# o/ H! {9 Nurea nitrogen, creatinine, and calcium all were
* _4 u7 F8 j9 |) d2 @( p; _within normal range for his age. The concentration
+ n1 ]5 S+ }/ F. Y3 t2 c- p( \of serum 17-hydroxyprogesterone was 16 ng/dL
x* ~3 H, t K: u3 ]% }% u(normal, 3 to 90 ng/dL), androstenedione was 209 \6 Q C- b$ E5 S1 {1 T3 B2 l
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
# ^' t% \% e0 P% C0 D! R2 _% kterone was 38 ng/dL (normal, 50 to 760 ng/dL),( d7 s2 n/ X+ O+ A
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
' z" \$ ^( ]3 ]5 J% E' N49ng/dL), 11-desoxycortisol (specific compound S)
' M# U8 ^6 H* P4 {/ A2 M7 G( _was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-5 F! X0 p% [! M. W8 s4 w9 A
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total6 e) k2 ?6 P$ a, ~# D/ B/ O; e+ P, B
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
4 n; `3 K: c/ D" D$ p0 C" Kand β-human chorionic gonadotropin was less than
* \3 C1 d! X4 o/ r0 N6 O5 mIU/mL (normal <5 mIU/mL). Serum follicular) D/ p/ Y B% ?* H! g8 p2 G1 A
stimulating hormone and leuteinizing hormone7 R" m2 n8 T/ K- S( U. W) Q$ P) j
concentrations were less than 0.05 mIU/mL& x6 E9 C g% t1 r+ T
(prepubertal).
J$ x( {. _2 B$ b" F9 l+ gThe parents were notified about the laboratory
" F1 Q7 F0 ]% m# ?results and were informed that all of the tests were
4 `( |# e* t3 F6 gnormal except the testosterone level was high. The# L" B5 Z) m9 X3 \9 P- f' P
follow-up visit was arranged within a few weeks to
% k5 ^$ }: n! p+ f" B4 M$ [obtain testicular and abdominal sonograms; how-
6 d% O7 R' U8 J- D' Yever, the family did not return for 4 months.
' V/ n0 i4 m8 v: M( o2 q* @Physical examination at this time revealed that the
5 E" x! u0 c; t7 y0 I4 Schild had grown 2.5 cm in 4 months and had gained
, [7 D, M1 e8 P& O0 X" F2 kg of weight. Physical examination remained$ F, h0 V2 d( a3 O$ c
unchanged. Surprisingly, the pubic hair almost com-
- r4 z4 _5 h* b/ A( j# i) M3 m7 Jpletely disappeared except for a few vellous hairs at
$ a* w+ f. Z ~0 J9 s; n2 [the base of the phallus. Testicular volume was still 2
, b K/ W6 R& p0 emL, and the size of the penis remained unchanged.1 D- t5 `- G. S
The mother also said that the boy was no longer hav-+ A8 H3 C) e" @ n* b
ing frequent erections.! ?+ B7 P' T( y2 b6 A! g
Both parents were again questioned about use of; U% H$ Q m/ b
any ointment/creams that they may have applied to# y5 B; W. Y* f+ U7 P5 Q
the child’s skin. This time the father admitted the/ R( f. `. ]9 H% d1 K3 ~) Z( A
Topical Testosterone Exposure / Bhowmick et al 5416 c/ X) F) N1 j" e# V. s
use of testosterone gel twice daily that he was apply-, L( C4 E% m5 i- \# X# ^9 A1 u
ing over his own shoulders, chest, and back area for
# i4 O# e* i- a6 r* ]a year. The father also revealed he was embarrassed
3 V: |6 F" e {" \2 S# ~to disclose that he was using a testosterone gel pre-2 z4 W6 P, K, l6 c2 Y4 g. j
scribed by his family physician for decreased libido9 j2 o+ J+ Q. x" I) o
secondary to depression.
# ]; L" K8 K: o+ w! VThe child slept in the same bed with parents.
- e9 N" Y7 u7 o% G: F- PThe father would hug the baby and hold him on his
T, S9 H# X# P$ ^. z) j: Zchest for a considerable period of time, causing sig-
9 P( ~! ?1 A2 H) p1 S# @nificant bare skin contact between baby and father.
% n M7 f5 @3 Y' M! }( y4 TThe father also admitted that after the phone call,
0 K* y: W: ~6 z. t/ n5 o# a1 ~# ywhen he learned the testosterone level in the baby9 ?( C& s8 K' l Y1 k
was high, he then read the product information0 U2 c9 g( F' N9 n4 e- O b1 w% S
packet and concluded that it was most likely the rea-: O9 T* w# Z. L
son for the child’s virilization. At that time, they
, S% A. J( \( z: ^: c% v9 qdecided to put the baby in a separate bed, and the4 t0 g. } Y0 [
father was not hugging him with bare skin and had
; {* a. G* ^1 l; B- `) ybeen using protective clothing. A repeat testosterone$ G! F1 C q+ N/ V
test was ordered, but the family did not go to the6 ~- U6 w y0 z9 {/ T% Z- U6 v U+ I
laboratory to obtain the test.
7 d* k9 P0 v, Q! _Discussion; ^, O: g: s4 G$ A
Precocious puberty in boys is defined as secondary
n" ^) J. a2 H, A6 f5 Q a1 Isexual development before 9 years of age.1,4
" x" T+ u- n; l. |Precocious puberty is termed as central (true) when, Q e/ c# _* |0 T
it is caused by the premature activation of hypo-
1 c6 C2 b& A. Q( k4 ?thalamic pituitary gonadal axis. CPP is more com-
7 Z1 H7 h _7 R1 q+ D! q) `mon in girls than in boys.1,3 Most boys with CPP% W' U# M6 e9 H: u" i
may have a central nervous system lesion that is' A [4 i6 A, o9 u. T ~0 m7 }+ L
responsible for the early activation of the hypothal-
7 p r2 d1 E& f5 |- s5 samic pituitary gonadal axis.1-3 Thus, greater empha-' w; R1 Z3 |/ @7 B. s! s, o6 g
sis has been given to neuroradiologic imaging in
, [* v* L2 T+ W* h2 M& B7 M8 Aboys with precocious puberty. In addition to viril-) F: x! S+ B# L; N+ J
ization, the clinical hallmark of CPP is the symmet-% R8 x3 q, U6 z* Q
rical testicular growth secondary to stimulation by
6 Z' ~, [; W8 J6 f& N1 rgonadotropins.1,3: V2 Q: n( O X6 R
Gonadotropin-independent peripheral preco-6 B: @9 \) H! m% K+ z, `$ m% R4 |
cious puberty in boys also results from inappropriate
q$ c' ~/ Z& l$ [& I8 r& `androgenic stimulation from either endogenous or
( G, I1 f8 ]# i' |) mexogenous sources, nonpituitary gonadotropin stim-9 l4 d }! H+ x/ L) U X5 G
ulation, and rare activating mutations.3 Virilizing3 S- e/ D; i" n o" V4 S: P5 t
congenital adrenal hyperplasia producing excessive: V8 J) I9 o6 ~! ^4 a$ p
adrenal androgens is a common cause of precocious7 D. W' ]4 W: I2 y/ G( K
puberty in boys.3,4
+ U- j- q7 d' `5 Z1 PThe most common form of congenital adrenal
6 r$ y! k% o, R. z: Yhyperplasia is the 21-hydroxylase enzyme deficiency.+ `* b9 g5 | F0 J+ o+ [2 ]
The 11-β hydroxylase deficiency may also result in6 E$ L9 h7 d- x+ ^
excessive adrenal androgen production, and rarely,
! T7 S. D) Q& San adrenal tumor may also cause adrenal androgen% n- V- B$ l) Z6 m# q9 o) g
excess.1,3
* I4 _; Z6 r+ x( E0 v% E* lat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from- c# t* H) m2 _4 O/ O8 q
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007( _6 @* B& m2 b8 N
A unique entity of male-limited gonadotropin-7 \4 C! E% \9 _& e; o
independent precocious puberty, which is also known8 f7 P- W0 }2 s6 T, @+ r. t
as testotoxicosis, may cause precocious puberty at a+ j. F3 s2 r# k$ _9 A9 J" m0 k
very young age. The physical findings in these boys9 S1 c+ }6 n6 {4 \7 ^
with this disorder are full pubertal development,( _: s i6 y/ m: }- b
including bilateral testicular growth, similar to boys! m0 v) L+ t, G7 S
with CPP. The gonadotropin levels in this disorder
9 [+ w* l" Z6 u3 B/ |8 t1 ~% q# Lare suppressed to prepubertal levels and do not show
5 m! B2 z) m: b. dpubertal response of gonadotropin after gonadotropin-, k' j7 R; S# w/ K1 f d
releasing hormone stimulation. This is a sex-linked+ Y) r+ E5 n* d) N: R6 r
autosomal dominant disorder that affects only) N9 i0 S- F U
males; therefore, other male members of the family6 m% P8 s, r! q8 U/ q0 O2 [# d
may have similar precocious puberty.3& ^0 v# T( ^/ u
In our patient, physical examination was incon-( Z; n. }- T t6 w: a; L W0 O
sistent with true precocious puberty since his testi-
, ~: d& z3 X9 V. Y8 hcles were prepubertal in size. However, testotoxicosis2 r1 V- T1 @( B# {' a1 o
was in the differential diagnosis because his father9 I3 Z: | a, o; y- O( d
started puberty somewhat early, and occasionally,0 t- S/ k% ], `$ ]6 t4 I% M
testicular enlargement is not that evident in the! n, I' l2 i* x+ O
beginning of this process.1 In the absence of a neg-
* X4 s& O( R: W" Q! Qative initial history of androgen exposure, our4 T: @: n- p+ m
biggest concern was virilizing adrenal hyperplasia,
5 H: ~1 M6 S! E+ peither 21-hydroxylase deficiency or 11-β hydroxylase
% g& E: a( N9 q5 L" ~+ G) z+ _deficiency. Those diagnoses were excluded by find-+ C0 N9 i+ h: v1 K" V* J3 r; d/ R/ F
ing the normal level of adrenal steroids.1 w( `9 Z S' ]" k* Z, [5 X
The diagnosis of exogenous androgens was strongly
! @1 G! x, k4 U1 Esuspected in a follow-up visit after 4 months because4 i" O+ T/ z f3 h$ \
the physical examination revealed the complete disap-0 y) D; x! g B6 F2 x' H5 Q1 }( N
pearance of pubic hair, normal growth velocity, and
: Y8 f8 O" t( S9 Kdecreased erections. The father admitted using a testos-: d% I' Z! N- B4 p/ ?7 ?, F! p4 w
terone gel, which he concealed at first visit. He was. I: q; h8 o. R7 R/ |, d3 S J
using it rather frequently, twice a day. The Physicians’
) u7 X* D* f5 b3 lDesk Reference, or package insert of this product, gel or* X- R" d" b( F8 M( `+ M' Q+ Y* _
cream, cautions about dermal testosterone transfer to0 C8 i, l9 Y* }# {! G9 {
unprotected females through direct skin exposure.- Z" O' W1 }) \3 o2 b
Serum testosterone level was found to be 2 times the( c" m; i2 S: S1 O
baseline value in those females who were exposed to
$ Q1 }/ | v- c% e9 S# ~even 15 minutes of direct skin contact with their male3 S( S; n% g0 K# j2 ?$ _& D- ?' E
partners.6 However, when a shirt covered the applica-# h. W# X7 P$ ~5 k2 L
tion site, this testosterone transfer was prevented.% l# N. U9 [0 W$ o' N1 [# A x, V5 B F
Our patient’s testosterone level was 60 ng/mL,4 J% i: V: i8 \
which was clearly high. Some studies suggest that
% g. E, j. \; ^; k$ edermal conversion of testosterone to dihydrotestos-. C6 H8 j0 U7 o0 ^% `- X" D# t
terone, which is a more potent metabolite, is more
0 k' ^6 _. U& U+ bactive in young children exposed to testosterone4 p- R- P) }; i' I* C* u; Z2 ^- E/ Y
exogenously7; however, we did not measure a dihy-' w2 q$ ~+ G ^
drotestosterone level in our patient. In addition to, i' }/ I) r3 u w' K' E @
virilization, exposure to exogenous testosterone in# j" h; u8 \3 F$ h
children results in an increase in growth velocity and
3 C; `, e8 Q1 @advanced bone age, as seen in our patient.
9 g% x2 |" o1 wThe long-term effect of androgen exposure during9 W2 n+ T! L4 w# b* ]! x' w
early childhood on pubertal development and final
# A0 j' @4 _0 s1 {7 c' y, w% Sadult height are not fully known and always remain
1 U! O; }6 \0 [9 A2 b/ t( Ca concern. Children treated with short-term testos-) g* H0 ]1 w% e, C+ y, L2 B
terone injection or topical androgen may exhibit some
) l2 }1 [8 g- X) P1 E& F; {acceleration of the skeletal maturation; however, after
6 c8 \0 _& u" d! _, [cessation of treatment, the rate of bone maturation* w- u1 l' i% R
decelerates and gradually returns to normal.8,9; ?4 F& {$ s" O( ~3 j8 T0 |
There are conflicting reports and controversy0 O% J; k- ]# W
over the effect of early androgen exposure on adult
1 r* J% P$ U. Q8 r* Xpenile length.10,11 Some reports suggest subnormal+ y3 ^3 [- \! \6 O0 B! t' o
adult penile length, apparently because of downreg-+ L v+ L( h0 w' D7 T
ulation of androgen receptor number.10,12 However,& Y$ ^; k+ q1 m2 l# v( p1 B! h
Sutherland et al13 did not find a correlation between
- k- W! Q" d# cchildhood testosterone exposure and reduced adult, @8 i% u, h6 o$ r
penile length in clinical studies.( x! L+ u5 y3 ~0 _
Nonetheless, we do not believe our patient is" k- K6 C8 |9 t
going to experience any of the untoward effects from
+ k( l- x A+ |4 X2 T) \* Q* Itestosterone exposure as mentioned earlier because( }7 N; R! N- K
the exposure was not for a prolonged period of time.2 ?6 r/ p/ g3 i# K( x8 B D
Although the bone age was advanced at the time of
; |: F9 ]6 v, q5 Cdiagnosis, the child had a normal growth velocity at. s* i$ h5 W! _: b- ^/ X
the follow-up visit. It is hoped that his final adult$ b! I2 B* b! B* _, r& b5 z2 N
height will not be affected.7 Y9 M7 v+ v4 N. ]- K8 D) l
Although rarely reported, the widespread avail-
4 f4 P7 d) k1 b: s# f t/ u: Sability of androgen products in our society may
8 X, p( v6 c! ^/ b/ o% ]indeed cause more virilization in male or female2 @+ w" z2 r4 `6 r4 i7 k
children than one would realize. Exposure to andro-
0 X5 H1 }' {/ o* H# cgen products must be considered and specific ques-) G4 i( A8 J8 H4 \$ z8 @
tioning about the use of a testosterone product or G+ O3 Z' Y+ a; P/ y
gel should be asked of the family members during
8 h* ^, `4 h0 l, |: dthe evaluation of any children who present with vir-* b# v' @$ e" V+ F3 z7 k- E4 l1 U
ilization or peripheral precocious puberty. The diag-
: `* w7 U/ _6 w0 A8 w) {. y8 k8 Knosis can be established by just a few tests and by6 U m4 |. H# C: B9 B7 q
appropriate history. The inability to obtain such a
- s% A D4 g$ ohistory, or failure to ask the specific questions, may) w, P! G$ b+ b2 Z8 Q/ D! v7 c
result in extensive, unnecessary, and expensive' N; _4 f0 m5 O; F# L% }9 S+ p9 X2 \
investigation. The primary care physician should be
3 W4 K7 ~1 ]5 w* c" X @/ S7 @aware of this fact, because most of these children
& w/ O, o ~8 @# x* L5 Dmay initially present in their practice. The Physicians’
% q1 Q. g6 l: Y8 e* l' BDesk Reference and package insert should also put a" |+ q; l: V0 A, a }) h) _
warning about the virilizing effect on a male or" q5 F3 v( C, x6 b$ }8 R
female child who might come in contact with some-1 ?- E( U! \- q' w. O C& S
one using any of these products.
) g$ ?( m: Q% l8 G3 RReferences; A: E4 \- c# N
1. Styne DM. The testes: disorder of sexual differentiation
5 q0 H9 u) A) x" E( ?( A. land puberty in the male. In: Sperling MA, ed. Pediatric
( |$ B! [- X" T. D3 C' K& iEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
9 {8 ~9 j! m$ I0 N6 B2002: 565-628.
! | D9 S3 y4 i0 b; o2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
: ]+ D8 `; j# O" ~0 Hpuberty in children with tumours of the suprasellar pineal |
|