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Sexual Precocity in a 16-Month-Old
% }* A1 ~- q! L7 TBoy Induced by Indirect Topical6 o/ t" I& u' d
Exposure to Testosterone
/ P X }( X. u6 q! B: cSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,23 j# f- z- R/ u
and Kenneth R. Rettig, MD1' R# |9 {2 Y% p4 B4 [( E) ~6 S
Clinical Pediatrics0 w2 Z! A# T6 m* v
Volume 46 Number 6, ]0 y' Z x' m4 E+ U
July 2007 540-543: r5 Q0 x5 K) L/ K5 @7 S) Y1 |( `( p
© 2007 Sage Publications
4 @/ `1 D: q# c( g2 W10.1177/0009922806296651' e! d4 y% l) D! n2 `! g
http://clp.sagepub.com
8 P8 j: _8 V8 s. Y0 `hosted at
# r t& A" ]# N$ Z* N5 X4 E3 K: ehttp://online.sagepub.com2 A C- Y2 I% a2 r
Precocious puberty in boys, central or peripheral,2 S5 y; T2 V* M8 z) W3 i
is a significant concern for physicians. Central
) k+ J' I7 h u }* e! H8 }precocious puberty (CPP), which is mediated
2 }+ a6 G: K9 g' Q3 ^- r& J2 vthrough the hypothalamic pituitary gonadal axis, has8 y' e7 N7 a: U8 P L5 ^
a higher incidence of organic central nervous system
/ b6 b0 g, T+ J& h8 z* H% O$ ilesions in boys.1,2 Virilization in boys, as manifested3 T2 j. ^& `5 b3 w( F8 L' o
by enlargement of the penis, development of pubic
# r, [* Y+ E4 \% @ ?+ p2 o n, Dhair, and facial acne without enlargement of testi-
/ t/ p7 z1 z' t! e6 Dcles, suggests peripheral or pseudopuberty.1-3 We9 h; ] @/ Y8 E4 n1 h. j* T
report a 16-month-old boy who presented with the6 c1 H) [9 }' [+ {1 q# D
enlargement of the phallus and pubic hair develop-5 \1 Q# }! c' C' @/ I t D
ment without testicular enlargement, which was due R6 ~& Z# b5 d
to the unintentional exposure to androgen gel used by% d0 D$ X0 F, _3 v
the father. The family initially concealed this infor-
9 J9 T7 C- D2 y% `! H" A7 p4 N# Omation, resulting in an extensive work-up for this# O2 ?* w6 I& R
child. Given the widespread and easy availability of
" T* z/ M! S4 _" k- b. Utestosterone gel and cream, we believe this is proba- \9 _8 ~$ c$ ?8 t, Z2 X
bly more common than the rare case report in the
. v5 F/ i1 H. E4 y% ?- Z nliterature.42 n# ?$ y- U; o( `( g% W& L3 m! {) i
Patient Report
d7 S$ P! \% i* ?$ q; l2 Q. M9 LA 16-month-old white child was referred to the
* w* z( ^4 m5 h& C1 hendocrine clinic by his pediatrician with the concern
7 M5 _' C- N# y' n8 `) ^" M) Oof early sexual development. His mother noticed& a6 g) r( Z9 A- |+ D: A
light colored pubic hair development when he was
& f* }/ N0 V# I( L mFrom the 1Division of Pediatric Endocrinology, 2University of% m, W: _, @. `5 | ~$ C/ s3 @
South Alabama Medical Center, Mobile, Alabama. r( C& ?2 ^& Z- R* n' `. y
Address correspondence to: Samar K. Bhowmick, MD, FACE,* u5 ~0 S5 T; J( c; n1 _$ c8 j
Professor of Pediatrics, University of South Alabama, College of- B& v9 j2 x0 r- ]1 ]6 ^
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
) X( W. ?; \0 F4 }e-mail: [email protected].# N2 O) Y9 q ^7 {! r
about 6 to 7 months old, which progressively became9 H& i3 A& @2 ?7 s) p# K D& X0 v8 Z
darker. She was also concerned about the enlarge-1 z0 j- x4 Q$ ?/ T, [
ment of his penis and frequent erections. The child/ |3 ~( z/ W/ i7 C! l. ~
was the product of a full-term normal delivery, with
7 z- |% U4 |0 |& Aa birth weight of 7 lb 14 oz, and birth length of
1 T( m7 _& f( P+ q& _1 n! D" W20 inches. He was breast-fed throughout the first year, P. y- j$ R7 B* t" N F2 h4 D
of life and was still receiving breast milk along with
6 d4 E5 w( z% Zsolid food. He had no hospitalizations or surgery,
1 B& y; e; a$ X. x$ }and his psychosocial and psychomotor development2 ]3 Q# D6 c! O. D/ [2 a
was age appropriate.5 |! T! V# @/ w
The family history was remarkable for the father,8 O" C/ n! R3 ?8 s5 c9 ]
who was diagnosed with hypothyroidism at age 16,
1 y3 C% j3 j7 U& |, Dwhich was treated with thyroxine. The father’s: v/ \$ i/ F+ v" @: d" p6 t
height was 6 feet, and he went through a somewhat
$ I+ y- a4 q/ ?3 nearly puberty and had stopped growing by age 14.
( R r* z7 g& D B& IThe father denied taking any other medication. The6 D) J% A$ y2 s0 t8 P
child’s mother was in good health. Her menarche1 G& o5 @3 b* D r& k t& n
was at 11 years of age, and her height was at 5 feet" ?! J! g2 g, M! K0 W$ B
5 inches. There was no other family history of pre-
( L- i# ]7 ^# `4 ^" j+ h1 ]cocious sexual development in the first-degree rela-; D4 i t& H; T; ^! Q' u
tives. There were no siblings.1 T1 x1 r, I" \$ I4 P, y% O: q
Physical Examination
' R; l h. f( w' aThe physical examination revealed a very active,
3 a3 D0 o$ h) H' p5 }5 kplayful, and healthy boy. The vital signs documented# U- P' \0 c4 ]( z* d5 Y) U
a blood pressure of 85/50 mm Hg, his length was+ m3 W9 B) ~, y, C( G
90 cm (>97th percentile), and his weight was 14.4 kg% i4 |- a* O: a7 c9 K) x' P
(also >97th percentile). The observed yearly growth
3 }- {+ a$ _. C2 J- ~" bvelocity was 30 cm (12 inches). The examination of
0 S7 j9 q" _2 u; U0 \, O ~" x3 e8 Rthe neck revealed no thyroid enlargement.
* K. g1 L9 Q% e3 `The genitourinary examination was remarkable for8 |$ Z. i5 k% N* l# w8 R" g. S4 E
enlargement of the penis, with a stretched length of
( t6 q+ m1 f; l7 [( n7 f8 cm and a width of 2 cm. The glans penis was very well
; J' f6 p% D& n+ Qdeveloped. The pubic hair was Tanner II, mostly around
5 P: X: |/ i( i( g! Z* v8 l540) q# k$ y' i6 Q6 c
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from N9 T- X. f5 M2 N+ w# `
the base of the phallus and was dark and curled. The0 z' I d2 J0 a+ T" y
testicular volume was prepubertal at 2 mL each.
: h( ^" w8 u7 I6 c+ t) q: k. ?$ |5 X) _The skin was moist and smooth and somewhat' w; k% X% u) I: V8 A- n( K
oily. No axillary hair was noted. There were no& l) ~ f3 \! t; J
abnormal skin pigmentations or café-au-lait spots.( n2 A; t/ S1 O7 V5 \+ {# \
Neurologic evaluation showed deep tendon reflex 2+8 U* E7 C2 X$ L" T- R+ @4 N- _
bilateral and symmetrical. There was no suggestion
. M6 Y1 J1 i# R; @' j% v3 }of papilledema.
5 @) g3 l7 T0 X& ]. H& q) `Laboratory Evaluation, y' K' a8 H% d6 I/ q+ V
The bone age was consistent with 28 months by0 e) C% Y: R2 Q% ~# h1 P
using the standard of Greulich and Pyle at a chrono-
5 W8 E1 M3 }) ^ J) N6 T; Q! z- P3 s$ Tlogic age of 16 months (advanced).5 Chromosomal
4 _- e3 r. i$ J: N! C! f6 |karyotype was 46XY. The thyroid function test
6 z" s9 m. J6 V4 W8 S: l$ y! O+ u/ }showed a free T4 of 1.69 ng/dL, and thyroid stimu-6 U/ Y. |9 j7 B6 N! m' L
lating hormone level was 1.3 µIU/mL (both normal).' ~ s; ~! l S+ I
The concentrations of serum electrolytes, blood( U2 B5 J' W4 p8 ?. F
urea nitrogen, creatinine, and calcium all were" c* F( i$ T0 p `/ g2 y5 S5 E
within normal range for his age. The concentration6 B, P4 W% S+ n& ]" g# ~& Z) Z
of serum 17-hydroxyprogesterone was 16 ng/dL& L( A& c, K$ v9 e
(normal, 3 to 90 ng/dL), androstenedione was 20' L- a- p! R+ }4 e) D4 M1 A
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-0 b- ^2 V) v" |
terone was 38 ng/dL (normal, 50 to 760 ng/dL),. }! ^% l7 ^& @" l5 z& F- K" m
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
" [# I- i; m! k* i8 m* T. a49ng/dL), 11-desoxycortisol (specific compound S)
; J6 Q, p4 J1 P/ [6 jwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
% T/ b- E0 X L3 F. ttisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total) o* f1 U( Z- {+ l H0 H" E
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),& Z% S" L7 X. m
and β-human chorionic gonadotropin was less than
' f: e$ Z9 t& M8 O- L5 mIU/mL (normal <5 mIU/mL). Serum follicular
$ n+ ~( b: j; t3 N1 @% @! Mstimulating hormone and leuteinizing hormone
& u8 Y& \# ~! Oconcentrations were less than 0.05 mIU/mL$ w/ q( y* O M
(prepubertal).
% B4 ?: c# y) g- H3 T3 ^: HThe parents were notified about the laboratory+ ]+ K+ A7 f+ H$ t1 O
results and were informed that all of the tests were
% ~0 F2 c1 u' G; _3 inormal except the testosterone level was high. The
5 |$ r! J6 ?5 @" i" o ufollow-up visit was arranged within a few weeks to, A5 C% c1 {7 L( f
obtain testicular and abdominal sonograms; how-5 y% T" z- O E3 _% P9 o' \: u
ever, the family did not return for 4 months.! W0 b; m4 q& c$ M' Z1 U+ q1 C
Physical examination at this time revealed that the
# M- o* K9 W, ]) M6 ^/ v) {" K. gchild had grown 2.5 cm in 4 months and had gained
, @# a( X2 N$ F2 kg of weight. Physical examination remained
+ f$ K) T% b/ N6 A P% Uunchanged. Surprisingly, the pubic hair almost com-* J: g1 B; H; n( G* j) v
pletely disappeared except for a few vellous hairs at
% [ d* G( p5 ^& V' Z/ ?9 lthe base of the phallus. Testicular volume was still 2* j9 z; K7 B1 Q
mL, and the size of the penis remained unchanged.) W/ w" b' {7 J3 A* Y* c
The mother also said that the boy was no longer hav-
2 U6 r! c7 `3 P9 ning frequent erections.
, W. n( L3 }4 m0 }Both parents were again questioned about use of& {5 x S! p% ?' T. N$ J
any ointment/creams that they may have applied to
~4 k* A$ x$ `5 D; y4 O& Pthe child’s skin. This time the father admitted the
& \3 w6 ?/ G b4 `$ ]+ W4 n5 ATopical Testosterone Exposure / Bhowmick et al 541
4 c a1 |% i* X* y7 X% E; w3 Z Kuse of testosterone gel twice daily that he was apply-
$ a* _+ ]- n7 t* A! oing over his own shoulders, chest, and back area for' q! q' V% ~) W( ]0 F
a year. The father also revealed he was embarrassed5 O3 w- g, t e& }) ?. [. x
to disclose that he was using a testosterone gel pre-
) [' D5 F8 l( {1 Rscribed by his family physician for decreased libido
4 o: ]% @" S* X8 }secondary to depression.
) E' l; F7 E6 d. c* IThe child slept in the same bed with parents.) n# A! o# B! a5 ?' }
The father would hug the baby and hold him on his ? u6 H8 H9 ~2 G% C
chest for a considerable period of time, causing sig-
, Z/ d/ I3 b; N- [6 \1 s6 ^nificant bare skin contact between baby and father.% E. V6 P! ` p0 p$ |
The father also admitted that after the phone call,
6 L3 j4 w2 d1 L* c3 _; Jwhen he learned the testosterone level in the baby+ @9 M7 i) B" @- T/ {
was high, he then read the product information3 U- a2 G/ F1 v m* g
packet and concluded that it was most likely the rea-
1 n1 F( D! V7 W+ R% V9 sson for the child’s virilization. At that time, they% d# f5 o6 d9 n0 u) m5 n
decided to put the baby in a separate bed, and the
. Q p# D! m6 t8 z- r U T1 V9 zfather was not hugging him with bare skin and had( F/ H) A: i$ S! X' E
been using protective clothing. A repeat testosterone9 ~0 U) f0 M0 R0 n% R* Q
test was ordered, but the family did not go to the! s! N$ x. b, }) T" p
laboratory to obtain the test.- e0 a) t9 q. a6 K
Discussion
/ q9 c H. S$ IPrecocious puberty in boys is defined as secondary
4 y, c- U, ~# xsexual development before 9 years of age.1,4
8 {3 b% m/ F8 S8 X4 APrecocious puberty is termed as central (true) when
* a& ~* N$ w( e. m1 V: `it is caused by the premature activation of hypo-
& T% I0 n/ g' Q. i" U+ e( U) w5 athalamic pituitary gonadal axis. CPP is more com-+ H5 H! W& p' c) Z0 c7 j
mon in girls than in boys.1,3 Most boys with CPP3 |6 K. Q4 U( E- i y
may have a central nervous system lesion that is
; @0 j+ _. \/ [' K8 M' {responsible for the early activation of the hypothal-
+ w$ b6 o* q0 J; t" m; o" H0 ]$ A5 wamic pituitary gonadal axis.1-3 Thus, greater empha-
. q- Z; E- g% l i1 psis has been given to neuroradiologic imaging in
1 @5 g( w7 w5 k7 u3 Nboys with precocious puberty. In addition to viril-
3 U: @; d( ` z8 P _1 Kization, the clinical hallmark of CPP is the symmet-% \6 Q" @0 b; Q: e, R
rical testicular growth secondary to stimulation by! f* o( B$ h B. D1 @4 Q
gonadotropins.1,3, _7 o, {3 v) G: {
Gonadotropin-independent peripheral preco-) m0 c" T4 q& T/ E
cious puberty in boys also results from inappropriate
' a! v6 e2 i1 H. j+ jandrogenic stimulation from either endogenous or, T, F6 Y/ l: ^
exogenous sources, nonpituitary gonadotropin stim-
; ^6 D" x/ Q: r& X0 u2 Q; w) julation, and rare activating mutations.3 Virilizing
4 R2 T' [8 v2 }" s( ucongenital adrenal hyperplasia producing excessive: q0 [# x1 Q6 `. E/ \
adrenal androgens is a common cause of precocious. M! C- @& W0 ^& i
puberty in boys.3,4- y* i2 B( ]8 A6 ?; T6 _
The most common form of congenital adrenal2 j, j/ ~) X, U( |
hyperplasia is the 21-hydroxylase enzyme deficiency.
1 b' I1 y2 q- f) l. HThe 11-β hydroxylase deficiency may also result in+ Z, D1 H& r" F: Y$ {
excessive adrenal androgen production, and rarely,0 c% X2 e+ N% l$ ?% ~# K- w2 Y7 |3 _
an adrenal tumor may also cause adrenal androgen/ |, `5 |5 [% h$ H, ~( ~' H# e/ o
excess.1,3
) X$ z6 P& t2 c1 L$ L: c. v% E8 |at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
, G9 H. n. ~' z$ c w2 p+ j542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
+ j, F' r2 Z3 k1 }3 hA unique entity of male-limited gonadotropin-
1 u W; d& w' T8 X* S6 Zindependent precocious puberty, which is also known$ m, K& M' |2 h/ s7 ~) f
as testotoxicosis, may cause precocious puberty at a
% i( K0 A, U. u7 svery young age. The physical findings in these boys) z! b. `1 k5 M; G
with this disorder are full pubertal development,
# S1 j! S4 r D5 Y# `, H3 uincluding bilateral testicular growth, similar to boys
+ U# h8 v5 T, q, X% Nwith CPP. The gonadotropin levels in this disorder: f9 d3 m3 ^$ v. }7 F6 ^) {
are suppressed to prepubertal levels and do not show
) ? F, I' h. F% j! g7 K* i1 Bpubertal response of gonadotropin after gonadotropin-
" i# k, p. T- {( w* Z$ U2 o5 Mreleasing hormone stimulation. This is a sex-linked, S& p& K( ]6 |) E9 Z* V* X6 [
autosomal dominant disorder that affects only
: D) m9 }' V; K+ _0 xmales; therefore, other male members of the family; d! q( p; U6 }+ i* t2 j
may have similar precocious puberty.3
4 A# O) e: J2 s5 D2 k/ OIn our patient, physical examination was incon-* h: L# `" K' a
sistent with true precocious puberty since his testi-) C; h$ R5 [% H$ b7 p" X8 k
cles were prepubertal in size. However, testotoxicosis
0 I- Z z5 m( [ mwas in the differential diagnosis because his father
, S7 e' o' z: S7 E6 istarted puberty somewhat early, and occasionally,
~7 Z# Y6 G6 g) P0 s! c! E, g3 Y2 ?testicular enlargement is not that evident in the
& @8 t' U$ P) S/ i& Bbeginning of this process.1 In the absence of a neg-
, D, M+ k4 ~# ] G2 p- P+ wative initial history of androgen exposure, our- g6 P1 Y. H: R/ q
biggest concern was virilizing adrenal hyperplasia,
2 |1 M; v3 K, J* \$ ?, C' Aeither 21-hydroxylase deficiency or 11-β hydroxylase
# e8 v) s2 b: Q5 k" ~8 gdeficiency. Those diagnoses were excluded by find-9 F( ^$ ?% e" D2 r y' U: W5 m/ X
ing the normal level of adrenal steroids.
; T, K+ u( \& S9 m. BThe diagnosis of exogenous androgens was strongly8 P$ S8 r- p- {1 \! L
suspected in a follow-up visit after 4 months because, ?4 }6 V$ y+ ^/ t7 v
the physical examination revealed the complete disap-' A |( d# p2 f: m
pearance of pubic hair, normal growth velocity, and7 u% w- l6 O1 a
decreased erections. The father admitted using a testos-5 @0 d F3 k% f, A* Q
terone gel, which he concealed at first visit. He was* @. I7 `8 [ _; a9 X8 C3 N
using it rather frequently, twice a day. The Physicians’
. r/ o' n( c' \- u: a/ eDesk Reference, or package insert of this product, gel or: u" T2 j v6 o1 K
cream, cautions about dermal testosterone transfer to
0 K0 z: Q( G( y7 f: bunprotected females through direct skin exposure.
6 S. c8 b/ J5 W% E% J6 f* V; }9 vSerum testosterone level was found to be 2 times the
5 `7 y6 P [* `3 g4 qbaseline value in those females who were exposed to
$ W2 Z; _/ q( A+ w8 Reven 15 minutes of direct skin contact with their male& Z1 @# }1 z$ L* l' ?7 l# C
partners.6 However, when a shirt covered the applica-. p: U- t2 `0 t6 h, `( x p' Y' I2 I
tion site, this testosterone transfer was prevented.6 S' u6 v* i$ R. I* L1 u, t) _
Our patient’s testosterone level was 60 ng/mL,; X- W; B' j& E0 k; z- e
which was clearly high. Some studies suggest that% W/ i$ O7 ]4 J8 l
dermal conversion of testosterone to dihydrotestos-- S/ q k6 u `
terone, which is a more potent metabolite, is more1 C4 Z- e9 b6 G0 }$ U; q1 O9 ^8 n7 n
active in young children exposed to testosterone' F( d1 C g: A7 z8 y
exogenously7; however, we did not measure a dihy-
1 D% m) p! D+ X% W* zdrotestosterone level in our patient. In addition to9 P7 h: g( a2 s) t; Q5 o
virilization, exposure to exogenous testosterone in
) S; p$ ?$ j3 E. l2 rchildren results in an increase in growth velocity and2 ]. G9 T) x( ? y ?* N
advanced bone age, as seen in our patient.! _8 M/ d) L/ @# O5 ?1 \, w
The long-term effect of androgen exposure during
0 }5 _ D. S, {! H+ M& a, Yearly childhood on pubertal development and final; b$ R" j0 W( R- b7 D8 |% i2 l
adult height are not fully known and always remain
. f+ C+ j& {# ~, `! }3 @) V4 W; S& Qa concern. Children treated with short-term testos-- l4 ]+ z% D y0 E2 ?# J( h; \
terone injection or topical androgen may exhibit some) o, D/ Z/ B' H4 \ o+ v3 ]' J k# @
acceleration of the skeletal maturation; however, after
: }0 T4 E& b/ W1 K; q* fcessation of treatment, the rate of bone maturation9 b! f! [" |0 o9 ]+ U! F$ ^( }
decelerates and gradually returns to normal.8,93 y4 g0 G4 D6 @3 Z, M
There are conflicting reports and controversy
l) a# p7 L1 s* tover the effect of early androgen exposure on adult
' B; ^- x8 Z. l. P& h0 Wpenile length.10,11 Some reports suggest subnormal, x, u; h r! c$ b8 }$ t! }
adult penile length, apparently because of downreg-) x* A! T s, s6 Q/ ]: [: I% y) r, I
ulation of androgen receptor number.10,12 However,2 S C2 K1 X, e- S& |% B; o
Sutherland et al13 did not find a correlation between- W# Q1 j* C6 C% D
childhood testosterone exposure and reduced adult
# P; Y; `2 H4 L9 t0 rpenile length in clinical studies.! N- H" j1 x2 a( [
Nonetheless, we do not believe our patient is6 h( A6 i6 ^2 q' `4 l1 K3 V4 X1 J
going to experience any of the untoward effects from
9 p: e4 z+ T) U5 a4 v% stestosterone exposure as mentioned earlier because
; \" y$ n" x) Wthe exposure was not for a prolonged period of time.* H- q+ X0 a+ i2 v' e$ w4 e$ x3 a) O
Although the bone age was advanced at the time of
3 Q0 a! g9 N0 c: Gdiagnosis, the child had a normal growth velocity at5 R, R ~- V! ]' x; K2 w0 L2 _/ L
the follow-up visit. It is hoped that his final adult
' C; w& P" c4 ~$ Y6 W9 D' Iheight will not be affected.7 j* v0 {$ z. Z. \" _6 @# h
Although rarely reported, the widespread avail-" l+ b; J0 E( R; Q; I$ B
ability of androgen products in our society may
7 y& }$ ]1 p3 L/ mindeed cause more virilization in male or female
$ h6 q7 }! I9 Q* wchildren than one would realize. Exposure to andro-
- M% X. B/ p; f" B- j5 J; Qgen products must be considered and specific ques-
2 [ X+ [* @+ ]; ~% z! o$ T' Ftioning about the use of a testosterone product or5 U+ w3 }( g" v3 a. X
gel should be asked of the family members during) Q: H6 Y- _ Q, E& A
the evaluation of any children who present with vir-+ @, ^8 `# }9 C" E
ilization or peripheral precocious puberty. The diag-
' I8 p }6 i5 @; W) Z) Vnosis can be established by just a few tests and by: H4 x: U: c+ S4 U3 q7 w# |' Y3 X
appropriate history. The inability to obtain such a5 }7 v ]7 l6 c0 {' O9 ^* D- M6 z
history, or failure to ask the specific questions, may
4 {" P* ?* F @) ^* M9 J! K* cresult in extensive, unnecessary, and expensive
O1 n& V7 |- x( U* o+ `( N& s ^investigation. The primary care physician should be7 i, \1 b4 J4 ?; j$ q( O
aware of this fact, because most of these children! Z, a) Y/ M% ~8 J" y6 I$ m
may initially present in their practice. The Physicians’
+ | C" t6 Q. y0 v: kDesk Reference and package insert should also put a1 S7 F) G( N% V; m$ R2 J
warning about the virilizing effect on a male or
$ P! X; i( x+ O- L3 ]. ffemale child who might come in contact with some-
" P* E0 H' _% S6 T# R4 _one using any of these products.
* f u2 ?+ W5 ^2 p7 X6 qReferences
& T, m. Z6 R8 t4 C1. Styne DM. The testes: disorder of sexual differentiation6 l6 p) r5 w& D
and puberty in the male. In: Sperling MA, ed. Pediatric0 ^2 q4 |1 c. ^* s! L3 ?" e; N- P
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
, y/ t5 r* f; H5 p- f2002: 565-628.4 i- }4 q, Z/ \6 g7 S
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
' w; t0 B' s, Gpuberty in children with tumours of the suprasellar pineal |
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