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Sexual Precocity in a 16-Month-Old" q8 m. L1 f& I2 o% S
Boy Induced by Indirect Topical
& p2 c1 q! J; d9 H2 LExposure to Testosterone4 a4 s' H/ [& o, m4 I: B
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2/ O" T8 Z" b Z9 \2 t0 b: z' g
and Kenneth R. Rettig, MD1
( S4 `$ y- z' [3 H+ M* RClinical Pediatrics* z7 H" P+ e- W" m, _' P
Volume 46 Number 6
! h1 x0 ~ V. V I8 `' S4 yJuly 2007 540-543; _ `" v u/ ]6 f
© 2007 Sage Publications
& G$ u$ n; h/ M/ D7 t" g5 N! E10.1177/0009922806296651
1 j8 t, I0 ?% u" p6 _http://clp.sagepub.com
: i) m, k! ^; L% B/ E9 h9 lhosted at
( O( C, l B" \8 uhttp://online.sagepub.com# q0 c: o: n9 K+ s7 A! H4 q
Precocious puberty in boys, central or peripheral,- p+ T# R' k6 M7 v8 q- W
is a significant concern for physicians. Central
: L, ?9 L" p* ]precocious puberty (CPP), which is mediated' ]' |! f. m& F
through the hypothalamic pituitary gonadal axis, has
- O5 K j9 U8 l- [5 b2 ha higher incidence of organic central nervous system% K- q" N9 b& j3 l. R
lesions in boys.1,2 Virilization in boys, as manifested
- E8 Q. R' c, Z* M% O- Vby enlargement of the penis, development of pubic2 X3 p4 E4 ?8 m1 ]0 V( m) N
hair, and facial acne without enlargement of testi-8 H' X6 w* _" u& f) I- F
cles, suggests peripheral or pseudopuberty.1-3 We# O- p- c- ~- C9 Q/ J5 K5 s1 a
report a 16-month-old boy who presented with the
& M: {4 P- F ]* q0 m$ M# wenlargement of the phallus and pubic hair develop-
/ X* z1 S' Y% R4 u* ^$ P/ W/ Iment without testicular enlargement, which was due
) U/ M2 E: A$ z1 u( {to the unintentional exposure to androgen gel used by) d3 d0 n) H& s: `& d7 O/ ?" `$ O! l
the father. The family initially concealed this infor-
" z5 N# x' F: q3 Omation, resulting in an extensive work-up for this
7 N5 Z: B f) d; j6 Q2 qchild. Given the widespread and easy availability of
+ f7 p% S: D' a5 {: wtestosterone gel and cream, we believe this is proba-8 w0 x9 `9 Q2 Q" L5 h
bly more common than the rare case report in the) q) I# ^2 @$ J5 y4 x4 h
literature.4
9 P4 `5 F6 Q: h5 `7 _, v; s7 X pPatient Report
$ @" `- [5 H1 o, h: v1 aA 16-month-old white child was referred to the
$ o+ ]8 n# @8 T P+ ]( p" X8 kendocrine clinic by his pediatrician with the concern" t0 G, ]! {, Z' \
of early sexual development. His mother noticed
3 `5 j7 d! C3 n3 [9 p) Rlight colored pubic hair development when he was
0 i. X( k4 w9 F8 SFrom the 1Division of Pediatric Endocrinology, 2University of/ G/ a% {: I. ]1 l, w' U& N+ A
South Alabama Medical Center, Mobile, Alabama.
7 {1 `1 p! U0 g }Address correspondence to: Samar K. Bhowmick, MD, FACE,
% ~1 N+ W( K Y: h" u( KProfessor of Pediatrics, University of South Alabama, College of6 J$ f2 [% b9 i- T1 l" B# `3 G: ~
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
3 n( L& H$ _3 H& s! me-mail: [email protected].
O6 p# W% L- g3 |* F& Y9 I* jabout 6 to 7 months old, which progressively became, T7 {# r: z& G* M. P
darker. She was also concerned about the enlarge-
, R; @# E( `2 d$ i* [ment of his penis and frequent erections. The child
1 ^6 w5 n1 H5 d0 x2 rwas the product of a full-term normal delivery, with
$ j4 C. u: w9 z) X* a0 h/ K* H0 Fa birth weight of 7 lb 14 oz, and birth length of: e: ]; M- F$ ~( l/ P; b
20 inches. He was breast-fed throughout the first year* l$ A: D0 z; Y; j
of life and was still receiving breast milk along with; G- s: {+ S% s/ Y
solid food. He had no hospitalizations or surgery,
0 |7 h6 b% t% _6 n {- |6 p& Cand his psychosocial and psychomotor development
+ O- {& h9 ?, f8 i: o1 W) h7 Dwas age appropriate.
! v& M& Z# M1 \# X% YThe family history was remarkable for the father,2 q# m4 f& o8 X+ I3 V' D" s4 F
who was diagnosed with hypothyroidism at age 16,
+ L1 T. a) ]! Z$ V# Mwhich was treated with thyroxine. The father’s
. z% D! A$ v2 Theight was 6 feet, and he went through a somewhat
, M$ s s+ [+ a+ ?# Wearly puberty and had stopped growing by age 14.! _# \/ {8 ?( T+ u0 w8 y/ s; [
The father denied taking any other medication. The
' j8 o3 |5 I' T4 I! E3 y6 Zchild’s mother was in good health. Her menarche* W% J& h/ }9 x6 W4 k7 f p0 B
was at 11 years of age, and her height was at 5 feet" g4 G. `9 J; `" j7 K* [- _% q2 Y
5 inches. There was no other family history of pre-
! h9 O! I$ O+ P( _1 Acocious sexual development in the first-degree rela-* A, A6 e O0 Q& J9 A/ I
tives. There were no siblings.# } n- _* `0 Q* P _+ e
Physical Examination0 H# _. V2 B5 }. W
The physical examination revealed a very active,3 v6 r3 M z/ ?% K
playful, and healthy boy. The vital signs documented1 z& C; U2 y9 Z
a blood pressure of 85/50 mm Hg, his length was
# ?5 R0 B4 ^) O! ]2 _% A- L90 cm (>97th percentile), and his weight was 14.4 kg
: N8 Y2 q6 r- w* g/ X0 t(also >97th percentile). The observed yearly growth
0 `( O8 V0 k4 C1 K* v/ e' Mvelocity was 30 cm (12 inches). The examination of
# [+ y3 } ^, i- g! Bthe neck revealed no thyroid enlargement.
. I7 k) E6 D' w# C, \8 k P% sThe genitourinary examination was remarkable for
2 z3 r/ s6 f G$ {* q8 }+ Z: K; H: ienlargement of the penis, with a stretched length of
6 \. h# S% Y# l# y. c* l" F8 cm and a width of 2 cm. The glans penis was very well
6 A, E5 R! M$ A5 I1 G& Fdeveloped. The pubic hair was Tanner II, mostly around
2 d6 q/ B5 ^" ?3 R540" Q( ?8 q! W* F$ W6 i
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
+ Q4 k) K! b( Y! n" A3 F' uthe base of the phallus and was dark and curled. The5 R& Z# O# f" N% k+ }
testicular volume was prepubertal at 2 mL each.& {+ U7 ^- p* r. |7 C
The skin was moist and smooth and somewhat
g% K7 e; [; w& woily. No axillary hair was noted. There were no
1 o1 u# }. N; A6 labnormal skin pigmentations or café-au-lait spots." T3 o2 |4 ^* ~: |
Neurologic evaluation showed deep tendon reflex 2+0 @8 b1 n1 b. j
bilateral and symmetrical. There was no suggestion# t }0 r9 b, o8 l/ i8 N: m5 P
of papilledema.) H3 o- K5 p( T
Laboratory Evaluation% B9 `+ H7 W# h: L. v
The bone age was consistent with 28 months by
5 N/ l! I) b( g# t q7 Iusing the standard of Greulich and Pyle at a chrono-6 D0 u/ h2 X& Q' U
logic age of 16 months (advanced).5 Chromosomal) B) c8 g2 D/ {5 r7 J5 `% X
karyotype was 46XY. The thyroid function test1 p2 s- K' P5 b' E* S! o
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
' _, C5 B2 e& Plating hormone level was 1.3 µIU/mL (both normal)., E# I1 R0 v0 k/ ^
The concentrations of serum electrolytes, blood
9 m. g" B9 D" ^& G yurea nitrogen, creatinine, and calcium all were7 g' K& e6 |/ p+ \3 @ ]) ~2 T0 \/ P* U& Z
within normal range for his age. The concentration
3 ~) ^3 f o1 W& j7 `" Vof serum 17-hydroxyprogesterone was 16 ng/dL. \# U2 x) {1 j+ F* q
(normal, 3 to 90 ng/dL), androstenedione was 20
$ y& |- N( H S! A( c& hng/dL (normal, 18 to 80 ng/dL), dehydroepiandros- ?/ A: P8 V. a
terone was 38 ng/dL (normal, 50 to 760 ng/dL),' ~( b6 x: z: S/ J: U* W' \
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
# H; Y4 G: |: n5 I49ng/dL), 11-desoxycortisol (specific compound S)3 j' K9 q7 Q1 H7 \
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-* v" X6 R: E: w! J
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
4 W* B5 C c1 Ntestosterone was 60 ng/dL (normal <3 to 10 ng/dL),. w* T8 g! p7 u' P/ [4 w
and β-human chorionic gonadotropin was less than# N7 E- S2 e) ~; a
5 mIU/mL (normal <5 mIU/mL). Serum follicular
4 L8 c1 G( u' }" E* b& U+ Qstimulating hormone and leuteinizing hormone
3 m% L7 F9 u; Z" M( ^+ H8 X, Xconcentrations were less than 0.05 mIU/mL% d0 m* k/ J' q2 ~/ y Z I
(prepubertal).
3 }" Z- A3 e3 aThe parents were notified about the laboratory
" m$ T& e; Q9 w3 b) h3 y% Zresults and were informed that all of the tests were
; M2 q* }, a1 z9 G pnormal except the testosterone level was high. The
$ ~- o& L# h5 @+ l3 h2 |+ ofollow-up visit was arranged within a few weeks to8 j, B/ n' a% u" P" w
obtain testicular and abdominal sonograms; how-
( V7 I" [: a/ Dever, the family did not return for 4 months." u0 s7 w! N! G. ^
Physical examination at this time revealed that the! Y7 l" o5 \% \2 s2 X; @
child had grown 2.5 cm in 4 months and had gained# @" m# u1 g4 V" c9 }
2 kg of weight. Physical examination remained1 i3 h5 @7 `$ z J' c. ^
unchanged. Surprisingly, the pubic hair almost com-
- B0 A8 Z: I3 C/ E; e; v. Q$ Opletely disappeared except for a few vellous hairs at
: H* o& x7 ?! m+ s( T; tthe base of the phallus. Testicular volume was still 2. T% c7 Q0 T2 u6 Y' P
mL, and the size of the penis remained unchanged.; @0 y2 t7 ~- B/ Z6 S
The mother also said that the boy was no longer hav-
9 w; H6 p! N% i- C9 ^ing frequent erections.. G3 x4 M$ z! O2 u+ ~7 i
Both parents were again questioned about use of
+ d4 ]& ^1 C R8 ~/ Fany ointment/creams that they may have applied to
0 B, B' \0 ?3 k x* Zthe child’s skin. This time the father admitted the0 a! x6 I. u, r
Topical Testosterone Exposure / Bhowmick et al 541
7 |5 p$ a6 X: h. Z' Z! v, N6 fuse of testosterone gel twice daily that he was apply-
; I" _; X8 `5 `0 Q) j! { sing over his own shoulders, chest, and back area for
* _# v& U& _. M1 W4 s: b! ]5 Oa year. The father also revealed he was embarrassed6 \! q9 u$ ?* t, R8 J: a$ y" O( V
to disclose that he was using a testosterone gel pre-
# P1 ?0 ~6 Y4 h" P9 I6 S6 hscribed by his family physician for decreased libido! j' S+ k' h4 ^7 c8 H9 f! R: P
secondary to depression.
0 P& T; v* C# D- ^9 A7 h$ @1 x2 gThe child slept in the same bed with parents.% h w1 |+ H+ C0 R
The father would hug the baby and hold him on his+ t# q$ S0 a0 G% h7 g; @* P0 j2 ]
chest for a considerable period of time, causing sig-- E& o$ n3 l2 l, i
nificant bare skin contact between baby and father.
i) @& ?/ l7 i% j, X& |The father also admitted that after the phone call,7 ?, n! x% ]1 a5 ^6 I) ?9 t; J$ ]
when he learned the testosterone level in the baby7 a& D" C3 b+ p+ }* K& y
was high, he then read the product information
1 ^+ Y2 u& h: T: Ppacket and concluded that it was most likely the rea-* s! g7 Q" b& E" i
son for the child’s virilization. At that time, they
3 \6 @3 e A# @0 j/ \, A; Wdecided to put the baby in a separate bed, and the: p w8 |% t$ F4 ~. k' v
father was not hugging him with bare skin and had
: |5 g$ r3 u% Jbeen using protective clothing. A repeat testosterone
. G% y! e8 h9 `3 ttest was ordered, but the family did not go to the# C s8 D0 G: {+ B7 h
laboratory to obtain the test., m |$ @0 Q) b$ q; k" s" C3 R; M
Discussion
. m5 B/ v$ L3 h# S% [- \( {$ QPrecocious puberty in boys is defined as secondary
! s9 L' D, X( ~' gsexual development before 9 years of age.1,45 U1 Y: m6 R$ Q5 z( ]
Precocious puberty is termed as central (true) when! E5 \( |+ A$ ]9 u/ S& S8 d
it is caused by the premature activation of hypo-. t: y/ D7 ^; T6 c
thalamic pituitary gonadal axis. CPP is more com-9 X$ k$ V& E- Y. V. l% @* u R
mon in girls than in boys.1,3 Most boys with CPP- r4 O1 k F9 u0 J7 H
may have a central nervous system lesion that is/ ~" A6 `- C$ N* X: Z. f$ \
responsible for the early activation of the hypothal-
2 \! j$ k% H ^& Jamic pituitary gonadal axis.1-3 Thus, greater empha-" r0 e! x! D5 U9 \
sis has been given to neuroradiologic imaging in, b4 Y" V) n2 ~4 K( b6 @, _
boys with precocious puberty. In addition to viril-; O* F5 R9 Z4 F; t1 F' k: J
ization, the clinical hallmark of CPP is the symmet-
* x5 J7 p" ^" d6 Krical testicular growth secondary to stimulation by( Q9 N \$ v( `% S3 [
gonadotropins.1,3
! ~( z1 `) M% t% p! X* lGonadotropin-independent peripheral preco-+ Q$ Z |7 V8 O( k; t- N
cious puberty in boys also results from inappropriate% I* g6 O# l! S3 H5 G
androgenic stimulation from either endogenous or6 [" m. O( H( d( u0 L& X+ J
exogenous sources, nonpituitary gonadotropin stim-
9 W( x' a6 t! I- Sulation, and rare activating mutations.3 Virilizing5 i% @2 Q M1 R6 W/ @. w& b
congenital adrenal hyperplasia producing excessive7 n9 m1 f, s3 P$ w3 r8 K4 O; f4 C, p/ ]
adrenal androgens is a common cause of precocious
* v$ ~* H* ]$ u; J: F$ D) x! xpuberty in boys.3,4
4 U& W1 x/ m0 uThe most common form of congenital adrenal2 z6 C+ N: |' e( ?6 ~8 Q7 b
hyperplasia is the 21-hydroxylase enzyme deficiency.
3 j2 {; K2 I3 C7 mThe 11-β hydroxylase deficiency may also result in0 R) B7 ~& R! A" o6 L' Y t7 Z$ @
excessive adrenal androgen production, and rarely," g9 t9 d: j! P$ W4 B
an adrenal tumor may also cause adrenal androgen" S- N! B- D: ]# ~# ~0 O
excess.1,3
6 H9 T9 O+ j# e$ Z4 eat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
, H0 @% x) O) G6 R542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
0 q, X, b! w3 u2 pA unique entity of male-limited gonadotropin-6 \: f3 K: a( l2 |( e
independent precocious puberty, which is also known
8 _! x6 b- s5 C) i4 @# M* }as testotoxicosis, may cause precocious puberty at a- R9 P/ y0 P$ \. w' x- _, g J! L
very young age. The physical findings in these boys
$ M0 J& k: c! Awith this disorder are full pubertal development,
% ]* \/ Y' c0 }2 m- p6 C; Jincluding bilateral testicular growth, similar to boys. B; t* o. M3 Z+ k
with CPP. The gonadotropin levels in this disorder; w) {; P8 k: w3 C9 W$ P6 f
are suppressed to prepubertal levels and do not show
7 u$ g) Z" J# F8 G* ~& U9 w3 wpubertal response of gonadotropin after gonadotropin-
5 t$ \8 h. R8 z0 `) [releasing hormone stimulation. This is a sex-linked
; v( q! w# Q6 v! d3 J1 ]! v1 \) Gautosomal dominant disorder that affects only
: C+ e: K1 Y4 d2 ]* h& H8 Umales; therefore, other male members of the family
; z, n1 I$ L: L' q; Q! X8 G' Gmay have similar precocious puberty.3
1 l3 Y& G) F1 K2 K5 U+ KIn our patient, physical examination was incon-
c l$ Z- I5 y" B1 ^+ qsistent with true precocious puberty since his testi-
% G) k! K2 h' |: b3 tcles were prepubertal in size. However, testotoxicosis* B% h$ N0 d/ x+ b, v
was in the differential diagnosis because his father; z4 k( k' H, |. @. m$ ?0 ?0 k4 I
started puberty somewhat early, and occasionally,
5 r# k1 K4 @ j/ G+ z7 ytesticular enlargement is not that evident in the9 g% B! ], x8 I4 z
beginning of this process.1 In the absence of a neg-3 g- e5 s* P( W! m$ F' s9 Q9 B9 O
ative initial history of androgen exposure, our/ x5 \0 r4 H5 P" m! i2 q: w1 Z
biggest concern was virilizing adrenal hyperplasia,! C" ]' J6 ~% c4 A1 s: C
either 21-hydroxylase deficiency or 11-β hydroxylase
$ v. m8 F9 s9 r) l% K2 bdeficiency. Those diagnoses were excluded by find-
0 K8 L' m* j( C+ G( u( ]. fing the normal level of adrenal steroids.
0 z$ ?6 R8 k. t# B/ i0 \The diagnosis of exogenous androgens was strongly
% Q' t4 N# }4 m( O! q. D# {8 M0 Fsuspected in a follow-up visit after 4 months because
e9 R; L1 G# t" Wthe physical examination revealed the complete disap-
* f t+ ?- F1 }/ @/ {% ^# C+ Opearance of pubic hair, normal growth velocity, and) z( |6 Z- p V* y. s m% L( t
decreased erections. The father admitted using a testos-
r7 K- G1 p+ K& b0 zterone gel, which he concealed at first visit. He was( m4 Y7 ~& B1 B0 @* {3 F
using it rather frequently, twice a day. The Physicians’
0 |) x3 G6 O8 q- e4 J d- TDesk Reference, or package insert of this product, gel or
1 ^& k* D1 _: Q4 e. J) \cream, cautions about dermal testosterone transfer to. |3 k( S, }4 |3 T: ^, W
unprotected females through direct skin exposure.6 V3 u% x+ o7 C5 | ^& B. k
Serum testosterone level was found to be 2 times the
' ~; ?1 A! c% i' k& y6 C) Vbaseline value in those females who were exposed to
2 o- K% v4 Y$ }+ w/ yeven 15 minutes of direct skin contact with their male% O$ v% N4 u, n. d- U: T
partners.6 However, when a shirt covered the applica-: R4 B" i5 C& l& Y0 m
tion site, this testosterone transfer was prevented.7 z& E# {) u* V i/ K2 G3 f3 I& d9 k3 F
Our patient’s testosterone level was 60 ng/mL,. F0 G- S# [# J o9 m) Y7 p
which was clearly high. Some studies suggest that
7 i# l; n* d* n8 I- G+ i5 j( ]dermal conversion of testosterone to dihydrotestos-
9 I6 ?1 ~+ E" fterone, which is a more potent metabolite, is more) w1 t5 b0 `! ]/ U* j. Y
active in young children exposed to testosterone- g, i1 q0 y3 p: h
exogenously7; however, we did not measure a dihy-5 F1 X( }! O6 D* X/ Q9 P
drotestosterone level in our patient. In addition to
$ K, m6 z$ T1 Q" g$ U" uvirilization, exposure to exogenous testosterone in {5 x6 j3 o1 J9 w6 H5 q
children results in an increase in growth velocity and
! u$ j$ k, _5 T1 |9 C# T8 [advanced bone age, as seen in our patient.
7 B0 O/ r) ?9 h8 Z" G! R) mThe long-term effect of androgen exposure during
5 }. y; v) [2 x8 xearly childhood on pubertal development and final2 [& e; o, d# N
adult height are not fully known and always remain. ^' f: l# h/ e8 F9 G M! A. s: M$ ]1 n
a concern. Children treated with short-term testos-
# E0 S7 |$ v7 @terone injection or topical androgen may exhibit some
% x7 ^9 B, y+ `) ?acceleration of the skeletal maturation; however, after& r6 L1 l1 z$ T, Q
cessation of treatment, the rate of bone maturation
4 l2 N2 ^4 Z% P) [% M4 a' \decelerates and gradually returns to normal.8,91 j5 e8 h6 ~, n; a; d0 ^, l- X) C
There are conflicting reports and controversy" }& j, n+ m) ]; O1 b8 z$ M( O4 y
over the effect of early androgen exposure on adult
7 e& J N" L0 G* C( [# M6 fpenile length.10,11 Some reports suggest subnormal
: F, z) I5 m, |0 cadult penile length, apparently because of downreg-3 L+ Y" x( ` K. ]1 H% R# V
ulation of androgen receptor number.10,12 However,, v e/ u+ A; |8 v& L+ p- y
Sutherland et al13 did not find a correlation between3 j& U9 f6 B3 h6 P! f! ^7 o
childhood testosterone exposure and reduced adult
' `4 R5 @+ S5 t( E/ u4 b: rpenile length in clinical studies.: P* d( c2 Q5 i! p; E0 F, L
Nonetheless, we do not believe our patient is2 b/ M/ d& P; i% E
going to experience any of the untoward effects from: o/ s+ u" I$ p5 T0 ?
testosterone exposure as mentioned earlier because! {) Z$ t) J; v) g* q( o; v( ~
the exposure was not for a prolonged period of time.9 L3 ^3 v7 B( t
Although the bone age was advanced at the time of
! ? Z R @4 n; i; l6 [7 w7 ^2 s4 Cdiagnosis, the child had a normal growth velocity at
5 M3 a& ?, S! [$ N! B8 m dthe follow-up visit. It is hoped that his final adult
4 v( N( G/ |, I% t ^height will not be affected., j7 j! E: |) X$ i, Y5 u; j) v! H. ^! z
Although rarely reported, the widespread avail-
' e7 o- O$ M$ [& kability of androgen products in our society may
1 Y# ]. r: \- W# e; ~0 @indeed cause more virilization in male or female
& ]. U" Z2 f3 P. Tchildren than one would realize. Exposure to andro-
1 o7 n/ ^9 h0 w* V+ @; i. Mgen products must be considered and specific ques-9 d$ {, c5 a1 h( @) h3 L& o
tioning about the use of a testosterone product or
, l6 ^/ J I8 P: A! y6 h3 kgel should be asked of the family members during
$ k! _* F8 {; S: kthe evaluation of any children who present with vir-7 o* P; ^! o, s! H$ O& o
ilization or peripheral precocious puberty. The diag-9 J! J: o8 s& i2 d0 v
nosis can be established by just a few tests and by
5 i! X: I1 s: v1 @- Dappropriate history. The inability to obtain such a9 }. Z$ U! v! h9 c% K# E8 p
history, or failure to ask the specific questions, may
; B8 D- c3 v# R, T( [% K/ I- ]result in extensive, unnecessary, and expensive/ ~4 I4 g: g. @; ~( U
investigation. The primary care physician should be
' Y7 m6 E" t: [. ?, U; e$ T! Caware of this fact, because most of these children6 J& L2 S7 F! m, n
may initially present in their practice. The Physicians’
! H2 o* T; s! ^% x0 L- |5 I/ Z3 _7 b& JDesk Reference and package insert should also put a; r# ]+ u% f: [ e
warning about the virilizing effect on a male or0 i1 x0 U' R4 K' f0 ~! N$ }" r
female child who might come in contact with some-
2 x: ^2 k) L7 none using any of these products.8 X6 o1 ?, z; N- ?5 M0 r$ [, q
References9 M2 k. {5 ]/ z5 P/ i
1. Styne DM. The testes: disorder of sexual differentiation
& u4 J* c& N/ v$ H0 G5 B+ eand puberty in the male. In: Sperling MA, ed. Pediatric
/ W3 @% |/ ^; c6 v8 X: P2 n3 fEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;8 w v* H) v) `- d& `0 i
2002: 565-628.
- c2 d( v+ j) [# }/ \2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious8 o* O: V. T: e6 j
puberty in children with tumours of the suprasellar pineal |
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