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Sexual Precocity in a 16-Month-Old
& P2 ]9 ?& Q/ Z: e. oBoy Induced by Indirect Topical
5 R. p4 T/ ^5 w. q `* t% qExposure to Testosterone
+ n/ P! c r3 o$ \, g) B; JSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
9 X. }7 b% [3 G7 l+ Zand Kenneth R. Rettig, MD1
1 ?$ u7 B! h& U# C _& g w0 ]* oClinical Pediatrics: E- u4 R9 J7 q3 j, W7 n n
Volume 46 Number 6
, s# F; S5 _( W& N* x6 F4 ZJuly 2007 540-543
% O( a* N3 |: h* W# ?4 w- a L© 2007 Sage Publications! |0 ` V# O) K! ~# h# u0 Y
10.1177/0009922806296651+ U ? ~4 ^0 w/ ]; O, {
http://clp.sagepub.com& @4 X8 R6 O5 f) L
hosted at' W$ `7 Z# f: q. W* C
http://online.sagepub.com+ H* z/ Y: L2 b. I3 c
Precocious puberty in boys, central or peripheral,/ L8 F' p9 {3 t" D: O0 Z3 C
is a significant concern for physicians. Central
% h) D# m+ w+ q4 q0 {7 j% xprecocious puberty (CPP), which is mediated
2 C8 J9 M) }! ^0 F: ~. n$ h& ]6 ?through the hypothalamic pituitary gonadal axis, has7 ?" b5 h. E& M* J8 ^
a higher incidence of organic central nervous system4 T; s+ t1 B7 q0 z
lesions in boys.1,2 Virilization in boys, as manifested
' s& H3 C: D. H nby enlargement of the penis, development of pubic
! i, a. |3 z8 Jhair, and facial acne without enlargement of testi-
( g$ g' f! ]% J7 G8 N( Hcles, suggests peripheral or pseudopuberty.1-3 We1 k" S2 B( ^+ [& a! N
report a 16-month-old boy who presented with the
& C6 I# d) N, g, c, A0 R, R6 Oenlargement of the phallus and pubic hair develop-4 D. K$ Q$ ~/ n- R/ a
ment without testicular enlargement, which was due
2 d. e: S& P' C+ h$ O5 fto the unintentional exposure to androgen gel used by
. A. l' h* C- {0 k4 V. [5 ]the father. The family initially concealed this infor-! t* I6 i/ k/ {7 K& Y
mation, resulting in an extensive work-up for this( K' [. C/ A0 ^$ q4 S; s
child. Given the widespread and easy availability of
' n. H* J# _; _testosterone gel and cream, we believe this is proba-3 [+ H, S1 ]# Q, B4 O6 K, _
bly more common than the rare case report in the
# Z6 {! y" C' }4 w8 \literature.4' w9 W0 ^( Z7 m/ t0 d9 A
Patient Report
5 w+ x5 `# ]3 J' E5 u @1 D2 `A 16-month-old white child was referred to the) P3 V3 U: F' j# U( ]0 \" `, y. A
endocrine clinic by his pediatrician with the concern# @7 D% G4 L( o/ {* ]+ P) O
of early sexual development. His mother noticed2 A2 o- c9 q6 n5 k s2 V" \4 T# C3 [
light colored pubic hair development when he was. _0 w# ^) F4 J1 x6 F" ~1 w* L
From the 1Division of Pediatric Endocrinology, 2University of
, I% d8 Y; Y8 vSouth Alabama Medical Center, Mobile, Alabama.; X* b A+ \$ J
Address correspondence to: Samar K. Bhowmick, MD, FACE,
; V9 X8 S3 g! @8 ] H* EProfessor of Pediatrics, University of South Alabama, College of* r2 O' p0 x3 ]& [; R. V
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
|! T- b, d' f8 W& c* fe-mail: [email protected].
7 l7 r* \* N8 E( m) S; @' Iabout 6 to 7 months old, which progressively became
9 A- A- t n$ H% `# u1 H- Xdarker. She was also concerned about the enlarge-
( \1 l: L2 O. Yment of his penis and frequent erections. The child
- L9 J8 `9 e7 }8 }! }- Gwas the product of a full-term normal delivery, with
/ b' K& n7 d5 X- {) La birth weight of 7 lb 14 oz, and birth length of, U* t$ ^$ c M/ ]
20 inches. He was breast-fed throughout the first year2 `: p) c& Y }; @4 J
of life and was still receiving breast milk along with; {4 E7 i/ H2 i/ F& @+ W" I, h
solid food. He had no hospitalizations or surgery,# z. v/ O9 V n0 v8 P+ k
and his psychosocial and psychomotor development
, W7 Y2 D7 k- ^2 wwas age appropriate.3 A- o1 T. D( x# i: u; [
The family history was remarkable for the father,4 W8 C5 W. }- c# u, l
who was diagnosed with hypothyroidism at age 16,& I; _( E2 G2 I5 y6 ~' B
which was treated with thyroxine. The father’s
6 M! b8 G1 \0 I# Cheight was 6 feet, and he went through a somewhat5 ?8 e6 h. b0 q
early puberty and had stopped growing by age 14.5 ^/ v6 ?2 X* D7 P+ K
The father denied taking any other medication. The1 G0 N1 Y! k" P1 J: U
child’s mother was in good health. Her menarche6 l0 v+ _% r9 ^8 R/ @
was at 11 years of age, and her height was at 5 feet
3 c1 x6 j3 t, L4 U: I G5 inches. There was no other family history of pre-
9 S z9 N: Z, o8 d% ccocious sexual development in the first-degree rela-9 J& S2 R- w* e+ I
tives. There were no siblings.
+ m! W9 N( n' C" T; e. Y7 gPhysical Examination, e8 B# A/ O5 c) h+ o. B, b9 d
The physical examination revealed a very active,9 u5 Z3 F6 @* m- q8 y" E- g+ C
playful, and healthy boy. The vital signs documented
' F7 d) o0 Q/ @: [a blood pressure of 85/50 mm Hg, his length was( f9 H( _2 s, x0 [% L
90 cm (>97th percentile), and his weight was 14.4 kg
0 n" H; `: Q/ y* D. a# W% {% e% E7 P# q(also >97th percentile). The observed yearly growth( |/ F. y* B0 |5 m/ q* W
velocity was 30 cm (12 inches). The examination of; D6 T' }9 t8 Z# i
the neck revealed no thyroid enlargement.
$ o! G1 H( W8 j- l# d% b% tThe genitourinary examination was remarkable for, t" i* D! a! a. B" V: e
enlargement of the penis, with a stretched length of" `/ J% z8 h5 P2 V
8 cm and a width of 2 cm. The glans penis was very well' k$ ]" o4 }9 r. b
developed. The pubic hair was Tanner II, mostly around: Q+ o6 M3 G0 H0 y" V
540/ d; b* P7 S$ ?, T) |3 d! e* g# Q
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
( j( I7 c8 }' r& Zthe base of the phallus and was dark and curled. The
. {1 U2 F* J: V: Dtesticular volume was prepubertal at 2 mL each.- G5 J5 I/ ~+ Q
The skin was moist and smooth and somewhat' [! D/ [; t( e7 T8 `
oily. No axillary hair was noted. There were no
* F( k( @4 W5 [2 C7 \5 habnormal skin pigmentations or café-au-lait spots.
8 ^: d3 k& `# U" O7 fNeurologic evaluation showed deep tendon reflex 2+
% Z m+ u5 {+ Pbilateral and symmetrical. There was no suggestion9 ^# n) i4 P6 l+ n. P4 y) E. [$ d
of papilledema.3 b' D% _) l/ _
Laboratory Evaluation
/ V, {3 c6 u/ kThe bone age was consistent with 28 months by0 H, p0 ^( r. ?7 m8 |0 `1 ]- V
using the standard of Greulich and Pyle at a chrono-/ i+ R6 ]' |) k( }0 T* L
logic age of 16 months (advanced).5 Chromosomal
& L2 p) {+ C/ Q3 U! o/ @+ Hkaryotype was 46XY. The thyroid function test9 u' P! H, s, T+ t+ @# j
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
J- |6 X D; ?9 V# v) |lating hormone level was 1.3 µIU/mL (both normal).
9 ^3 i3 ~0 ^/ R$ A' \The concentrations of serum electrolytes, blood- Z2 X( h8 \/ P" Q4 O/ ]! V6 }
urea nitrogen, creatinine, and calcium all were# x2 ^% t" ~2 p2 q$ q
within normal range for his age. The concentration
6 b' v2 e3 \6 h+ v" G& d, k1 Sof serum 17-hydroxyprogesterone was 16 ng/dL
% D8 B1 O+ f" a- I F& w+ s- @(normal, 3 to 90 ng/dL), androstenedione was 20
( l h7 u9 K/ F8 T+ i4 A% Eng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-+ B6 ^* k; [ e$ F! C% Z5 L3 F
terone was 38 ng/dL (normal, 50 to 760 ng/dL),3 i& {6 x! H8 V( r) d
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
7 `8 Z" I8 U1 I* s& P9 W# {; P49ng/dL), 11-desoxycortisol (specific compound S)
9 [* m/ d3 j" ywas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-. p, x7 e8 Y1 I# `; B) R
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total/ F7 Z. u5 v- B9 a. b' i
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
% l& b- T2 j( h. `7 B3 q$ Gand β-human chorionic gonadotropin was less than
4 a) \( s! B# B5 mIU/mL (normal <5 mIU/mL). Serum follicular4 @% H8 s7 I, d; W) b' Q5 {
stimulating hormone and leuteinizing hormone0 j: W# }! J/ P. A# c `! m# u
concentrations were less than 0.05 mIU/mL; [5 O" F: X5 _
(prepubertal).
6 M9 t# V# }4 c6 I' R1 RThe parents were notified about the laboratory- g9 N6 a( K) E* Z' }9 s
results and were informed that all of the tests were
K) W- i; ^8 q" [% d9 P. W$ ?; T; qnormal except the testosterone level was high. The
! H1 j, l* f4 Q' ofollow-up visit was arranged within a few weeks to
& H! Z8 k7 O$ L; g- Qobtain testicular and abdominal sonograms; how-4 y, A# D0 k7 u& M* _( Z' O. m. x
ever, the family did not return for 4 months.
$ C t5 t: I2 p: k5 SPhysical examination at this time revealed that the
; z: K. \7 z- y9 x. Kchild had grown 2.5 cm in 4 months and had gained
. n+ d2 r+ x' W0 f; p9 M2 kg of weight. Physical examination remained
) C% r( X5 J( C3 N6 B7 _unchanged. Surprisingly, the pubic hair almost com-) u" d% i' a* \! Q, d2 H* W. S
pletely disappeared except for a few vellous hairs at
" a) c& I: p5 X# f1 `; Othe base of the phallus. Testicular volume was still 2# J- \5 `( F* d/ q
mL, and the size of the penis remained unchanged.- I) Z, Q; h" G* P5 l
The mother also said that the boy was no longer hav-7 x& k- G% ]! p' c8 _
ing frequent erections.
0 W6 S- g% F) `+ g1 V- r; ? \Both parents were again questioned about use of
0 K6 K! b$ O' G# L" \# t$ Z) l1 }any ointment/creams that they may have applied to; O2 @* r) h8 F9 J: G( Y) B
the child’s skin. This time the father admitted the
R" Z; K1 C& [8 b7 [+ {Topical Testosterone Exposure / Bhowmick et al 541) c5 N% \, i# @ C" [% o0 U
use of testosterone gel twice daily that he was apply-1 B# e; Q% t9 U7 o% b( V) W# u2 i
ing over his own shoulders, chest, and back area for4 f2 N; @/ s# v* d. L8 p8 v
a year. The father also revealed he was embarrassed7 P" U! O: I/ r8 N$ T
to disclose that he was using a testosterone gel pre-3 M5 A- n% T; q0 _1 f( Q: ~3 f
scribed by his family physician for decreased libido& G1 N" j# N3 k! v2 I% u+ U
secondary to depression.
/ S- r) A4 d; g. [) q5 s CThe child slept in the same bed with parents.% r s$ L, L2 i0 o' j) [! _
The father would hug the baby and hold him on his% C) R l$ C2 H+ j1 x
chest for a considerable period of time, causing sig-' }, J" N0 j$ H k' S7 ?5 w
nificant bare skin contact between baby and father.* W) O+ \+ ^, \& [- [
The father also admitted that after the phone call,
4 g* u6 w ?, p1 R- _1 zwhen he learned the testosterone level in the baby+ F3 e- _ H7 y- H Q9 j0 }
was high, he then read the product information
6 k! W9 z, l, o7 X5 Z% f1 opacket and concluded that it was most likely the rea-+ L/ r. ]( k: t; J! n6 L
son for the child’s virilization. At that time, they
' W2 M5 C7 W Mdecided to put the baby in a separate bed, and the2 j: J2 \5 f* ?
father was not hugging him with bare skin and had' Y2 T' I- q1 @( B6 P, F
been using protective clothing. A repeat testosterone" b* L$ N: x+ k# K& b5 c- R1 |
test was ordered, but the family did not go to the% T8 f, x7 Y6 x
laboratory to obtain the test.
M2 I$ E' [$ Y, D$ l$ r) U0 g* YDiscussion( ?5 b0 O6 l3 e' V3 W
Precocious puberty in boys is defined as secondary
! M9 |5 g2 \9 C( g% E# asexual development before 9 years of age.1,4
! w3 A+ m% c" z, BPrecocious puberty is termed as central (true) when
k4 b4 Z/ g) y8 @. K& u: S' I+ N, Vit is caused by the premature activation of hypo-
. f9 P4 X9 q/ D5 U! P. P4 ]$ W( Vthalamic pituitary gonadal axis. CPP is more com-
- V, n+ o c" D+ W/ p; r! gmon in girls than in boys.1,3 Most boys with CPP t: q L/ X7 ]
may have a central nervous system lesion that is: L1 H* N- A- a: `* r, s
responsible for the early activation of the hypothal-
. `4 f2 [6 ~4 ?- c( r* m) F1 Damic pituitary gonadal axis.1-3 Thus, greater empha-0 z* T* [+ x d6 U
sis has been given to neuroradiologic imaging in
! e& B% {2 c+ i3 Q; _" V4 w2 n$ zboys with precocious puberty. In addition to viril-
2 ~8 I. x8 K$ {/ W* T6 {+ \2 ?/ cization, the clinical hallmark of CPP is the symmet-" {( N0 I7 s0 {8 B! L, ~/ ^. F
rical testicular growth secondary to stimulation by
# T3 p$ S# n' C/ m! |' j* \gonadotropins.1,3
+ c- v- d6 Q' w' r3 B. s7 }4 N* pGonadotropin-independent peripheral preco-
: i# F; b: W" G6 o z: a2 m) Ycious puberty in boys also results from inappropriate
8 g5 }2 B T+ j+ i: Vandrogenic stimulation from either endogenous or! k$ R' M+ Y8 D( ], I
exogenous sources, nonpituitary gonadotropin stim-
; ^7 p" @$ Z7 X5 K# ^" j; j9 nulation, and rare activating mutations.3 Virilizing5 u! p* d7 g2 v: z+ z
congenital adrenal hyperplasia producing excessive
3 ]9 J+ c% L0 z4 \9 [# N2 ?adrenal androgens is a common cause of precocious
$ e& P! x- D3 f# B, {puberty in boys.3,4
3 a, ^0 R/ J$ d& s; o k( v: pThe most common form of congenital adrenal, T Q3 ~1 j# b* L. E
hyperplasia is the 21-hydroxylase enzyme deficiency.
7 K; f$ l1 E6 vThe 11-β hydroxylase deficiency may also result in" v1 `+ t+ { }2 S6 w: X
excessive adrenal androgen production, and rarely,- l z8 v4 j, v5 v1 j- {
an adrenal tumor may also cause adrenal androgen
7 O; [/ O9 c! y" |" ^, ]. ^0 p" Aexcess.1,3
. x& L7 I3 ~- d# V7 Y ^at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from% t0 X/ M, d# z/ u( I8 O
542 Clinical Pediatrics / Vol. 46, No. 6, July 20075 Z9 U8 L" R) a# D% y% M, K- H; w7 q
A unique entity of male-limited gonadotropin-
0 X4 P; r- F. Y; Zindependent precocious puberty, which is also known9 z7 b2 S* z: Z
as testotoxicosis, may cause precocious puberty at a
. s0 _" G( f5 K5 ?' ivery young age. The physical findings in these boys1 Q+ U0 f9 I6 g* H: X4 s& N
with this disorder are full pubertal development," a0 O& C6 z. Z+ y u: ^ ^
including bilateral testicular growth, similar to boys4 i/ g V& P% f, d" K2 J/ t
with CPP. The gonadotropin levels in this disorder
3 v. f5 K& d' ^5 Jare suppressed to prepubertal levels and do not show6 T: V1 }( X- v4 A# y* f
pubertal response of gonadotropin after gonadotropin-
$ A* a, a, X, X2 F; ereleasing hormone stimulation. This is a sex-linked: i; a% n! _1 {3 z9 L& p
autosomal dominant disorder that affects only
* e/ O& O( ~4 |9 i* T+ r5 Rmales; therefore, other male members of the family8 _) \0 d; K+ G6 J2 Q
may have similar precocious puberty.3) G& v1 m( o! ^, O/ ]6 \) g4 o
In our patient, physical examination was incon-
- v; @4 G: s3 tsistent with true precocious puberty since his testi-
6 {5 t* D2 g8 @% l5 bcles were prepubertal in size. However, testotoxicosis
, m8 q2 D; D8 c! c4 @! u* @/ Rwas in the differential diagnosis because his father
4 ~4 \7 E/ k0 L8 B% Rstarted puberty somewhat early, and occasionally,& [6 ^- m) G, C
testicular enlargement is not that evident in the; e) ]8 `1 H( _4 N; [
beginning of this process.1 In the absence of a neg-
9 R% o A$ Z0 \) q" ?ative initial history of androgen exposure, our
6 C" @1 @( `' R rbiggest concern was virilizing adrenal hyperplasia,
[- p3 N( n; Z% P1 r8 @- neither 21-hydroxylase deficiency or 11-β hydroxylase! r& D' P, ?* w" H/ e6 t
deficiency. Those diagnoses were excluded by find-
! u. Y+ ?# y) @! Q8 t: Fing the normal level of adrenal steroids.
" c' u$ f6 L. y% Z0 g' H- cThe diagnosis of exogenous androgens was strongly1 j" M6 \- U! G& l
suspected in a follow-up visit after 4 months because
) L! ~. O* D* J+ l: |! Uthe physical examination revealed the complete disap-3 |, x' H' z+ @1 X+ G
pearance of pubic hair, normal growth velocity, and9 F8 c" S) K2 T5 ?% n6 \
decreased erections. The father admitted using a testos-
6 U# ?4 [0 J9 ^' F1 ~8 ?terone gel, which he concealed at first visit. He was
4 \- c! U, H4 d0 Lusing it rather frequently, twice a day. The Physicians’0 o" P" M4 i( N9 ]% M0 ~: q
Desk Reference, or package insert of this product, gel or
5 W9 I# _" T; n3 }1 O1 ?cream, cautions about dermal testosterone transfer to& ~2 x9 N( \0 H2 ~1 b9 N: {
unprotected females through direct skin exposure.
& c4 H7 r$ N# ?5 _' l2 S. zSerum testosterone level was found to be 2 times the
, Q* F! O z# l9 ~0 f; `baseline value in those females who were exposed to' Y8 N y# w1 Y7 F, Z7 H
even 15 minutes of direct skin contact with their male, E6 b6 d' {/ {
partners.6 However, when a shirt covered the applica-
! S" B) q7 j- I& M+ [: g3 s( ztion site, this testosterone transfer was prevented." R8 c# u f) V4 m
Our patient’s testosterone level was 60 ng/mL,
9 r. h' b: p' ]/ Swhich was clearly high. Some studies suggest that# G0 W/ K+ Z3 T! m( b6 S8 d
dermal conversion of testosterone to dihydrotestos-- v3 p& R* t" O* ~% F$ c! ]
terone, which is a more potent metabolite, is more: v5 J/ K0 ?- J5 c- i+ O
active in young children exposed to testosterone3 b' j0 b3 w) g3 x+ l# v! ]
exogenously7; however, we did not measure a dihy-2 S6 L, g7 {- Z) B1 W. X1 I
drotestosterone level in our patient. In addition to
. ]$ b9 M0 C6 g% v5 a7 l. @/ J# Uvirilization, exposure to exogenous testosterone in
9 ^9 O7 u# U0 ?" T1 @6 Rchildren results in an increase in growth velocity and z2 k; F6 ^0 N; v" N
advanced bone age, as seen in our patient.
+ ~0 `0 |9 B# Q1 ~1 O& BThe long-term effect of androgen exposure during" W5 ~% g0 J' F( p. ?6 O7 d
early childhood on pubertal development and final, `! R' _) ?1 {1 {- `3 C
adult height are not fully known and always remain Q# L7 x5 \: L, R. f
a concern. Children treated with short-term testos-
) K8 X9 v; W8 ]: Lterone injection or topical androgen may exhibit some- [5 [1 R6 _# G' s$ s
acceleration of the skeletal maturation; however, after
) L) ?' W, ~, R) y) e' kcessation of treatment, the rate of bone maturation
; L7 L. ~6 h% d$ o( c8 ]) }decelerates and gradually returns to normal.8,9
& m; V, ` a' A$ QThere are conflicting reports and controversy& ~* A6 Q! t( n0 z
over the effect of early androgen exposure on adult, w2 I# A! k! U5 f
penile length.10,11 Some reports suggest subnormal5 E% e; J6 j' o! p7 l
adult penile length, apparently because of downreg-
% E2 o- X9 ^, D9 Uulation of androgen receptor number.10,12 However,
/ c6 d1 f* V9 N' `4 FSutherland et al13 did not find a correlation between
& b6 j& @- ?2 T# r, t5 b" E$ O% Uchildhood testosterone exposure and reduced adult7 i1 d3 V; i7 M+ ]
penile length in clinical studies.( B7 ?! d! W: W$ ~; L5 C& o8 ^
Nonetheless, we do not believe our patient is
0 Q. ^0 \6 B# v: Xgoing to experience any of the untoward effects from/ H) ~- j+ L3 k* x" a
testosterone exposure as mentioned earlier because" Q2 X" z! [" A% L& t
the exposure was not for a prolonged period of time.0 @$ {2 F0 w4 |4 t; \7 B
Although the bone age was advanced at the time of. U" h; J5 ~4 K+ t* ^8 _
diagnosis, the child had a normal growth velocity at* s2 A6 K" i6 c8 Q: o8 B9 X; {/ ~: h4 [
the follow-up visit. It is hoped that his final adult
, l5 w% D$ K9 rheight will not be affected.9 O- Q) O5 [% D* i% p z2 i
Although rarely reported, the widespread avail-! A2 b$ ]3 `3 X0 z/ Y+ \ i- m
ability of androgen products in our society may' ?: ?7 L: p. L/ ]" |+ Y/ N, E
indeed cause more virilization in male or female
6 x' o1 V' v% P! s% R9 i% L% W# Nchildren than one would realize. Exposure to andro-
3 ?( P6 ^) C6 D& N1 {8 p" x! [gen products must be considered and specific ques-2 Z; Z- i# l; R- y, G; ?; A
tioning about the use of a testosterone product or8 p) H6 m7 f/ W* A
gel should be asked of the family members during
$ [! y T5 P9 L$ m3 M2 Zthe evaluation of any children who present with vir-
# e: a) ~4 h$ a6 Z3 Hilization or peripheral precocious puberty. The diag-
# j; x* U t- q- x0 l9 Dnosis can be established by just a few tests and by0 J& c `$ `, m$ |3 m$ M
appropriate history. The inability to obtain such a! _" c3 L! R5 D2 m; }
history, or failure to ask the specific questions, may
) H N% g, q1 d8 k5 _& k- b3 }3 tresult in extensive, unnecessary, and expensive
5 E" [* O0 |* L0 w9 `investigation. The primary care physician should be
" a6 {8 Z' d! Y+ F" F5 Taware of this fact, because most of these children4 f9 x+ J# A6 M& O( A
may initially present in their practice. The Physicians’
; q# M) c1 ], f: r+ T; xDesk Reference and package insert should also put a
' q' z0 F# E* _- z- o) i# Kwarning about the virilizing effect on a male or
$ D6 s. ?0 S$ T; Hfemale child who might come in contact with some-2 r1 A' V- J- ~+ A/ n2 ^% O
one using any of these products.* a3 K+ l" T4 S1 m
References
# I. M7 H, I/ w) u1. Styne DM. The testes: disorder of sexual differentiation
, p6 B" I# G7 k, B- s5 s' o; V) ^and puberty in the male. In: Sperling MA, ed. Pediatric
: P0 m9 B" h- x' n( |! _, Z7 Q' qEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;9 I8 h# Y" {& A; N, \4 C4 y
2002: 565-628.
# T1 Z5 ` Y2 g% V; r" L# u/ u2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious2 `9 X. M d8 Y" y
puberty in children with tumours of the suprasellar pineal |
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