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Sexual Precocity in a 16-Month-Old
* U6 g# Y& P6 h+ y; \Boy Induced by Indirect Topical0 [5 w6 R! W! u3 N
Exposure to Testosterone7 p1 w' k7 `' E1 G, [
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2 i% t2 e4 S9 g; ]7 e( j( v. w
and Kenneth R. Rettig, MD1
' Z& r' }+ Q0 ]0 _" e5 gClinical Pediatrics' C9 J* [+ M+ V# X5 @
Volume 46 Number 6
5 y7 @3 b. v2 l" A0 nJuly 2007 540-543
9 P! x# ?5 F% o© 2007 Sage Publications
; M9 l5 s# z' H7 h' k2 _6 h10.1177/0009922806296651
8 s6 W: c/ {4 t8 s$ w& Ghttp://clp.sagepub.com4 q" Q x- B. z/ n. V, k) K) `
hosted at
4 a* u J' S2 J L* d5 lhttp://online.sagepub.com
9 x4 }. K/ b% N2 Q; mPrecocious puberty in boys, central or peripheral, j* S5 W& a4 r" g
is a significant concern for physicians. Central5 Z5 {9 p! N6 A$ X" P
precocious puberty (CPP), which is mediated
7 ]! N; @/ @& y. r' g$ d% uthrough the hypothalamic pituitary gonadal axis, has
% ?% m; q; \5 {% Z/ G: c4 aa higher incidence of organic central nervous system! B& `" W- f; C6 l; b7 R
lesions in boys.1,2 Virilization in boys, as manifested
6 ?# X" ~( B7 w( Dby enlargement of the penis, development of pubic
$ D [5 L) t8 a3 Q7 e- chair, and facial acne without enlargement of testi-2 \" ?9 x& Y4 R: V' `9 E7 P) L
cles, suggests peripheral or pseudopuberty.1-3 We* E$ I* B2 G( ~( s( Y
report a 16-month-old boy who presented with the: x. S; z$ o+ b3 V6 x4 i2 U% y
enlargement of the phallus and pubic hair develop-
/ E: }, a, ?* G1 t0 Tment without testicular enlargement, which was due
' A; A& Z* a" T# a/ b, Q5 \to the unintentional exposure to androgen gel used by$ w) \- k7 M) g5 z$ u0 \
the father. The family initially concealed this infor-
: z. _2 |; ?0 P2 }/ A" \; h: B: gmation, resulting in an extensive work-up for this
2 l6 S' D( z2 h/ I2 n9 Fchild. Given the widespread and easy availability of
) W5 F) H8 ~) xtestosterone gel and cream, we believe this is proba-
! m* r: d1 z' y% N# R: H; ~9 ebly more common than the rare case report in the9 P. c6 K- b! T4 I
literature.4* y5 B$ O2 j% `& c
Patient Report' \; }% v6 X; B: m$ B
A 16-month-old white child was referred to the3 M5 o# ?8 C+ Q# C S& z/ ?
endocrine clinic by his pediatrician with the concern& y3 m9 s- j% |& @9 }
of early sexual development. His mother noticed* X0 n& X$ Y. }1 L) a& g
light colored pubic hair development when he was9 k. P0 h9 T/ c( }2 t" l
From the 1Division of Pediatric Endocrinology, 2University of0 \ S) g' ~: v8 ]
South Alabama Medical Center, Mobile, Alabama.1 L; _# N4 _) ~+ H5 R
Address correspondence to: Samar K. Bhowmick, MD, FACE,0 i6 E* B% h2 J
Professor of Pediatrics, University of South Alabama, College of6 V- P7 r/ x; V$ t; ]- R' C) y5 T( s o
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;- g: }; B: E# G9 Y8 a" Z$ a: Q: _
e-mail: [email protected].
6 b' [6 ^3 n R0 @$ v: I' habout 6 to 7 months old, which progressively became
" @4 V! D" o5 s- M. Pdarker. She was also concerned about the enlarge-
* W, t1 w8 V- V; ?3 y9 w( \ment of his penis and frequent erections. The child
x# Z# c- m& w3 g( Z5 y z' Rwas the product of a full-term normal delivery, with
1 x7 ]- P5 |: x" h% ~& r& ka birth weight of 7 lb 14 oz, and birth length of
% U$ U3 i# w. p& c3 I4 g20 inches. He was breast-fed throughout the first year( ~, Y5 i& e5 I, T
of life and was still receiving breast milk along with3 N$ h. N9 Q8 w Y w J7 S
solid food. He had no hospitalizations or surgery,
, {7 H r1 F0 U* M/ Q( d1 Yand his psychosocial and psychomotor development
% w% M, _! a: O4 h5 `7 Z. ]2 [was age appropriate.
0 Z8 Q9 t d0 T; vThe family history was remarkable for the father,3 Z( @) j( ~: u
who was diagnosed with hypothyroidism at age 16,0 a% |: ]0 l6 |9 I
which was treated with thyroxine. The father’s7 [9 k) w4 N6 k. i
height was 6 feet, and he went through a somewhat
) |- {" |3 E0 G' G" [% L- x4 e* A, c5 ~early puberty and had stopped growing by age 14.- L% n5 |! s' a$ M
The father denied taking any other medication. The
3 _: p* y' |" |$ z8 P9 w5 q; tchild’s mother was in good health. Her menarche
6 e# m( x& i3 C+ P/ B6 C. p* i9 I# T' owas at 11 years of age, and her height was at 5 feet
* S+ \. s2 U! g& ~5 U5 inches. There was no other family history of pre-
, H6 }- C/ d6 e. P5 Dcocious sexual development in the first-degree rela-! g8 N7 H1 X! H- P- j* k. g9 M# I& ~. y
tives. There were no siblings.5 C3 u4 V) s3 M/ ^
Physical Examination# U; T9 [0 x' |) {" r! G- ]6 \
The physical examination revealed a very active,
+ z5 v9 }1 u E' x: @: f- nplayful, and healthy boy. The vital signs documented8 p4 \9 |. A# M- u& D# j J1 b1 J
a blood pressure of 85/50 mm Hg, his length was
1 T/ Y( p' y9 w5 U% u- d90 cm (>97th percentile), and his weight was 14.4 kg
* o2 v Q5 K$ {, }2 v# E; Y) V f: L(also >97th percentile). The observed yearly growth
2 q$ J# E. w; Y' S H% vvelocity was 30 cm (12 inches). The examination of- f" b2 V) W0 D2 Q3 q$ H
the neck revealed no thyroid enlargement.
9 L. w: N( I3 \ VThe genitourinary examination was remarkable for
6 z6 p0 g- o9 @( m. w: N9 i/ \enlargement of the penis, with a stretched length of
7 b' r$ n$ a9 N* J& A7 w, C8 cm and a width of 2 cm. The glans penis was very well
! q# q) F& ^6 B" b8 sdeveloped. The pubic hair was Tanner II, mostly around
W9 ?1 K) @% q! o540
T {0 M3 v+ o/ K. Q, Nat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from0 Y2 b+ W# B+ x9 q o* t9 D
the base of the phallus and was dark and curled. The: ~& y6 ~+ k' w7 v$ t+ ~1 [" L
testicular volume was prepubertal at 2 mL each.
+ p+ z0 u; v# X8 B0 a% i8 mThe skin was moist and smooth and somewhat
' H. N' W. Z( O1 y/ Qoily. No axillary hair was noted. There were no+ ?! d9 g7 k. h9 s. M
abnormal skin pigmentations or café-au-lait spots.' E0 M7 O, d* {$ F/ A5 i
Neurologic evaluation showed deep tendon reflex 2+5 E7 n! G- P, ` `
bilateral and symmetrical. There was no suggestion
$ k6 U& s6 e: `# S2 d: gof papilledema.
! W6 q3 L+ E* S- h0 sLaboratory Evaluation" H8 O u8 A/ w0 }# G
The bone age was consistent with 28 months by
$ @8 g* t& {4 t \using the standard of Greulich and Pyle at a chrono-. e5 [6 l- |. |0 Y3 x; @$ C/ D
logic age of 16 months (advanced).5 Chromosomal
% [6 o/ e$ A% wkaryotype was 46XY. The thyroid function test. j. e. l5 D. g3 R
showed a free T4 of 1.69 ng/dL, and thyroid stimu-7 y) b8 n5 ?) Z& Q. Q, J
lating hormone level was 1.3 µIU/mL (both normal).$ J* p3 U( Z9 I W4 ], f8 @4 W3 ?
The concentrations of serum electrolytes, blood
% O/ R6 ~7 c7 }5 m2 i1 v P* Qurea nitrogen, creatinine, and calcium all were
7 ]* R6 d- y. c2 G8 R# Awithin normal range for his age. The concentration
8 x1 C( I: w" W; s. jof serum 17-hydroxyprogesterone was 16 ng/dL; m- ~" H# k4 r$ \
(normal, 3 to 90 ng/dL), androstenedione was 20
2 y% P3 _4 _% [2 \9 b& [: o& n5 s$ ^ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
3 _5 e. J# S$ xterone was 38 ng/dL (normal, 50 to 760 ng/dL),* n4 ^+ k, V' K3 j
desoxycorticosterone was 4.3 ng/dL (normal, 7 to+ S/ M( X% b& M, P' Q
49ng/dL), 11-desoxycortisol (specific compound S)
; j7 V' L: T7 L ?8 K; ^2 Awas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-- b2 v. A/ l) @/ [9 e
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
" g( E. W; _" `testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
* O! I& n2 T6 }3 W% U+ t3 j8 K; X/ ~and β-human chorionic gonadotropin was less than
3 ^6 C# q/ M, n$ R0 }3 y* n5 mIU/mL (normal <5 mIU/mL). Serum follicular
* B- G! t) }; H4 dstimulating hormone and leuteinizing hormone
1 E/ d/ I0 f( Y& oconcentrations were less than 0.05 mIU/mL
/ y& J0 o( M! c9 e' l(prepubertal).
6 i+ r# z9 T5 Q, _( D: @The parents were notified about the laboratory
1 p# \* X( ?) k5 C9 dresults and were informed that all of the tests were
5 X: g8 L+ q* p: |3 q3 p; Gnormal except the testosterone level was high. The
3 r. y! m+ k# V% |0 l# f: Lfollow-up visit was arranged within a few weeks to
0 \5 b J2 S, f0 E8 `obtain testicular and abdominal sonograms; how-
2 o- q+ C% {7 c- E7 @1 never, the family did not return for 4 months.
7 j" z+ l# i' WPhysical examination at this time revealed that the
3 ~5 ]+ L1 B: K) ?. }child had grown 2.5 cm in 4 months and had gained
+ Q$ ^# R- g/ Q" d _2 kg of weight. Physical examination remained9 n% k- r" h6 ~& V( J3 I
unchanged. Surprisingly, the pubic hair almost com-
! X4 [- J- s2 \7 T) g1 {4 H) Dpletely disappeared except for a few vellous hairs at6 @! y5 V" [4 a3 T) O
the base of the phallus. Testicular volume was still 2
& L& o! K' |: |: M1 pmL, and the size of the penis remained unchanged.
6 U- \9 K) ^* F, @" M [The mother also said that the boy was no longer hav-
/ Y% I3 @0 V, M: ]) E' V8 ^; \ ming frequent erections.
/ ^0 R! s# Q- ?0 w# F$ Y5 oBoth parents were again questioned about use of
0 g" e+ a) W d# S, F* Eany ointment/creams that they may have applied to% t& ]" s4 ^5 T8 B1 v, c
the child’s skin. This time the father admitted the o2 N# y$ {& J) N; [% I# F5 Y
Topical Testosterone Exposure / Bhowmick et al 541
. ?2 k E& K. s. ?" Z& O' U$ E- J6 duse of testosterone gel twice daily that he was apply-
+ w- J% D, m3 E$ g9 u7 Bing over his own shoulders, chest, and back area for
, X- ^' H& c! X/ Q$ u. G! }8 Ra year. The father also revealed he was embarrassed# v3 Y) P' a% |
to disclose that he was using a testosterone gel pre-
+ z, b" Q$ f. n# Z$ m* F2 |: Mscribed by his family physician for decreased libido
5 z1 t; o, B @( ysecondary to depression.
+ @1 M5 Y6 B* u3 O6 Y" kThe child slept in the same bed with parents.' C) ~% @" Y8 c0 J5 Q6 ]( g
The father would hug the baby and hold him on his
' R* _4 \% K2 z1 F/ U4 echest for a considerable period of time, causing sig-
4 Q# Q2 ]& D% ^% Onificant bare skin contact between baby and father.: P) @5 t: u- s9 f/ Y6 |# l# U' Y
The father also admitted that after the phone call,! T( V3 e; H$ V# b; L* }
when he learned the testosterone level in the baby
( d! a1 ]# w0 dwas high, he then read the product information1 Q2 W0 J; H, u
packet and concluded that it was most likely the rea-$ ~6 E; w" w; I9 a
son for the child’s virilization. At that time, they
! u* N7 N* {, }) t$ L gdecided to put the baby in a separate bed, and the
$ l" o* B/ d% ?/ p6 F( F( ifather was not hugging him with bare skin and had
* k! R( k9 x4 dbeen using protective clothing. A repeat testosterone6 d9 U* x5 r/ e( k$ j K
test was ordered, but the family did not go to the
. q7 a6 \$ o" a8 ulaboratory to obtain the test." D$ @! h8 D0 D3 `' b/ m7 l. v
Discussion
$ d2 Q5 V* W5 X, s6 A6 @; M1 ^Precocious puberty in boys is defined as secondary$ Q3 _6 { u. t% H4 z2 p
sexual development before 9 years of age.1,4
2 K9 g8 c. a5 P) i5 p! w" v' [) MPrecocious puberty is termed as central (true) when
. `. c6 {! D% vit is caused by the premature activation of hypo-. @' P1 v9 U( m6 M
thalamic pituitary gonadal axis. CPP is more com-$ k; c' X# T: b
mon in girls than in boys.1,3 Most boys with CPP, [" ?' x6 L" Y$ O' O; Q
may have a central nervous system lesion that is
# H" z/ I6 L% `) r9 Nresponsible for the early activation of the hypothal-# B5 c% H H4 O# r
amic pituitary gonadal axis.1-3 Thus, greater empha-
5 I- T) m3 F p6 }3 ~7 G9 E3 Bsis has been given to neuroradiologic imaging in" `% Z, L- s& ?9 N" P
boys with precocious puberty. In addition to viril-
% `! O- p3 `/ Nization, the clinical hallmark of CPP is the symmet-, o* R$ _4 Z5 n. ]: ?! a
rical testicular growth secondary to stimulation by
C8 K2 M2 j4 b6 t2 {* \: Y# F2 jgonadotropins.1,3
: x7 y! ]' n8 ?$ {! A2 n5 j$ R1 _Gonadotropin-independent peripheral preco-
8 \" w0 [) B, A$ }cious puberty in boys also results from inappropriate: G! H- ~0 m) L, @ w
androgenic stimulation from either endogenous or
* C' O0 ]# K& ]7 O U/ ]2 G) Zexogenous sources, nonpituitary gonadotropin stim-, F% s. ]8 q2 L# a9 I+ j- Q
ulation, and rare activating mutations.3 Virilizing
5 z, k d$ c4 K; x' `congenital adrenal hyperplasia producing excessive
- O7 ^% Z7 X! E; n* ]1 cadrenal androgens is a common cause of precocious
0 m6 P0 g0 @2 ?- L {puberty in boys.3,49 h. ]3 J9 k# F$ A" K2 H, w- F. X F7 |
The most common form of congenital adrenal
, f% R h% B2 J' X. xhyperplasia is the 21-hydroxylase enzyme deficiency." i0 D' A# W- M# [ U! N
The 11-β hydroxylase deficiency may also result in% q1 ~2 T9 H4 y" S8 q$ C& _) ?
excessive adrenal androgen production, and rarely,8 ?* I6 C+ c8 g; l
an adrenal tumor may also cause adrenal androgen
% `! u( [8 U4 v4 W T0 oexcess.1,3
* v8 @1 b. p& P. e0 Qat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
' K* s" r, L( J8 K/ y1 x% U" v542 Clinical Pediatrics / Vol. 46, No. 6, July 2007( @. ^5 ~7 i8 F7 E
A unique entity of male-limited gonadotropin-7 \& [) { D$ C6 P* d/ |1 G
independent precocious puberty, which is also known
# T" s6 o- e3 q( ?& Yas testotoxicosis, may cause precocious puberty at a2 t9 V% _% @8 ?9 A' U
very young age. The physical findings in these boys
2 o6 G; }' m7 Zwith this disorder are full pubertal development, i+ D4 ]0 ?/ ~- ?7 O; S
including bilateral testicular growth, similar to boys$ r; W- f: V, u8 M* J% [: u
with CPP. The gonadotropin levels in this disorder. K! Y# s9 M% i! h& k: N0 s( o4 H
are suppressed to prepubertal levels and do not show9 [* s6 d2 s4 N* S* }: e& _4 L
pubertal response of gonadotropin after gonadotropin- b; V7 S, I5 Y% n0 i2 w
releasing hormone stimulation. This is a sex-linked
/ l. c4 F9 R( i' ?1 N: W% lautosomal dominant disorder that affects only0 q! }8 G1 I7 z* ]5 }$ ]
males; therefore, other male members of the family4 t: ?1 q3 o% d2 M, ?
may have similar precocious puberty.3; ?& H8 Q+ e2 }: x% W
In our patient, physical examination was incon-: L9 O5 h0 l( X/ s `1 P
sistent with true precocious puberty since his testi-" v/ J4 g5 \! @+ G
cles were prepubertal in size. However, testotoxicosis
6 ^. y Y$ c2 mwas in the differential diagnosis because his father
6 U0 V% q3 ^# E4 O. n( s! z8 dstarted puberty somewhat early, and occasionally,
3 E4 Z$ @1 I6 e6 [; g- O' v. ztesticular enlargement is not that evident in the
, g+ J- F5 i& y3 @: E5 g% tbeginning of this process.1 In the absence of a neg-
( h% m- L& S2 i- D$ o% Wative initial history of androgen exposure, our8 B! y5 X( _/ O
biggest concern was virilizing adrenal hyperplasia,. @* ^9 B; t I* Q) K* E/ O; [2 h- x
either 21-hydroxylase deficiency or 11-β hydroxylase
( p P$ Y" T4 d5 ^& g$ ~deficiency. Those diagnoses were excluded by find-+ j1 j! n- ?/ E, P2 ]9 j
ing the normal level of adrenal steroids.- \+ X9 T9 a; L1 m# {
The diagnosis of exogenous androgens was strongly
( r0 P4 y. E: u2 T6 lsuspected in a follow-up visit after 4 months because
* [6 b8 i# a7 Y5 N+ |the physical examination revealed the complete disap-$ y8 c3 ?: |) E' E) T- l% \2 w, `: a6 Z9 E
pearance of pubic hair, normal growth velocity, and6 m+ [8 v* a( F, z2 h$ b" G
decreased erections. The father admitted using a testos-& a& p& o; v, {& L, {8 d
terone gel, which he concealed at first visit. He was; k4 I+ e& P, j- n: @. T8 R
using it rather frequently, twice a day. The Physicians’
2 M; Z2 N! |! e( G9 SDesk Reference, or package insert of this product, gel or# |( z" s, {: k: q% q
cream, cautions about dermal testosterone transfer to
& f% p- Q' J8 \, ?3 x. junprotected females through direct skin exposure.
7 d0 n: {7 m8 G8 I% a9 xSerum testosterone level was found to be 2 times the3 l4 j$ p, k0 H; h6 L( V
baseline value in those females who were exposed to
% C, A2 L* _- `& x0 j0 ?even 15 minutes of direct skin contact with their male
% V& G( q7 V! r) Bpartners.6 However, when a shirt covered the applica-
! s7 @! X. J& @3 I* I) ttion site, this testosterone transfer was prevented.- i) }* k. u4 M( D. Q
Our patient’s testosterone level was 60 ng/mL,* |% p! P7 A. f7 a* k4 d9 L$ h
which was clearly high. Some studies suggest that2 q8 F: t4 ~) X z; n
dermal conversion of testosterone to dihydrotestos-2 m- F: x2 B+ T: I
terone, which is a more potent metabolite, is more
+ r {1 y* x+ o Tactive in young children exposed to testosterone! H3 Y9 D J! y; U
exogenously7; however, we did not measure a dihy-3 x, z! Q* L6 _, Q
drotestosterone level in our patient. In addition to' b3 H9 |1 D# d
virilization, exposure to exogenous testosterone in5 l8 A0 e+ s7 M8 f- P0 G+ a L
children results in an increase in growth velocity and
5 Y% Q7 A1 l1 u# J; x- nadvanced bone age, as seen in our patient.
- d4 X& B6 a3 T% t( HThe long-term effect of androgen exposure during% A: O! _. i8 W9 b/ O2 _
early childhood on pubertal development and final% V! R# b x, r. b9 D' ^$ ~
adult height are not fully known and always remain
5 t- S$ v- b4 ~+ z0 g8 d9 ta concern. Children treated with short-term testos-+ Z" C% C! ] i& g, o' o
terone injection or topical androgen may exhibit some R( X: i8 L, n
acceleration of the skeletal maturation; however, after
0 K5 |4 q- X/ X5 ?" y1 @cessation of treatment, the rate of bone maturation
: c. P7 B7 x6 }, b5 b1 kdecelerates and gradually returns to normal.8,9
$ r- K1 P- w" s4 c5 s8 V1 rThere are conflicting reports and controversy
5 X' }% X+ n+ \! \( gover the effect of early androgen exposure on adult
K# Q/ J7 ~1 u( Epenile length.10,11 Some reports suggest subnormal& U$ w; G( P4 ^# Q# l; F- D# g
adult penile length, apparently because of downreg-# m, V7 j d0 H- h F2 _6 x. `
ulation of androgen receptor number.10,12 However,1 X: l# g% E3 ~ \8 k0 e+ u
Sutherland et al13 did not find a correlation between+ {) N2 v+ r) e h
childhood testosterone exposure and reduced adult
+ o5 y3 f4 Y# Z' a7 q/ }$ _penile length in clinical studies.
, K+ x; S8 T" k* H6 T' zNonetheless, we do not believe our patient is. g R' W' Q) ^5 G& {. o" P" E
going to experience any of the untoward effects from5 D- j- z- D# Y7 N6 w( h
testosterone exposure as mentioned earlier because- ]/ T8 L# n6 P
the exposure was not for a prolonged period of time.2 P# U3 w+ Z+ c! r5 v! y
Although the bone age was advanced at the time of' `6 E$ F, R# m) t! n @
diagnosis, the child had a normal growth velocity at
2 a" h4 i) ~! m( c* k' Qthe follow-up visit. It is hoped that his final adult7 u# k' F* B" S7 b! m
height will not be affected.4 a) b1 D: `0 J+ M4 ?' x: P6 u
Although rarely reported, the widespread avail-: S' r- c6 O! ^& S
ability of androgen products in our society may
3 ?+ k7 s: E9 N" w" g+ Cindeed cause more virilization in male or female
. k9 V4 P6 @4 P- I* r2 S- echildren than one would realize. Exposure to andro-' g, D9 p* m* u5 l& z
gen products must be considered and specific ques-
( {3 B8 f0 W9 u0 e8 M- L- t8 @tioning about the use of a testosterone product or
% O. r$ p0 s8 Q9 s3 w3 y. k5 }6 L2 [gel should be asked of the family members during& [* L+ ~3 s0 W' x+ Y
the evaluation of any children who present with vir-: k$ u; R$ u6 i/ G5 e: V' }4 S9 x( M
ilization or peripheral precocious puberty. The diag-
5 t6 ?+ F- J$ Wnosis can be established by just a few tests and by
7 _3 E/ b. L7 |; P; }, ]* B4 c$ ?appropriate history. The inability to obtain such a4 H3 v7 a; C8 Y& X) m! E" H3 x
history, or failure to ask the specific questions, may
* [; y* g" c* ]5 Yresult in extensive, unnecessary, and expensive
Y @5 f' P( p4 i/ J Finvestigation. The primary care physician should be
* D9 T. e9 E3 |aware of this fact, because most of these children
9 l5 y4 \- o* W3 _/ T# t) H fmay initially present in their practice. The Physicians’
8 h: ]0 @" T: k& j1 n E! ~. wDesk Reference and package insert should also put a
) ~# z, t; A; ^5 a6 Vwarning about the virilizing effect on a male or
, {* Q) h& y% y4 e+ H- i; ]female child who might come in contact with some-! l, F+ ^! g( b- T5 ~( V
one using any of these products.
0 c; \0 M. ?* c8 ~; I: D9 ~/ KReferences4 `3 b+ M0 {' R. l4 G6 a5 l
1. Styne DM. The testes: disorder of sexual differentiation
+ e$ C1 Q3 _- ^2 Q% n+ Y. t( Z4 gand puberty in the male. In: Sperling MA, ed. Pediatric5 e2 Z. X/ \" @( G6 `% Y2 ]" Y& Y
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;! d# b, j$ p$ _4 k8 a' t
2002: 565-628.
. g* L( E0 @5 f, V2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
4 c7 b9 \# G$ N j( ^puberty in children with tumours of the suprasellar pineal |
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