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Sexual Precocity in a 16-Month-Old5 B% e# Q) v, y
Boy Induced by Indirect Topical6 s" a8 _3 @( O4 o; J
Exposure to Testosterone
" I+ U+ x; ` Z, d, x. Z4 d+ [# p. mSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,29 N" k& y5 }- N# M! n
and Kenneth R. Rettig, MD1
$ @; M# I; H5 j% p6 RClinical Pediatrics0 `, a9 Y* p4 T% }
Volume 46 Number 6# Z7 ^. h5 O& Y
July 2007 540-5431 Z+ J/ x5 G4 r/ u. o' O% V
© 2007 Sage Publications
; T9 @, s8 t4 ~1 R/ u+ g# ]* r* v10.1177/0009922806296651$ f6 b- l; b- z4 Z
http://clp.sagepub.com4 n. q9 |3 k' i2 Q* T+ F2 R
hosted at/ Z( i! }" a8 {3 `
http://online.sagepub.com
4 f, _9 h# H1 I* y: a7 m$ m. ZPrecocious puberty in boys, central or peripheral,5 c; A, y* B: @6 W
is a significant concern for physicians. Central2 j* [5 C! Z5 D. o6 @1 Q9 B+ O
precocious puberty (CPP), which is mediated6 W# _1 W Q) J7 S# w* L3 g( m6 g! K$ `
through the hypothalamic pituitary gonadal axis, has
+ V# m5 \$ j% W9 X2 v* |# ?a higher incidence of organic central nervous system
% d% S: P3 c: u: _+ ulesions in boys.1,2 Virilization in boys, as manifested
8 s" E. n: G' U4 e2 r3 }1 vby enlargement of the penis, development of pubic
# N3 L6 R3 X! t+ p J) R+ ?3 shair, and facial acne without enlargement of testi-+ o1 e8 k6 L1 s. l3 g7 S
cles, suggests peripheral or pseudopuberty.1-3 We
/ T, t! r1 D) i+ z: u& V5 preport a 16-month-old boy who presented with the
, i! X3 j% n* u4 }enlargement of the phallus and pubic hair develop-
, F+ \2 h* ]/ z5 F0 {ment without testicular enlargement, which was due% }& W* {% f x! q- C+ C+ U
to the unintentional exposure to androgen gel used by
- K# y1 N6 k( D0 U% i" z+ `# P/ e3 gthe father. The family initially concealed this infor-* V$ I- w' M D, W8 X( M
mation, resulting in an extensive work-up for this
% n; g9 a9 C O8 l b8 V8 gchild. Given the widespread and easy availability of% R/ u4 a7 @% l6 |/ s9 H& B
testosterone gel and cream, we believe this is proba-
6 \/ f6 F( C7 nbly more common than the rare case report in the
% ?6 S& o# W; a5 T2 f( r6 Nliterature.4' i4 n: c$ E7 |& C
Patient Report
' J& x* _& p$ A3 ~2 @* c R) eA 16-month-old white child was referred to the% G5 W9 U" @. Z T% h! r- N- i
endocrine clinic by his pediatrician with the concern- R/ q5 e9 |5 p3 M& N" ?4 c& B# }4 E+ w
of early sexual development. His mother noticed' j: O+ A$ \0 C# E8 P# E# d+ \
light colored pubic hair development when he was* x. J- [! Y4 w6 j+ @
From the 1Division of Pediatric Endocrinology, 2University of
! k8 ]" B4 Q2 s; u- LSouth Alabama Medical Center, Mobile, Alabama.% F! o! y6 H& t5 H; N5 q2 x' j
Address correspondence to: Samar K. Bhowmick, MD, FACE,
$ {8 {1 g/ L+ \3 f4 jProfessor of Pediatrics, University of South Alabama, College of. y Y+ C. B* n! m* h' V4 n
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;9 ?) Z! X3 P a
e-mail: [email protected].9 _" t% H V0 F5 g$ F$ \
about 6 to 7 months old, which progressively became
$ T! `$ y. M5 ?- M! \darker. She was also concerned about the enlarge-
/ f4 B" e) k; \7 pment of his penis and frequent erections. The child2 w4 q9 h3 F# v, B1 {" G4 Z
was the product of a full-term normal delivery, with/ ~; W! K* z3 W# m" f9 y
a birth weight of 7 lb 14 oz, and birth length of. B$ Z3 w8 p) z; j
20 inches. He was breast-fed throughout the first year
: ]5 v7 [ o7 H7 q2 wof life and was still receiving breast milk along with; K* v8 p$ A _) \) [! `7 i& w5 X
solid food. He had no hospitalizations or surgery,
8 e* N. z1 o# U6 Q, G. C( i' g$ A& ~and his psychosocial and psychomotor development9 _. e& |( M- Y: C# h
was age appropriate.3 g0 u; L) \# z9 w
The family history was remarkable for the father,& e5 m( q, R& ^( l$ s' `( ~# I- P
who was diagnosed with hypothyroidism at age 16,
5 D" k- p) ~0 a! G- Dwhich was treated with thyroxine. The father’s& W) [) e v0 @- r' s
height was 6 feet, and he went through a somewhat
. O% o( b# z e. F, G. Aearly puberty and had stopped growing by age 14.
6 V8 Q+ v7 q# E8 x4 \6 r! XThe father denied taking any other medication. The) }# Z( @ p F9 ]/ T: x% e$ a0 d
child’s mother was in good health. Her menarche
% w( |4 M; C. w- swas at 11 years of age, and her height was at 5 feet
1 C% r- `) P2 h# j8 j5 inches. There was no other family history of pre-6 z2 S0 t$ s2 W0 L0 w- W
cocious sexual development in the first-degree rela-9 A7 @ z. ~2 }* `" e: |, |
tives. There were no siblings.
+ a* ?! e# ~: {& z# Z6 |0 oPhysical Examination3 C7 J% E5 l' T3 q) M- ^
The physical examination revealed a very active,
6 J7 W% q( S2 J' }playful, and healthy boy. The vital signs documented; ~$ A! N0 \% B0 S* |. M/ G
a blood pressure of 85/50 mm Hg, his length was
# X" Q" J. z' X( J5 w# n s90 cm (>97th percentile), and his weight was 14.4 kg
+ e: }5 \0 h3 p/ u(also >97th percentile). The observed yearly growth
7 s' p. \% Z) v6 k9 fvelocity was 30 cm (12 inches). The examination of
[# x- Z! m, b, V- i, [the neck revealed no thyroid enlargement.
) h5 B& o; g4 T8 y* a j+ oThe genitourinary examination was remarkable for4 m) R( w; V% G7 \8 Q/ U
enlargement of the penis, with a stretched length of- Z0 p% z6 a8 @8 V4 W4 l
8 cm and a width of 2 cm. The glans penis was very well5 g; i1 Z4 X! Z! L7 y$ s3 C; |
developed. The pubic hair was Tanner II, mostly around
3 K& Z" y+ W9 @540% D+ s# T( U& D' p+ ? D
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from. D/ S* l, L! @. R# Z. h% z2 E
the base of the phallus and was dark and curled. The7 o3 v+ Z L+ Z3 a3 Z0 c t2 v
testicular volume was prepubertal at 2 mL each. B5 a. H3 J7 P; h9 n- N7 c
The skin was moist and smooth and somewhat
: Q/ z, T, q5 c9 C, E# y7 Boily. No axillary hair was noted. There were no6 a* m# R- x4 M
abnormal skin pigmentations or café-au-lait spots.
7 ^' U* y6 H% ?$ W" V- cNeurologic evaluation showed deep tendon reflex 2+
8 P1 u. P3 D$ b$ `0 i/ Rbilateral and symmetrical. There was no suggestion
& \: ~2 ]7 K( S+ r6 }9 Zof papilledema.1 k; ^7 i! F3 l
Laboratory Evaluation
6 d7 u. Z+ n4 S d+ D/ [9 {) S/ oThe bone age was consistent with 28 months by6 e" S) q& M K* R& P+ }' _
using the standard of Greulich and Pyle at a chrono-
" M9 R% P Q% K7 ~& slogic age of 16 months (advanced).5 Chromosomal# b6 x% H+ G& N$ J4 T
karyotype was 46XY. The thyroid function test0 t" d6 u/ w. h( i3 g f# _8 j
showed a free T4 of 1.69 ng/dL, and thyroid stimu-8 b# [$ i* E6 k `0 ]" p6 E. u! [
lating hormone level was 1.3 µIU/mL (both normal).4 I! o Q0 O( \: w" [" {. {' a7 O4 c
The concentrations of serum electrolytes, blood9 B! k' w7 \. ?2 R
urea nitrogen, creatinine, and calcium all were+ F% i4 g1 _1 b2 F; `6 Z! L
within normal range for his age. The concentration
4 s+ \" m$ z |5 u: cof serum 17-hydroxyprogesterone was 16 ng/dL
) D# Z5 f* u" P. s% w% t(normal, 3 to 90 ng/dL), androstenedione was 20 v1 X& C: e4 O
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
) G, j+ m) W+ e& nterone was 38 ng/dL (normal, 50 to 760 ng/dL),8 Q. A* F- h, `" Z2 @3 e7 Q
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
( M7 w0 F+ U/ c: G f49ng/dL), 11-desoxycortisol (specific compound S)# w6 h4 K! Q3 M
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-* e, y l2 [3 u: [3 c
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
; c& I M0 d1 q- B h& K# T$ d* W1 u+ Ptestosterone was 60 ng/dL (normal <3 to 10 ng/dL), D5 E% H+ q9 ~8 O
and β-human chorionic gonadotropin was less than' }: R7 O. m$ G9 f) G' [5 @: _8 |1 j
5 mIU/mL (normal <5 mIU/mL). Serum follicular% n: J i) R: l; A
stimulating hormone and leuteinizing hormone( f7 n/ s" P6 M# u" a2 Z* N
concentrations were less than 0.05 mIU/mL
, l1 M3 K/ W7 l3 z(prepubertal).8 c: [/ p5 k1 p) m3 ^
The parents were notified about the laboratory
, L8 J% _# A* n7 ]2 Y/ ^+ T8 \results and were informed that all of the tests were) i% U7 J* ^- A; A( l
normal except the testosterone level was high. The/ R4 i( Z$ [+ H) I7 P4 Z5 \3 ?
follow-up visit was arranged within a few weeks to2 H7 k+ s; y- f: C; R9 d0 F: u0 P \
obtain testicular and abdominal sonograms; how-
2 e& L! `1 b& n" q( M% Iever, the family did not return for 4 months.: K, g0 O* [& @. T" c0 \9 P! D
Physical examination at this time revealed that the6 C- {4 q( Z* W" ?3 g& X' [
child had grown 2.5 cm in 4 months and had gained) ~- Z9 H: C Z, k2 y# P* B! Z' J% j8 d
2 kg of weight. Physical examination remained
8 x, s% O$ \5 i9 p5 Lunchanged. Surprisingly, the pubic hair almost com-
! N) u/ ^* E( q4 ~3 u% ypletely disappeared except for a few vellous hairs at5 B3 e$ f% J% m* }9 m, F! h7 m
the base of the phallus. Testicular volume was still 2" ~4 C( O2 G; t; J9 w h) z: {6 T
mL, and the size of the penis remained unchanged.7 u8 }$ E, B' F& c! V o. q
The mother also said that the boy was no longer hav-
1 v# e. Z0 o/ r) v: K! wing frequent erections., x& P; v$ I7 c- {+ [# X
Both parents were again questioned about use of
3 E3 D# E& @8 ~any ointment/creams that they may have applied to9 C- N7 B0 e+ G& H1 { N4 `
the child’s skin. This time the father admitted the2 U/ D; H* _0 Q( i( o7 A
Topical Testosterone Exposure / Bhowmick et al 541
, R5 x( {( a0 G/ w# }8 wuse of testosterone gel twice daily that he was apply-
( Z7 U: h9 Q$ _; ~ing over his own shoulders, chest, and back area for& |3 c+ u0 U; Z6 i& O' x2 }, T1 b
a year. The father also revealed he was embarrassed
4 U1 e/ l( h3 Pto disclose that he was using a testosterone gel pre-
c; Z) g9 ?4 dscribed by his family physician for decreased libido
& d1 c: `3 u, W8 o' z% P$ j4 gsecondary to depression.
( r' a" X1 h, a4 HThe child slept in the same bed with parents.# G' l/ |. t9 H* ^$ ?
The father would hug the baby and hold him on his1 i% W0 k! Y- u- p; P7 z5 g4 J! Z
chest for a considerable period of time, causing sig-
3 _* O5 t9 f6 h; dnificant bare skin contact between baby and father.) _( t; P2 X) J) H. r+ s; d
The father also admitted that after the phone call,
* m( i9 X; @2 awhen he learned the testosterone level in the baby
' @7 I- T( o' E: v3 Z* W2 ewas high, he then read the product information* H Z, K! U2 s) E" w- {% k5 U7 O( _1 B
packet and concluded that it was most likely the rea-$ a) \2 N( C0 N; n8 U3 _
son for the child’s virilization. At that time, they
7 O# o* s1 M( q5 ldecided to put the baby in a separate bed, and the
9 W. j1 o! r; e. J! lfather was not hugging him with bare skin and had) s8 {, Q# N! m9 C) q
been using protective clothing. A repeat testosterone
0 x2 Z" Y" j7 K0 N) ]# e" K& Xtest was ordered, but the family did not go to the4 ?9 D1 {. \: t3 F3 u: t& b+ _
laboratory to obtain the test./ k0 ~3 H' W- M) _
Discussion3 n0 z8 ?- }* U, n. D
Precocious puberty in boys is defined as secondary6 N+ d8 D9 S" r0 f2 K
sexual development before 9 years of age.1,4
G6 T; L6 m+ d# HPrecocious puberty is termed as central (true) when
' V, `% z2 b5 {it is caused by the premature activation of hypo-
2 x, h3 L% R0 J2 W/ Lthalamic pituitary gonadal axis. CPP is more com-: j- O2 i7 M) j2 U# B
mon in girls than in boys.1,3 Most boys with CPP
/ ~$ F$ L' E2 | P: s+ R& h) rmay have a central nervous system lesion that is5 S8 ^0 B" ^( D K
responsible for the early activation of the hypothal-6 T6 K) u* F4 P8 E# J4 s: z
amic pituitary gonadal axis.1-3 Thus, greater empha-
) c: O. t; x; O- I4 Hsis has been given to neuroradiologic imaging in
5 [9 n- Z4 }+ p* m, W, R" ]boys with precocious puberty. In addition to viril-
4 N" v7 k9 n0 w) {% _" Y! I j! D4 Z, C9 nization, the clinical hallmark of CPP is the symmet-; ]. Y' w( `- P$ m& [
rical testicular growth secondary to stimulation by% k7 ^1 q8 m" z! H% b/ V+ {
gonadotropins.1,3
4 u& X0 M5 k I) sGonadotropin-independent peripheral preco-& |7 x6 ?) u$ ]" o
cious puberty in boys also results from inappropriate
+ g+ O( ^' g/ }% d( ]4 G2 E$ uandrogenic stimulation from either endogenous or) M' L6 n9 Y4 Q! V% R! E5 {, Q
exogenous sources, nonpituitary gonadotropin stim-+ K$ Z: J U/ k! g
ulation, and rare activating mutations.3 Virilizing5 d# O' a0 j3 T
congenital adrenal hyperplasia producing excessive
* t+ |+ L9 L* H7 t1 L# J% {4 ]( oadrenal androgens is a common cause of precocious
+ q7 \4 }. Q8 d0 v$ }- \puberty in boys.3,4
, f) |% C1 f* J+ x3 V* dThe most common form of congenital adrenal
2 z/ M: w* r1 x7 Zhyperplasia is the 21-hydroxylase enzyme deficiency.+ t) a, a& v7 D$ u4 z
The 11-β hydroxylase deficiency may also result in
4 n# E8 D0 ]* l! t: zexcessive adrenal androgen production, and rarely,/ y; e, m) Z7 j; h* Q3 T
an adrenal tumor may also cause adrenal androgen% A7 R* @5 J/ @8 R8 V- ?+ { L0 |
excess.1,3
$ m+ d; R8 @; Kat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
& `; Z0 r _4 A9 K. C9 ]542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
" Z C) n, Y1 R; w, }A unique entity of male-limited gonadotropin-6 \& Y: h5 X/ m/ g |
independent precocious puberty, which is also known" l5 E3 s# @7 v3 Q6 h6 e8 r# o) U
as testotoxicosis, may cause precocious puberty at a4 ]% i, q8 R" a6 D% ]4 L
very young age. The physical findings in these boys
, J6 c6 p: M3 j5 E8 Z& swith this disorder are full pubertal development,( k+ V7 H1 A$ q- F( n
including bilateral testicular growth, similar to boys! x) J( C9 ~8 D2 S+ k
with CPP. The gonadotropin levels in this disorder) g& V: K) h7 ?3 ]6 o, w; L7 U p+ }7 D
are suppressed to prepubertal levels and do not show
5 \2 Z1 x. l* m3 z* M9 O# kpubertal response of gonadotropin after gonadotropin-% X2 h/ c. k+ }/ N8 T( ~0 r* `
releasing hormone stimulation. This is a sex-linked* q0 n7 c+ z' r7 X( j: m0 Y9 a
autosomal dominant disorder that affects only
$ o; R$ ~; e* F) v0 vmales; therefore, other male members of the family4 P% j( l- N7 ]8 [3 p$ _' L
may have similar precocious puberty.3
) W9 n, k' r( }# e1 qIn our patient, physical examination was incon-
& Z4 ~% X1 z- K, U8 }* Isistent with true precocious puberty since his testi-+ e9 k& ]& G& ^- L# t
cles were prepubertal in size. However, testotoxicosis) d) ]* u5 j9 ~" C( m& ?
was in the differential diagnosis because his father
1 H, E$ u# e6 t, D8 a1 d. R" Pstarted puberty somewhat early, and occasionally,) g5 `% s8 E) U
testicular enlargement is not that evident in the
0 ^& U% b; x' `: v/ Qbeginning of this process.1 In the absence of a neg-
) d6 j! ~" V$ M' Z. c( M8 s4 k" Mative initial history of androgen exposure, our. i5 ~* o0 z8 ^* D( Z5 q6 @( P# z
biggest concern was virilizing adrenal hyperplasia,( Y6 X/ I* v* k+ _
either 21-hydroxylase deficiency or 11-β hydroxylase
4 ]8 j# |; F& u0 t1 R+ sdeficiency. Those diagnoses were excluded by find-
) B B0 \ U) ]ing the normal level of adrenal steroids. T6 D( D7 z) B5 r+ }
The diagnosis of exogenous androgens was strongly+ O! D/ u- u/ A }
suspected in a follow-up visit after 4 months because
' ?- n6 q' Z# q" v$ qthe physical examination revealed the complete disap-' m0 ~" W3 |9 x, p1 x2 k7 d2 `6 z
pearance of pubic hair, normal growth velocity, and
6 r- t! X! e E/ Odecreased erections. The father admitted using a testos-
g) g: ]! P6 |# jterone gel, which he concealed at first visit. He was/ i% w; y0 m6 E+ v3 J' X$ A
using it rather frequently, twice a day. The Physicians’
N" i4 o, {) a) t+ Q- tDesk Reference, or package insert of this product, gel or" j& y4 X3 e# U9 v
cream, cautions about dermal testosterone transfer to
- h% l& m$ \5 q: ?unprotected females through direct skin exposure.# L- F) r" d2 G$ X) B. L
Serum testosterone level was found to be 2 times the# e1 U1 U& Q* y' t# v& P. S9 k
baseline value in those females who were exposed to
; ?2 M2 { E2 s% { [, v- o9 U. l" Eeven 15 minutes of direct skin contact with their male2 A: R$ W, ]( T
partners.6 However, when a shirt covered the applica-6 @' X8 o& U' Q/ L4 y/ N
tion site, this testosterone transfer was prevented.- G: a4 |. s. N3 o0 F
Our patient’s testosterone level was 60 ng/mL,
9 k8 t3 j3 |! q$ S m, ]which was clearly high. Some studies suggest that. s) `8 a8 f( R) Q
dermal conversion of testosterone to dihydrotestos-2 S' b6 t+ C6 O' G# ~
terone, which is a more potent metabolite, is more
8 R& S% H: A" dactive in young children exposed to testosterone
2 b* u. @5 e2 eexogenously7; however, we did not measure a dihy-' ~8 Q4 |5 ~% @0 \1 n: E% _9 [* c
drotestosterone level in our patient. In addition to1 q+ O; [5 E: a7 o$ V9 I7 O
virilization, exposure to exogenous testosterone in9 G# ^$ M+ {% S
children results in an increase in growth velocity and# Z1 H; u/ E, u$ t' |
advanced bone age, as seen in our patient.
1 j. B, S7 N9 V( NThe long-term effect of androgen exposure during& j/ r0 k4 x6 H, b! R4 ~
early childhood on pubertal development and final. h- C+ p$ H9 F5 V8 _/ b# `
adult height are not fully known and always remain% _: W) }3 c9 I, _+ E1 c
a concern. Children treated with short-term testos-
" X' W6 b% z9 m5 m0 S+ Fterone injection or topical androgen may exhibit some
( W( v) @$ \ g- }4 m6 tacceleration of the skeletal maturation; however, after7 _6 C) H b+ ~3 I0 h2 W! z- O# u, Z
cessation of treatment, the rate of bone maturation L/ H1 T+ h9 `% ^
decelerates and gradually returns to normal.8,9
- \( P: {! M, x. ^4 b5 j3 t3 q' \There are conflicting reports and controversy o: t+ F. E* p; N1 J/ X7 @4 i
over the effect of early androgen exposure on adult
( w6 H$ a0 r4 d) x5 ?# U; upenile length.10,11 Some reports suggest subnormal6 \9 k( h# Z) f4 P3 a
adult penile length, apparently because of downreg-/ [% x9 p% _% p) P# ~
ulation of androgen receptor number.10,12 However,) D! P$ X( C) n
Sutherland et al13 did not find a correlation between
- }9 q7 F) a; e' m. Dchildhood testosterone exposure and reduced adult
% u1 Y2 Z4 P" @: E$ n0 }penile length in clinical studies.
! v2 A3 p, b3 K: cNonetheless, we do not believe our patient is. a8 [3 y0 r3 h' H
going to experience any of the untoward effects from3 ?( j/ _( m+ g
testosterone exposure as mentioned earlier because( }, A- J$ c* F8 k, t4 T
the exposure was not for a prolonged period of time.+ n7 T" L- [1 {' M
Although the bone age was advanced at the time of' A y A% V$ a3 ~2 R4 J. F
diagnosis, the child had a normal growth velocity at
6 B0 J8 M8 F1 N% g! Jthe follow-up visit. It is hoped that his final adult
+ z2 T* U9 _' C& j' q7 m" B4 Aheight will not be affected.
+ L$ Q( I+ Z2 `' Z2 \% e+ D+ NAlthough rarely reported, the widespread avail-
2 T6 m! J1 t K) N8 w. hability of androgen products in our society may
6 ?' d2 o. @6 Z# c; g8 K# lindeed cause more virilization in male or female* U0 {8 {0 G$ y# k
children than one would realize. Exposure to andro-# S! _( ^* D9 }: Y+ o, R7 S7 W
gen products must be considered and specific ques-, {0 r6 I9 M/ c0 k( g0 k5 ?
tioning about the use of a testosterone product or4 R9 i" M; b% i5 f* e
gel should be asked of the family members during
- c6 @# e5 J. j0 U& r Y9 Q# cthe evaluation of any children who present with vir-
6 c0 t2 {4 N6 z% M, F. N: ?ilization or peripheral precocious puberty. The diag-9 I4 v( J+ x6 y% D% ?% _
nosis can be established by just a few tests and by5 U1 I# L$ A+ w/ F) v% v- O# ]
appropriate history. The inability to obtain such a; ?2 N X/ E# F2 B% O- U/ z7 i
history, or failure to ask the specific questions, may
2 B/ q9 W A7 ?. }result in extensive, unnecessary, and expensive. ]" O& X" P D3 h
investigation. The primary care physician should be
) {: r; t" g; o; R6 N0 c. @aware of this fact, because most of these children
4 i* I3 U- f# O$ ~ y' smay initially present in their practice. The Physicians’
0 _7 V( F K% }3 H2 n& ~1 LDesk Reference and package insert should also put a' y3 i( C7 b @0 C
warning about the virilizing effect on a male or9 s, M4 ?/ y; v# c
female child who might come in contact with some-
8 ?9 n- ]' i7 C; ?2 `2 uone using any of these products.) o! Q! D* D8 E2 ~* ^
References
6 K* Z- m5 V/ ~) J0 v1. Styne DM. The testes: disorder of sexual differentiation
" |. q0 Q8 {5 u* V/ ]; pand puberty in the male. In: Sperling MA, ed. Pediatric: D/ T& S/ G0 Y- E, \/ O
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
5 F% b4 F4 X: G2002: 565-628.3 k) V" L$ d0 ?, F$ p% N1 e
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
/ j" j- B2 d7 a# _2 Ipuberty in children with tumours of the suprasellar pineal |
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