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Sexual Precocity in a 16-Month-Old
" F; w4 G1 Z; T; x7 WBoy Induced by Indirect Topical
9 H" {5 h, E9 a7 ^' d+ zExposure to Testosterone
: _4 v! {% a6 `2 b# XSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
; M7 N4 N( I: c1 A) ^and Kenneth R. Rettig, MD1
2 h& ?* y( e' K' n" iClinical Pediatrics( M, g) z6 o" u# v/ y4 p
Volume 46 Number 6, E& N, h: B$ c2 V8 R( }3 K
July 2007 540-543
0 h. C4 O, J! c6 v0 X© 2007 Sage Publications
5 T- Y" K; c, I4 Q10.1177/0009922806296651: c3 a, Y! o# F/ X1 u \$ Z
http://clp.sagepub.com
2 T' |7 Y; ]7 O+ U" Q1 G3 E7 ^7 Hhosted at
) V" @7 ?3 x0 H# j: Ohttp://online.sagepub.com: u1 M3 Q. r2 f
Precocious puberty in boys, central or peripheral,/ `/ Y& B( j1 Z
is a significant concern for physicians. Central# }, C; o' t. d1 v' S! x% ]
precocious puberty (CPP), which is mediated" B& z0 V$ e! x+ e/ `
through the hypothalamic pituitary gonadal axis, has
: |+ ^4 I4 ]' f) d" M/ r Ta higher incidence of organic central nervous system& Y8 p- n7 v3 E) B! i
lesions in boys.1,2 Virilization in boys, as manifested/ }, x* U( T& g5 a
by enlargement of the penis, development of pubic. Q8 q8 Z. K' Q K
hair, and facial acne without enlargement of testi-
0 |! r8 ~1 M( x F+ @cles, suggests peripheral or pseudopuberty.1-3 We
+ I2 m: ]" j2 O" O' W& I. b! ureport a 16-month-old boy who presented with the
4 `8 E2 _0 M6 b8 o& C8 }enlargement of the phallus and pubic hair develop-1 c n. C" Z- a6 P- h# A1 _" ]
ment without testicular enlargement, which was due
d9 E% H3 T- B$ u( {to the unintentional exposure to androgen gel used by
) j7 U7 Y3 N, `3 G3 J) kthe father. The family initially concealed this infor-: k. Q- s4 ^5 s3 b8 @: X( [1 S
mation, resulting in an extensive work-up for this
! ~# b( `, J- Vchild. Given the widespread and easy availability of' l( C1 e) N9 W" G* l1 V2 k
testosterone gel and cream, we believe this is proba-
* s6 c- i8 Y# p2 X% k: q4 {* N0 fbly more common than the rare case report in the
. z0 `% Z9 U$ m5 v( \% x& l! Rliterature.4' R b' h: B) g* R! ^' o0 ~
Patient Report) _, t' M E' O/ z, P: M4 s/ ~
A 16-month-old white child was referred to the
9 v* `+ g" V; L* @, ]4 W. }endocrine clinic by his pediatrician with the concern( \2 u& S5 X% \3 A
of early sexual development. His mother noticed1 D$ M# f/ U. _, \$ [
light colored pubic hair development when he was) X, T$ ~0 m9 o# e0 u
From the 1Division of Pediatric Endocrinology, 2University of2 K9 b/ T! {; x" [1 b- R9 l- r
South Alabama Medical Center, Mobile, Alabama.! _8 H) g- c: S! a% ^! G) H: H0 s
Address correspondence to: Samar K. Bhowmick, MD, FACE,
# L; X- {# w [+ [9 n( cProfessor of Pediatrics, University of South Alabama, College of
+ i& L. w/ s* ^+ q v# eMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
- a- ]! B0 m+ |. Y6 P7 ve-mail: [email protected].! ]5 s) ^" {: H0 V
about 6 to 7 months old, which progressively became, _/ v& u( U4 S" R6 D4 C
darker. She was also concerned about the enlarge-3 q4 y! R( L9 c6 H, L& r; e
ment of his penis and frequent erections. The child
. M* I( C: m/ w, |: {& L$ z4 b$ P6 Nwas the product of a full-term normal delivery, with
7 X9 Q5 h: f; _8 Ja birth weight of 7 lb 14 oz, and birth length of+ d1 \, e, R+ }9 _
20 inches. He was breast-fed throughout the first year
7 K: q; T6 ?3 h3 a; L2 P+ Zof life and was still receiving breast milk along with( y1 u ?% v# n) N
solid food. He had no hospitalizations or surgery,: ^: U3 g- r* }9 u* ^+ j; g
and his psychosocial and psychomotor development/ k; z5 ?7 L8 _( ^
was age appropriate.9 W% z' C2 e: K; c" n, S
The family history was remarkable for the father,5 o5 c5 L5 {: _/ H4 J: h9 z
who was diagnosed with hypothyroidism at age 16,
5 t% z0 x' L* a) zwhich was treated with thyroxine. The father’s
F5 B) t7 A/ Bheight was 6 feet, and he went through a somewhat4 c# a( J( x3 x! P$ y2 ~0 H
early puberty and had stopped growing by age 14.0 z7 D# x j/ N0 N$ r
The father denied taking any other medication. The
( I4 y6 ~* z w- N; q! t: kchild’s mother was in good health. Her menarche
/ [+ W/ O' B5 h2 {- i4 swas at 11 years of age, and her height was at 5 feet
6 M; H2 E6 b/ W& I$ e5 n$ u5 inches. There was no other family history of pre-3 B4 K! g# ]* `- K. K1 }+ ^. G
cocious sexual development in the first-degree rela-. N5 J) i0 r" v8 Z: s3 _; P
tives. There were no siblings.% K8 Q- k- X+ T1 p6 P, ]
Physical Examination
* W1 Z1 l, a7 g' C5 V% F7 H) hThe physical examination revealed a very active,5 l( b+ G( B7 n5 F+ G- ~3 h5 P
playful, and healthy boy. The vital signs documented
$ o# B: E, d4 Z4 v* b4 ba blood pressure of 85/50 mm Hg, his length was, S& `* E# g6 A* ?) D- Y5 o
90 cm (>97th percentile), and his weight was 14.4 kg* \- I( y( |5 M5 Q! o! I R
(also >97th percentile). The observed yearly growth8 S9 C8 \. t0 _9 o* \3 {6 \0 z" c
velocity was 30 cm (12 inches). The examination of. w% ]$ N5 ^2 T5 y2 m8 I& J$ x
the neck revealed no thyroid enlargement.
# @7 _0 |) |" @The genitourinary examination was remarkable for
2 A, M* g( K8 |# G# _! Cenlargement of the penis, with a stretched length of
5 L0 T7 P& e3 w# Q8 _7 K8 cm and a width of 2 cm. The glans penis was very well. s4 t, Y. h/ ~9 p/ l2 N8 v
developed. The pubic hair was Tanner II, mostly around% E8 F& p3 Y8 I
540
6 h! k& d3 \3 v, U9 a ^- cat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
9 I2 t# ]3 g! q; g& Zthe base of the phallus and was dark and curled. The
. q# A1 I# Y: V! u8 itesticular volume was prepubertal at 2 mL each.
( [, C. ?: |9 a8 J# o3 g" J) hThe skin was moist and smooth and somewhat9 f8 K0 A8 h) @% U t
oily. No axillary hair was noted. There were no
0 M$ g7 D$ d1 m8 j( R- Fabnormal skin pigmentations or café-au-lait spots.
% l0 |2 J* ^: z& O: B4 ^Neurologic evaluation showed deep tendon reflex 2+$ \, d# W+ O" \8 G0 ^3 g: ^: A3 `
bilateral and symmetrical. There was no suggestion1 H, G# F9 C$ N7 ~
of papilledema.
U0 }6 c' N2 q; i% f8 yLaboratory Evaluation; V1 e1 v5 O; s N p0 g
The bone age was consistent with 28 months by
) y/ e. e" g# M6 S, a5 ] H4 Kusing the standard of Greulich and Pyle at a chrono-2 }& X& R" ]5 G- Q" s3 y' s
logic age of 16 months (advanced).5 Chromosomal/ ]4 r4 r$ t6 J, A" w. P
karyotype was 46XY. The thyroid function test) W `; v+ n0 k3 C; R d( S
showed a free T4 of 1.69 ng/dL, and thyroid stimu-, s M2 U+ L W& Y: v* m+ D
lating hormone level was 1.3 µIU/mL (both normal).$ {1 |' Q, V' e: |/ g# u! A
The concentrations of serum electrolytes, blood
6 e. S& o1 z% A! Xurea nitrogen, creatinine, and calcium all were
3 T6 K R5 `0 F% l; owithin normal range for his age. The concentration1 e5 J* {" I" } @- r5 {& C8 ]" G: Y7 e
of serum 17-hydroxyprogesterone was 16 ng/dL7 S: _* `! Q8 } K, D
(normal, 3 to 90 ng/dL), androstenedione was 20
+ L6 m1 B* }/ M- |9 yng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-- e4 @8 `. m$ i7 M9 ~; o
terone was 38 ng/dL (normal, 50 to 760 ng/dL),* D# C$ i/ s/ O" ?& k
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
6 ]4 g: Y# J6 [$ w; P/ B/ e% Z0 ~49ng/dL), 11-desoxycortisol (specific compound S)9 i( h0 q$ f( ]* e2 `. b" o9 A) T* x
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-* e' y8 U$ o5 X) X4 y' v
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total& J# r/ ~) c& k, a4 X1 z3 `
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),/ O# s0 |6 Y4 @$ l
and β-human chorionic gonadotropin was less than p' T/ M( v0 F: t! M
5 mIU/mL (normal <5 mIU/mL). Serum follicular
& g( s9 J' B& l+ n+ ostimulating hormone and leuteinizing hormone
/ k" P8 a6 g3 i0 F2 Bconcentrations were less than 0.05 mIU/mL% x# N1 b5 q* L6 p, D7 }
(prepubertal).
2 p& X# s2 K) GThe parents were notified about the laboratory
) c5 y3 A! q2 A/ xresults and were informed that all of the tests were7 }8 k) m1 `- @7 ^
normal except the testosterone level was high. The8 |8 x0 w1 m4 f+ D1 D; o
follow-up visit was arranged within a few weeks to4 R) S, a5 n. N' b. o: D6 t# H
obtain testicular and abdominal sonograms; how-
( y$ S }5 M/ n% T/ c) iever, the family did not return for 4 months.( Z- S+ E& ~1 ?; }, m7 x( K$ f
Physical examination at this time revealed that the
/ t8 j |7 B" t) S. A" {2 F/ d+ ?child had grown 2.5 cm in 4 months and had gained8 t X* w9 t2 Z
2 kg of weight. Physical examination remained0 @- J3 }$ B, A
unchanged. Surprisingly, the pubic hair almost com-
- A! i- N7 g, Z) S, R. T% \pletely disappeared except for a few vellous hairs at
1 N+ O8 S* V; |0 d' }8 n. N; `4 {/ bthe base of the phallus. Testicular volume was still 2! e4 q; N2 j) W
mL, and the size of the penis remained unchanged.1 o3 x, I$ p( f8 C A
The mother also said that the boy was no longer hav-
$ X/ X4 u, m/ W8 S5 g, K# {ing frequent erections.! {8 O- X2 Y% h A: b
Both parents were again questioned about use of0 ^# B9 H! f7 x0 ]% x& l) S& ]/ C
any ointment/creams that they may have applied to
1 z0 K( c* V3 f0 \the child’s skin. This time the father admitted the* N- K! {& l1 d- d' E: X' t0 y
Topical Testosterone Exposure / Bhowmick et al 541
5 Q p4 t5 F9 Kuse of testosterone gel twice daily that he was apply-! o0 X1 ]1 o4 Q/ m; e
ing over his own shoulders, chest, and back area for
1 _- n+ g/ ?" H1 o5 X4 w Q- \) Ua year. The father also revealed he was embarrassed) T, [; ^: p& Z! G
to disclose that he was using a testosterone gel pre-
( Q" j& R; F- ~: H& Cscribed by his family physician for decreased libido) P% c1 h0 E! J* s+ U6 u; F0 o
secondary to depression.
. _, p4 x+ i3 Q- P% R# uThe child slept in the same bed with parents.. B9 B2 _+ {. c
The father would hug the baby and hold him on his
& g: X) n+ q( T, r" |chest for a considerable period of time, causing sig-
' S. N1 x0 ], N: x! Anificant bare skin contact between baby and father.
n) u( g& S# ]. J$ [The father also admitted that after the phone call,
- i: Z' [+ Z6 l( l- I% x1 }when he learned the testosterone level in the baby; O6 W. @- ~+ H, M3 q5 _: ~- K6 T% v2 W
was high, he then read the product information6 l) i% {4 j) F4 u1 e4 [) B
packet and concluded that it was most likely the rea-/ }9 f8 D/ O* [4 `
son for the child’s virilization. At that time, they) O7 |7 g3 c% Q# e; e) B
decided to put the baby in a separate bed, and the8 y7 N; B0 _1 N3 k6 `
father was not hugging him with bare skin and had+ p2 t& H3 k* s( _+ A' C
been using protective clothing. A repeat testosterone
6 c- K* |2 ]; W: I6 r! jtest was ordered, but the family did not go to the+ B8 F# U' Y9 k
laboratory to obtain the test.) }/ `. w8 `+ p- E; A; K
Discussion
1 p9 B: ?: D: E3 iPrecocious puberty in boys is defined as secondary& d0 k! N7 h& c+ |+ s$ v
sexual development before 9 years of age.1,42 y3 h/ T( W; T& j" N, |
Precocious puberty is termed as central (true) when
) O$ R9 s+ R9 g/ iit is caused by the premature activation of hypo-
5 Q# ~; j1 v+ B8 `# a; n4 C4 M. ~- othalamic pituitary gonadal axis. CPP is more com-
* V: e: Y4 U: F3 amon in girls than in boys.1,3 Most boys with CPP
q+ @, E; ?: f; J" h+ ]may have a central nervous system lesion that is: x7 ?6 B6 D6 @4 P* O8 d6 w) N
responsible for the early activation of the hypothal-$ H- C4 {' j# j4 V, Q
amic pituitary gonadal axis.1-3 Thus, greater empha-
0 r& n5 s& k! K5 `sis has been given to neuroradiologic imaging in3 Z9 S' R5 A/ c' I9 X4 I8 a. G g
boys with precocious puberty. In addition to viril-
3 F D$ [ x, l; ]ization, the clinical hallmark of CPP is the symmet-
& f" ]5 S! S$ q3 J% |7 Xrical testicular growth secondary to stimulation by: o( B. W! ~3 }9 I Z- K; z
gonadotropins.1,3
- i$ m$ A$ ^6 |% c) ^$ ?& X- gGonadotropin-independent peripheral preco-
/ K% @4 M: j w, k: |8 bcious puberty in boys also results from inappropriate3 h$ i( W; z2 v$ ~" w
androgenic stimulation from either endogenous or
3 C: V1 {' x* n+ t- r, Gexogenous sources, nonpituitary gonadotropin stim-
e+ k( Z5 h& F nulation, and rare activating mutations.3 Virilizing, q* B& J/ q. x3 D& `( f
congenital adrenal hyperplasia producing excessive1 f4 }. @0 ]8 S( _$ J4 N( `) A
adrenal androgens is a common cause of precocious- m! B* ^9 I$ ]+ S0 c; {5 }
puberty in boys.3,4
3 L9 V: g7 @$ G _8 ?9 n+ tThe most common form of congenital adrenal$ u5 k1 c; Y& ^, Z
hyperplasia is the 21-hydroxylase enzyme deficiency.+ P+ o/ y1 u- u+ ?7 Z
The 11-β hydroxylase deficiency may also result in( t9 B, k2 N& {" R4 K6 V3 B
excessive adrenal androgen production, and rarely,
4 b- i) q- n n0 u. O7 o5 X4 Man adrenal tumor may also cause adrenal androgen* w5 e" d6 a- U8 F% E
excess.1,3; F5 w5 z) x; C; [0 K3 f. S
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from. g% j* e; |9 w- C' d0 K
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007. j( T% ]- S4 k6 |, d; V
A unique entity of male-limited gonadotropin-$ V! x0 h! e, j9 J
independent precocious puberty, which is also known
# ^5 I- g8 ]5 J1 \0 Q4 G1 ?: U2 ras testotoxicosis, may cause precocious puberty at a3 U% v1 `! i s& g, j* D% g
very young age. The physical findings in these boys
9 u& _3 U' c# _with this disorder are full pubertal development,
/ u$ ^ R- m/ u& a( J% K/ u! b7 v; Lincluding bilateral testicular growth, similar to boys! ~9 |1 i, {% C, }6 n2 g
with CPP. The gonadotropin levels in this disorder
2 P9 m9 u5 N% d" C n# E6 ~7 k+ tare suppressed to prepubertal levels and do not show
- I1 x, O& V; m0 U8 ~pubertal response of gonadotropin after gonadotropin-
1 H. B- }+ q+ ]; I% Areleasing hormone stimulation. This is a sex-linked0 F) l x1 u; i% D, K% x* u
autosomal dominant disorder that affects only2 }0 t4 `$ h4 L8 ]1 t
males; therefore, other male members of the family
8 N: U- o$ v. n9 W% P% @! Umay have similar precocious puberty.3
% {, m+ V7 l& R& E0 ?2 bIn our patient, physical examination was incon-
* t/ d) O4 }/ x; g; Ssistent with true precocious puberty since his testi-2 Y0 ]* t( Q' F& ]0 U$ B! r
cles were prepubertal in size. However, testotoxicosis- ~, G5 T0 P1 W9 b$ p+ B- W+ {
was in the differential diagnosis because his father
3 |* j" Y' v# e; W7 Tstarted puberty somewhat early, and occasionally,1 R& G, O" Q4 ^8 m4 [4 _* ]- F: E
testicular enlargement is not that evident in the
5 \2 W/ x- p2 gbeginning of this process.1 In the absence of a neg-
8 v' O' M1 c* E4 O5 U o2 T( ^& O; Rative initial history of androgen exposure, our- S9 J7 V a0 n k! M. k0 {7 y
biggest concern was virilizing adrenal hyperplasia,' M% e% f( t9 [! ^2 C
either 21-hydroxylase deficiency or 11-β hydroxylase
5 U# [% q) Q0 B! O. C7 jdeficiency. Those diagnoses were excluded by find-2 ` d: E! g$ I/ E' j) X+ c
ing the normal level of adrenal steroids.; r8 w' S8 y: e0 I y7 n; q0 Y
The diagnosis of exogenous androgens was strongly1 |; m4 {- I4 p0 v' }1 @
suspected in a follow-up visit after 4 months because% R3 g' [0 C2 A; O6 O5 {
the physical examination revealed the complete disap-/ y6 X" o- s8 \
pearance of pubic hair, normal growth velocity, and3 m( l6 ]( [$ L. C" \, J
decreased erections. The father admitted using a testos-
4 z# k) |5 R; D, ^" C7 V) `0 D# Dterone gel, which he concealed at first visit. He was' M* q/ L9 e4 h! c% S
using it rather frequently, twice a day. The Physicians’9 \, B' _# q) e' m3 K
Desk Reference, or package insert of this product, gel or* @. E6 P1 o7 v8 c, s
cream, cautions about dermal testosterone transfer to7 p% W) P8 N9 @8 i- c
unprotected females through direct skin exposure.
; D$ z1 G* O/ @Serum testosterone level was found to be 2 times the
: s/ d# b& D+ z8 L- Pbaseline value in those females who were exposed to
& H9 l: N6 Q: i5 [' ^even 15 minutes of direct skin contact with their male+ L; V) b7 b( @
partners.6 However, when a shirt covered the applica-% ~7 j0 Z3 \1 D( }
tion site, this testosterone transfer was prevented.5 U- V" x) V+ N8 j3 T
Our patient’s testosterone level was 60 ng/mL,
: Q+ u5 ~) o; ^5 Ewhich was clearly high. Some studies suggest that! o1 O: c2 X1 L/ a
dermal conversion of testosterone to dihydrotestos-$ [5 k+ c* k) @1 T. \) X, E
terone, which is a more potent metabolite, is more( G: u5 }% c: z# f" c$ t. V
active in young children exposed to testosterone
/ G l2 \# Y9 d; h9 U2 h* S3 ~exogenously7; however, we did not measure a dihy-
4 y2 A" X- i5 i2 y% Jdrotestosterone level in our patient. In addition to% }' m8 ~8 Y5 c( l1 E2 z* S$ F
virilization, exposure to exogenous testosterone in
; T$ |9 o4 ~$ Z5 M+ e. ?children results in an increase in growth velocity and9 u _1 x0 M; V) }& o1 [
advanced bone age, as seen in our patient.5 P! c) ]# v- F& R+ P0 M4 [
The long-term effect of androgen exposure during; \0 Q# X/ f+ X0 l5 H
early childhood on pubertal development and final! V/ l! O$ n! J4 m& i
adult height are not fully known and always remain
5 T$ e% N3 R: {& }% Va concern. Children treated with short-term testos-
+ [& n# h% ^8 [/ h( Kterone injection or topical androgen may exhibit some. k7 S7 a/ E% g4 c5 D$ D+ M1 k
acceleration of the skeletal maturation; however, after% m+ D4 ]( J$ ~# e1 q: I6 [8 o
cessation of treatment, the rate of bone maturation
" M% l% }0 [- p( g. K |decelerates and gradually returns to normal.8,9
, T4 c* @ Z/ q8 E4 KThere are conflicting reports and controversy+ X" z! j/ N7 y- H- G, s+ g. i7 t
over the effect of early androgen exposure on adult. V( b( l9 I d3 {- [0 x y% v6 s4 Z
penile length.10,11 Some reports suggest subnormal
- A) _0 _9 h9 \' R# |adult penile length, apparently because of downreg-) h% h7 g B# S( U; [( |
ulation of androgen receptor number.10,12 However,
8 F8 U9 k: }9 T+ PSutherland et al13 did not find a correlation between% ]) Y+ r G0 l' Y
childhood testosterone exposure and reduced adult' g" f# `, O5 Z& q3 A5 T4 U! b
penile length in clinical studies., ~& O/ _9 _. ]* b- r: L
Nonetheless, we do not believe our patient is+ d# M. `1 S7 R0 R
going to experience any of the untoward effects from
9 i$ z7 T. {$ |+ P1 {testosterone exposure as mentioned earlier because) U, `1 R5 s6 V
the exposure was not for a prolonged period of time." g7 w& ]& }7 k }+ }% ?% X/ L( Z
Although the bone age was advanced at the time of8 Z9 j; r( D3 W h; s; c- p7 w
diagnosis, the child had a normal growth velocity at9 ]; Y6 c' { @+ r( S) b6 Y
the follow-up visit. It is hoped that his final adult5 e7 b. F) k+ J' J* M$ Z& G9 X
height will not be affected.9 L0 ]: R0 D9 V$ ~% _6 V# Y+ k
Although rarely reported, the widespread avail-0 |# D4 O% n; Z( t+ t% d
ability of androgen products in our society may& W* W7 g; V# w
indeed cause more virilization in male or female8 H3 ^* s1 d5 b. K
children than one would realize. Exposure to andro-' w( f5 K% t! z3 Y
gen products must be considered and specific ques-
J! n$ j7 s% Itioning about the use of a testosterone product or
, { h# N8 F) Hgel should be asked of the family members during% g, ~# T; c( y1 B/ p8 A
the evaluation of any children who present with vir-
8 k( z. W! |- J/ j9 m( E0 z/ Jilization or peripheral precocious puberty. The diag-
: ^- T/ ^7 v+ E* ?nosis can be established by just a few tests and by
- [% e3 n6 C* N' Fappropriate history. The inability to obtain such a
+ F8 ?" h0 r" C) ?5 [3 r: ^history, or failure to ask the specific questions, may
- E4 g0 }" G/ @) f3 L# Presult in extensive, unnecessary, and expensive
" Y: J) E+ ?' m( Tinvestigation. The primary care physician should be
- m1 x: q# j2 u/ taware of this fact, because most of these children
+ M% f: T2 [, rmay initially present in their practice. The Physicians’
@" g0 M+ v! v8 a& h. U* mDesk Reference and package insert should also put a
& f3 ]% ?$ m/ |# E& T3 ]6 z, e$ Uwarning about the virilizing effect on a male or" O' t& L! P' E
female child who might come in contact with some-
- }& P \% T( rone using any of these products.0 a" h5 _: ]; Z) D$ \/ ?
References5 c- M5 f+ i5 o
1. Styne DM. The testes: disorder of sexual differentiation' R( v2 b8 k0 P6 |" D
and puberty in the male. In: Sperling MA, ed. Pediatric
) F- ] q: K# t6 ~$ y5 ]$ \/ TEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;% S% [! m1 V- ]
2002: 565-628.
& ?) ~: d q! X% |2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious0 |) V1 B7 h, t: c: i$ x* n. E
puberty in children with tumours of the suprasellar pineal |
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