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Sexual Precocity in a 16-Month-Old: i9 R+ b6 ~$ f( ]
Boy Induced by Indirect Topical
9 G2 @5 g' l9 N9 ~( RExposure to Testosterone0 }$ Z( }' l7 X1 {0 G8 ^
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
+ A; \- u1 s( B& m U3 N9 _' o& ^and Kenneth R. Rettig, MD1 i C0 M6 G9 ]+ j! w# |* B1 J
Clinical Pediatrics
2 ]: s _' r, Q" Q/ xVolume 46 Number 61 g. B6 n) \; ]/ O; D8 ~
July 2007 540-543
- ~2 O+ X" G$ s2 b/ r( W7 R; i© 2007 Sage Publications! u) X) q, v% E
10.1177/0009922806296651$ N. o* T- Z* A0 x2 }
http://clp.sagepub.com1 G! k# L2 E$ Y
hosted at" q4 F( \# y9 A5 g
http://online.sagepub.com
6 y7 h4 i. I! ]2 N7 e7 k* ePrecocious puberty in boys, central or peripheral,) o3 s' H; F D) T4 m
is a significant concern for physicians. Central
$ @% u3 T* j: F1 I p0 Aprecocious puberty (CPP), which is mediated8 M9 e, d, T3 W9 M! _" A
through the hypothalamic pituitary gonadal axis, has
8 j: B0 i4 P4 g% G2 G" R' Qa higher incidence of organic central nervous system' p* A6 h7 \/ I
lesions in boys.1,2 Virilization in boys, as manifested& P; M( D1 q3 [& W. `3 f
by enlargement of the penis, development of pubic. X; R9 V' B6 {9 h
hair, and facial acne without enlargement of testi-- T, y) m( @7 X
cles, suggests peripheral or pseudopuberty.1-3 We* S/ a- P: {) D1 O5 @. i7 {7 j
report a 16-month-old boy who presented with the
* Q/ _, A& F2 L6 n) i2 g+ e. Henlargement of the phallus and pubic hair develop-4 m, c3 v7 a: N% |3 s9 E
ment without testicular enlargement, which was due9 G( L7 a5 e% `2 `# a. V% }8 e& |
to the unintentional exposure to androgen gel used by
, \6 |1 |; o U5 ?: m# A' mthe father. The family initially concealed this infor-! a7 G% P3 g4 K+ d
mation, resulting in an extensive work-up for this
7 z" R8 _( q# M" Y3 x' {child. Given the widespread and easy availability of3 \; V" e3 V% u& L% D
testosterone gel and cream, we believe this is proba-0 n, s/ J& Q* r p9 w' k
bly more common than the rare case report in the. w2 Z+ ?: U, _ B! A. z- H
literature.49 E$ J& x2 I1 i. C/ z
Patient Report$ @( R3 B5 ?% h, L! Q
A 16-month-old white child was referred to the
. T8 q' z# C; r; dendocrine clinic by his pediatrician with the concern
$ I# D5 v1 e2 k8 ]( L6 ^of early sexual development. His mother noticed; M" I8 E; c% U& o5 J
light colored pubic hair development when he was
( ^7 z. k3 c* k( \* s6 J) vFrom the 1Division of Pediatric Endocrinology, 2University of
' c* Z9 {/ e' ?& |; [+ nSouth Alabama Medical Center, Mobile, Alabama. r# S' @1 ?. G* K6 s
Address correspondence to: Samar K. Bhowmick, MD, FACE,6 H& g% X1 q* ]
Professor of Pediatrics, University of South Alabama, College of
6 N% x3 d' P5 Z: _Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
Z7 K' k9 ~! e" x. @2 Le-mail: [email protected]./ `1 F! \; N; r3 w+ g
about 6 to 7 months old, which progressively became" @2 A( t, V4 N! U* ~' m5 Q' I: L
darker. She was also concerned about the enlarge-- f0 F! I) D. x2 R+ A
ment of his penis and frequent erections. The child7 t3 J0 [/ X h$ d" C0 l- b. w
was the product of a full-term normal delivery, with# p6 q7 F3 `( j7 H2 b
a birth weight of 7 lb 14 oz, and birth length of7 K1 ~: Y4 x# Z$ ~& y9 S( t
20 inches. He was breast-fed throughout the first year6 ~! M# B" e; m/ _2 y: E/ H" k
of life and was still receiving breast milk along with- _; K3 p9 p5 P4 q; a+ s/ @
solid food. He had no hospitalizations or surgery,
" q$ _- K9 b3 S9 u5 Y. n; I7 Wand his psychosocial and psychomotor development% _: f$ ?3 F1 A" ^
was age appropriate.
5 V% x2 P6 _9 S( u$ g; ?$ u+ A+ UThe family history was remarkable for the father,7 L d! C; c; |' S- r
who was diagnosed with hypothyroidism at age 16,# z7 l8 m. e* Y: U( F, K
which was treated with thyroxine. The father’s
# P' l2 j; l/ C4 _height was 6 feet, and he went through a somewhat$ x& l k' U! v( A
early puberty and had stopped growing by age 14.: i* g; }: q/ d2 C) i( ^
The father denied taking any other medication. The u0 `6 [+ C( ^6 p8 d- r
child’s mother was in good health. Her menarche
- z: h0 j$ ~+ G: gwas at 11 years of age, and her height was at 5 feet
9 Q( q: p+ c6 M, r/ w6 O5 inches. There was no other family history of pre-
( T6 l. O9 [" H" `1 `cocious sexual development in the first-degree rela-" W- Z& G$ @1 {
tives. There were no siblings.% E/ d' A1 C. v/ o* ?* S
Physical Examination N; A- ]# j2 V
The physical examination revealed a very active,/ o$ b+ z) T u% ^5 r1 ?' k$ F
playful, and healthy boy. The vital signs documented4 o/ ~" u' i' y7 {& @) l
a blood pressure of 85/50 mm Hg, his length was
/ s! G9 Z' ~2 d9 m- e- N/ ?5 \# Q; S) D90 cm (>97th percentile), and his weight was 14.4 kg
8 B/ y. @) Z1 v3 O(also >97th percentile). The observed yearly growth; S! `, f1 {, r( @9 r
velocity was 30 cm (12 inches). The examination of
+ B+ M- {8 x! L6 U5 V, ~the neck revealed no thyroid enlargement.! `7 ^( W6 m" s. d6 |1 e
The genitourinary examination was remarkable for
& t+ s6 w* r! x6 x. V) v: renlargement of the penis, with a stretched length of; s" f' ~% J6 Q) i0 [
8 cm and a width of 2 cm. The glans penis was very well
. G! S" U4 k7 o# L8 v/ o0 w- pdeveloped. The pubic hair was Tanner II, mostly around
3 P! Y; ?! G. F540
, r; q% n9 o' J; \" oat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from. k4 b1 `: A; W8 S, P
the base of the phallus and was dark and curled. The5 M7 \$ p: [* m" I7 p3 \
testicular volume was prepubertal at 2 mL each.
& m. n. Y! e* H3 \* d6 hThe skin was moist and smooth and somewhat
- Z; U1 m0 o* w; xoily. No axillary hair was noted. There were no
3 B0 o1 V4 m, s3 z8 O& oabnormal skin pigmentations or café-au-lait spots.
4 x1 B" a3 @* }- S$ n4 |, KNeurologic evaluation showed deep tendon reflex 2+
% ^: {, f6 W, `9 C0 L, Lbilateral and symmetrical. There was no suggestion; ], w6 x$ K, ]% H- R
of papilledema.
: ] B$ S l0 n8 \, l7 {Laboratory Evaluation4 B; L5 S: ^# n* ~% p) V
The bone age was consistent with 28 months by1 d" v0 z4 h' s' ]$ `
using the standard of Greulich and Pyle at a chrono-) h, j4 q9 `0 l M; T# B
logic age of 16 months (advanced).5 Chromosomal
' _% g3 H+ U. R3 s4 ~0 qkaryotype was 46XY. The thyroid function test
) e3 B% ~- `+ w; yshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
4 P, J$ l8 T" e J3 w% {lating hormone level was 1.3 µIU/mL (both normal).
6 X, [1 V+ Y8 IThe concentrations of serum electrolytes, blood
) v, n( u7 e, L) L, Xurea nitrogen, creatinine, and calcium all were
5 I: A8 ~) l3 Q3 V j& o5 ewithin normal range for his age. The concentration
, d6 B5 S4 H. Q; [of serum 17-hydroxyprogesterone was 16 ng/dL4 u4 {) y# r' _# T, n3 i; d
(normal, 3 to 90 ng/dL), androstenedione was 20- n% O& ?& d5 ?& d! b
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
6 z8 b3 ?) |8 b2 ^terone was 38 ng/dL (normal, 50 to 760 ng/dL),, x1 M5 E: q& X) x9 c* ~
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
1 O# Q; n1 U% s8 W- N, ]) y& z( A49ng/dL), 11-desoxycortisol (specific compound S)
% R9 y; T* d! F8 R! u3 c e- f# C9 wwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-, r+ E2 J" c. L$ W( D1 f
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
3 f& b3 v+ Y$ M) |& Itestosterone was 60 ng/dL (normal <3 to 10 ng/dL),8 h) M7 ?; \6 x( y; q ?
and β-human chorionic gonadotropin was less than
* W/ U+ j: p& m- _' i7 ^5 mIU/mL (normal <5 mIU/mL). Serum follicular
! F$ j3 x' M- e8 L( g) cstimulating hormone and leuteinizing hormone+ Q, O1 K1 y8 Q* k( {4 y3 S
concentrations were less than 0.05 mIU/mL
$ M# L5 f. g, Q1 {8 p8 w: Z1 E(prepubertal).9 }, m5 `- I+ c1 Q) t, C
The parents were notified about the laboratory
, s8 N% T; V; Mresults and were informed that all of the tests were
- \* J _! R; w. O+ snormal except the testosterone level was high. The
7 o+ T3 n- F9 P7 K+ ]follow-up visit was arranged within a few weeks to
3 n3 R; z7 x* ?/ ?# L$ wobtain testicular and abdominal sonograms; how-+ E9 ]/ h3 M) Q# c/ R; x
ever, the family did not return for 4 months.8 \+ M' V* O! X5 H# [" e
Physical examination at this time revealed that the
4 p/ u6 g/ P V' G0 {0 X* Z( Pchild had grown 2.5 cm in 4 months and had gained
" ^5 F, {0 w& \0 Y8 K2 kg of weight. Physical examination remained r' ?( m8 w' L7 M, ~: Y K9 }
unchanged. Surprisingly, the pubic hair almost com-' G: h+ C$ |+ z7 B; W2 {! n
pletely disappeared except for a few vellous hairs at
5 M. c3 d& a: w7 Kthe base of the phallus. Testicular volume was still 2
/ @' E' I y" A$ RmL, and the size of the penis remained unchanged.% ]+ L J7 p( G8 ]# R4 J
The mother also said that the boy was no longer hav-) K+ O+ T- y5 ]5 X) C( _4 ^( J" h
ing frequent erections.5 m; |3 A _2 Z" ^: L. A2 S
Both parents were again questioned about use of
% H3 s/ [* Q/ A7 `* { _/ Nany ointment/creams that they may have applied to
% m5 ?7 A5 [7 C8 nthe child’s skin. This time the father admitted the* M- S" H6 s/ f0 Y- ]
Topical Testosterone Exposure / Bhowmick et al 541
8 l1 O: \+ y) E9 uuse of testosterone gel twice daily that he was apply-. D; ]0 O2 |; P* b1 W- J* z3 x
ing over his own shoulders, chest, and back area for
' [2 W/ e% i2 c6 M0 ea year. The father also revealed he was embarrassed
9 C/ q- j" C. P7 \3 Uto disclose that he was using a testosterone gel pre-
9 z6 K1 k2 T$ ^0 s2 u# u6 v1 k* cscribed by his family physician for decreased libido+ [4 @- o2 t7 H7 V
secondary to depression.2 F" D% x' p' A- ^4 G
The child slept in the same bed with parents.9 J6 Q; M: N2 J
The father would hug the baby and hold him on his7 C( _9 Z: @4 j8 A0 O
chest for a considerable period of time, causing sig-) B# `/ K" V* R) e u0 y' S2 j# y" E
nificant bare skin contact between baby and father.! F' n" ~- w2 |( v; |/ J. @/ h; Q
The father also admitted that after the phone call,
: ~. c4 ?" l* N* gwhen he learned the testosterone level in the baby
. o. V. _; x9 ?' H7 I2 |! wwas high, he then read the product information
1 U9 R" D! U% f! ypacket and concluded that it was most likely the rea-+ p& ^% X6 X) }" Q
son for the child’s virilization. At that time, they
- _ I* ]! Y0 y J2 ?9 [decided to put the baby in a separate bed, and the
/ v( ~4 x* n2 w- m1 q* {# ifather was not hugging him with bare skin and had
7 f) Q B$ B# i3 t7 e3 f; G* V( u' abeen using protective clothing. A repeat testosterone
' J K! e" j4 ]! w6 K5 ?& l9 _test was ordered, but the family did not go to the
9 O# ~3 Z7 t: U4 w3 x* C) Plaboratory to obtain the test.
# A. x, w$ ^: L; C7 a, p6 cDiscussion
1 }" w6 q5 W5 \! ] rPrecocious puberty in boys is defined as secondary5 m8 x$ N3 C1 d- {: }' @8 N }
sexual development before 9 years of age.1,42 J$ E, ^3 f" {0 ?8 C1 l3 ^0 d
Precocious puberty is termed as central (true) when
7 y4 i1 t3 K# o2 ~( t$ M: \/ Xit is caused by the premature activation of hypo-
4 l8 r2 K0 p) F! u; B* Y/ othalamic pituitary gonadal axis. CPP is more com-
$ g6 n' V! G' Z, p( Qmon in girls than in boys.1,3 Most boys with CPP
8 X/ d l9 M" tmay have a central nervous system lesion that is" ^* u, I# ]) {: b4 B
responsible for the early activation of the hypothal-# ]* n# h, b0 I [
amic pituitary gonadal axis.1-3 Thus, greater empha-+ E U7 s: E4 b o
sis has been given to neuroradiologic imaging in
5 V$ o9 H2 a2 @$ m0 Y0 m5 H8 @boys with precocious puberty. In addition to viril-
, A0 X) ^* b% I$ q( hization, the clinical hallmark of CPP is the symmet-7 q# }) x/ ` I& p) j
rical testicular growth secondary to stimulation by/ Q% ]. r$ e; o: R- ?0 Y9 b6 x# \
gonadotropins.1,3. R3 {5 q0 D1 `) R% E* }" Z' S
Gonadotropin-independent peripheral preco-
* I! ^' j' x% W) dcious puberty in boys also results from inappropriate; y% n+ ?% ?6 `& i6 z
androgenic stimulation from either endogenous or
9 [ \* z0 B6 v$ y; G1 Z! yexogenous sources, nonpituitary gonadotropin stim-
/ X: n+ a: @) B9 |: t: pulation, and rare activating mutations.3 Virilizing, a4 k5 i9 N% U
congenital adrenal hyperplasia producing excessive5 n4 h V% r, R7 g
adrenal androgens is a common cause of precocious
+ U% g3 [6 f( \* ^: }; j- T5 ppuberty in boys.3,4
: Z# R/ G: J* ?9 P+ SThe most common form of congenital adrenal) {7 {$ E0 C7 D" j+ [
hyperplasia is the 21-hydroxylase enzyme deficiency.
* e/ f. n3 j6 x2 |The 11-β hydroxylase deficiency may also result in; I4 a' b# z- S6 k2 k7 y
excessive adrenal androgen production, and rarely,
0 A: b) ^/ v$ }an adrenal tumor may also cause adrenal androgen& e! {. Q* L# i" t O
excess.1,3" s9 W0 F& ]6 a! G; ` n N0 E- L3 |) l
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from' R$ a; s0 s0 s5 |' t
542 Clinical Pediatrics / Vol. 46, No. 6, July 20073 M4 ^* e2 O/ l4 _; @+ K
A unique entity of male-limited gonadotropin-
8 `7 B$ J$ q- Aindependent precocious puberty, which is also known8 K' d: y U7 c7 f) [, ?
as testotoxicosis, may cause precocious puberty at a
& u: l3 ~" k+ E8 N9 j9 N5 Yvery young age. The physical findings in these boys
% u/ v9 @3 R3 U0 Nwith this disorder are full pubertal development,
' H3 b4 A- W9 s( F6 T! X; r1 gincluding bilateral testicular growth, similar to boys4 G' `$ c1 j5 P
with CPP. The gonadotropin levels in this disorder
6 n0 A7 L; |8 L; Zare suppressed to prepubertal levels and do not show
" W3 X* ]& t; Y- o0 x6 opubertal response of gonadotropin after gonadotropin-
+ d% W# A& _" u% j; ireleasing hormone stimulation. This is a sex-linked; d. Z2 f9 Q2 [ V! N1 e
autosomal dominant disorder that affects only
; J, x$ {) B: t2 }* c9 Kmales; therefore, other male members of the family8 C0 d% }3 R: h8 B$ l
may have similar precocious puberty.3
2 n3 j0 o( t+ f9 E9 c& u& lIn our patient, physical examination was incon-& w+ o3 q) o4 e) i: F Q
sistent with true precocious puberty since his testi-
7 m! V) h( B% U2 q6 L9 p# {% ]cles were prepubertal in size. However, testotoxicosis' i- i/ B+ o0 L7 E
was in the differential diagnosis because his father
" Z$ ?* {) G. ^$ ^; y. r: g7 M: g+ kstarted puberty somewhat early, and occasionally,
* I5 u& s* u$ ~* k, C9 rtesticular enlargement is not that evident in the
1 ]( O, K0 _6 h5 K2 vbeginning of this process.1 In the absence of a neg-
& B% V% ]7 J j9 b+ e& ?ative initial history of androgen exposure, our3 D( h$ F2 g2 q! e5 K9 H0 i! V
biggest concern was virilizing adrenal hyperplasia,
I; [+ z7 m4 L6 P: {+ Geither 21-hydroxylase deficiency or 11-β hydroxylase
- ?# O2 h% K) Z# c% i' j. Ndeficiency. Those diagnoses were excluded by find-; t) r: l% w7 C8 V% ~
ing the normal level of adrenal steroids. v6 z7 i! |4 [4 i
The diagnosis of exogenous androgens was strongly ] q" n- b+ E/ A7 \
suspected in a follow-up visit after 4 months because3 T5 r; u8 B! |' v4 ~0 c: `
the physical examination revealed the complete disap-* {5 N h8 L. X' ~* W
pearance of pubic hair, normal growth velocity, and
: d; f$ p- \, r9 G- k& k, E# _decreased erections. The father admitted using a testos-
; o. f2 D) W+ i0 j: n N$ Oterone gel, which he concealed at first visit. He was
1 d% c' l5 Y7 l% {" ousing it rather frequently, twice a day. The Physicians’9 O- `; a. K$ ?0 b0 l6 O" Z
Desk Reference, or package insert of this product, gel or
: [2 J. x3 p- ]0 X3 ]+ d5 Y3 ?! U) ocream, cautions about dermal testosterone transfer to y: c+ e* q' g5 a, }( W
unprotected females through direct skin exposure.0 ~( E3 O3 F% S- o* v
Serum testosterone level was found to be 2 times the
9 T8 z3 I2 d* ^& Q6 @0 _baseline value in those females who were exposed to9 k d7 N9 y0 Z, W
even 15 minutes of direct skin contact with their male! {& V6 Q0 H, L: [7 `' D" I2 w$ a
partners.6 However, when a shirt covered the applica-
0 J$ [6 @/ r, |tion site, this testosterone transfer was prevented./ I- K1 a. \. |) L
Our patient’s testosterone level was 60 ng/mL,
8 g6 i6 M/ ~+ N2 m3 R1 Wwhich was clearly high. Some studies suggest that
9 w; R$ O# @- _0 W% O, Udermal conversion of testosterone to dihydrotestos-3 c F S }7 G( d- w
terone, which is a more potent metabolite, is more+ E0 j | m; u$ `* ?* _6 m8 A
active in young children exposed to testosterone+ U- G8 K$ d0 t. ]
exogenously7; however, we did not measure a dihy-
5 ^& x9 z# S0 d5 f* u7 ^8 wdrotestosterone level in our patient. In addition to
1 @& Q( P0 `0 Q& yvirilization, exposure to exogenous testosterone in
; e2 }- x/ G3 I7 Z" ^4 ?# Y [ ~2 Gchildren results in an increase in growth velocity and2 h, U" v* z' Q2 R! G$ v
advanced bone age, as seen in our patient.
3 |2 m! G5 M4 z; s9 S9 `8 oThe long-term effect of androgen exposure during
, W" O7 u, U2 W- ~' L, R- kearly childhood on pubertal development and final1 x9 S0 V' O) L; K* [ i: P t
adult height are not fully known and always remain4 z* `1 g7 v1 I: Y8 U. `
a concern. Children treated with short-term testos-
6 q6 `5 m! e9 G" ~terone injection or topical androgen may exhibit some
4 d! v. T, b. V% o6 H7 l1 n; lacceleration of the skeletal maturation; however, after8 R8 |/ a* F6 I/ F! `6 B8 q
cessation of treatment, the rate of bone maturation% O7 E/ u/ G; S9 A
decelerates and gradually returns to normal.8,94 I$ D) @2 Y' R" R% @) k1 g
There are conflicting reports and controversy
, \4 m( \! ~" D$ b3 V' @over the effect of early androgen exposure on adult
: Y2 \( T( F( x% }1 @6 zpenile length.10,11 Some reports suggest subnormal( k# x: n9 M, e. ~$ o
adult penile length, apparently because of downreg-9 i" @2 I0 @2 m$ Y. j- T* L8 q O
ulation of androgen receptor number.10,12 However,& u3 e" V7 u5 ^5 a. y' t
Sutherland et al13 did not find a correlation between
- w4 U( s' `4 C8 q. G9 F' X6 ?childhood testosterone exposure and reduced adult
- ]. q Q- T2 [8 H$ X) \# [: |penile length in clinical studies.
3 {) f7 S8 C2 L& E7 `5 W. h( hNonetheless, we do not believe our patient is
0 h. f5 R/ Y3 f4 T* ygoing to experience any of the untoward effects from
' M# I0 p( U* }) n! Rtestosterone exposure as mentioned earlier because
+ w) m1 g; t7 \3 l1 n9 w4 Athe exposure was not for a prolonged period of time.
4 m/ G# P, L( f9 P8 B: HAlthough the bone age was advanced at the time of# u4 ~+ I; N' i: o" I4 i9 e
diagnosis, the child had a normal growth velocity at
N1 w, R& g( f0 u5 P9 D% l/ Mthe follow-up visit. It is hoped that his final adult
& X. }( d; ~! q) xheight will not be affected.
/ g" Q) H0 X$ _* j k& CAlthough rarely reported, the widespread avail-
; ]5 |6 F& V$ t: rability of androgen products in our society may3 R; }$ i2 b' W, l
indeed cause more virilization in male or female
5 k/ o% {+ l0 w% f! _children than one would realize. Exposure to andro-) o; i3 D$ ^( s0 @! n% d0 ~
gen products must be considered and specific ques-. R. m/ A* B& V
tioning about the use of a testosterone product or
2 D( v0 R. Q" `1 }; P+ m1 Qgel should be asked of the family members during
Q4 P' W9 n2 w! `* O, {' Othe evaluation of any children who present with vir-) x7 n3 w) ~9 k* e# ^+ g
ilization or peripheral precocious puberty. The diag-
; R% W9 e9 Q- n* n* T8 Mnosis can be established by just a few tests and by. o& \+ m8 e0 V% U+ _1 A
appropriate history. The inability to obtain such a9 T8 W9 M) W$ J/ K1 L
history, or failure to ask the specific questions, may" B2 Y7 U8 w, \0 I7 D, L
result in extensive, unnecessary, and expensive7 h8 Q& S r3 r: ?% `
investigation. The primary care physician should be
, o3 ~9 M. ^7 m* Y( O- saware of this fact, because most of these children
6 G$ @% D0 f! \# R6 _ o+ P4 rmay initially present in their practice. The Physicians’
+ a6 s: Y4 ^2 S6 X b6 T- `* n5 KDesk Reference and package insert should also put a# a. g2 W0 C3 O1 W" h6 i, M
warning about the virilizing effect on a male or. I+ V! h- y- s; g/ h" p8 W8 L
female child who might come in contact with some-( F n7 u7 ~* l; i
one using any of these products.
4 e+ b' h! z/ VReferences! ]' j5 U) J" o& ]$ X0 m
1. Styne DM. The testes: disorder of sexual differentiation
9 p7 p9 M E& F7 ]! oand puberty in the male. In: Sperling MA, ed. Pediatric/ p! i; }. N; }5 J; Z3 ~ W4 z
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;9 g5 w( n6 b \6 Q5 U2 v
2002: 565-628.
; @* r' o7 J9 z' I2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
+ Z9 ]5 g- F" }' z4 r2 \& tpuberty in children with tumours of the suprasellar pineal |
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