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Sexual Precocity in a 16-Month-Old" g" l. c7 W# Z7 Z- d$ `( }
Boy Induced by Indirect Topical A' y( ~) o* i! @$ Z+ O6 d2 Z
Exposure to Testosterone
0 F5 G" N. V2 a2 v+ O5 V, KSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
5 p+ u2 i, b0 p( sand Kenneth R. Rettig, MD1- z9 J& E3 u' ?$ J6 N5 X0 k0 j
Clinical Pediatrics
; G+ ~ Z6 |% RVolume 46 Number 6
+ T9 D; o( F* s' W1 AJuly 2007 540-543
; f9 n3 n* q% X K© 2007 Sage Publications
6 O$ Q( k7 {( T: e S% \10.1177/0009922806296651
" L5 I/ I7 b0 N2 F. hhttp://clp.sagepub.com
- I' G$ _0 f% chosted at
$ Y7 b, {( B9 d; g6 R2 `: |3 Q3 Nhttp://online.sagepub.com# i5 w' o( ]% C, k0 p6 v4 K* v/ a
Precocious puberty in boys, central or peripheral,
! G) ~; T H( {- i% Y+ P9 eis a significant concern for physicians. Central( m- r0 F4 ~# p' e/ l Y
precocious puberty (CPP), which is mediated W2 h0 R4 R9 W( ]/ W; t
through the hypothalamic pituitary gonadal axis, has
/ k/ P+ r' E9 a! I* j Ha higher incidence of organic central nervous system
: S; Q9 A, z7 blesions in boys.1,2 Virilization in boys, as manifested
, O2 g: Z1 K. N _5 `by enlargement of the penis, development of pubic
- e, }# o% j8 S* y% `6 @. d2 Phair, and facial acne without enlargement of testi- ?; e' U0 J# U9 v8 d
cles, suggests peripheral or pseudopuberty.1-3 We, Y6 K$ U# g0 g+ I4 X
report a 16-month-old boy who presented with the
2 y0 T+ p0 i' N; Z5 eenlargement of the phallus and pubic hair develop-
4 Z; o X q$ G7 k3 S, g/ wment without testicular enlargement, which was due
( g$ o* R% x& ~' j% zto the unintentional exposure to androgen gel used by
0 x4 W; x, p; z# J1 U, ] {9 Z2 Vthe father. The family initially concealed this infor-
0 [0 j/ [1 _' ?( z0 Y) lmation, resulting in an extensive work-up for this
: t2 g4 n; w! Z& [$ e! u( n* Lchild. Given the widespread and easy availability of
/ p7 a/ K( K& ?testosterone gel and cream, we believe this is proba-- e$ h+ g6 }8 F# f( U
bly more common than the rare case report in the: C' e$ r( ]' l' m' y, X$ i
literature.4* K4 g0 {$ H: {) s" _
Patient Report0 S. T& r: ?1 O9 o7 z) b( @' ?
A 16-month-old white child was referred to the
" e, g1 L" @2 S/ { Q: gendocrine clinic by his pediatrician with the concern
8 S8 ?; {' {5 _0 q2 wof early sexual development. His mother noticed
* `4 B) ]( }7 L+ K. dlight colored pubic hair development when he was
' g# v# Z- I5 O X( X: SFrom the 1Division of Pediatric Endocrinology, 2University of8 y: x, V# |. o6 t
South Alabama Medical Center, Mobile, Alabama.
& @3 k1 j; q" }& |Address correspondence to: Samar K. Bhowmick, MD, FACE,
) }7 _) \' s+ t: F, BProfessor of Pediatrics, University of South Alabama, College of1 l' S9 ?5 v& a* v+ u. ^! z
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
# M- Z) s0 |* ]+ xe-mail: [email protected].
: g: W8 M( B3 O- o) X! ], eabout 6 to 7 months old, which progressively became, ]/ z/ g4 ^" e
darker. She was also concerned about the enlarge-
& n* [1 A% n, q4 r: J6 x! Gment of his penis and frequent erections. The child
1 y0 \, w4 B4 s& lwas the product of a full-term normal delivery, with g1 z. F2 P- F' W4 |) X6 D9 _
a birth weight of 7 lb 14 oz, and birth length of2 d& c$ c% t- ]* l
20 inches. He was breast-fed throughout the first year
" U- S1 ~* C1 [. C8 v& `of life and was still receiving breast milk along with
* W7 l0 O- y" ^3 s$ s F3 _7 Usolid food. He had no hospitalizations or surgery,5 q3 a( j4 U" y
and his psychosocial and psychomotor development
0 k: N9 l6 X! @$ Wwas age appropriate.
6 N, L- o# Q* B; M2 EThe family history was remarkable for the father,
/ O+ k( Q7 Z/ P5 F! O) d4 \6 ~/ Ywho was diagnosed with hypothyroidism at age 16, l1 }" j7 k1 A6 r# i, R: V
which was treated with thyroxine. The father’s; Q- F+ Y, B" ?9 o% @2 ~
height was 6 feet, and he went through a somewhat, }+ Y0 K* y2 W7 E/ `3 U7 a u
early puberty and had stopped growing by age 14.' [, i2 ~% z3 k, B* U# F& X
The father denied taking any other medication. The
+ G, s! i4 I5 V) G& achild’s mother was in good health. Her menarche+ T+ z( \, |/ `$ Y* ~0 G
was at 11 years of age, and her height was at 5 feet
7 A5 B" z: M% ~5 inches. There was no other family history of pre-6 m% i# z8 {5 j$ h. p! i; m
cocious sexual development in the first-degree rela-
' e+ e, t; c; t( `, i- x7 I0 E. {tives. There were no siblings.
2 y( B1 P9 B0 sPhysical Examination: ^; u7 {( q: f) @* ]* L
The physical examination revealed a very active,
" S7 j2 z; S% s' rplayful, and healthy boy. The vital signs documented
2 ?1 D4 c7 O' a8 Y) {/ \ b! ta blood pressure of 85/50 mm Hg, his length was/ J; G$ |0 @1 w
90 cm (>97th percentile), and his weight was 14.4 kg
+ r: `5 C+ N' S; |( M$ D# W/ u(also >97th percentile). The observed yearly growth! }! Q G4 H- L
velocity was 30 cm (12 inches). The examination of
+ h3 Y& ~+ ~, m' c0 v) v$ n, Gthe neck revealed no thyroid enlargement.1 R$ R0 I9 e# `4 p% m
The genitourinary examination was remarkable for
8 d5 K" P4 k0 [; K6 E6 Y6 Q. Fenlargement of the penis, with a stretched length of
( V2 ]! ^& x1 A& ?8 U, l8 cm and a width of 2 cm. The glans penis was very well
6 F4 Q# S# y, E$ E4 Z: qdeveloped. The pubic hair was Tanner II, mostly around
( L- e# X9 B6 L. T. ^5405 I0 p/ D) u% p, k- Q/ h/ {- O* H
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from; Z' A0 V l1 O3 b8 ~
the base of the phallus and was dark and curled. The d/ R: a7 `* `5 J2 k3 S
testicular volume was prepubertal at 2 mL each.- J* ^" P3 y9 |, |: x! A" G
The skin was moist and smooth and somewhat
x) `( q4 S% O0 w& Coily. No axillary hair was noted. There were no, s. B6 g1 g# y/ T$ W" Q0 g
abnormal skin pigmentations or café-au-lait spots.
( V; ?( ^/ V: O- p& Y) P# iNeurologic evaluation showed deep tendon reflex 2+$ M/ m) I9 M* |; g V
bilateral and symmetrical. There was no suggestion
' x2 g9 A9 O Rof papilledema.
+ N9 z6 S. {7 l; Z; iLaboratory Evaluation8 s1 @' _! y) a
The bone age was consistent with 28 months by
$ b. U) `1 F& ~" L/ vusing the standard of Greulich and Pyle at a chrono-
5 n" A+ D7 \& o% X! ~1 t' t' k" k# wlogic age of 16 months (advanced).5 Chromosomal6 c& `% p9 K" R6 R6 U$ a
karyotype was 46XY. The thyroid function test
" |1 \" r1 `$ F6 r% F6 p$ Rshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
9 V4 Q( Z ?% j% J# }( v0 B0 clating hormone level was 1.3 µIU/mL (both normal).
" f* e4 P i `; B" R* _7 k3 R5 LThe concentrations of serum electrolytes, blood
! q1 p% l& u0 Z7 ~- k5 \& ?- jurea nitrogen, creatinine, and calcium all were
0 q7 N' Y& V9 \- D" L) W) iwithin normal range for his age. The concentration. ^. o" T7 t! e3 N6 p1 {4 u0 H( Z
of serum 17-hydroxyprogesterone was 16 ng/dL# {1 w h) }/ L; I& K! Q
(normal, 3 to 90 ng/dL), androstenedione was 20
% A) f0 l9 \, C$ p1 V3 l& Hng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-5 e4 a. q! |4 U4 X4 T; a
terone was 38 ng/dL (normal, 50 to 760 ng/dL)," J+ ]7 k4 [( W4 j9 K( I" t
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
: Z N4 F, k* L8 h) y/ b6 L49ng/dL), 11-desoxycortisol (specific compound S)
- Y2 e b f. D" lwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
2 t( Q: U8 F: p0 R& \tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
n) c( W: Q" J$ k. X6 b' j; jtestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
& N5 d: |8 y4 @# n! Y5 G c# kand β-human chorionic gonadotropin was less than
+ G7 O: ?' r: b0 ^, T9 n2 ^+ k5 mIU/mL (normal <5 mIU/mL). Serum follicular" K* l3 y" X4 ?
stimulating hormone and leuteinizing hormone
& L+ h" u1 m7 {* ]& q1 nconcentrations were less than 0.05 mIU/mL7 Q# }) S. ^. @7 k4 s- N+ c
(prepubertal). p7 {: Z! Q$ d) v5 P$ P
The parents were notified about the laboratory1 S0 `1 S4 ?9 D
results and were informed that all of the tests were
m' Q; ?' l' k( |& l' N+ U; _+ gnormal except the testosterone level was high. The
" c" d- {( u6 ifollow-up visit was arranged within a few weeks to
; \+ f% T4 z5 D8 uobtain testicular and abdominal sonograms; how-( H6 ^8 |4 M3 S- z0 P
ever, the family did not return for 4 months.
4 B% Z6 K j7 Q4 \: _) r1 nPhysical examination at this time revealed that the- m; K. X9 D& W% M! D
child had grown 2.5 cm in 4 months and had gained. I( t+ G- O" h8 J0 y& C: B
2 kg of weight. Physical examination remained
6 p0 z! w& m3 e; w Munchanged. Surprisingly, the pubic hair almost com-
) ^; D! H4 M0 Bpletely disappeared except for a few vellous hairs at9 O X1 @2 f7 K Z+ v2 v
the base of the phallus. Testicular volume was still 2
3 O7 k4 o+ [- y2 D# N' n5 w/ BmL, and the size of the penis remained unchanged.
$ v1 a; T0 L; _6 _0 Q8 Y' JThe mother also said that the boy was no longer hav-3 c& ^6 H7 Q' q0 e. ~
ing frequent erections.5 G5 |( C/ p# O& \
Both parents were again questioned about use of
* o J; d, e. Oany ointment/creams that they may have applied to
2 j5 x# @9 i* Y$ N; xthe child’s skin. This time the father admitted the- r% a X2 f" \. K
Topical Testosterone Exposure / Bhowmick et al 541
3 W! v" J5 ]3 `4 H8 u4 P- ^use of testosterone gel twice daily that he was apply-
- D0 _1 @: V/ F6 I" H# G& @. Oing over his own shoulders, chest, and back area for8 Q' q6 g. |) R6 g6 ?# n
a year. The father also revealed he was embarrassed
) z9 g- E6 W0 s8 c) xto disclose that he was using a testosterone gel pre-
* i; R2 w: F B3 C9 a! I: h, Y! g. kscribed by his family physician for decreased libido
* n2 d x& ` {% x) f4 Isecondary to depression.
) p. z- H6 i1 YThe child slept in the same bed with parents.
; i& R! {- Z. \8 X. n9 mThe father would hug the baby and hold him on his
# G% [4 \8 j5 h; \+ `chest for a considerable period of time, causing sig-6 p& I! ]. B5 E2 I' k& x8 c0 p6 f- k/ v
nificant bare skin contact between baby and father.
/ ~9 ^! b* G" y. x" T6 Y. H5 iThe father also admitted that after the phone call,# A/ o- z) j' Z3 D
when he learned the testosterone level in the baby
2 _5 j, n* A" n- c4 k4 R0 g, Zwas high, he then read the product information
% `* m2 Z) N/ b5 g) {packet and concluded that it was most likely the rea-( |5 j% ~9 s9 g! o2 h
son for the child’s virilization. At that time, they
( Y! q* ?7 V+ Z* V2 kdecided to put the baby in a separate bed, and the
0 R9 N C' n3 I; h) Y! n+ O% Cfather was not hugging him with bare skin and had4 t2 ~ f, ^/ S- t0 d
been using protective clothing. A repeat testosterone
- w; Q1 R, h( `test was ordered, but the family did not go to the
1 k5 Z5 ?; |% z3 C: K& Ulaboratory to obtain the test.
1 |2 r8 Z5 B+ O4 p' W: FDiscussion% f! |; X& D! |! q0 k8 N' W9 F
Precocious puberty in boys is defined as secondary8 S/ T3 { r9 z" r3 l' M& l9 J4 K
sexual development before 9 years of age.1,4. p. B8 F# H) O0 X, `. x. K4 \
Precocious puberty is termed as central (true) when
* g" b7 U& h' ], y' P( ?it is caused by the premature activation of hypo-
6 O# _ P( l* c3 }thalamic pituitary gonadal axis. CPP is more com-& h/ ?: e2 l- x1 K9 b' n4 Z
mon in girls than in boys.1,3 Most boys with CPP
, G* i, g- m+ u/ k6 I% pmay have a central nervous system lesion that is1 B7 |( _2 D% D( X: \5 W6 G/ |
responsible for the early activation of the hypothal-$ { H& @7 B* Z! E- J
amic pituitary gonadal axis.1-3 Thus, greater empha-. S8 z/ h0 g; g8 q$ D0 k- v
sis has been given to neuroradiologic imaging in
2 \& ?( K* p! D$ M8 A s) O) F/ oboys with precocious puberty. In addition to viril-8 n0 t9 b! r% E* @
ization, the clinical hallmark of CPP is the symmet-! p1 r' [; _" G+ s
rical testicular growth secondary to stimulation by( x# `+ c |+ a) M
gonadotropins.1,3/ N3 _( y1 \' [/ ?& J, v& D7 n
Gonadotropin-independent peripheral preco-" L* ?: T+ J2 f7 N S4 R Q
cious puberty in boys also results from inappropriate2 h. u1 z- q, S3 r6 F
androgenic stimulation from either endogenous or
8 g- L7 W5 E( v1 K! h2 iexogenous sources, nonpituitary gonadotropin stim-
- u9 |, @8 O1 F; T n9 vulation, and rare activating mutations.3 Virilizing
" a8 ~, D9 a, Dcongenital adrenal hyperplasia producing excessive
- Q! @& T6 K d ], e2 Oadrenal androgens is a common cause of precocious
. M$ K) `) @. u9 v( B8 A& c5 j9 {# Dpuberty in boys.3,4
' Z: I0 {2 r7 U4 ]9 B+ j# BThe most common form of congenital adrenal! A, u- C! h0 D6 y& P' t k
hyperplasia is the 21-hydroxylase enzyme deficiency.3 c' R0 }, ~6 W' f4 |) o" [
The 11-β hydroxylase deficiency may also result in
; m- b4 e2 F5 d: y* E* P7 Hexcessive adrenal androgen production, and rarely,1 ^: c* H# g& _* R" w
an adrenal tumor may also cause adrenal androgen5 N' o( F7 I$ n" k
excess.1,3
/ v: }" |# p3 A4 z% f% tat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
9 d# F* ~% W, A/ b: ]; f8 y542 Clinical Pediatrics / Vol. 46, No. 6, July 20075 \7 y& C9 P& \( S0 v
A unique entity of male-limited gonadotropin-
, e! [& T; J1 _9 N$ I6 n H9 Jindependent precocious puberty, which is also known
# w" v9 R, |! Z7 h' W- tas testotoxicosis, may cause precocious puberty at a7 O! ^# z0 {1 L x, c" q
very young age. The physical findings in these boys1 w0 \" O1 G% p1 \& T9 i
with this disorder are full pubertal development,
" j- Z# X0 w4 m9 P$ i7 Gincluding bilateral testicular growth, similar to boys# @& U; T K/ k O: p u
with CPP. The gonadotropin levels in this disorder
$ K" M+ O4 c; u! M7 X. q$ vare suppressed to prepubertal levels and do not show/ U+ h+ |0 `& b& ?2 d! w/ g3 v3 B
pubertal response of gonadotropin after gonadotropin-7 [5 L6 I! z G' t1 W
releasing hormone stimulation. This is a sex-linked$ G' K2 d! [0 ~( `
autosomal dominant disorder that affects only" d# ?/ F1 u' m3 U8 U
males; therefore, other male members of the family0 X: Z- J9 D# h: w. X
may have similar precocious puberty.3, z3 G! d$ A0 Q5 Z ^/ U, K$ W; w
In our patient, physical examination was incon-( P E8 u# U# r. t( C {, D
sistent with true precocious puberty since his testi-. a8 G) M5 \7 x4 s, y* a3 a
cles were prepubertal in size. However, testotoxicosis# d Y7 W) ~( n1 Q0 j
was in the differential diagnosis because his father. k' _. U2 v# A* J
started puberty somewhat early, and occasionally,/ \) |% L7 P i K% ?3 s
testicular enlargement is not that evident in the
# T0 z" |7 O: ^6 y! i) t' J* N' h/ Xbeginning of this process.1 In the absence of a neg-/ C: q4 G. y/ C. w
ative initial history of androgen exposure, our
$ S- |6 M; K9 u2 k5 d) h0 ^, gbiggest concern was virilizing adrenal hyperplasia,
% g6 F& K6 U& f0 neither 21-hydroxylase deficiency or 11-β hydroxylase( ^+ x% R4 G; f) {0 x! _: B
deficiency. Those diagnoses were excluded by find-% |7 j; y; M$ e3 l
ing the normal level of adrenal steroids.
4 `1 s* X' s: ]& l. v. S; c5 ]The diagnosis of exogenous androgens was strongly( s- l7 B. S4 H9 S) z1 o
suspected in a follow-up visit after 4 months because4 i- J. ^4 ]* h: }, z
the physical examination revealed the complete disap-0 Y' N. i. Z4 ^( z; p; \' X. k
pearance of pubic hair, normal growth velocity, and. G$ j% [2 o. G+ k& k0 [$ G( U
decreased erections. The father admitted using a testos-- |" w0 i2 _ T8 H
terone gel, which he concealed at first visit. He was# a) V( i+ v. p" V z$ E$ @8 n
using it rather frequently, twice a day. The Physicians’8 Q3 Q C" l7 }
Desk Reference, or package insert of this product, gel or
1 z3 P# P0 e, M! \( Ccream, cautions about dermal testosterone transfer to
6 [ F3 O0 }1 n! n* `unprotected females through direct skin exposure.) o3 U! Z+ a. a
Serum testosterone level was found to be 2 times the6 j6 u: t! P: h: C9 I. Z
baseline value in those females who were exposed to
7 t: ]" y4 q7 P, [2 P6 Reven 15 minutes of direct skin contact with their male
& g0 x: U5 N m; I9 z. zpartners.6 However, when a shirt covered the applica-
2 k" S/ \5 F6 ~, O% Ntion site, this testosterone transfer was prevented.: H+ H' {: \+ Q8 y; `* \
Our patient’s testosterone level was 60 ng/mL,
( {, I1 V# Q2 C6 U7 ?$ Nwhich was clearly high. Some studies suggest that- I$ }2 J' f: V2 Z; x, Z# c
dermal conversion of testosterone to dihydrotestos-9 m+ E) p! o" `- m; E1 b; T
terone, which is a more potent metabolite, is more
- C% Z& r4 g. Sactive in young children exposed to testosterone
2 c5 }, X# P2 ]; Y/ @exogenously7; however, we did not measure a dihy-. t# A- T8 @9 P' A' b
drotestosterone level in our patient. In addition to
2 B! ~5 p4 ?4 ]" @virilization, exposure to exogenous testosterone in1 J8 Q# w/ h- C' \5 ?
children results in an increase in growth velocity and5 W7 l1 e3 G6 p% W4 k
advanced bone age, as seen in our patient.+ n/ d( _2 K/ i; m
The long-term effect of androgen exposure during
! y6 ?/ m8 E; V% M/ {% mearly childhood on pubertal development and final
' P+ k/ ~7 O% V5 {/ y* Dadult height are not fully known and always remain7 o$ @ J# {+ \- o3 \
a concern. Children treated with short-term testos-
6 N% n3 N& I+ ~1 R, G! Y, K+ N. Oterone injection or topical androgen may exhibit some- g1 h: m) x7 g3 i$ H# l
acceleration of the skeletal maturation; however, after$ q: V1 W9 `% V! A7 a+ A
cessation of treatment, the rate of bone maturation
4 v; N- L: b8 H; H, @0 Wdecelerates and gradually returns to normal.8,93 V! _5 s9 O& N4 n& g1 d
There are conflicting reports and controversy/ j* H0 t- F; }
over the effect of early androgen exposure on adult# M7 W* \: P( y9 c& d: z3 R* x
penile length.10,11 Some reports suggest subnormal/ e2 J8 F, k: t& Q. d2 s4 ?1 r
adult penile length, apparently because of downreg-
+ T7 o8 V/ o o! dulation of androgen receptor number.10,12 However,
2 m9 S. ] ]$ ]6 d8 V- ESutherland et al13 did not find a correlation between
, w6 D7 M! Z3 Y% s+ ^childhood testosterone exposure and reduced adult0 u W- L, I) D7 A$ B2 Q/ w* h
penile length in clinical studies.
# T( l+ h3 E& s8 h$ D2 _3 @Nonetheless, we do not believe our patient is% O; H2 @9 Z5 D/ y' o$ @. \" b5 ?, I
going to experience any of the untoward effects from
8 L, `& d6 s" W ^# p9 Ltestosterone exposure as mentioned earlier because
2 W9 f+ \% {& U( U0 V. J' A) _7 ythe exposure was not for a prolonged period of time.9 V. s- C0 I" u, e5 E! e
Although the bone age was advanced at the time of
6 |% h' I8 o/ b8 m/ Ldiagnosis, the child had a normal growth velocity at5 `' k0 Y6 S/ |- U8 d
the follow-up visit. It is hoped that his final adult- R. u+ T. Z0 k1 T1 m, v& Q
height will not be affected. k* c" {& }5 _. A
Although rarely reported, the widespread avail-
2 Q3 s" V) b7 B/ X3 b$ ~0 M5 x( cability of androgen products in our society may
7 K: ]& S# V: s; F4 K( windeed cause more virilization in male or female
- |! b+ I6 t' R8 {5 n4 Lchildren than one would realize. Exposure to andro-' ~; ^" I$ t& W% }( C
gen products must be considered and specific ques-% O; \" \7 W1 e3 L9 M. a( J
tioning about the use of a testosterone product or
, N1 u' t& ~( Dgel should be asked of the family members during
9 s( K/ d) s9 Pthe evaluation of any children who present with vir-
e, P: l0 {) `8 b" j1 E0 k* Wilization or peripheral precocious puberty. The diag-
9 d. X& }9 f5 k E$ snosis can be established by just a few tests and by2 h) P- c0 i% v* A0 y d
appropriate history. The inability to obtain such a+ t$ q! V1 k0 u
history, or failure to ask the specific questions, may
& p' A9 ^" b# t {8 ]result in extensive, unnecessary, and expensive
' d( _7 f% M; E: d2 j( Vinvestigation. The primary care physician should be1 J$ ?9 F9 Y. r+ f* B% ?" m0 b8 C
aware of this fact, because most of these children
1 N; I6 K9 r( U& X3 s/ N5 Q8 Dmay initially present in their practice. The Physicians’0 R* e( T. q) Z( I
Desk Reference and package insert should also put a
( j, f% H! ?0 ~% c( y7 nwarning about the virilizing effect on a male or) l& p8 x% P. d$ b! B
female child who might come in contact with some-
# L0 ]$ d1 I. b9 G% C5 ?one using any of these products.
) U% D& \$ ]0 p, l# M' pReferences5 z9 ]! ]7 [6 P' t( O |1 ~! G
1. Styne DM. The testes: disorder of sexual differentiation3 b- Z i0 g/ f
and puberty in the male. In: Sperling MA, ed. Pediatric, \/ D5 L b* h: q/ Q
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
5 \4 ~ ~! u. Q: B7 \2002: 565-628.
% `: O& X' h" E! Z% o8 y+ B7 n2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious. V, a/ f+ C" w
puberty in children with tumours of the suprasellar pineal |
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