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Sexual Precocity in a 16-Month-Old1 N2 s( u* \, P
Boy Induced by Indirect Topical
' D+ I7 a, G3 f3 N! r, N# vExposure to Testosterone
0 P% r6 [6 @# }4 \ cSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
i9 m' A3 V* a8 A% w$ e. C# ?3 Wand Kenneth R. Rettig, MD1# k* i, S5 k% O" E+ ]
Clinical Pediatrics
9 b5 ~ n b, h& ~Volume 46 Number 6
3 ]3 ]: U; I8 ?: B/ V. M, C2 EJuly 2007 540-543
: \3 b) z @+ o6 O© 2007 Sage Publications% n0 M: d' k" r( V$ ]; f5 c6 [
10.1177/00099228062966519 r- T- f; {" x+ U* Z
http://clp.sagepub.com3 b% z; k* `9 ]' Z/ Q. l
hosted at+ F+ o/ L2 Q4 w/ p1 W9 O4 ^
http://online.sagepub.com
" k' {, J% O. L/ ^& _' A' w6 `Precocious puberty in boys, central or peripheral,; ^8 G' ]! v7 G
is a significant concern for physicians. Central- Q+ J! k0 f: N$ j+ ?8 z& I9 N
precocious puberty (CPP), which is mediated4 k: ~ b) @- D. O* _
through the hypothalamic pituitary gonadal axis, has- P3 g! E9 x& s& @
a higher incidence of organic central nervous system
0 S3 W1 x& W8 C' Q/ M& A Qlesions in boys.1,2 Virilization in boys, as manifested
: y, E# R$ v1 t {6 O& L) `by enlargement of the penis, development of pubic, Q7 ~) r: |/ C$ P7 y7 n
hair, and facial acne without enlargement of testi-
% W' S* Z3 i$ _$ G# [# Rcles, suggests peripheral or pseudopuberty.1-3 We' t2 c# v) U* ?* U
report a 16-month-old boy who presented with the
3 m. e7 }9 A8 U; F. b, G1 genlargement of the phallus and pubic hair develop-0 j6 j4 `' x- z, V# i G% W3 E7 G% K
ment without testicular enlargement, which was due: V8 [' ~4 w' q2 u& G3 r% b; m: K8 {
to the unintentional exposure to androgen gel used by! l3 @+ ?& B7 ?; ]& y' E# s' u. |. b
the father. The family initially concealed this infor-6 Y) o4 u: }6 ~6 ~0 U8 l
mation, resulting in an extensive work-up for this) b5 b" x+ N3 S
child. Given the widespread and easy availability of
9 }' ~4 d+ Q4 \0 F" S$ b0 v2 |testosterone gel and cream, we believe this is proba-
& p3 ^* u$ j, p8 \! S! Z2 `bly more common than the rare case report in the
$ j7 Y; z- e0 C& \# fliterature.4
. y& c* ]4 h) Z3 I- DPatient Report+ ^8 ?1 L7 W; ?
A 16-month-old white child was referred to the7 G- v4 m. j0 d% n
endocrine clinic by his pediatrician with the concern; H# a" P: x: [/ f3 L, l
of early sexual development. His mother noticed5 n; m1 j. Y; b, C+ a1 M6 `
light colored pubic hair development when he was' g2 O) g# k" Q
From the 1Division of Pediatric Endocrinology, 2University of
3 C& a& B$ M4 c$ F" b4 OSouth Alabama Medical Center, Mobile, Alabama.
" \4 k: t# B' w$ y8 T9 ^- HAddress correspondence to: Samar K. Bhowmick, MD, FACE,
; s- Y, O/ o1 A1 w+ ZProfessor of Pediatrics, University of South Alabama, College of0 s1 z# h! s7 n. H$ |6 v' @7 p- H9 C
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
1 W3 \9 o& ^+ S; ge-mail: [email protected].
6 K1 o2 O$ w$ W5 ~3 _about 6 to 7 months old, which progressively became! u3 O+ O) z0 s5 D- E
darker. She was also concerned about the enlarge-8 l$ E J. Z1 g) d
ment of his penis and frequent erections. The child
8 F8 J. o2 f" S* L# [$ W- J! uwas the product of a full-term normal delivery, with
7 ^7 E+ a( v1 m1 U3 A7 l& b" Za birth weight of 7 lb 14 oz, and birth length of
* m3 w! A. I4 q$ V20 inches. He was breast-fed throughout the first year
# z, m9 K) P9 f# Qof life and was still receiving breast milk along with2 ^% o8 r3 Q& c- G. F; }
solid food. He had no hospitalizations or surgery,
7 X' Z' H/ \% F& J& b3 Cand his psychosocial and psychomotor development0 [3 ^2 t& D% C& |
was age appropriate.
{" ^: I5 W& M4 kThe family history was remarkable for the father,7 K# a9 _, P# n) r
who was diagnosed with hypothyroidism at age 16," ]/ N# j# z- m% {; \
which was treated with thyroxine. The father’s( N" d o$ A4 Q+ D: E6 W" b+ M
height was 6 feet, and he went through a somewhat; E9 P+ C5 P" J# _3 w: B
early puberty and had stopped growing by age 14.
: b+ t% f: L v l( K% C) ?The father denied taking any other medication. The m' N: w% K' ^- Z, t; ?: y) X, q
child’s mother was in good health. Her menarche" l K3 ~* ^! j0 w4 N
was at 11 years of age, and her height was at 5 feet* n+ Y* b, K+ a8 @6 r7 v# G
5 inches. There was no other family history of pre-' V+ d" F( W7 i" |5 {* Z# y
cocious sexual development in the first-degree rela-
# Z1 z$ }4 \7 Y+ s' btives. There were no siblings.
y6 Q; Z/ e! a) P! RPhysical Examination
4 o2 d4 j6 A9 d" I3 |, h8 e2 kThe physical examination revealed a very active,9 v5 Y0 r9 l; @
playful, and healthy boy. The vital signs documented
1 m$ K- D$ Y) B2 O7 a) N% @a blood pressure of 85/50 mm Hg, his length was
. b! P( W0 i) b90 cm (>97th percentile), and his weight was 14.4 kg1 }* V# [, `- z
(also >97th percentile). The observed yearly growth
3 m! @2 T, S! R% [6 d' g* Ivelocity was 30 cm (12 inches). The examination of' \% [- ^3 F3 c! b$ [1 ?+ \% B
the neck revealed no thyroid enlargement.
8 {5 }0 z8 G# k5 n" v. @/ M, u4 e0 gThe genitourinary examination was remarkable for
9 J, |+ U f3 D& y3 y' Senlargement of the penis, with a stretched length of3 k& @$ F* ~3 D
8 cm and a width of 2 cm. The glans penis was very well; [! F9 S! a1 Y9 M2 B
developed. The pubic hair was Tanner II, mostly around# o4 N' H' Y' R! O: M
540
5 u6 i) ^2 b, |% nat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
: @) G- k4 X) ?: h, q6 qthe base of the phallus and was dark and curled. The) R- |8 C- [3 J& T
testicular volume was prepubertal at 2 mL each.
, v" {1 a) `" x; qThe skin was moist and smooth and somewhat! U/ [% p+ M) c' n3 Z
oily. No axillary hair was noted. There were no
" y: S- m" u% V; h: Q0 e( G% e& cabnormal skin pigmentations or café-au-lait spots.
' y1 c! q$ E) K( I! q7 W4 b% [Neurologic evaluation showed deep tendon reflex 2+8 A0 t! Y! U7 }! f
bilateral and symmetrical. There was no suggestion
9 ^- U# [5 i M- Q7 V2 Sof papilledema.
4 u! H2 | d* l. c0 @Laboratory Evaluation
/ o' [4 o. [ I2 t% |The bone age was consistent with 28 months by
& o& |, d0 V4 t1 ^1 ~! P! Gusing the standard of Greulich and Pyle at a chrono-/ [. \# C) t( e1 n& U
logic age of 16 months (advanced).5 Chromosomal
8 f" E0 B; q( U; i- n5 }/ ekaryotype was 46XY. The thyroid function test3 H. N( H+ Q* g5 r3 h+ v% D
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
_- K' l% D! P% n( i' F, j0 flating hormone level was 1.3 µIU/mL (both normal).
A$ ?. X* A+ r2 y9 tThe concentrations of serum electrolytes, blood$ X/ o: t: b. V4 p% z
urea nitrogen, creatinine, and calcium all were
( O& e: M5 P- _' x; uwithin normal range for his age. The concentration# }# P- ]7 _8 S+ Y
of serum 17-hydroxyprogesterone was 16 ng/dL
/ i' }0 v4 e+ y& o, H(normal, 3 to 90 ng/dL), androstenedione was 20
; V) {5 y$ g# U5 }2 Dng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
- q1 f: c' a, |$ l& Z3 x/ Q8 L! p% qterone was 38 ng/dL (normal, 50 to 760 ng/dL),1 L, z5 v* _+ }6 k# X
desoxycorticosterone was 4.3 ng/dL (normal, 7 to9 t$ u. ~* q0 G' p3 ]
49ng/dL), 11-desoxycortisol (specific compound S)
6 ?/ ]% }6 n: Y# x9 jwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
. n; B, t: ]4 D4 s0 a( C1 Qtisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
3 \5 B) X$ Q+ e- `3 Htestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
( J! ]; @2 b$ _. K Gand β-human chorionic gonadotropin was less than
. [ O; \! Y# R. ?& f' t2 t5 L5 mIU/mL (normal <5 mIU/mL). Serum follicular9 q/ c( A4 ?; z
stimulating hormone and leuteinizing hormone
3 `) T7 o7 ~' Tconcentrations were less than 0.05 mIU/mL
9 Q0 u; i2 a2 Q' n(prepubertal).0 x9 m5 q1 y$ \: j
The parents were notified about the laboratory
6 J, w1 C2 @0 Jresults and were informed that all of the tests were' j& _6 Q+ M# |8 B4 x
normal except the testosterone level was high. The' e/ n. M& K. K( X
follow-up visit was arranged within a few weeks to, G/ H7 X3 N4 v; ?4 u
obtain testicular and abdominal sonograms; how-
/ F' w3 |7 w2 K8 r% p7 q, }ever, the family did not return for 4 months.
, R- p) a* j0 l8 S! m& t8 ePhysical examination at this time revealed that the9 t) S4 L, h% d+ Z, n+ h- m
child had grown 2.5 cm in 4 months and had gained
; @4 Q+ z. Y+ B% L" d& A3 `) M, E2 kg of weight. Physical examination remained. O! p s* @- k$ q% k; A) a3 E& _( P8 n
unchanged. Surprisingly, the pubic hair almost com-. ]7 c i) T3 L4 _% l8 b2 u! i
pletely disappeared except for a few vellous hairs at; W5 K2 Y- k" z8 m8 \9 h
the base of the phallus. Testicular volume was still 2
2 V: _8 o: m- Q; F4 ?* imL, and the size of the penis remained unchanged.
- M1 y3 K8 _ _3 {) V8 d# K% EThe mother also said that the boy was no longer hav-8 P! T! y2 I8 x
ing frequent erections.- W/ t: R4 E( N$ o* s) u
Both parents were again questioned about use of4 M8 q4 p" F$ ?7 ~) ?" Y8 u. @
any ointment/creams that they may have applied to7 b; D8 @2 {) `# B# R6 n' q- q
the child’s skin. This time the father admitted the
! U! C5 a$ @7 @3 BTopical Testosterone Exposure / Bhowmick et al 541
7 E- E+ Z( F+ o y& y4 duse of testosterone gel twice daily that he was apply-
+ j3 @, t/ \( Ding over his own shoulders, chest, and back area for
+ @# |# h4 D+ Ia year. The father also revealed he was embarrassed
+ F# c/ ^ K( l' |+ t4 h5 w! mto disclose that he was using a testosterone gel pre-
6 F' ]2 _5 ], ^6 n. tscribed by his family physician for decreased libido
7 ^0 a* k7 F- e3 ^. q$ Asecondary to depression.
: l( W, ?4 H9 oThe child slept in the same bed with parents.
3 z) ]5 D0 q9 l x1 [. w: D9 S9 O: CThe father would hug the baby and hold him on his4 i6 ?6 ?" g) z
chest for a considerable period of time, causing sig-
2 ]& M! @! q1 a/ G; X$ Fnificant bare skin contact between baby and father.5 H. A4 b, i; @+ F. m
The father also admitted that after the phone call,. c. Y. g. _/ U1 m/ L* [2 P
when he learned the testosterone level in the baby
8 o8 `7 G# H/ N% H/ M$ ]1 ~8 n3 Twas high, he then read the product information
% `; e7 T$ J, N. f4 v9 vpacket and concluded that it was most likely the rea-* T& {! E! t# ]( P) {/ ?' }$ Q
son for the child’s virilization. At that time, they
3 {$ U- @ M9 Pdecided to put the baby in a separate bed, and the
7 ]) M: p d' F/ ?0 B' _& n" xfather was not hugging him with bare skin and had
1 R6 [) U: l) U, ^( Nbeen using protective clothing. A repeat testosterone
" a: z: W" N8 ~: @% p7 jtest was ordered, but the family did not go to the
/ l- u7 o3 `% |( llaboratory to obtain the test.
+ B7 `7 e8 y. p% j5 eDiscussion; G" ?5 k5 ~# y7 i+ ]' j9 Q" t% d
Precocious puberty in boys is defined as secondary
, b* v. S9 X3 ?" f1 isexual development before 9 years of age.1,4
# R1 w" h* ~: O: r. rPrecocious puberty is termed as central (true) when5 l7 l" }/ @6 d) y) [% T i& `
it is caused by the premature activation of hypo-/ ^% x/ l; K7 y6 }% ?
thalamic pituitary gonadal axis. CPP is more com-/ M& M5 `9 q- A' x2 R$ D# @6 F% n
mon in girls than in boys.1,3 Most boys with CPP
3 h* i/ N; ^8 s K5 N2 k0 u& imay have a central nervous system lesion that is* s9 v6 U0 ?( R; f7 t" R w1 W: ]
responsible for the early activation of the hypothal-0 L9 f0 T1 J" Y9 H% B$ b* C
amic pituitary gonadal axis.1-3 Thus, greater empha-
. _/ B q2 {3 R$ ]; Usis has been given to neuroradiologic imaging in
, j0 ]% U- c; G& x0 \7 u( q( Rboys with precocious puberty. In addition to viril-) I: ]) o' I" ~, \3 m# z
ization, the clinical hallmark of CPP is the symmet-: G8 R! I' b3 S4 A; X
rical testicular growth secondary to stimulation by0 i* l9 d) ?% Y( ]# e, P
gonadotropins.1,3' b& Z# H8 i: y
Gonadotropin-independent peripheral preco-0 i, O& h1 {; |7 r
cious puberty in boys also results from inappropriate
# o" Q5 y1 K7 e! a- i6 {6 A! D0 j& ]androgenic stimulation from either endogenous or: X# F2 x0 o5 p) |* Y
exogenous sources, nonpituitary gonadotropin stim-5 Z1 v, |1 K6 W7 l& d/ B; `3 P! O8 ~; E
ulation, and rare activating mutations.3 Virilizing! f1 K/ x8 U' j# @! v+ |* W
congenital adrenal hyperplasia producing excessive
- E& p( G9 p2 w& T. {0 X+ Y8 ?adrenal androgens is a common cause of precocious' P% ~% p0 t5 t6 X# I
puberty in boys.3,4; X& A D6 R1 e @. ]
The most common form of congenital adrenal
1 u# s2 i% G s) }6 [hyperplasia is the 21-hydroxylase enzyme deficiency.
5 s" N! q( z) l) K' n' LThe 11-β hydroxylase deficiency may also result in
; @; _ X7 ^0 g5 s# j! Zexcessive adrenal androgen production, and rarely,4 k" ]* M8 n* P3 P9 E) m
an adrenal tumor may also cause adrenal androgen0 w* A( ?4 }$ G% _6 y
excess.1,3! \0 _7 m! j! e# E- M
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from! x2 s: O o; Z4 _' a& a
542 Clinical Pediatrics / Vol. 46, No. 6, July 20070 G! }( S! ^+ P3 G
A unique entity of male-limited gonadotropin-
8 @- E7 c+ K8 H: ^* U1 ~. Windependent precocious puberty, which is also known
$ J' N* P. ]! Cas testotoxicosis, may cause precocious puberty at a3 p! T0 S ^+ c* F% s/ z
very young age. The physical findings in these boys
7 J4 a, E' y9 @* |6 @/ E! b- j/ pwith this disorder are full pubertal development,
; L8 g: ], C. f& a' [$ K- ?( zincluding bilateral testicular growth, similar to boys/ Z, |, `( _. F2 S: ]) F T% @" M
with CPP. The gonadotropin levels in this disorder. k" t1 z$ n, u& w$ R4 `
are suppressed to prepubertal levels and do not show: @) J# \- F* @! D+ p
pubertal response of gonadotropin after gonadotropin-
$ z; ~$ {7 Z9 p' d4 mreleasing hormone stimulation. This is a sex-linked5 {0 P2 \3 Z* k, L0 N# A
autosomal dominant disorder that affects only( q' \3 A0 z, M' j) G( e
males; therefore, other male members of the family2 a' ^/ J( ?( s2 j6 \. E' g
may have similar precocious puberty.35 H0 p, b8 n$ N8 @' Y, I- O1 w
In our patient, physical examination was incon-8 d1 f, l5 M1 |9 a1 c
sistent with true precocious puberty since his testi-
2 R, d0 I) H1 t& E& @0 Ncles were prepubertal in size. However, testotoxicosis: j9 l0 e6 x9 \
was in the differential diagnosis because his father
3 a5 G+ j' T/ M+ Z V. w- O' Ystarted puberty somewhat early, and occasionally,/ l. {& n o& d' j# V& t
testicular enlargement is not that evident in the
. }! }; B4 W @* a. kbeginning of this process.1 In the absence of a neg-
{# m1 v# U& b' O/ B: O" s* bative initial history of androgen exposure, our
* e0 i# X6 Z% M: @% r! `1 ?6 Ubiggest concern was virilizing adrenal hyperplasia,
6 a& K5 r8 n' B6 j s- Ceither 21-hydroxylase deficiency or 11-β hydroxylase2 Q0 a% ? C. h! N
deficiency. Those diagnoses were excluded by find-9 _% r; o( G$ H0 G
ing the normal level of adrenal steroids.0 a T: D3 ^/ ]) G
The diagnosis of exogenous androgens was strongly8 g; y7 A( B$ g6 v( g
suspected in a follow-up visit after 4 months because* l7 N8 g \7 ]* |/ J5 L
the physical examination revealed the complete disap-
6 E6 K7 x0 Q5 t0 ~6 e3 [0 g( v' R+ _pearance of pubic hair, normal growth velocity, and% b4 c% d* z) W' P5 ]- t* ?
decreased erections. The father admitted using a testos-
2 ]9 g: q7 q l6 uterone gel, which he concealed at first visit. He was8 Q, P7 X. v j! D; `- Y8 x% _5 k& V
using it rather frequently, twice a day. The Physicians’
s8 t* ?6 k$ A# ^% v1 t9 [Desk Reference, or package insert of this product, gel or
; j7 Q9 w: l X& b$ w) g- Ncream, cautions about dermal testosterone transfer to/ N" i& X, ?5 i2 H" k
unprotected females through direct skin exposure.
* I2 I+ O6 V3 M- A7 X- n9 ^Serum testosterone level was found to be 2 times the
( a( N: g+ D7 L2 z Pbaseline value in those females who were exposed to
G2 k' o$ W% heven 15 minutes of direct skin contact with their male+ n, n# T6 P7 @( h
partners.6 However, when a shirt covered the applica-0 N- l) U/ X- p# h
tion site, this testosterone transfer was prevented.
+ l7 u x# g: g5 U ^1 n$ `Our patient’s testosterone level was 60 ng/mL,. ~2 e4 o7 O8 [+ x$ h% W( F0 C
which was clearly high. Some studies suggest that. @5 Z9 X: j$ j5 Z& Z
dermal conversion of testosterone to dihydrotestos-
! @3 `8 q8 y1 l. b' C2 h' \terone, which is a more potent metabolite, is more) V$ R3 h3 Q: a0 x" I' b6 G% |
active in young children exposed to testosterone
0 _7 l+ b+ D+ wexogenously7; however, we did not measure a dihy-
/ l+ J# X2 A7 Kdrotestosterone level in our patient. In addition to
# F: g9 K8 C8 d) A% Wvirilization, exposure to exogenous testosterone in
6 @1 g- Q( m5 n" y/ Rchildren results in an increase in growth velocity and
' H1 K8 I! q- v, a9 Q* l9 Wadvanced bone age, as seen in our patient.
- b+ Z3 m. S% ?8 aThe long-term effect of androgen exposure during
7 E0 b* j a& z5 ~3 ]early childhood on pubertal development and final
6 }1 I. l% r4 j {adult height are not fully known and always remain& q4 W& x7 T, E
a concern. Children treated with short-term testos-+ q$ b. Z ?4 K
terone injection or topical androgen may exhibit some
% w+ a) `; c. i1 Sacceleration of the skeletal maturation; however, after
+ p& z5 E, i6 o2 e3 v7 D: R0 B( |cessation of treatment, the rate of bone maturation
/ v7 L! e3 P _- B2 e* T+ fdecelerates and gradually returns to normal.8,9
# E9 g% t3 ]$ n0 PThere are conflicting reports and controversy
1 ?% e: \. @' A5 v6 x4 U& Dover the effect of early androgen exposure on adult/ V, n. n4 @; b' V+ j9 ]
penile length.10,11 Some reports suggest subnormal
$ |' i# D" F: F' X, I* v* iadult penile length, apparently because of downreg-! y, e" k: t/ M, [& y" [. @
ulation of androgen receptor number.10,12 However,
- |# d o1 R6 SSutherland et al13 did not find a correlation between* T7 s, Q8 v, e- \0 y( K
childhood testosterone exposure and reduced adult. k+ ?) r4 D% B( e- O' ~
penile length in clinical studies.( \* X3 ~) ~ s: V& t( b
Nonetheless, we do not believe our patient is
& D& b2 V% j. U9 |' ^& sgoing to experience any of the untoward effects from
L0 I' }) t7 B- [ G' Q: Etestosterone exposure as mentioned earlier because! m1 b$ M0 k% V: o4 W7 e. {
the exposure was not for a prolonged period of time.
5 T* \' _$ \& c& RAlthough the bone age was advanced at the time of
3 M1 x: W% `4 V# h1 |diagnosis, the child had a normal growth velocity at& P9 ^; w* R' J$ A( x
the follow-up visit. It is hoped that his final adult
$ n4 w3 e% M5 Y7 g7 Iheight will not be affected." }* c: I' T5 _/ H3 v. w- z
Although rarely reported, the widespread avail-
( t! `$ }$ j% E2 ^ability of androgen products in our society may
+ a& O& p! [ m3 v: o; x1 D% Bindeed cause more virilization in male or female
) }# @& b! E0 B3 ]& X5 a; l6 Rchildren than one would realize. Exposure to andro-2 T' V( ^4 X. }1 G1 p( r; o- a; l
gen products must be considered and specific ques-
4 J, H3 v( O. Otioning about the use of a testosterone product or. ~+ f4 k- f, p: w% Y. H1 u) r, V
gel should be asked of the family members during% J, M+ o0 E. U' K' g! E: j# m8 m- ^( Z
the evaluation of any children who present with vir-. a8 k. M! ^( ]* `2 H5 e+ s4 }
ilization or peripheral precocious puberty. The diag-- W) A0 I6 _! o3 ~8 C0 }' k
nosis can be established by just a few tests and by% ^/ `$ R$ ], l7 Z! r* O
appropriate history. The inability to obtain such a
: h! p7 Z; h, U0 ?history, or failure to ask the specific questions, may
! j1 H' W- Z" S0 y- ~result in extensive, unnecessary, and expensive& i" s Z1 H8 f/ z' @ {
investigation. The primary care physician should be I- B) ^2 a1 |, A$ W) m B
aware of this fact, because most of these children1 ~' ~) r& |: A3 N
may initially present in their practice. The Physicians’
' s$ s* g6 e4 l" G" xDesk Reference and package insert should also put a
* K4 Y9 C( N Q+ P. a4 E/ `' lwarning about the virilizing effect on a male or& `; G T" \3 ?# v
female child who might come in contact with some-
3 p& \4 f& m; p4 a! {. Yone using any of these products.
/ u e" Z3 q* o! `References
) \ Z- ` G2 F) R! J1. Styne DM. The testes: disorder of sexual differentiation5 |$ ]; A6 N9 f$ Y' R3 W
and puberty in the male. In: Sperling MA, ed. Pediatric
6 b- l3 E0 _7 z* NEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
3 B' f7 T. \7 [ r; b6 u; b, h- t2002: 565-628.
. q, v2 z0 k) l8 b/ Z3 B2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious; t' S# M- X" C9 O y( a. g0 N
puberty in children with tumours of the suprasellar pineal |
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