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Sexual Precocity in a 16-Month-Old/ q/ H' m" G) e* L% z
Boy Induced by Indirect Topical
+ q( @4 l2 C2 ^* K7 j- N5 \4 GExposure to Testosterone8 q/ `/ b. p; s, D8 v
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
: w: R8 g" I" m9 G2 dand Kenneth R. Rettig, MD1
' e% P) u" T; q6 [Clinical Pediatrics6 y9 Z# T' B+ S9 S9 A- f
Volume 46 Number 6
/ O& n9 V: I x4 l! B+ r- O6 xJuly 2007 540-5432 E5 V) c6 M# Z3 s$ U# g
© 2007 Sage Publications
; L3 U! h! Z8 N6 U+ D$ e9 j10.1177/0009922806296651
7 S6 B$ g8 U) j8 ]/ X# V& e8 T5 Ehttp://clp.sagepub.com
3 e) E) c/ W- f R" ?: Ihosted at
8 H0 ?; y, w9 D4 w- q. {( \http://online.sagepub.com
! y6 n7 Y# t$ u" U- Z' J2 `Precocious puberty in boys, central or peripheral,
7 W5 [4 D6 j% H/ b8 Vis a significant concern for physicians. Central
9 L2 z" m8 t; x! I# N, Dprecocious puberty (CPP), which is mediated0 L: Q4 w6 O1 Z2 L0 T5 i
through the hypothalamic pituitary gonadal axis, has
4 ^/ `( y/ k: _a higher incidence of organic central nervous system5 b/ f' ~" d7 T
lesions in boys.1,2 Virilization in boys, as manifested2 E( q- r7 i& j
by enlargement of the penis, development of pubic
O; u% q- Z, yhair, and facial acne without enlargement of testi-1 w# E* A4 B- M1 D
cles, suggests peripheral or pseudopuberty.1-3 We
2 X; e$ ?* \% P6 J( sreport a 16-month-old boy who presented with the
9 D. ~6 J9 {1 B: N4 P( d, N4 Cenlargement of the phallus and pubic hair develop-% y! E" K2 @9 D9 T" _: B9 k
ment without testicular enlargement, which was due
$ w3 P8 E' e- j7 q, `9 c) wto the unintentional exposure to androgen gel used by
8 D# \6 Q, W y7 |; s; gthe father. The family initially concealed this infor-" L5 @" Q; o' e% b4 X' l+ J
mation, resulting in an extensive work-up for this
. _+ d) g. G- Q2 ~child. Given the widespread and easy availability of+ }# K0 k8 h4 r% x5 y( U1 Z& k; f% D
testosterone gel and cream, we believe this is proba-( W* g) h! d+ B# ~
bly more common than the rare case report in the2 _% l+ L" K: s$ `* e. B; b$ Z
literature.49 @ i" p6 [1 z$ w4 l
Patient Report# Z4 t" M/ Y& C0 C! k) m
A 16-month-old white child was referred to the2 O, ~# {# o4 h& \- |
endocrine clinic by his pediatrician with the concern
0 e/ _( Z( ^+ E6 d3 j* @& ]of early sexual development. His mother noticed
( S$ @: Q7 Q1 s$ n( K8 z8 Jlight colored pubic hair development when he was7 s7 I3 x* K7 W" v- S7 B
From the 1Division of Pediatric Endocrinology, 2University of" y( J3 F5 Y4 W6 U' c: ^" ^4 W- r
South Alabama Medical Center, Mobile, Alabama.
. E5 @- Z, [# Z5 o9 t' lAddress correspondence to: Samar K. Bhowmick, MD, FACE,
1 a4 [8 H/ b$ o- k/ i; @( RProfessor of Pediatrics, University of South Alabama, College of W, Z- v! a7 w2 s" x
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;* T9 v3 v2 R8 b6 v, B8 B
e-mail: [email protected].7 e* t6 h k! `9 w7 J9 {$ l
about 6 to 7 months old, which progressively became* u, e# r; a( i9 w- [2 j5 T" p9 j3 M
darker. She was also concerned about the enlarge-$ b4 b. t7 [/ V. Q3 c5 R
ment of his penis and frequent erections. The child
# c; [ I s6 y/ G/ ^2 cwas the product of a full-term normal delivery, with
( l8 Z1 \' F. ?) s5 Ta birth weight of 7 lb 14 oz, and birth length of
' H0 p$ I; b7 m% W l3 M" V20 inches. He was breast-fed throughout the first year( P$ H8 `6 g# Q; e: O- K# P0 Z
of life and was still receiving breast milk along with
: V. j0 t3 A( G# B, Z* _solid food. He had no hospitalizations or surgery,
- }: X5 m. k& tand his psychosocial and psychomotor development
, }6 G5 n4 \' \6 Q$ uwas age appropriate.! ?# ~8 [; g9 c2 P
The family history was remarkable for the father,
?4 q5 a6 ~+ [9 rwho was diagnosed with hypothyroidism at age 16,
* N1 E N1 h3 Uwhich was treated with thyroxine. The father’s% |) ^& ?& ^2 u
height was 6 feet, and he went through a somewhat
0 n# Q+ W% Q% ?% g; oearly puberty and had stopped growing by age 14./ u0 p q( ], v: I y4 f8 ^
The father denied taking any other medication. The; g F: m, D; |) W
child’s mother was in good health. Her menarche, W8 Y; I, \/ @( ], R4 m
was at 11 years of age, and her height was at 5 feet
! b, j/ C3 [- A' ^4 N0 ?5 inches. There was no other family history of pre-, o( f7 j6 u( ]) Z8 @; n; X
cocious sexual development in the first-degree rela-% B$ Z3 U! r7 ?- Z$ W
tives. There were no siblings.6 ^9 T7 `1 l$ ]
Physical Examination
' e; \1 ~% t. R2 Z# P- gThe physical examination revealed a very active,
5 q8 u' |8 ^# k% k1 Lplayful, and healthy boy. The vital signs documented
& b" k7 U+ K- q+ K( m; _8 Y0 Ta blood pressure of 85/50 mm Hg, his length was" j8 Y9 N$ H2 Q% O
90 cm (>97th percentile), and his weight was 14.4 kg$ k# O s$ J6 c$ o1 I# u+ L
(also >97th percentile). The observed yearly growth" w' `" Y9 l3 u* O
velocity was 30 cm (12 inches). The examination of( f: K( D) M/ }$ f, n% h. \
the neck revealed no thyroid enlargement.
' e9 ~: Y' D0 Q" b1 s4 \The genitourinary examination was remarkable for* j s! u* |' O6 s2 r$ z
enlargement of the penis, with a stretched length of
6 v- e0 a m/ c8 cm and a width of 2 cm. The glans penis was very well: u% _8 e/ ~6 ]
developed. The pubic hair was Tanner II, mostly around$ P" ]8 C9 N/ c% v1 f: \5 V9 d
5404 H6 S* _) G; n3 q2 E( P& r& a
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
7 X+ Z$ M7 m/ `, G0 q% F( }the base of the phallus and was dark and curled. The
, v6 C! f5 i9 L; q7 H0 l- F7 @testicular volume was prepubertal at 2 mL each.' b( Q2 }! {1 E$ W9 _
The skin was moist and smooth and somewhat( Z; x+ ^: ^! c) y5 G
oily. No axillary hair was noted. There were no p: @( g6 n; X4 ?1 g
abnormal skin pigmentations or café-au-lait spots.
3 I4 t0 o, U- s7 ?) O, z/ YNeurologic evaluation showed deep tendon reflex 2+2 x7 r) l6 X( f+ v
bilateral and symmetrical. There was no suggestion& W4 y) e, ~/ L. f3 }8 E& L# ~1 Z
of papilledema.& T/ R; W+ }1 s, t
Laboratory Evaluation
( T3 q0 a6 J; a* y/ d6 u0 HThe bone age was consistent with 28 months by
9 \3 M9 Q3 E* o$ t2 dusing the standard of Greulich and Pyle at a chrono-
: m6 ]- }# [6 W4 X, x! h7 Hlogic age of 16 months (advanced).5 Chromosomal4 w5 \. D% C" X4 L/ q
karyotype was 46XY. The thyroid function test
' G9 m2 Z1 N# R" b, @; F9 r- Wshowed a free T4 of 1.69 ng/dL, and thyroid stimu-/ \/ J% {- U# d7 Z
lating hormone level was 1.3 µIU/mL (both normal).
, t. M2 [) \! p! N" {* w! L$ Q. v& `# [The concentrations of serum electrolytes, blood3 M7 L: I/ D ?0 S
urea nitrogen, creatinine, and calcium all were. d4 W% H8 a8 Y, w
within normal range for his age. The concentration5 W0 V i, C1 K/ O' R, g+ v
of serum 17-hydroxyprogesterone was 16 ng/dL, j/ O2 A! B- x- `5 I2 v/ m& [' O
(normal, 3 to 90 ng/dL), androstenedione was 20
_+ G. |2 X+ ^ Rng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
! B7 x) m8 E/ ]' W+ D' @1 W* q% Tterone was 38 ng/dL (normal, 50 to 760 ng/dL),
1 G2 G1 x( F8 v. L U2 tdesoxycorticosterone was 4.3 ng/dL (normal, 7 to0 f8 t1 r% n- I3 i& D+ y) x
49ng/dL), 11-desoxycortisol (specific compound S)
" A0 o5 M$ \! z( t* u$ M# g' Gwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
; i# X" x& P& |% rtisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total& V7 K3 J8 S& J% B/ c2 s% s9 i
testosterone was 60 ng/dL (normal <3 to 10 ng/dL)," X2 l2 v$ m2 V0 N/ r
and β-human chorionic gonadotropin was less than& ]2 E9 J: J; \, \. T5 U1 h) }
5 mIU/mL (normal <5 mIU/mL). Serum follicular8 l' i9 s; H; r& z: l
stimulating hormone and leuteinizing hormone
+ y! z; u2 ]; Lconcentrations were less than 0.05 mIU/mL( W2 Y0 j$ s! [ M( x+ A; c0 r4 A- Z
(prepubertal).
# p; V: o# \ x6 z2 k" `5 sThe parents were notified about the laboratory( Z2 e" p2 B& X3 e
results and were informed that all of the tests were8 K( }$ V; o8 A) ^0 P5 f
normal except the testosterone level was high. The
1 @4 U* U) ^8 u& Qfollow-up visit was arranged within a few weeks to
( t8 {. y( K3 q2 I J' xobtain testicular and abdominal sonograms; how-
! j) p: { y$ t3 o: O' Lever, the family did not return for 4 months.
: ~; r$ A2 L% Z. jPhysical examination at this time revealed that the
2 ^ Q1 A2 ?7 A6 Kchild had grown 2.5 cm in 4 months and had gained3 i2 H1 n5 b4 e2 J- v! s" L" s- s
2 kg of weight. Physical examination remained
* ~) l' y u! Q' L4 Xunchanged. Surprisingly, the pubic hair almost com-
; U4 Q6 E4 U* [2 E0 i5 @pletely disappeared except for a few vellous hairs at) y" H% z' I$ Q
the base of the phallus. Testicular volume was still 2( L& ~1 ^( O+ a% y: Q+ @; T
mL, and the size of the penis remained unchanged.- q6 K% \/ ^5 V6 y, x/ \
The mother also said that the boy was no longer hav-. C7 d* j% i; Y! |1 ]+ U
ing frequent erections." z! u. @# |8 ]. l
Both parents were again questioned about use of
$ A8 X% O% E: q' @any ointment/creams that they may have applied to# j/ a2 C) k& E, g
the child’s skin. This time the father admitted the$ v4 ]& e! Q% d# Y {' h) r/ Z
Topical Testosterone Exposure / Bhowmick et al 541; c5 N* R; u, t3 B& y' o2 a
use of testosterone gel twice daily that he was apply-: ^$ K# w4 o6 S9 R- C2 I8 J G
ing over his own shoulders, chest, and back area for
3 Z: a, C6 U! F- P G7 o9 q* T, ~a year. The father also revealed he was embarrassed
$ q% ~& R- v" R4 K) r$ }to disclose that he was using a testosterone gel pre-- [5 L+ g* Q/ p' c$ i
scribed by his family physician for decreased libido
9 I) T* S+ _' q% Vsecondary to depression.5 |- |5 j: x7 @) W; A
The child slept in the same bed with parents.
( r+ E" k* x) @, M, f& _The father would hug the baby and hold him on his* w" O8 W7 ~: G; {( m
chest for a considerable period of time, causing sig-
6 y5 A$ P3 C( k/ }/ ~nificant bare skin contact between baby and father.+ U6 v- u) a- f7 \' b
The father also admitted that after the phone call,) l0 F% ]% p! {) V% O2 r% H" j* k
when he learned the testosterone level in the baby- A/ E: ]( K% D2 F l( D0 ~$ ]
was high, he then read the product information
2 j- t' \! K; V0 x& y- A9 ^packet and concluded that it was most likely the rea-9 \6 x" V- n( ]& t8 Z) G. m: X
son for the child’s virilization. At that time, they, J: l% u6 p( f; O/ ]' A9 |
decided to put the baby in a separate bed, and the
: B" j. f+ ?1 `9 @9 [father was not hugging him with bare skin and had
& V5 Z) f4 b2 L- [) n; g, S" X& jbeen using protective clothing. A repeat testosterone2 _( i9 X$ W5 e2 u! O' L# a, X2 @' y
test was ordered, but the family did not go to the2 R9 }; I8 \; W4 c
laboratory to obtain the test.' `, J9 I/ e( G4 k6 v* e
Discussion
( }" K0 |: s5 V7 \* \Precocious puberty in boys is defined as secondary
! I6 y5 _, X0 psexual development before 9 years of age.1,4
( F& X! w; V9 HPrecocious puberty is termed as central (true) when: z. o# `, M( m# H% ?. h- g
it is caused by the premature activation of hypo-
) ?1 ^' z/ L2 A. A& B) {5 ]% Kthalamic pituitary gonadal axis. CPP is more com-, M, i9 v! Q% A" A5 E0 P0 r
mon in girls than in boys.1,3 Most boys with CPP+ t( l2 _* e F$ |* S' O' x
may have a central nervous system lesion that is S; Y3 I8 {1 K: ^3 g2 \& z; u
responsible for the early activation of the hypothal-
7 o f7 ~" Z3 c( q0 d7 y$ ^amic pituitary gonadal axis.1-3 Thus, greater empha-
: C! r" K3 x }6 a, K7 ^; fsis has been given to neuroradiologic imaging in, B5 Y8 B1 T0 ^6 ?2 z) [$ T% T3 I& Q' W
boys with precocious puberty. In addition to viril-
/ u4 ?1 o2 k. R1 ~# p ?ization, the clinical hallmark of CPP is the symmet-8 _# V0 h, P. Y9 \1 M/ ?! @
rical testicular growth secondary to stimulation by
5 N: m( ~' e7 t" t; ngonadotropins.1,3
% @, [, |7 |' FGonadotropin-independent peripheral preco-
" x O4 R6 z S1 y6 t1 t, [- z. Dcious puberty in boys also results from inappropriate
% e$ k$ N( R* n0 k" V* pandrogenic stimulation from either endogenous or/ x+ W3 T3 D2 C
exogenous sources, nonpituitary gonadotropin stim-
" E- g& ~. h7 T: E8 eulation, and rare activating mutations.3 Virilizing
: K. t8 i2 p8 q1 {6 gcongenital adrenal hyperplasia producing excessive
! ~: G; { _* }adrenal androgens is a common cause of precocious
/ C. E4 R$ I8 u% r% Vpuberty in boys.3,4
# V( ~0 F& P4 B r T; O/ u. iThe most common form of congenital adrenal
?4 H# \9 O2 Rhyperplasia is the 21-hydroxylase enzyme deficiency.( L% }, ]" r X I6 d B p
The 11-β hydroxylase deficiency may also result in
7 ]% O; J s' P0 C4 o. w5 pexcessive adrenal androgen production, and rarely," M9 c' Q7 y- m# [; n* V8 H# }
an adrenal tumor may also cause adrenal androgen {0 k* H7 k$ d4 B% O6 ~' u
excess.1,3( v" I) }: i2 u
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from/ t! i& h% c6 M/ b
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
3 m& n8 U) j8 Q( MA unique entity of male-limited gonadotropin-
: t( I( Z; y$ ?0 r( N3 ~) ?independent precocious puberty, which is also known5 \( {* E5 l- l
as testotoxicosis, may cause precocious puberty at a
- T) f B4 J. y& F7 i7 _5 o3 @very young age. The physical findings in these boys
! N' b. Y+ l: P+ p1 Hwith this disorder are full pubertal development,) X3 {* C: V2 j7 r) M
including bilateral testicular growth, similar to boys! z& Z9 @4 B( U, A& D+ g1 Y
with CPP. The gonadotropin levels in this disorder: z* h" G6 D4 y4 [, Q7 a
are suppressed to prepubertal levels and do not show" m% X! c4 Z& x' k; J
pubertal response of gonadotropin after gonadotropin-0 W. `8 ^6 l1 ~$ i+ J8 {' P7 L/ @ B
releasing hormone stimulation. This is a sex-linked
: u: ?2 u R) u" ~$ X& pautosomal dominant disorder that affects only( I& T" ]: W! G" w9 g5 |
males; therefore, other male members of the family
% q4 [$ s' v% `$ Z. \( tmay have similar precocious puberty.3' t- F4 D9 E1 ~1 i3 p' q/ I9 o6 I
In our patient, physical examination was incon-
6 @+ |/ j3 }/ A+ S( l* i' {5 xsistent with true precocious puberty since his testi-* C3 a( d: D0 i9 e. {3 `1 k3 l
cles were prepubertal in size. However, testotoxicosis
7 G. H9 ]1 X3 C' h0 P) wwas in the differential diagnosis because his father' i2 C8 E) p8 K$ n [+ E8 a
started puberty somewhat early, and occasionally,
2 Y# d |! |0 S- t% a, ptesticular enlargement is not that evident in the8 W! p+ M8 w! A) r/ h, L5 S
beginning of this process.1 In the absence of a neg-/ J2 x8 m- K+ L6 T: N
ative initial history of androgen exposure, our8 P/ R+ g0 V% X+ F
biggest concern was virilizing adrenal hyperplasia,
/ w" }% C& \% J6 F9 T ~4 ^either 21-hydroxylase deficiency or 11-β hydroxylase, I6 x4 @+ c" H- m$ n
deficiency. Those diagnoses were excluded by find-
0 Q6 g! R) n+ T" W3 j4 _ing the normal level of adrenal steroids.
* \ p% ]4 j# V* i V/ RThe diagnosis of exogenous androgens was strongly3 [0 T1 u% t$ ]3 E7 g3 e9 s+ J- L% g* q3 v
suspected in a follow-up visit after 4 months because
( I, J3 M( G) Kthe physical examination revealed the complete disap-
( X8 g$ }* I; ^4 t: z% }pearance of pubic hair, normal growth velocity, and0 W8 _' e& z9 s/ @* O
decreased erections. The father admitted using a testos-) C' }$ b0 m9 E4 s- o
terone gel, which he concealed at first visit. He was
- e7 H+ w0 h4 v8 C* gusing it rather frequently, twice a day. The Physicians’- q# x( ?) V' e9 K) C5 G& j6 _' _
Desk Reference, or package insert of this product, gel or
! Q* I) r; S/ D& I+ U& [cream, cautions about dermal testosterone transfer to
" y) B5 f1 `8 m' z' i8 A( {$ Eunprotected females through direct skin exposure.9 s6 C/ K4 }7 x
Serum testosterone level was found to be 2 times the; Q4 l2 X) k: u3 s8 D3 R) a
baseline value in those females who were exposed to
5 Z: g5 c4 Y4 ?, a$ F6 Reven 15 minutes of direct skin contact with their male2 I- C0 m7 z' [0 c* h; m/ q
partners.6 However, when a shirt covered the applica-
. a* B' ]7 B+ Z, n" n I+ X# r1 qtion site, this testosterone transfer was prevented.- C; L; t- B/ o$ u) f( n
Our patient’s testosterone level was 60 ng/mL,, C( A, [7 J3 z) {# Q- i
which was clearly high. Some studies suggest that
* k/ s; y! M/ B- _4 |1 _dermal conversion of testosterone to dihydrotestos-
. z6 m. o# h6 R' D) v0 lterone, which is a more potent metabolite, is more D% @/ o' x& C7 w7 D: h3 m4 q9 ]
active in young children exposed to testosterone, p" b8 k& T' |+ J- S
exogenously7; however, we did not measure a dihy-3 v: N- D( u) U
drotestosterone level in our patient. In addition to
" u6 T) v. {3 ~; O8 c9 @9 \virilization, exposure to exogenous testosterone in9 v, Y. f% t& P8 F- F
children results in an increase in growth velocity and
8 x# ?1 H p ?, W6 D; iadvanced bone age, as seen in our patient.+ n& Z& V% H+ G+ n+ b# F: D j
The long-term effect of androgen exposure during5 T8 I! k# d2 |/ f8 [6 d1 f' f
early childhood on pubertal development and final
' a$ V' f" l$ N: V0 k3 nadult height are not fully known and always remain; k& ~, Z! D0 h3 A
a concern. Children treated with short-term testos-9 J& W: Z5 e( i& n4 c- a0 I
terone injection or topical androgen may exhibit some. t6 U! @+ U% e$ a: J6 b& C
acceleration of the skeletal maturation; however, after: f# c- k+ s6 I7 n
cessation of treatment, the rate of bone maturation
3 p. R* l3 K8 e6 \decelerates and gradually returns to normal.8,91 _, i) y9 N# G8 N6 N8 W4 u
There are conflicting reports and controversy9 b& @3 S* `: x2 M3 T+ i [
over the effect of early androgen exposure on adult* }) G; j0 E$ u" o: M' G5 q" r
penile length.10,11 Some reports suggest subnormal6 |5 c4 {8 [4 D" Z: S: Y8 s3 X
adult penile length, apparently because of downreg-
2 {0 B. F4 j* Uulation of androgen receptor number.10,12 However,
) ?3 G- Z. U! v" K) H hSutherland et al13 did not find a correlation between2 G& b( U% Y# Y5 ?, ^) T8 s, e
childhood testosterone exposure and reduced adult* b. P. v1 x: Z4 l. Y2 h4 G
penile length in clinical studies.
, t/ Z# L2 m, q4 q" b/ `Nonetheless, we do not believe our patient is
) A" U8 q0 T9 P' Qgoing to experience any of the untoward effects from
- b2 H: y9 ~: ^+ B1 \5 Ltestosterone exposure as mentioned earlier because
t. z% x- Q; v5 Zthe exposure was not for a prolonged period of time.
: r' d$ H' ~) A! N7 U3 l! v( NAlthough the bone age was advanced at the time of
9 L# r9 X/ w% R! }& |6 I+ udiagnosis, the child had a normal growth velocity at& U1 s( _( D# q0 a
the follow-up visit. It is hoped that his final adult2 H& M' Y+ n! h: C
height will not be affected.. s& h( \& M: t
Although rarely reported, the widespread avail-
8 b5 _; D3 l+ y7 ^+ T' i' K Kability of androgen products in our society may
7 y6 E/ c' v e% u* kindeed cause more virilization in male or female
: q2 V+ z5 h7 D1 O- p: s9 nchildren than one would realize. Exposure to andro-
* u) P1 @: r7 I6 e( @6 C# J+ Ugen products must be considered and specific ques-
: _/ M5 g& E8 w5 M$ e( Ctioning about the use of a testosterone product or2 _. s1 n) I9 K" i R, @
gel should be asked of the family members during- l" i& X* }/ h1 P' g
the evaluation of any children who present with vir-
G; P+ t9 I; q4 Y9 Nilization or peripheral precocious puberty. The diag-
8 S! A+ R$ r3 ^- U* Enosis can be established by just a few tests and by
6 Y, w! x5 v' @! E1 @, `appropriate history. The inability to obtain such a& A; y/ P. i; Y1 s
history, or failure to ask the specific questions, may
3 T' M C9 B4 j$ f3 o5 _result in extensive, unnecessary, and expensive7 k9 D8 r/ {# y+ Q
investigation. The primary care physician should be0 F' j" [, w& L2 w( l; B
aware of this fact, because most of these children' l$ k- N7 u6 E z. d0 }. x
may initially present in their practice. The Physicians’3 ]/ M: \9 N4 \2 \" f( k5 t
Desk Reference and package insert should also put a
7 d6 L5 \4 f4 N1 Hwarning about the virilizing effect on a male or9 s4 H+ Y4 t* |: [% ?- \! U; w
female child who might come in contact with some-2 S' X$ q$ U, V# P) g8 y! k
one using any of these products.
3 E9 P# p: M; D" t# e( NReferences! g) S3 F3 n9 c/ d" B, G0 C1 y" a
1. Styne DM. The testes: disorder of sexual differentiation Z$ v6 z1 W: p' C7 V
and puberty in the male. In: Sperling MA, ed. Pediatric
0 p! v: Q4 a9 L _' P' }Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
; {. v$ D" x* `. p9 y9 P2002: 565-628.
& @ G- k! [/ X2 [2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious! z' B& H! c# X+ g. S L
puberty in children with tumours of the suprasellar pineal |
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