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Sexual Precocity in a 16-Month-Old
0 k( O _0 o X0 fBoy Induced by Indirect Topical
0 |0 W3 ~& O' `: p) F# ]Exposure to Testosterone' F% ]8 {& |. r" m' V
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
0 c' e' B9 _) z0 u: Pand Kenneth R. Rettig, MD12 M2 N2 T7 f. L1 m
Clinical Pediatrics
0 [7 Y) c# K$ f) O1 E$ d' aVolume 46 Number 6% s6 I1 t. A& U! j, w" G& {
July 2007 540-5433 c' k" g3 Z; j# \+ g7 ~
© 2007 Sage Publications& c- S" u9 m4 S2 u$ [
10.1177/0009922806296651- \0 ^. R! j9 [% e6 o
http://clp.sagepub.com- T/ _2 g! R) e ^ P* ~9 C
hosted at' V4 \6 a+ v# q* |7 _, R' F% Q$ J
http://online.sagepub.com
, m& q `0 |0 @0 M& KPrecocious puberty in boys, central or peripheral,4 R" u5 k% M: i* R( s
is a significant concern for physicians. Central
, D; N0 ]: ]- K7 \6 x- J5 m" F/ Eprecocious puberty (CPP), which is mediated5 Z8 J1 R+ d: M& _0 |( z) l4 y
through the hypothalamic pituitary gonadal axis, has
1 V% {5 [7 L/ Y; Ta higher incidence of organic central nervous system1 |# z0 @3 I: m' U+ P, {4 f
lesions in boys.1,2 Virilization in boys, as manifested
; z$ t7 Q0 i# }by enlargement of the penis, development of pubic
% i, z1 m% W! n# m( H, Shair, and facial acne without enlargement of testi- d$ m# }, V' e) w
cles, suggests peripheral or pseudopuberty.1-3 We
; @( x, k1 }2 J& F% i/ D, O6 |: breport a 16-month-old boy who presented with the1 l2 f* U3 w; s& W6 A7 {: u
enlargement of the phallus and pubic hair develop-
! ]# Q" T3 }2 e/ Sment without testicular enlargement, which was due q: [! _! \7 q( f
to the unintentional exposure to androgen gel used by
: h4 z4 l2 Y6 ^& Z5 \! z/ c3 \the father. The family initially concealed this infor-
$ M* V& K0 ]" O+ |+ v5 U/ R% k. W, @mation, resulting in an extensive work-up for this" E$ b3 x2 l+ B% U- H. c* g& R
child. Given the widespread and easy availability of1 |1 t1 @* C8 n
testosterone gel and cream, we believe this is proba-
, s' l3 ?% N8 v1 A$ k% x. Hbly more common than the rare case report in the
) [4 q# l" I6 @! O0 w7 f3 l( cliterature.48 @5 M t3 e; ~" N' ~0 \& L& i
Patient Report0 W/ @. a3 Y8 V0 z
A 16-month-old white child was referred to the3 D) |' T: B5 v; K0 W
endocrine clinic by his pediatrician with the concern
( P4 x8 I* U# q4 L0 E, Eof early sexual development. His mother noticed
9 _1 B7 Z3 r7 ^; wlight colored pubic hair development when he was- k9 \: D& z: i
From the 1Division of Pediatric Endocrinology, 2University of0 U- L: V3 r1 y4 s; K, p, o
South Alabama Medical Center, Mobile, Alabama.
0 R6 O' p* u6 l- e+ D4 J! KAddress correspondence to: Samar K. Bhowmick, MD, FACE,
% L# v2 H- @+ X+ y( k: z9 nProfessor of Pediatrics, University of South Alabama, College of" H5 ~8 k$ l" y+ G! f& H
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
+ R4 w _% K; q. Ce-mail: [email protected]. k# p2 u6 Y& N6 w
about 6 to 7 months old, which progressively became
. U' h7 T: R0 j) n( V5 F3 R- Jdarker. She was also concerned about the enlarge-7 n: n E: T4 r c' `% z) P
ment of his penis and frequent erections. The child
+ o7 o* E) E+ ]2 }/ jwas the product of a full-term normal delivery, with
# R2 D0 c* O3 {# t2 Ia birth weight of 7 lb 14 oz, and birth length of( \, t: Q- z5 a6 b$ x% B
20 inches. He was breast-fed throughout the first year( I! K5 c, ^! V) h5 a* |$ B
of life and was still receiving breast milk along with! B, G- K3 {% x
solid food. He had no hospitalizations or surgery,
7 T" T6 w+ |5 p: d$ P+ kand his psychosocial and psychomotor development ^$ ~1 i7 H# S1 {, g) X Y
was age appropriate.
, n* L5 Y2 w1 Y0 M: dThe family history was remarkable for the father,
- _+ ~5 N. ]. T$ Ewho was diagnosed with hypothyroidism at age 16,
7 J, u! Z! @7 n0 T7 u# H5 `1 Uwhich was treated with thyroxine. The father’s" f5 O$ J8 U8 ], z2 I/ x
height was 6 feet, and he went through a somewhat
: m6 Y) J( m- W( E2 Wearly puberty and had stopped growing by age 14.
/ C0 Y. |4 a3 q: FThe father denied taking any other medication. The1 F/ N0 k4 w. ^
child’s mother was in good health. Her menarche! e- m, U7 c- C# Q
was at 11 years of age, and her height was at 5 feet
5 h7 S4 y: W ]5 inches. There was no other family history of pre-
" u/ }: R( v! d& j( Xcocious sexual development in the first-degree rela-3 v; l; @: T; T
tives. There were no siblings., ], O: i2 V% F& Z6 F( h
Physical Examination1 p S0 |7 [# |( u
The physical examination revealed a very active,
3 Y7 v8 Z3 P R/ }1 _% mplayful, and healthy boy. The vital signs documented( a, U+ O3 o4 `2 k; P6 g
a blood pressure of 85/50 mm Hg, his length was/ j4 d1 x0 Q! v& `
90 cm (>97th percentile), and his weight was 14.4 kg- t! G! [+ V9 T, Q& m5 [/ Z
(also >97th percentile). The observed yearly growth; j: \: _" W* x, ?4 S/ v, e l
velocity was 30 cm (12 inches). The examination of5 \+ T t# S7 P/ c; m' Z
the neck revealed no thyroid enlargement.* K8 [1 o4 n2 j( o, n
The genitourinary examination was remarkable for
/ d3 ~3 s- X9 l) g7 @enlargement of the penis, with a stretched length of
+ G3 k& P8 o! J, G: b8 cm and a width of 2 cm. The glans penis was very well
( X6 Q7 a! i7 Y! V6 K% R; xdeveloped. The pubic hair was Tanner II, mostly around
0 R# B+ Q3 m2 M" Q w540' P+ D8 m( I( ^
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
) E0 R% ]* _: ~8 P% Y9 I+ Pthe base of the phallus and was dark and curled. The7 h0 q& w& m5 r; n
testicular volume was prepubertal at 2 mL each.
- ?% }4 W4 v7 D' x6 D( {The skin was moist and smooth and somewhat
2 K8 Y. c8 @! G* J g! soily. No axillary hair was noted. There were no: Y. o3 D. w% N3 e2 x! e
abnormal skin pigmentations or café-au-lait spots.% H) x7 ^& @5 Y; i8 [4 \
Neurologic evaluation showed deep tendon reflex 2+
9 ~" g& w6 ]* v. Wbilateral and symmetrical. There was no suggestion
$ z6 i7 \( @. t# Y; {+ uof papilledema." A; |3 a# h, x2 i& E: r2 x( G
Laboratory Evaluation: g" n4 `! d8 R5 |% z" k! \- C
The bone age was consistent with 28 months by2 w! C' j$ P# g( U' R( z& B
using the standard of Greulich and Pyle at a chrono-
i8 n: w/ R' a3 x1 Flogic age of 16 months (advanced).5 Chromosomal
@& \5 M( R; m5 l A- M! ~karyotype was 46XY. The thyroid function test
" e, X9 [; x4 X% ~8 a* L+ _showed a free T4 of 1.69 ng/dL, and thyroid stimu-
1 c+ @7 c4 G$ N. e# q8 B4 tlating hormone level was 1.3 µIU/mL (both normal).
+ t% E5 ]* Z* C! I/ EThe concentrations of serum electrolytes, blood
7 i6 p4 \) s J8 `: C: Turea nitrogen, creatinine, and calcium all were4 @) s8 `4 ]8 W2 E+ n* ~+ ~2 f* |; ]
within normal range for his age. The concentration
1 w9 r$ |2 p) ?4 X7 @' ?$ @2 Zof serum 17-hydroxyprogesterone was 16 ng/dL
8 a, n- y+ J" N8 ^+ h(normal, 3 to 90 ng/dL), androstenedione was 202 S% f+ r# Y5 T# c: L6 c5 N
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
- b6 m( i2 ^/ [! Mterone was 38 ng/dL (normal, 50 to 760 ng/dL),
; f" {5 q; W+ P! ydesoxycorticosterone was 4.3 ng/dL (normal, 7 to
2 O6 s, S% C; x! b( M/ x49ng/dL), 11-desoxycortisol (specific compound S)* c$ b2 k7 n! \9 [3 n) ~! n
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
4 I1 i1 f2 Z, ]/ S4 x$ I0 r- p1 mtisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total. R1 z; _, e0 Z8 r/ o+ d* a
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),/ F. t4 P) j- D- o+ d5 p% T- R
and β-human chorionic gonadotropin was less than
3 T6 W! F) q! Z# u5 mIU/mL (normal <5 mIU/mL). Serum follicular; I! O) R3 Z( ?. @
stimulating hormone and leuteinizing hormone
4 X1 l( S% L/ b; P( e# W2 xconcentrations were less than 0.05 mIU/mL4 h/ N6 H) U7 T/ X# J
(prepubertal).
4 G4 u2 C3 D6 ?" C6 N7 P! `: y0 ?- ]The parents were notified about the laboratory
( G5 }) [; o* ] X, s0 S$ z K4 Jresults and were informed that all of the tests were
! }4 d7 d3 v! Y7 Snormal except the testosterone level was high. The
( g) l+ r% e2 H8 \, Lfollow-up visit was arranged within a few weeks to, ?- Z9 B. k, f' {( e& w) X3 h
obtain testicular and abdominal sonograms; how-! T" }5 i: c* v7 h! }
ever, the family did not return for 4 months.
" G, S! g! y; O( `4 ]Physical examination at this time revealed that the
5 N( O( B3 E1 ?: Y. ~child had grown 2.5 cm in 4 months and had gained. f& s/ S1 d2 n; @* ?* ]' B6 L, Q# H4 h
2 kg of weight. Physical examination remained4 [9 {0 _ y0 a
unchanged. Surprisingly, the pubic hair almost com-
% L1 K" H8 U; _+ ]7 w2 p2 Ppletely disappeared except for a few vellous hairs at
% l h4 o1 o# j; e/ w( e$ I8 l# sthe base of the phallus. Testicular volume was still 2
1 n! T6 a3 O, w/ A. ?3 j- w6 hmL, and the size of the penis remained unchanged.
3 a4 X8 k$ Z4 m l" ~( }- DThe mother also said that the boy was no longer hav-/ y4 @+ i' S% G- O3 D# k6 H
ing frequent erections.& t! O5 Z7 R2 o( w D' ?
Both parents were again questioned about use of
* A) p! ^) |6 H) T3 j- }3 jany ointment/creams that they may have applied to. b- t3 Q( U0 j* y1 A8 M
the child’s skin. This time the father admitted the0 o( a4 p r5 Y5 i5 j
Topical Testosterone Exposure / Bhowmick et al 541$ x0 s% v. l* `+ `+ ]7 }/ q, A
use of testosterone gel twice daily that he was apply-
# M0 ~2 o) P! U P( n0 J7 R0 wing over his own shoulders, chest, and back area for
. \) h( D' k* ?9 O7 }+ G+ Sa year. The father also revealed he was embarrassed
* y" h( G2 b& X* L/ b/ J Oto disclose that he was using a testosterone gel pre-; T) ^3 t$ x! }) \) t8 M1 h7 w4 E4 V! |
scribed by his family physician for decreased libido. l2 |6 ^8 }( k( i( T
secondary to depression.
3 {% j, A9 _" A0 S8 [% ]) F; n/ ]% FThe child slept in the same bed with parents.) g3 n* J1 a9 C% ]
The father would hug the baby and hold him on his5 l8 N( X1 s7 R& R
chest for a considerable period of time, causing sig-) e q3 L" z |' c/ z8 _
nificant bare skin contact between baby and father. E, c! q J$ _ p
The father also admitted that after the phone call,, Q$ L8 j% ?1 g! O3 j
when he learned the testosterone level in the baby
9 [! E# \- N) |was high, he then read the product information
' W3 l# V3 X* X4 l* g' Dpacket and concluded that it was most likely the rea-4 Y( I7 q2 g% F3 V# L: h
son for the child’s virilization. At that time, they1 z: H, H% c3 l5 H9 @+ y
decided to put the baby in a separate bed, and the
2 p g7 B1 X, Z# m9 N( Ffather was not hugging him with bare skin and had
- _9 f; \. T! ~) x; ]7 ^$ tbeen using protective clothing. A repeat testosterone' W0 ?3 j# u9 J) u+ m# _
test was ordered, but the family did not go to the6 E& V5 y! s/ Y7 H
laboratory to obtain the test.
0 ]/ r9 [1 F3 T; _6 L* ~4 KDiscussion
0 c" @, m+ L" C% t3 X4 p+ l6 BPrecocious puberty in boys is defined as secondary6 N8 Q( u- p3 w( b
sexual development before 9 years of age.1,47 ?+ _/ ~: a7 x& h2 Y9 f P
Precocious puberty is termed as central (true) when
* U# \' _, f/ N( X( G- s+ sit is caused by the premature activation of hypo-; {( c* u& ~7 X" x
thalamic pituitary gonadal axis. CPP is more com-
! @, \7 L3 y4 t+ S" |8 xmon in girls than in boys.1,3 Most boys with CPP
* w# r! R3 r! _0 P; y- C+ A& bmay have a central nervous system lesion that is
1 |8 O1 \, F4 ~responsible for the early activation of the hypothal-2 d' \' b" k+ H
amic pituitary gonadal axis.1-3 Thus, greater empha-2 B, t% p, e6 H% ^5 T
sis has been given to neuroradiologic imaging in
1 m/ s- x' D' m' E! q. ~$ p- qboys with precocious puberty. In addition to viril-3 T$ q7 N0 O2 ]& C2 ]
ization, the clinical hallmark of CPP is the symmet-
7 }. w% G I) O, [+ Crical testicular growth secondary to stimulation by
; F' g* G4 F! Ngonadotropins.1,3
- O* o7 U+ a" X4 \Gonadotropin-independent peripheral preco-% d7 n! `4 m( v1 @% g
cious puberty in boys also results from inappropriate
e! p. ~5 { ~androgenic stimulation from either endogenous or
$ @6 U6 w2 ^, T9 J4 u; z, [exogenous sources, nonpituitary gonadotropin stim-
3 T( G* B6 k/ ~ulation, and rare activating mutations.3 Virilizing
/ g5 b7 }+ h' P1 v3 L' f5 pcongenital adrenal hyperplasia producing excessive- x0 ^0 {! H2 m$ `+ \ B
adrenal androgens is a common cause of precocious0 e+ p, d7 ^3 J$ ]) |
puberty in boys.3,4
4 R# D8 b, K. z4 nThe most common form of congenital adrenal" ]0 M: k: r/ t) Q+ S1 S' x
hyperplasia is the 21-hydroxylase enzyme deficiency.7 A) [9 s$ U- S- v% c
The 11-β hydroxylase deficiency may also result in# [; Q1 P* U# g4 a9 t" ~- t0 d& Y
excessive adrenal androgen production, and rarely,7 d6 T6 D) O3 q6 \% K
an adrenal tumor may also cause adrenal androgen
! | Y- ]8 o$ Q+ _excess.1,3! ^" ]& Q! g6 O6 [
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
5 ?# @6 [4 J D( c542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
: t: M4 A3 R; e6 a1 u1 t% @0 ~A unique entity of male-limited gonadotropin-) G0 @6 k; A2 V* \9 X- P. x
independent precocious puberty, which is also known
3 d, k# t$ G4 l5 B, qas testotoxicosis, may cause precocious puberty at a4 P! e% B% o! Y. g& Q
very young age. The physical findings in these boys
6 n, y, M, U- O3 C S H& `6 mwith this disorder are full pubertal development,9 \5 J! E8 {, @6 x7 t# P# K
including bilateral testicular growth, similar to boys
8 O, P* |& ^2 _$ X( q% V" e8 V% hwith CPP. The gonadotropin levels in this disorder
7 x8 E/ n; b- _, l' n: d' }are suppressed to prepubertal levels and do not show* S' i9 b" `& \2 L7 p V1 e
pubertal response of gonadotropin after gonadotropin-
' B* Q, Q E0 ^" \9 w6 lreleasing hormone stimulation. This is a sex-linked0 |" x, Q7 B8 h% U) u9 v7 S9 n
autosomal dominant disorder that affects only
8 {& \' T, j$ w, W+ G9 \6 Cmales; therefore, other male members of the family
8 z$ g: h8 p# D( Y7 Y6 Bmay have similar precocious puberty.3
$ d% e$ X$ n, J% V' W$ [In our patient, physical examination was incon-
/ T- p5 E9 U$ F+ y) @sistent with true precocious puberty since his testi-9 d. n6 X: t' Z2 R, D6 A
cles were prepubertal in size. However, testotoxicosis: l, Z- q- M8 y/ O |, Y
was in the differential diagnosis because his father8 ^6 Q3 G" X' ], \0 x/ D
started puberty somewhat early, and occasionally,: n$ ^* S0 _) L$ l. F2 ^+ K7 s. W
testicular enlargement is not that evident in the8 {. `5 M3 k: b9 c" j+ F# X
beginning of this process.1 In the absence of a neg-5 h% S& j) G$ u- C5 W# Z- O0 b$ E
ative initial history of androgen exposure, our
* s I7 h) n% @; `; O+ y# \biggest concern was virilizing adrenal hyperplasia,
! V% n" o4 k' B5 Y3 V: Z/ ~! |" oeither 21-hydroxylase deficiency or 11-β hydroxylase, R5 J/ L5 h# X' `7 l6 j7 p: j
deficiency. Those diagnoses were excluded by find-: e5 S- B. _, V7 l4 h- \
ing the normal level of adrenal steroids.
- h2 M6 L8 Y4 \The diagnosis of exogenous androgens was strongly
" A4 T3 G( Y0 R% r! w9 F1 ~9 f& Z. U7 gsuspected in a follow-up visit after 4 months because6 C4 K( Z: L6 t* w3 C) V
the physical examination revealed the complete disap-
. \5 T ]( N3 ]4 o9 ]pearance of pubic hair, normal growth velocity, and
4 b) }, a( k2 K& C, Mdecreased erections. The father admitted using a testos-
\& A3 H, L1 M) k4 Y- p0 yterone gel, which he concealed at first visit. He was5 J! v" g# l0 U4 |8 z$ r' q
using it rather frequently, twice a day. The Physicians’8 _$ y$ T" Q- N8 I
Desk Reference, or package insert of this product, gel or, _' `# S% { i1 a
cream, cautions about dermal testosterone transfer to: w6 J. m) l) v: X& ^5 Z! r
unprotected females through direct skin exposure.
) l' N+ f9 `% uSerum testosterone level was found to be 2 times the
& k: C, v7 n3 D' d) Bbaseline value in those females who were exposed to& z) B: {9 E' @+ w# P! \
even 15 minutes of direct skin contact with their male
+ f( u) A- x& f3 Ppartners.6 However, when a shirt covered the applica-- d2 E* X, l: f" B9 ]
tion site, this testosterone transfer was prevented.
4 _$ G' \% x0 [5 JOur patient’s testosterone level was 60 ng/mL,3 @$ W- e$ @8 }" l7 c* u- ~
which was clearly high. Some studies suggest that, J) z- l1 I4 f% p
dermal conversion of testosterone to dihydrotestos-
$ }6 G9 c' C8 t8 W9 j) q9 oterone, which is a more potent metabolite, is more3 y5 q3 q4 `' F1 p0 I: z" Q
active in young children exposed to testosterone
! g; a% V i" f* [7 [5 Z2 Cexogenously7; however, we did not measure a dihy-
) y# o8 H7 u4 U$ ldrotestosterone level in our patient. In addition to
' H' T ~4 A% z/ u( ivirilization, exposure to exogenous testosterone in/ R8 v$ z! b. g2 x. ?
children results in an increase in growth velocity and' G D' ]9 c% B' l2 p" O. n
advanced bone age, as seen in our patient.- L; t- ?8 s* \* W# y$ b
The long-term effect of androgen exposure during
8 u8 c3 O; C5 l* F( _ W$ a$ u bearly childhood on pubertal development and final }" N T8 O- v' O% H
adult height are not fully known and always remain2 m$ e/ ~" R" Y
a concern. Children treated with short-term testos-* w+ [/ \. u/ {, K/ s D) T0 |1 _1 V
terone injection or topical androgen may exhibit some" }; P5 B# E; ^$ J
acceleration of the skeletal maturation; however, after# ~3 z+ s3 `. c, H4 w1 P$ O
cessation of treatment, the rate of bone maturation: P" g1 x: A# Y. d/ N
decelerates and gradually returns to normal.8,91 g+ w0 a' x8 A9 Y* ^
There are conflicting reports and controversy$ ]: L4 [2 ?: {2 F% s' ]# B, S
over the effect of early androgen exposure on adult
8 |4 Y4 H2 w: h+ X& _' d, Npenile length.10,11 Some reports suggest subnormal5 c! C4 p* w$ k# R
adult penile length, apparently because of downreg-
/ Y& l: t8 ^9 H' {ulation of androgen receptor number.10,12 However,& H- K% A* d, _) S4 \
Sutherland et al13 did not find a correlation between
* V" p' l0 V, ^2 m, Fchildhood testosterone exposure and reduced adult
0 y6 O% v+ a7 Y; N1 apenile length in clinical studies.3 V2 Y, m2 u, |! Q4 K6 `
Nonetheless, we do not believe our patient is1 G' Q. x% g( B, Q1 X
going to experience any of the untoward effects from, Y; M0 ?: I, y" G
testosterone exposure as mentioned earlier because0 J4 n1 N1 S; z) n* e; y5 j
the exposure was not for a prolonged period of time.# @+ p) U! P, ~9 ?2 f, a% Z
Although the bone age was advanced at the time of' Q: b1 Q/ P! S) @3 Z- }7 L
diagnosis, the child had a normal growth velocity at8 e* y& `4 l/ w; a
the follow-up visit. It is hoped that his final adult t; ]" e1 n. K5 I2 o. [$ g8 w! @
height will not be affected.6 }/ y' K/ H D5 E7 _0 v1 [" w
Although rarely reported, the widespread avail-/ x0 k/ e, G" A& {
ability of androgen products in our society may
, y4 r: u. m4 c& J: c; Yindeed cause more virilization in male or female
. O$ n2 a5 _8 {) G2 Pchildren than one would realize. Exposure to andro-
. J% r( ?, i+ H6 E) ggen products must be considered and specific ques-1 M" O) U! U1 @4 N; \
tioning about the use of a testosterone product or
# p$ M/ @6 v# x pgel should be asked of the family members during
7 `% h. q5 `6 nthe evaluation of any children who present with vir-' ?1 s" y' P. C2 I$ _1 k; v& S5 G
ilization or peripheral precocious puberty. The diag-
2 l' g6 i3 R$ w6 onosis can be established by just a few tests and by! l$ c# h+ [, D$ x- Q: S+ Z
appropriate history. The inability to obtain such a/ V7 Z' O o5 t8 a$ M: K; s4 _
history, or failure to ask the specific questions, may
- E5 F$ g! V% H. O3 K) vresult in extensive, unnecessary, and expensive
6 d/ J- g$ q6 \1 L! Sinvestigation. The primary care physician should be0 _# P$ a7 t" }3 r
aware of this fact, because most of these children
) {. F* f$ z: w7 ]7 N4 @: amay initially present in their practice. The Physicians’
, |: X) a1 r" s0 KDesk Reference and package insert should also put a1 b/ G8 V/ n% u( [! |. _
warning about the virilizing effect on a male or
2 Y# F5 ^+ _' e; ? |% V; y0 zfemale child who might come in contact with some-, C3 K; e7 q# y7 u* c) s
one using any of these products.
8 {- `" v0 F8 c; x0 @6 |References* ?7 M0 L: m; t
1. Styne DM. The testes: disorder of sexual differentiation" K7 k) R( }/ s
and puberty in the male. In: Sperling MA, ed. Pediatric
8 h N6 W( y9 [( Y. h: y! xEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
. U5 P" W7 K" s2002: 565-628.
* r" p) ^' c) d6 h2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious4 o. [2 R3 S( z# Q8 m' v
puberty in children with tumours of the suprasellar pineal |
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