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Sexual Precocity in a 16-Month-Old2 k$ c2 ^" ~4 I, @; Y* o" ^
Boy Induced by Indirect Topical
5 k8 w- q8 N( b: `. R3 D5 [8 IExposure to Testosterone
3 _5 G2 P9 ^6 c* X1 }Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,23 _& b- z) m% s8 l
and Kenneth R. Rettig, MD14 Y' V Y- |8 T# _
Clinical Pediatrics7 {; o* r. W' W7 X, N+ o
Volume 46 Number 6
4 U: N: R2 h! JJuly 2007 540-543
* g- @8 i4 N" t3 V/ j U* Y© 2007 Sage Publications
, @4 b: l' v- H6 I* Z& q) A10.1177/0009922806296651
3 h9 F% U% Y$ ^3 B# |6 A( J/ bhttp://clp.sagepub.com% V; x- u3 d- G) J
hosted at
* }) b' V) s7 Nhttp://online.sagepub.com
_. C6 c2 c1 MPrecocious puberty in boys, central or peripheral,
3 K4 n* K. E; B# T- q8 {$ T+ P" ois a significant concern for physicians. Central# u1 ~; ]% O3 `7 ^
precocious puberty (CPP), which is mediated
: I% {" K: m& v, p0 x: U8 F5 m. Gthrough the hypothalamic pituitary gonadal axis, has
% W# G$ |/ Z6 K2 q k; k) @. Ea higher incidence of organic central nervous system; z4 V# V6 [ p6 t. x. R
lesions in boys.1,2 Virilization in boys, as manifested
9 i" b' P) ~+ R3 v! pby enlargement of the penis, development of pubic& o& {: m1 U( C9 J# u9 x
hair, and facial acne without enlargement of testi-
+ \6 ?4 M5 f) ?! V; m! Y9 Gcles, suggests peripheral or pseudopuberty.1-3 We
; G/ `2 m6 z( ~3 {' S3 ureport a 16-month-old boy who presented with the3 A M+ O9 O1 F% ^" R
enlargement of the phallus and pubic hair develop-$ P: w% f; v& l. S% j
ment without testicular enlargement, which was due
4 R, i2 N3 J! i Q0 c6 b6 o; Oto the unintentional exposure to androgen gel used by* K1 l- Z# S1 `! C/ D6 j
the father. The family initially concealed this infor-
0 M5 A% ~# S1 ?8 `1 amation, resulting in an extensive work-up for this
* _- A6 y3 ^, Q, ]2 p! o9 A bchild. Given the widespread and easy availability of$ `+ A, V3 u7 D
testosterone gel and cream, we believe this is proba-
! \$ o7 \$ Q! b, E$ qbly more common than the rare case report in the Q6 w5 e; D8 E& y) E: y
literature.4& A, `# U$ s, R0 Y
Patient Report
7 s/ u4 d+ _; Z- ?6 Y" aA 16-month-old white child was referred to the1 f# y0 Y& `- V
endocrine clinic by his pediatrician with the concern9 D9 i- N0 R; V- ?2 X0 K
of early sexual development. His mother noticed6 i- o6 D' G# i# X. q' q& r
light colored pubic hair development when he was
2 D9 Z. G! P7 y7 c# C, W/ q" ]From the 1Division of Pediatric Endocrinology, 2University of
1 K1 o* e1 @, a7 x ASouth Alabama Medical Center, Mobile, Alabama.# A) T& Q2 |7 c, O3 i
Address correspondence to: Samar K. Bhowmick, MD, FACE,& p J6 Z1 @+ `, a) b+ d4 p6 R
Professor of Pediatrics, University of South Alabama, College of) I- U* ^: f4 W# u1 H4 m; l6 G2 k
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
8 n( a3 p( l" y) Ge-mail: [email protected].
% i, D9 E* p3 G. c- F- @; Eabout 6 to 7 months old, which progressively became
/ W/ q/ \5 r8 V0 c' x6 zdarker. She was also concerned about the enlarge-% S+ F& a9 ~1 N$ W3 }* a
ment of his penis and frequent erections. The child
3 n' O }1 L3 f- ]$ ^" B$ M! xwas the product of a full-term normal delivery, with7 ]$ E6 _. \) X# G* W. I1 D
a birth weight of 7 lb 14 oz, and birth length of
# N h% V4 s) |# {20 inches. He was breast-fed throughout the first year
/ A- v6 Z( H" n$ ^8 a4 j" c& Vof life and was still receiving breast milk along with
$ Y8 H. k0 b' t# h. V/ Vsolid food. He had no hospitalizations or surgery,! w) o) j5 M: o0 }& ~
and his psychosocial and psychomotor development
/ n8 D; }+ Q' ?0 R% T v, p" Xwas age appropriate.2 z5 t# |6 z( ]$ E% V: |8 Z6 O }
The family history was remarkable for the father,6 o: ~- o1 Q2 G" j8 R, N( i
who was diagnosed with hypothyroidism at age 16,5 @* q+ ], P% T/ @) m- H _8 m
which was treated with thyroxine. The father’s
. f5 H0 g; o8 O2 @, Iheight was 6 feet, and he went through a somewhat
& k1 H1 ?) d5 B+ I0 K; O3 }, Fearly puberty and had stopped growing by age 14.& y$ s5 m7 C6 J5 q
The father denied taking any other medication. The
" z' V2 m- m4 N/ |: o1 t9 Y$ Bchild’s mother was in good health. Her menarche; m7 ]5 g4 R1 X/ v/ V
was at 11 years of age, and her height was at 5 feet
& f" i/ w+ h6 A4 B" M9 r; S5 inches. There was no other family history of pre-
9 k( `; D% q2 ?/ lcocious sexual development in the first-degree rela-
7 b. k$ ]% T; Y- [ H; I8 A$ A9 Z- rtives. There were no siblings.) N8 x% W+ a0 `7 H' X$ g& G" ^' I
Physical Examination
! O6 v, i: {% e& u" {2 q4 wThe physical examination revealed a very active,
$ v5 ?* }% B$ F3 A4 T) N3 kplayful, and healthy boy. The vital signs documented5 ^7 B0 v d1 d2 N0 V4 B0 r5 b
a blood pressure of 85/50 mm Hg, his length was7 G: F2 P) T+ V, u: i6 @2 G( s
90 cm (>97th percentile), and his weight was 14.4 kg
" O2 u' \: S1 k) ?+ i& m(also >97th percentile). The observed yearly growth
0 y. u/ |" Q+ ]1 m9 wvelocity was 30 cm (12 inches). The examination of
1 b/ K: I! @$ d( b0 C6 a6 |- ` \the neck revealed no thyroid enlargement.
# o; Y5 B" z8 o; h7 \ a3 @The genitourinary examination was remarkable for
, @0 \$ s# ^/ \- X! r L$ _* Uenlargement of the penis, with a stretched length of
: f% H5 `" j( L9 ]8 cm and a width of 2 cm. The glans penis was very well H h) `6 i% V9 C7 W6 s
developed. The pubic hair was Tanner II, mostly around
$ h# d6 N& e8 J% G540
6 \& Y( M1 n; h E1 E x* Uat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
! U g' v5 c8 E7 sthe base of the phallus and was dark and curled. The. f# W9 p) W0 j. m5 J
testicular volume was prepubertal at 2 mL each.: @7 T0 l4 r$ I! d" |6 Z5 V1 p
The skin was moist and smooth and somewhat3 U! s3 s) I5 a/ w, c
oily. No axillary hair was noted. There were no
& N, g7 _1 [% m+ s! Q# ^" p. l8 p) Babnormal skin pigmentations or café-au-lait spots.
s* M$ G. N/ T% L, l" M2 D) E& G" t9 nNeurologic evaluation showed deep tendon reflex 2+
1 G$ N# [! g/ e% \* B ]" Q* D+ Jbilateral and symmetrical. There was no suggestion' ~- X% z( H8 H$ b; Z& x, h+ V
of papilledema.
4 l5 o6 t: Z0 x1 m$ F ?Laboratory Evaluation; X% G7 o2 X+ k F# k
The bone age was consistent with 28 months by
8 d# ~: s9 h7 Q) x$ o2 B4 ~; R+ Y( eusing the standard of Greulich and Pyle at a chrono-
! G7 j, Q3 i: b% n1 slogic age of 16 months (advanced).5 Chromosomal# b8 W: ^ p/ L+ f$ Z: _0 J
karyotype was 46XY. The thyroid function test
$ R; g% a% y3 R' R- ashowed a free T4 of 1.69 ng/dL, and thyroid stimu-
3 R7 ?6 o; s# u: y4 slating hormone level was 1.3 µIU/mL (both normal).0 o, ^. s- ~/ K% F, w
The concentrations of serum electrolytes, blood
6 c3 I, {7 a) R4 kurea nitrogen, creatinine, and calcium all were
4 D M5 T6 z% N1 ]$ w8 g2 h* hwithin normal range for his age. The concentration# B9 u; @, {; Y, T: p/ E
of serum 17-hydroxyprogesterone was 16 ng/dL. o: k% H% m' A0 ^. R
(normal, 3 to 90 ng/dL), androstenedione was 20
; g# l! Y4 l8 x8 Ing/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
( i, L8 {3 v4 X1 p* pterone was 38 ng/dL (normal, 50 to 760 ng/dL),
z& n( H; t1 b0 P4 t! W) r$ \0 Qdesoxycorticosterone was 4.3 ng/dL (normal, 7 to5 c6 h/ O2 ], I! K m8 Q" x
49ng/dL), 11-desoxycortisol (specific compound S)" ?1 d5 ~3 L v' E3 Q) v( B
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
t4 |3 r1 k8 q l* ?" |, v% Ctisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total5 C* X* N; {4 W) U ^+ r1 F
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),/ z. ?. w0 g0 Q' h' h2 R. S6 u
and β-human chorionic gonadotropin was less than+ H5 D2 L) h3 f8 @- k/ ]5 ?* {
5 mIU/mL (normal <5 mIU/mL). Serum follicular+ {3 M4 N3 {& q' o
stimulating hormone and leuteinizing hormone1 n4 i: d5 Q; G8 `& t
concentrations were less than 0.05 mIU/mL) ?' S' h+ V' k1 W y$ V
(prepubertal).0 x9 h% s r3 b. c0 O! J
The parents were notified about the laboratory
* o, u" F7 ?( r( k* gresults and were informed that all of the tests were1 l; A2 J/ {+ V% H. R* L4 A
normal except the testosterone level was high. The I5 O8 e4 }4 V; i0 @2 j9 R
follow-up visit was arranged within a few weeks to# j( K* B5 a$ l+ P4 {& {# H1 V
obtain testicular and abdominal sonograms; how-* t2 R, q2 ?1 y" k
ever, the family did not return for 4 months.
( j {! z& y: X4 L+ XPhysical examination at this time revealed that the) n5 P& t$ {/ G8 E: {
child had grown 2.5 cm in 4 months and had gained3 `. j1 l& P; G% G+ ?
2 kg of weight. Physical examination remained
7 f5 u( |# I& w3 junchanged. Surprisingly, the pubic hair almost com-
; ]) \: ~, k$ Kpletely disappeared except for a few vellous hairs at
+ T. j: N4 E" G" y- U0 uthe base of the phallus. Testicular volume was still 2' R& F: H& r/ @; v/ t0 }4 d, S6 K
mL, and the size of the penis remained unchanged.1 N! m2 e3 p& P/ i( ?& f& p8 r
The mother also said that the boy was no longer hav-. Z$ N( h+ c3 s( \: ~1 E5 n
ing frequent erections.# ]1 ~7 ]2 E, c
Both parents were again questioned about use of
( k' P- B6 b) o Q+ v5 Pany ointment/creams that they may have applied to3 p5 Z. `" b y0 s- O0 W
the child’s skin. This time the father admitted the' U) ~# u; N# g' c: c& @8 |! z+ u9 o
Topical Testosterone Exposure / Bhowmick et al 541
" |( G: F: w" |) ~use of testosterone gel twice daily that he was apply-* ^3 M+ s0 m9 `+ H S7 p2 P
ing over his own shoulders, chest, and back area for, a+ E# K5 ^, M* M, \1 e
a year. The father also revealed he was embarrassed
$ f7 p3 f( C8 N% kto disclose that he was using a testosterone gel pre-
7 j& o4 H% T9 Kscribed by his family physician for decreased libido/ l% w5 I# s$ D. H5 Y' L, ?
secondary to depression.
" B" t: v* a ~! K6 Y: |0 m: qThe child slept in the same bed with parents.
" F) L. q l R: F0 |/ C2 YThe father would hug the baby and hold him on his+ C# R1 {8 B9 m5 m! U
chest for a considerable period of time, causing sig-. }) B* I2 b, I9 O. O
nificant bare skin contact between baby and father./ ]8 L/ W8 y7 F; p6 H, {
The father also admitted that after the phone call,
" A5 |; D2 K: V1 Mwhen he learned the testosterone level in the baby$ m% W' o. n1 }. B9 j7 K
was high, he then read the product information0 E+ B+ j$ ]* {# T! F4 Z
packet and concluded that it was most likely the rea-0 @' ]' k. X/ l
son for the child’s virilization. At that time, they* G, n- t0 B6 y% i# C) P2 Z: H4 c f
decided to put the baby in a separate bed, and the% N+ z% }8 v5 ~" s u1 H1 D" }9 P
father was not hugging him with bare skin and had$ L4 @6 k, E; K
been using protective clothing. A repeat testosterone4 s1 ^3 E- ~% O( c# o, t3 \. L
test was ordered, but the family did not go to the y# ^8 t' g: n' [
laboratory to obtain the test.
: D6 }: f* K# K2 g3 h7 P0 tDiscussion
# N3 Q0 C! }+ X/ y8 kPrecocious puberty in boys is defined as secondary/ ?7 y# ^ o0 O3 C0 \# Q3 y' D
sexual development before 9 years of age.1,4. e0 I1 ?% \8 @
Precocious puberty is termed as central (true) when3 [; N; p' P' E. Z" ]7 ?
it is caused by the premature activation of hypo-
! x5 ?+ j- j0 @" A1 jthalamic pituitary gonadal axis. CPP is more com-; w& h) H$ y, C0 i
mon in girls than in boys.1,3 Most boys with CPP
, s4 e& M3 P/ ^0 H7 G Emay have a central nervous system lesion that is
, n# A5 ~4 q+ e( xresponsible for the early activation of the hypothal-
! e* Q3 j* q) f% ~% E* Tamic pituitary gonadal axis.1-3 Thus, greater empha- }; k. ?. h7 q6 O
sis has been given to neuroradiologic imaging in6 C$ |& B1 }' K1 P- f' M
boys with precocious puberty. In addition to viril-: {9 h7 q- B+ P. [3 C" m% |6 f
ization, the clinical hallmark of CPP is the symmet-% _' b' Q0 Q! I3 y% B
rical testicular growth secondary to stimulation by
- N" H3 a5 P1 K" }gonadotropins.1,3
S$ z% E& X' ?) s; P( f& BGonadotropin-independent peripheral preco-% N. t: A; q( b, l
cious puberty in boys also results from inappropriate
: N2 F+ G) l. aandrogenic stimulation from either endogenous or5 ~% x! E4 @4 B+ Z
exogenous sources, nonpituitary gonadotropin stim-1 O+ g _& ~( z
ulation, and rare activating mutations.3 Virilizing
# H; w% O) @! X ~7 h0 Hcongenital adrenal hyperplasia producing excessive" N% f6 ?$ M8 r. ^
adrenal androgens is a common cause of precocious
6 O( B q* c+ gpuberty in boys.3,4
/ @& H& l2 m; T' EThe most common form of congenital adrenal3 ?+ B$ n7 ~( `; P: l3 s3 J7 l
hyperplasia is the 21-hydroxylase enzyme deficiency.1 Q4 m) ^! s: q, y' x
The 11-β hydroxylase deficiency may also result in4 Q5 [2 o$ f) ?5 l$ L
excessive adrenal androgen production, and rarely,0 z4 ~6 P: f8 S1 c
an adrenal tumor may also cause adrenal androgen( M+ j3 {. u: z( L
excess.1,3& O: `+ W$ q# T8 R$ H% V+ t* [
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from# D& W7 W' x# j; a
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
' d! [, x# E" qA unique entity of male-limited gonadotropin-
( d3 P+ z. a% H9 Y; k3 Y; W. Rindependent precocious puberty, which is also known
( N A( ^. B$ N8 `5 E" m9 las testotoxicosis, may cause precocious puberty at a
* o4 O2 P" H& i! y9 R( c6 w2 zvery young age. The physical findings in these boys" \% j% S( V) R7 R
with this disorder are full pubertal development,
- a) I0 d. G. L4 [! Wincluding bilateral testicular growth, similar to boys
9 o3 y0 j. n) h) e6 Xwith CPP. The gonadotropin levels in this disorder
9 }% n: E f, q/ `) _( eare suppressed to prepubertal levels and do not show
* N2 ]! v2 m4 L# z1 _! fpubertal response of gonadotropin after gonadotropin-# a6 C; `% h0 U5 M, I9 E
releasing hormone stimulation. This is a sex-linked
# b" `# G, f& q& }2 zautosomal dominant disorder that affects only
( \) ^. @ m3 o" W. x# k- Rmales; therefore, other male members of the family
1 O, ~5 m4 B* ]" B9 w; {2 ]may have similar precocious puberty.3
9 D. Q* T$ H4 b/ F! bIn our patient, physical examination was incon-2 ~6 z+ t; i% [2 b1 c% z0 i5 g! S
sistent with true precocious puberty since his testi-/ b! N5 D2 |9 P8 x. o% b9 _
cles were prepubertal in size. However, testotoxicosis
& R* n( Q" E7 c! R( s* uwas in the differential diagnosis because his father# p2 S9 z7 {2 s9 a3 o
started puberty somewhat early, and occasionally,
: [0 ?5 q$ L8 ?+ Qtesticular enlargement is not that evident in the* _. D; \7 W* ^+ ]. e5 k; s
beginning of this process.1 In the absence of a neg- y5 j8 F9 T4 b2 {4 W" O
ative initial history of androgen exposure, our: I, i$ f) i1 r( ?9 J8 [% z) |
biggest concern was virilizing adrenal hyperplasia,4 `) w3 f9 w$ g- d! q j
either 21-hydroxylase deficiency or 11-β hydroxylase
! [, c: T/ o. T9 Mdeficiency. Those diagnoses were excluded by find-$ u ^4 Q; {. |
ing the normal level of adrenal steroids./ ?6 q" Y2 {+ D' C, F/ s+ K
The diagnosis of exogenous androgens was strongly2 j1 b' d8 U8 }# f3 s0 G, }% L7 |
suspected in a follow-up visit after 4 months because h* H4 o$ z1 f/ o$ h1 Z- F- ?
the physical examination revealed the complete disap-
& p/ b/ l1 l, Npearance of pubic hair, normal growth velocity, and0 E8 o; t2 B2 X
decreased erections. The father admitted using a testos-# r1 ]; a- P6 D% S5 ?! U' m O9 C
terone gel, which he concealed at first visit. He was2 l( t$ S: y1 m& L: B w
using it rather frequently, twice a day. The Physicians’' ?$ J0 M# o0 U7 q7 q' q
Desk Reference, or package insert of this product, gel or
5 y( u4 N6 y& V8 x: e" W5 ^cream, cautions about dermal testosterone transfer to
: Z# }, W7 P8 S& x cunprotected females through direct skin exposure.
4 q2 d% C' s3 i" ^9 ~0 XSerum testosterone level was found to be 2 times the3 [* `& v$ q, ~5 M
baseline value in those females who were exposed to6 E0 w! o/ M& C. _ L
even 15 minutes of direct skin contact with their male
; x2 ^" ^( {4 w' J9 ]& p2 hpartners.6 However, when a shirt covered the applica-0 q) S. ^, P, m+ @0 q% ]* [) V8 g
tion site, this testosterone transfer was prevented.3 A8 R* {/ o4 R$ b9 L- f; ]
Our patient’s testosterone level was 60 ng/mL,6 L. S6 H4 `! @/ b7 D6 d+ H% t
which was clearly high. Some studies suggest that
8 V* k( I( y4 u, ~% M3 K4 m: m2 S2 ^dermal conversion of testosterone to dihydrotestos-
' m/ D) T: Y* @3 _terone, which is a more potent metabolite, is more
r+ j8 w1 t$ Y& ~active in young children exposed to testosterone# O6 x) `! j1 ~1 d2 r% j
exogenously7; however, we did not measure a dihy-
3 G" c3 g2 j1 h u3 K6 y! @; Rdrotestosterone level in our patient. In addition to
4 k8 H7 O5 s4 @; T* X- Kvirilization, exposure to exogenous testosterone in
. z! O P2 B0 p- z7 v* {/ Y! Ochildren results in an increase in growth velocity and
$ E% F" h5 ?- Yadvanced bone age, as seen in our patient.9 Y# y8 h; y1 N4 l
The long-term effect of androgen exposure during
7 N" [9 c" v; c% V- @6 {. e* Rearly childhood on pubertal development and final
L: B2 Y) Z, @7 Y! Z- \* N. [adult height are not fully known and always remain! J% `0 i1 @5 D0 n1 P4 ]% b. r
a concern. Children treated with short-term testos-6 X4 j, g7 v' S! \. W3 |- p
terone injection or topical androgen may exhibit some! `3 H' K. W% @2 |, U5 ] Y F; \
acceleration of the skeletal maturation; however, after2 M: A! W% y3 _" C
cessation of treatment, the rate of bone maturation
2 g. D6 R7 f. Q9 K ]2 Q4 {/ Ndecelerates and gradually returns to normal.8,9
) |$ @5 }+ X, PThere are conflicting reports and controversy7 i A4 I5 x1 a. G
over the effect of early androgen exposure on adult
& j( n3 \3 v) p: ~4 b3 Kpenile length.10,11 Some reports suggest subnormal
* c4 X8 O- _ v6 H& q2 Q0 Fadult penile length, apparently because of downreg-4 {) w; d5 Y$ B, C4 d8 }
ulation of androgen receptor number.10,12 However,5 ~! U W" M" T8 g5 ~, H& k- d
Sutherland et al13 did not find a correlation between
& V( m# q4 k* ~6 k* ? `0 a0 g2 ~childhood testosterone exposure and reduced adult% k1 `6 Q. N2 l5 S) j
penile length in clinical studies.9 l% F/ A3 ]! o& W: ?
Nonetheless, we do not believe our patient is
7 G# Q$ }* y, X& r" B( q, V" Ygoing to experience any of the untoward effects from
- k# o7 l, P! Ttestosterone exposure as mentioned earlier because
9 { J% }9 g0 ?7 e1 R% ^( Ythe exposure was not for a prolonged period of time.
+ d# y4 V/ V f0 i6 fAlthough the bone age was advanced at the time of
$ F; r. X9 j* {! m' o8 u6 ^diagnosis, the child had a normal growth velocity at
/ Q, s5 a: S- I3 z6 E+ wthe follow-up visit. It is hoped that his final adult0 {/ m& [. x! Y9 z& _: j4 ]* c) f
height will not be affected.
5 ~5 i$ f# `, s3 q' EAlthough rarely reported, the widespread avail-* a$ [9 r4 G2 g$ Z+ A0 J' q
ability of androgen products in our society may
- `' n. P0 V/ \+ z( V1 v. r2 oindeed cause more virilization in male or female' Y0 r8 z0 S! `3 F' S% l
children than one would realize. Exposure to andro-) i E* L9 z- s
gen products must be considered and specific ques-
. |- r- Z8 w# ~' t% Qtioning about the use of a testosterone product or
" {& i2 d) X& Cgel should be asked of the family members during
3 _2 i# v T; V) g8 I, kthe evaluation of any children who present with vir-# S. g7 [8 R( h5 t
ilization or peripheral precocious puberty. The diag-! |- e# P4 H. e: V
nosis can be established by just a few tests and by
' g0 l% i) p( z- g8 @! Xappropriate history. The inability to obtain such a, c9 ?- b/ ]7 j8 O' {6 F
history, or failure to ask the specific questions, may
O9 x( F# h3 h6 u; O) l, qresult in extensive, unnecessary, and expensive( J0 R6 M9 R$ Y4 `" A
investigation. The primary care physician should be$ C7 N9 p" [, K% o
aware of this fact, because most of these children7 N) k9 F) h3 N* p6 N2 h
may initially present in their practice. The Physicians’9 x3 r+ M( \% G5 U( g+ W
Desk Reference and package insert should also put a
5 C) T, b+ a' w G; t- j% {0 wwarning about the virilizing effect on a male or# o5 G$ f4 v- }$ t' [- v" l! P" ^' Y
female child who might come in contact with some-
6 V7 c! y% j gone using any of these products.5 w, [+ l3 w. ^2 H4 P
References
( k5 r, V* f. c' |7 {5 e* h0 h1. Styne DM. The testes: disorder of sexual differentiation
* ^# q* V7 D% A( wand puberty in the male. In: Sperling MA, ed. Pediatric; e4 f3 @# h- d# b' z
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
# n- G/ m. M" n1 t3 E* m* Y2002: 565-628.
3 r# p- g( u! n2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious* I, y5 P$ l* B
puberty in children with tumours of the suprasellar pineal |
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