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Sexual Precocity in a 16-Month-Old
9 f# D' F% t+ q% U+ G" q N9 gBoy Induced by Indirect Topical
+ t7 N! x& n% u' sExposure to Testosterone" `$ m" _5 Q2 v
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2. D; R/ ~& [4 f. E9 E
and Kenneth R. Rettig, MD1& M2 c' M1 I6 C" o% r& e @0 b/ _
Clinical Pediatrics
# F0 ~- ]' l8 {3 o9 {" v wVolume 46 Number 6. X9 D/ c( Z5 {
July 2007 540-5432 e! T5 O1 X; o+ a! A
© 2007 Sage Publications
& ?" R: k8 r) d% Z1 K4 y! I10.1177/00099228062966513 r8 @$ b/ `" a- i. }) ^
http://clp.sagepub.com
$ u m) R4 t! K, Jhosted at: d* f$ K4 i8 G9 A4 ]& K
http://online.sagepub.com) t# Q7 }( t/ k6 `
Precocious puberty in boys, central or peripheral,/ ~: X: s9 d1 W4 }6 g2 ^' e
is a significant concern for physicians. Central8 M& t+ V: K) s) v# q( O- C" o
precocious puberty (CPP), which is mediated9 X1 G: w4 E' l
through the hypothalamic pituitary gonadal axis, has
* U: O! r; ^5 M- H& B+ La higher incidence of organic central nervous system
L' A- j1 i$ d9 t! Ilesions in boys.1,2 Virilization in boys, as manifested4 ~% j% y3 Z/ L0 K8 U2 z ~( s. z
by enlargement of the penis, development of pubic7 E, P/ q" F- m9 @
hair, and facial acne without enlargement of testi-
4 I8 T/ v4 L9 Mcles, suggests peripheral or pseudopuberty.1-3 We( a4 Z0 V1 G, V, b4 K0 N
report a 16-month-old boy who presented with the
4 d* q2 j; ?7 n6 u9 @enlargement of the phallus and pubic hair develop-4 u* v/ \$ @# g7 l; y, X m7 h
ment without testicular enlargement, which was due& I2 U( I: I$ D8 Q7 @7 O. e3 R' }) }
to the unintentional exposure to androgen gel used by
8 h9 \% B2 J) bthe father. The family initially concealed this infor-8 v! }# o8 e: P. D# ]
mation, resulting in an extensive work-up for this
6 ^+ z4 _+ s! m: Uchild. Given the widespread and easy availability of6 @8 h u2 S" \5 e' f
testosterone gel and cream, we believe this is proba-, @( I0 a" `$ M) J
bly more common than the rare case report in the
t0 r6 H: D1 X! Dliterature.4
4 B6 ^5 g1 `5 w' PPatient Report( J- \/ o& I# L( v3 g
A 16-month-old white child was referred to the0 c% {$ h0 J G! V/ U# e) v& H+ Y
endocrine clinic by his pediatrician with the concern* A. P8 g2 n2 O% s
of early sexual development. His mother noticed
# ~, S" b* T5 [3 q7 @9 R5 Flight colored pubic hair development when he was8 Z; I5 U! G7 F7 u) c8 s7 ^: u
From the 1Division of Pediatric Endocrinology, 2University of
! x. ?0 A- }! v/ wSouth Alabama Medical Center, Mobile, Alabama.
5 c+ \, S) A( j( k2 a5 FAddress correspondence to: Samar K. Bhowmick, MD, FACE,5 ?/ r8 Q0 X6 l+ k% I: M
Professor of Pediatrics, University of South Alabama, College of
* H" q n% y I) m7 bMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
, g9 p2 S" M, J1 c Fe-mail: [email protected].
+ t4 A) @0 e( n5 yabout 6 to 7 months old, which progressively became
r+ l# U# V$ C8 e7 G0 Vdarker. She was also concerned about the enlarge-
8 j! L( q! {$ k& fment of his penis and frequent erections. The child# Q4 P u- z& f4 t3 ~/ e
was the product of a full-term normal delivery, with2 l& m( z! H$ _/ t. f: E+ x+ j
a birth weight of 7 lb 14 oz, and birth length of
. M7 m& \# i7 V5 A; B w& z20 inches. He was breast-fed throughout the first year A8 t! G& \0 i# p. J1 l; A& ?
of life and was still receiving breast milk along with
+ f o( C% Y& x7 E2 ~- vsolid food. He had no hospitalizations or surgery,/ X8 \6 q& A1 O! ^/ j3 X3 _" D1 s
and his psychosocial and psychomotor development
- D L/ P) v, O+ G$ S; `: _. R1 T; @* qwas age appropriate.
0 Y& P! e7 n. o- q1 L9 j# W$ AThe family history was remarkable for the father,
8 H0 ^3 J7 B! S" h7 i4 l& ]who was diagnosed with hypothyroidism at age 16,
/ Y# k5 B6 X3 v mwhich was treated with thyroxine. The father’s& e% _, I6 L1 U9 K( M+ A
height was 6 feet, and he went through a somewhat) \! L" ]6 l- _, E8 C
early puberty and had stopped growing by age 14.
" Z# [" ^5 N( Q& C+ x! G1 x7 h: BThe father denied taking any other medication. The
$ ~% F+ ~3 G- t! l* c6 y( gchild’s mother was in good health. Her menarche' ]% U: m, _# J- z; L8 r8 V5 T
was at 11 years of age, and her height was at 5 feet2 M5 n0 c. j% \6 T
5 inches. There was no other family history of pre-7 w' w, p7 p8 Z! ^3 G z% ^- ?
cocious sexual development in the first-degree rela-
3 H% }# Q$ c. J" Y0 i, X5 V# B! ftives. There were no siblings.) e e% W3 X6 q$ g
Physical Examination
, v$ W- X: m) \) n+ Q/ @The physical examination revealed a very active,
# h# d% w4 ]$ T1 _playful, and healthy boy. The vital signs documented+ r, }: t, E: U; i% [7 C; b
a blood pressure of 85/50 mm Hg, his length was) S8 ]5 D1 c! T3 n. D$ V
90 cm (>97th percentile), and his weight was 14.4 kg! O( s, i. Y- C2 o
(also >97th percentile). The observed yearly growth
; G1 J* n- p; l: b* v uvelocity was 30 cm (12 inches). The examination of6 ~9 r5 G" y+ T5 U. ]' C
the neck revealed no thyroid enlargement.
. S; t4 R7 Z: [& IThe genitourinary examination was remarkable for; C3 {. Q4 O! a% D1 R/ a! Y/ d
enlargement of the penis, with a stretched length of
) i- K* @* g1 _2 u9 m: i$ w" X8 cm and a width of 2 cm. The glans penis was very well
) c- ^1 M, A: z! `developed. The pubic hair was Tanner II, mostly around0 u; f5 c5 k" F. @9 v
540
0 t) {2 Z _& V4 W2 |! @0 o9 Qat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from$ h6 U; N# v; \( ?. k
the base of the phallus and was dark and curled. The0 C" _+ ]' Q/ O* x! `% e0 n
testicular volume was prepubertal at 2 mL each.
$ M8 i( Q0 h/ v% D( w9 TThe skin was moist and smooth and somewhat6 q2 _) s2 L( s$ e
oily. No axillary hair was noted. There were no& K% Z* ]+ p2 |* \* ` l2 i+ f
abnormal skin pigmentations or café-au-lait spots.9 L2 ~. ~; Q/ ?+ @3 c* a" [
Neurologic evaluation showed deep tendon reflex 2+8 {$ R9 h5 ^4 R. J
bilateral and symmetrical. There was no suggestion
0 A5 |4 W* r/ @2 n5 Fof papilledema.7 Y0 \$ i" E$ x4 i+ z7 w
Laboratory Evaluation, d6 p, u9 T( t2 M; y# C5 ~
The bone age was consistent with 28 months by
, G8 ]' ^' U/ I musing the standard of Greulich and Pyle at a chrono-* p5 L% |+ i% r) f
logic age of 16 months (advanced).5 Chromosomal
# n/ E# R% Q# t2 N. W9 b1 Dkaryotype was 46XY. The thyroid function test
6 @# R. J$ I) h. yshowed a free T4 of 1.69 ng/dL, and thyroid stimu-) E! Z6 S& p8 C8 `
lating hormone level was 1.3 µIU/mL (both normal).* e- b* y1 ]2 I
The concentrations of serum electrolytes, blood5 h3 p) k+ O3 O4 q, W& h4 V2 P, z
urea nitrogen, creatinine, and calcium all were8 S2 Z, B$ ?; N
within normal range for his age. The concentration
0 }( z+ E- ~8 a4 Pof serum 17-hydroxyprogesterone was 16 ng/dL0 Y' o, ?, x$ V7 r' ]2 w1 M
(normal, 3 to 90 ng/dL), androstenedione was 20
6 G2 g R# s0 L4 Gng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-( c/ z/ \$ g% k6 C3 a# }
terone was 38 ng/dL (normal, 50 to 760 ng/dL),1 p G) U- ~6 t8 T+ i( G J
desoxycorticosterone was 4.3 ng/dL (normal, 7 to/ P0 X+ e0 [1 B& F( ^+ {( d) ~
49ng/dL), 11-desoxycortisol (specific compound S)
: \& B9 R' l: q6 C9 @" `9 Vwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
+ R- N7 L5 Q. U3 c9 b% @5 Ptisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total0 z, s8 b# D8 C7 t: ~0 a
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
8 z0 l2 b" P, U' ?' uand β-human chorionic gonadotropin was less than. X* j d' Q' W9 I6 i! b
5 mIU/mL (normal <5 mIU/mL). Serum follicular5 u7 r$ ~: {, ~2 [, x* j F
stimulating hormone and leuteinizing hormone" V3 `! r4 g6 s j: h4 Y" y* L
concentrations were less than 0.05 mIU/mL V X3 Q4 q4 j) s" J% @. s
(prepubertal).
9 \) N' E( t' c% E5 {. wThe parents were notified about the laboratory; \# C- e* Q6 c
results and were informed that all of the tests were
0 s0 [- e6 @" U4 C! t; t2 Z, b2 \normal except the testosterone level was high. The8 h6 \5 `) d1 E* ?
follow-up visit was arranged within a few weeks to
9 @* G, }, t. J4 y7 A! U2 Gobtain testicular and abdominal sonograms; how-: {3 @7 j- t3 X' q
ever, the family did not return for 4 months.1 x' t/ t6 C: j1 B' k1 _+ }
Physical examination at this time revealed that the( l5 h5 Y. J. i
child had grown 2.5 cm in 4 months and had gained) U. B& T3 o3 m0 D4 u/ ?
2 kg of weight. Physical examination remained
, r0 C0 x( o- I/ R d' ?unchanged. Surprisingly, the pubic hair almost com-6 C8 R2 Q% P I# N& O% o; s
pletely disappeared except for a few vellous hairs at
3 m! a* A/ l) Q5 D' O! i% Nthe base of the phallus. Testicular volume was still 2# q! o0 Q1 ], M. v( |! `5 W# B, w
mL, and the size of the penis remained unchanged.0 M5 T2 b% s2 w. ?) @% m: l
The mother also said that the boy was no longer hav-- x+ j7 @/ L% F5 n2 N
ing frequent erections.8 @& d! n' V0 C. t6 {" j/ j" F) W' w+ `
Both parents were again questioned about use of3 ?7 f) Q2 t/ u/ W( I
any ointment/creams that they may have applied to
) H: N! ?& }# r3 p) w7 ?the child’s skin. This time the father admitted the
0 p u6 L+ W+ NTopical Testosterone Exposure / Bhowmick et al 541
0 z, p, _8 c- Quse of testosterone gel twice daily that he was apply-: n0 q. Y! y+ Q& ?% P
ing over his own shoulders, chest, and back area for
2 y5 A" ?- t- Y% P: h9 K, `* xa year. The father also revealed he was embarrassed
9 y2 g0 r# s+ ~$ G9 m! ~( jto disclose that he was using a testosterone gel pre-3 U* |& Z2 w1 V) {6 ]
scribed by his family physician for decreased libido
/ n" K/ {1 P* \6 c- K3 M( Esecondary to depression.
' o& j& u$ l2 aThe child slept in the same bed with parents.
- d( @6 f3 K& QThe father would hug the baby and hold him on his$ \& q5 [5 p* w0 O
chest for a considerable period of time, causing sig-$ [! T7 j2 R$ G4 K, z7 d
nificant bare skin contact between baby and father.
7 [9 X) W3 o6 zThe father also admitted that after the phone call,
9 o3 H! C1 ]- A* s/ p% B8 gwhen he learned the testosterone level in the baby4 n# O) u9 ^) E: _
was high, he then read the product information0 b+ R3 s. {/ p v# r* S
packet and concluded that it was most likely the rea-
! @- Q- p; ]8 Qson for the child’s virilization. At that time, they
6 h @# i" s: E. z' Y. Wdecided to put the baby in a separate bed, and the
- v7 h# T }% u0 |father was not hugging him with bare skin and had
" |" B! e9 b& \6 I; gbeen using protective clothing. A repeat testosterone
5 \3 o( N$ V6 u! P& u5 M; {6 Ptest was ordered, but the family did not go to the% r3 f) m$ O# h( H7 ~
laboratory to obtain the test.$ h; Q1 K0 m9 p3 j$ W8 [
Discussion" `" p0 R% Z* o8 p# S T
Precocious puberty in boys is defined as secondary
, Z2 [2 ^, i. F; csexual development before 9 years of age.1,4
6 o# M: N6 z5 E6 k* u& q9 M3 mPrecocious puberty is termed as central (true) when3 J# M: O) z/ j5 G
it is caused by the premature activation of hypo-
; i; l% B2 u. K8 O/ f, G8 \thalamic pituitary gonadal axis. CPP is more com-
* h- p" P" T) L( w F# x Z; zmon in girls than in boys.1,3 Most boys with CPP9 s0 N e' O4 G) Z7 j! T2 T" ^
may have a central nervous system lesion that is
9 K+ a. D& S0 \( |: kresponsible for the early activation of the hypothal-
( V" r: j/ L% }; X C) B! Q1 F6 Namic pituitary gonadal axis.1-3 Thus, greater empha-4 C+ i6 w8 s4 \ P
sis has been given to neuroradiologic imaging in
. H" X* L, H" Q0 @$ v2 y/ J* Rboys with precocious puberty. In addition to viril-4 B# i+ P6 X' q7 b, T# W" U
ization, the clinical hallmark of CPP is the symmet-
. ]4 E# b! X/ I! drical testicular growth secondary to stimulation by' D c. g6 _% S* W0 F& y
gonadotropins.1,3! P4 W+ B9 \' H! M& n( V! M4 h+ l
Gonadotropin-independent peripheral preco-
$ v& B9 p* ]! R9 e+ x7 C# j9 Wcious puberty in boys also results from inappropriate
* l; {/ Y% ~# }8 Oandrogenic stimulation from either endogenous or
' `- I( e. \, g& b0 `6 e9 Gexogenous sources, nonpituitary gonadotropin stim-
) F5 T* C* e+ D& u& t, {0 b2 Y/ bulation, and rare activating mutations.3 Virilizing
0 Z+ v* H! M6 m2 s$ a! icongenital adrenal hyperplasia producing excessive
( d1 `3 e' Z4 [1 O" G/ I; Zadrenal androgens is a common cause of precocious
. |* C7 f# m# l* @; M! Tpuberty in boys.3,4
$ b1 t. p/ o+ iThe most common form of congenital adrenal
5 c- T; i7 H% x+ }0 f; Vhyperplasia is the 21-hydroxylase enzyme deficiency.6 H. r! a( c d' k! y. ~
The 11-β hydroxylase deficiency may also result in3 h+ G( ^, v. R& o& X
excessive adrenal androgen production, and rarely,3 a1 B9 ~4 O/ h2 o8 r8 b5 `
an adrenal tumor may also cause adrenal androgen7 X4 y- M- M6 ^# m% K2 K# U
excess.1,3
, o2 C( m; i3 N" E0 Hat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from8 F% M) R$ R# X- v5 z- p1 j
542 Clinical Pediatrics / Vol. 46, No. 6, July 20074 O& B5 N, P' @4 {& S4 d# y4 I' ?- b
A unique entity of male-limited gonadotropin-
6 F$ h2 {2 _$ F2 p1 h8 q3 Tindependent precocious puberty, which is also known$ n" Z8 [2 I6 Y! n* g( Y* F1 ~
as testotoxicosis, may cause precocious puberty at a
( k: Q4 P) J; i! ~/ ?3 R! v5 d6 e' Overy young age. The physical findings in these boys
* x) e1 [" b. k' ^9 awith this disorder are full pubertal development,. X1 x: y" M8 U, T' |0 g, J. s I
including bilateral testicular growth, similar to boys) k3 n; ^: P% i4 b1 L" M
with CPP. The gonadotropin levels in this disorder
r% {( f6 v$ A1 u9 o, Care suppressed to prepubertal levels and do not show' H/ U5 I+ ?8 ?: @4 H
pubertal response of gonadotropin after gonadotropin-
, L U+ |) Y) F% r0 D# X7 Creleasing hormone stimulation. This is a sex-linked
6 P s+ ?$ ]/ h! `8 G8 j O: ^- zautosomal dominant disorder that affects only( k$ B6 w- P8 `4 l
males; therefore, other male members of the family
; [% ?7 |" Y; y4 s: Xmay have similar precocious puberty.3
! H# ^( \0 K/ \7 G7 BIn our patient, physical examination was incon-0 ~, O" n: c; c) I9 U8 B7 W5 Q
sistent with true precocious puberty since his testi-" ]* b2 ]. T, N5 a' n
cles were prepubertal in size. However, testotoxicosis
" w& S% e2 A1 u% h4 [was in the differential diagnosis because his father3 @! X6 O: a$ G" i: r! [/ S1 H
started puberty somewhat early, and occasionally,% d* @+ a9 u- D' \- Z7 f R
testicular enlargement is not that evident in the8 h4 P2 l: z/ o2 v7 K! ~1 C- n+ p
beginning of this process.1 In the absence of a neg-3 N5 X$ c: r' m+ W
ative initial history of androgen exposure, our2 r3 p* V% Q/ H0 m+ v
biggest concern was virilizing adrenal hyperplasia,
8 o" ^0 G$ b1 j6 D% {; l$ jeither 21-hydroxylase deficiency or 11-β hydroxylase
4 Y) [6 o7 K6 f* u, J6 wdeficiency. Those diagnoses were excluded by find-# g% J( |2 s3 \
ing the normal level of adrenal steroids.
0 k% M+ w' D% X) ^. OThe diagnosis of exogenous androgens was strongly
+ S8 z% e. j) d/ h% p# Z8 N/ V: o# h* Asuspected in a follow-up visit after 4 months because
8 @* \2 \7 r% gthe physical examination revealed the complete disap-+ c r' b' a& ~
pearance of pubic hair, normal growth velocity, and) |; U/ W! ]4 G( E! m5 e) X* O
decreased erections. The father admitted using a testos-
/ K4 I( E8 v& f* w( c4 Cterone gel, which he concealed at first visit. He was
% K4 M# t. c6 [5 S8 h8 ?using it rather frequently, twice a day. The Physicians’& W/ P" f! A% b) q; \7 G
Desk Reference, or package insert of this product, gel or/ K6 e% [/ @/ g5 ? T6 n' a+ W
cream, cautions about dermal testosterone transfer to
; B, }5 x% w. Z" \- w5 Cunprotected females through direct skin exposure.
4 c% Y2 `: z( SSerum testosterone level was found to be 2 times the9 k; O; V4 [) h+ S' t: g) c' H
baseline value in those females who were exposed to1 H0 m R U9 y" H0 U0 q
even 15 minutes of direct skin contact with their male3 k* t$ z- y6 p4 a8 E
partners.6 However, when a shirt covered the applica-
! C3 N4 X' r. t8 l; Y2 dtion site, this testosterone transfer was prevented., v7 U. p$ U" @7 _& r( c
Our patient’s testosterone level was 60 ng/mL,0 r: r' h; X3 v
which was clearly high. Some studies suggest that+ M; ?" x* p1 J6 C! U8 o8 H
dermal conversion of testosterone to dihydrotestos-
% G& k( ^7 z- p" Hterone, which is a more potent metabolite, is more
2 [" g% T3 z5 O1 |& {7 dactive in young children exposed to testosterone
* E: ?8 r) s/ T3 Texogenously7; however, we did not measure a dihy-7 C. p, B4 k" w1 l
drotestosterone level in our patient. In addition to: V. v7 I# G+ B" J4 C4 E
virilization, exposure to exogenous testosterone in8 s& Z7 r' T- E# S$ S* z7 {# }; C
children results in an increase in growth velocity and
+ ]& i" w+ I, c8 S4 S o. v) Tadvanced bone age, as seen in our patient.
2 X& I. h3 f( Q; g$ j. P3 KThe long-term effect of androgen exposure during
2 F7 e6 o4 w( y2 k: ]early childhood on pubertal development and final+ e: W- m3 Z) T3 b! i$ M4 |5 O
adult height are not fully known and always remain2 e/ f& M$ v1 a$ I' g, U
a concern. Children treated with short-term testos-
9 g+ |4 @9 n1 C) T1 r/ Eterone injection or topical androgen may exhibit some
+ r% S; A+ g8 A- D+ nacceleration of the skeletal maturation; however, after$ H8 u' z/ x5 m- I
cessation of treatment, the rate of bone maturation
6 H m+ V. |( F2 M* D2 ldecelerates and gradually returns to normal.8,91 {- U5 s' Y; R0 Y5 t) w& z
There are conflicting reports and controversy
7 ]" ?+ a8 G: F- |* eover the effect of early androgen exposure on adult
/ [* s) _- U8 R- H/ l6 p- ?1 y0 V: zpenile length.10,11 Some reports suggest subnormal, }7 Y( c# o" G+ o% C5 ?
adult penile length, apparently because of downreg-1 N: T4 h+ J9 O
ulation of androgen receptor number.10,12 However,
' I( [9 R8 G1 \0 O+ k. E' C& zSutherland et al13 did not find a correlation between
V3 ~9 ^' x- \8 U: [% c3 |6 |childhood testosterone exposure and reduced adult
4 u! O! k2 S& q8 {; w/ Y8 f/ e, E5 G# ~penile length in clinical studies.& c; B; ^% m4 g3 y h! h1 x" c$ a
Nonetheless, we do not believe our patient is
/ W: Y1 X( J4 w7 `8 T) Mgoing to experience any of the untoward effects from
% s, [' H5 g/ K- y. C* ^8 ltestosterone exposure as mentioned earlier because
& X% R' }5 E/ ^( r$ b# v; A% b/ t5 w" fthe exposure was not for a prolonged period of time.
; a* E; f5 L# d& t4 RAlthough the bone age was advanced at the time of, Y" a( P! L( a6 B5 S. h
diagnosis, the child had a normal growth velocity at
8 Z+ f# O" U9 {- athe follow-up visit. It is hoped that his final adult7 u; C) u: k9 R* d7 R5 y; M% ]
height will not be affected.' l0 z7 j2 i* H* | S
Although rarely reported, the widespread avail-$ g0 z5 r1 M+ J8 [: Z. g
ability of androgen products in our society may
/ ^6 x0 b' M A3 n6 w( ^2 B; a& U- Cindeed cause more virilization in male or female
) e% O, R M4 `3 Z1 a; q$ c3 ~children than one would realize. Exposure to andro-
9 A! T" h1 p5 h6 W- \+ C# bgen products must be considered and specific ques-7 }# W2 L* v3 M, s- T. i
tioning about the use of a testosterone product or' g' V+ z: r6 {2 Y# g
gel should be asked of the family members during
0 y9 @* h! R) `. A* q1 ]" y. Vthe evaluation of any children who present with vir-
; U( B$ V' I; G6 {0 c& C& a N( iilization or peripheral precocious puberty. The diag-8 X) s' l, ]) B# C' b$ x8 e9 S. O
nosis can be established by just a few tests and by
0 ^1 |" d1 L; t3 K" {: c* H) Yappropriate history. The inability to obtain such a
$ N( ?/ i( E) F! |+ |history, or failure to ask the specific questions, may
9 M c4 k6 @, c/ k8 fresult in extensive, unnecessary, and expensive/ t. I6 J7 f0 c, O
investigation. The primary care physician should be2 D7 G$ O/ o* ~7 s* ^
aware of this fact, because most of these children
* K: B7 Y& Z/ R- u9 C1 g0 _0 ]& ~& Ymay initially present in their practice. The Physicians’1 r; D! g" o+ ?" Q$ t
Desk Reference and package insert should also put a
1 I( ]' d2 p; z# S( G5 y5 G# Awarning about the virilizing effect on a male or
* N' O: P! i+ |: j9 Xfemale child who might come in contact with some- m8 {2 q% \( P- B
one using any of these products., t, V& x! p$ o2 j7 ]7 B) ?' O
References
# p6 H7 E' R' Y0 z5 M' ^1. Styne DM. The testes: disorder of sexual differentiation6 `4 J. o' g4 ^
and puberty in the male. In: Sperling MA, ed. Pediatric
* Q$ o3 S. T* O) t6 L, i3 {Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
* a2 V; ~, d: @' q$ ]2002: 565-628.! J4 ~3 z; O/ T
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
$ U! |9 I0 h$ l( U5 Zpuberty in children with tumours of the suprasellar pineal |
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