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Sexual Precocity in a 16-Month-Old
" {, u E; s1 q, ]* P1 a3 w$ XBoy Induced by Indirect Topical
3 a# z9 D% m% k" S8 e5 ^Exposure to Testosterone
- m$ e" t% z9 ~1 h: v, F( k+ jSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
6 R$ C4 m! u; ^, q8 Oand Kenneth R. Rettig, MD1, K' j( p3 k- W& K3 \! q3 e
Clinical Pediatrics
+ U& s; k) c( u$ ^/ VVolume 46 Number 63 l# o, V& u: X! M. f4 U8 _7 }
July 2007 540-543+ g! z* a% V6 D5 H
© 2007 Sage Publications
3 |+ Y/ W: k5 q+ l P5 ]$ i9 B P10.1177/0009922806296651* L! Q: ?- s; l
http://clp.sagepub.com$ N: c+ ^$ l1 h5 y* h
hosted at" E' R1 T3 _: b! M, ^
http://online.sagepub.com
* [" x: y! R0 q- ]Precocious puberty in boys, central or peripheral,8 O( a% Y$ ~. c: ~0 {0 x
is a significant concern for physicians. Central0 L/ K7 R& |: ?# C+ k1 ^2 P
precocious puberty (CPP), which is mediated5 i9 v" |( X) M8 x
through the hypothalamic pituitary gonadal axis, has
1 z" p8 O: o: I9 e9 o& Oa higher incidence of organic central nervous system6 |- I+ F; ]1 @3 `1 c$ ]/ J& K
lesions in boys.1,2 Virilization in boys, as manifested
0 S) J( B3 C" y) d4 fby enlargement of the penis, development of pubic- Z: Y- j* H: _! ^3 k
hair, and facial acne without enlargement of testi-2 p J/ [" X) H6 C5 m6 T
cles, suggests peripheral or pseudopuberty.1-3 We
. o7 N* \, y4 o+ {+ n# f2 J% Xreport a 16-month-old boy who presented with the' k2 l1 ?% @1 l' x( t
enlargement of the phallus and pubic hair develop-& | U3 V2 I9 r0 U( E3 c& k
ment without testicular enlargement, which was due% x8 |: g1 q9 x; C: P3 u
to the unintentional exposure to androgen gel used by8 l# d8 x3 r* u' v& w. O4 w% z6 R
the father. The family initially concealed this infor-
& U! Q3 X2 x! t; pmation, resulting in an extensive work-up for this# l) U0 K0 C6 L `& c. V
child. Given the widespread and easy availability of
( s( g9 g% v* Y. u wtestosterone gel and cream, we believe this is proba- @! T) u( }# @% T4 a
bly more common than the rare case report in the( z$ y( p. O6 R
literature.4. |+ ^* ^# V1 N" R/ E" x1 H
Patient Report
5 J4 h0 g `" l! d+ GA 16-month-old white child was referred to the- C) i9 `0 C3 T- y" F7 J1 u) z
endocrine clinic by his pediatrician with the concern
+ G4 \. ?' J1 A6 X+ F, o( _$ Dof early sexual development. His mother noticed
0 H1 t: Q8 g% J2 d$ jlight colored pubic hair development when he was
( x& L, Z4 D$ w, x3 uFrom the 1Division of Pediatric Endocrinology, 2University of
% X- K6 J' z, ]South Alabama Medical Center, Mobile, Alabama.
, O5 \( C# w" D7 n+ Y* }) VAddress correspondence to: Samar K. Bhowmick, MD, FACE,
2 r; s9 G7 |, e) W# W8 K6 TProfessor of Pediatrics, University of South Alabama, College of8 t' _+ y* ~" O5 @# _$ g
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
4 y3 v4 _# s h" T; z4 m! C# ^e-mail: [email protected].8 f1 U# n4 {9 ~. F8 r& r) h
about 6 to 7 months old, which progressively became
6 V/ v& }4 O6 b3 M+ \darker. She was also concerned about the enlarge-& k6 z: q* B' P! P0 Y& _
ment of his penis and frequent erections. The child
7 l# G7 b6 D0 g/ G8 E0 A2 f, S; E8 Cwas the product of a full-term normal delivery, with3 y9 ]9 r1 e8 b& ^
a birth weight of 7 lb 14 oz, and birth length of
9 N5 S. S: M. e: Y {6 \/ ?" L20 inches. He was breast-fed throughout the first year, y. _ \. J$ f3 S! l- B
of life and was still receiving breast milk along with7 M1 K0 n3 X& ~! y* Y0 P% H
solid food. He had no hospitalizations or surgery,5 x; B! ~. Z v& E2 J1 t- e
and his psychosocial and psychomotor development
$ A$ E" z: c* R" C' Q+ m# Qwas age appropriate.
+ H' j0 Q7 O& aThe family history was remarkable for the father,
+ C! C- t! `8 t3 q. z" e9 Dwho was diagnosed with hypothyroidism at age 16,
5 T7 }, j; B# o7 R: X( V v6 twhich was treated with thyroxine. The father’s
3 |5 }) J; w1 s" D( a5 _height was 6 feet, and he went through a somewhat7 _% a4 U, n. z" H3 c
early puberty and had stopped growing by age 14." [4 u- x2 {' P* D/ e1 L6 ?7 O
The father denied taking any other medication. The
5 T0 Y- J1 f: R% i4 s4 Vchild’s mother was in good health. Her menarche9 I- T0 v; S. T: `. ?
was at 11 years of age, and her height was at 5 feet# d$ v* b7 n5 h. \0 {7 M' [
5 inches. There was no other family history of pre-, T% v9 w. A Z
cocious sexual development in the first-degree rela-2 [7 O1 }5 e" L% |8 }! m
tives. There were no siblings.% B; k; `" N$ W9 K8 i, u, w( D
Physical Examination0 ^/ S3 ^3 l4 Y
The physical examination revealed a very active,
9 T' A( E+ c ^6 d$ ?6 ^# ~playful, and healthy boy. The vital signs documented
" z$ k$ e, l5 A8 ba blood pressure of 85/50 mm Hg, his length was
" T8 s2 ]7 C0 f! a- X90 cm (>97th percentile), and his weight was 14.4 kg% C' \8 ]* T6 U; @9 v
(also >97th percentile). The observed yearly growth
/ R5 r e. U$ \velocity was 30 cm (12 inches). The examination of* S$ h. e! Q8 k
the neck revealed no thyroid enlargement.
2 I0 m2 W9 V. p% V& r+ s- }9 \The genitourinary examination was remarkable for/ g: }( ], H2 ^. [8 @8 h
enlargement of the penis, with a stretched length of
' m+ w2 ?0 k( L1 I& T% t8 cm and a width of 2 cm. The glans penis was very well% N- @. M) [: \; w$ T) }% O
developed. The pubic hair was Tanner II, mostly around8 p' A1 p, l" u$ R
540- G3 |8 ~$ g* M$ o% _, Q1 `
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from7 q+ D, q- d- i* | n' ^7 F
the base of the phallus and was dark and curled. The
' t2 A; A: T, b& dtesticular volume was prepubertal at 2 mL each.
% q" v! E9 Q% e4 [ S9 q4 b) ?The skin was moist and smooth and somewhat
- S% O8 C1 ?' c( ]. q: N7 aoily. No axillary hair was noted. There were no, O+ O: q& f' g: g3 \+ g; Q
abnormal skin pigmentations or café-au-lait spots.( H& S0 \' m: ]1 C$ M3 M& N# U
Neurologic evaluation showed deep tendon reflex 2+8 E; Q3 z2 ~) E9 Y
bilateral and symmetrical. There was no suggestion
- n: Q2 y5 S, r- v @! P6 Bof papilledema.+ V+ P% `; ~6 E; m! V- x9 v
Laboratory Evaluation/ a% ^% u7 [( v
The bone age was consistent with 28 months by5 W5 t) c* _7 C# `1 ?% P7 G0 u# M
using the standard of Greulich and Pyle at a chrono-0 N. w2 h1 b3 f6 O. e5 n/ M
logic age of 16 months (advanced).5 Chromosomal- W( M3 Z7 p+ \- Z' I, P
karyotype was 46XY. The thyroid function test
7 |+ D7 \9 t& h7 V1 Ashowed a free T4 of 1.69 ng/dL, and thyroid stimu-/ ~- o- j6 W. u! j2 k
lating hormone level was 1.3 µIU/mL (both normal).0 V; f/ p6 z$ T5 J3 N. o
The concentrations of serum electrolytes, blood8 Z' I0 O3 A! K5 T) \8 \' E
urea nitrogen, creatinine, and calcium all were/ O8 e9 s( ]' s5 r2 d" E4 D
within normal range for his age. The concentration8 e: p/ B% m2 P
of serum 17-hydroxyprogesterone was 16 ng/dL" z3 b1 S6 p$ J# C2 a% V$ u
(normal, 3 to 90 ng/dL), androstenedione was 207 Z; m4 c3 X$ ` x1 Q- N
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
' I4 |" R3 z& |2 }" r4 Zterone was 38 ng/dL (normal, 50 to 760 ng/dL),! C( S! ~4 R" j* J- G+ \. J
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
' t5 y& x& T7 b49ng/dL), 11-desoxycortisol (specific compound S)& J- h! A- ]' d' V4 `
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
- V( [8 \2 P+ q% q! T& Etisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
) C. R- E) L* H: D+ m8 U1 Xtestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
g$ j/ L' b9 w) h3 Band β-human chorionic gonadotropin was less than0 N, L3 ]8 |; i3 ^+ y" D
5 mIU/mL (normal <5 mIU/mL). Serum follicular
' ?4 W% ?! z0 g! Ostimulating hormone and leuteinizing hormone
3 n. [5 E6 w L, `+ G( Uconcentrations were less than 0.05 mIU/mL
2 ?6 h- ?5 N& s% h) O(prepubertal).3 E$ r' k" Y9 f0 O
The parents were notified about the laboratory2 r+ M$ |' _( A, R7 Z9 M0 d3 g
results and were informed that all of the tests were, I7 D5 I/ H: F
normal except the testosterone level was high. The' w- \( y4 X0 o6 D5 U$ a
follow-up visit was arranged within a few weeks to! _6 s# ^: F4 l8 K( S) U$ Z
obtain testicular and abdominal sonograms; how-3 r4 Z! B0 d# @1 ~$ P( H, R* T3 ]" z
ever, the family did not return for 4 months.- b2 g, G9 v& B/ P# X3 J) o( @9 o
Physical examination at this time revealed that the2 R' \3 i j. s. H- J8 v- l" M
child had grown 2.5 cm in 4 months and had gained3 J1 \0 q1 R' z3 C
2 kg of weight. Physical examination remained! @8 c5 P& f0 J5 ^* N* \" l
unchanged. Surprisingly, the pubic hair almost com-2 g \. |4 } w
pletely disappeared except for a few vellous hairs at) H% n7 S% m8 I2 C; b4 r" D/ T
the base of the phallus. Testicular volume was still 2, _- v& b& m+ \2 P- U, j( v
mL, and the size of the penis remained unchanged./ n6 E- N" ~( s0 a& i) [
The mother also said that the boy was no longer hav-; {) K. {5 ^5 t( |* q/ s
ing frequent erections.0 G, A6 Y' j& u9 z' T0 b
Both parents were again questioned about use of
: G9 U: h5 w: w A4 |$ jany ointment/creams that they may have applied to2 A, y: p- @* L3 a, ^
the child’s skin. This time the father admitted the
x, d+ m% C1 ]1 U7 @Topical Testosterone Exposure / Bhowmick et al 541/ r! X6 p- x. h
use of testosterone gel twice daily that he was apply-
: c ^; P3 b; o$ k1 fing over his own shoulders, chest, and back area for% d, l) u, E. Q. u- x, D" G! N& t
a year. The father also revealed he was embarrassed+ G9 T" m# d& @% W* b% g8 F
to disclose that he was using a testosterone gel pre-
! x0 T& @3 X3 r; _9 a8 pscribed by his family physician for decreased libido, F$ E/ V: N4 ?- N7 |6 D
secondary to depression.
5 V$ x' ^0 {+ ~) N& {% Y# U4 cThe child slept in the same bed with parents./ k" g \3 ^4 @. q6 v8 C: }
The father would hug the baby and hold him on his
; D$ @( @8 n: ~. J6 ]# w& @chest for a considerable period of time, causing sig-
0 k; d& M2 C0 m0 I" `nificant bare skin contact between baby and father.% d; z, ]/ g* c# W* J$ h7 \2 j
The father also admitted that after the phone call,7 {, C/ A) g8 A, o4 m9 _2 z$ _) D! t
when he learned the testosterone level in the baby
3 R, k- ~( \! f n4 ]! ~was high, he then read the product information6 B: s2 h. G `- W' a+ ^3 u# L
packet and concluded that it was most likely the rea-
; x, M5 T) E( Qson for the child’s virilization. At that time, they
& v9 ~: M$ f% L b! X* u$ l* _decided to put the baby in a separate bed, and the
% ^1 \4 a5 @3 q7 N8 dfather was not hugging him with bare skin and had
# v9 u2 N8 j1 q7 ]; |been using protective clothing. A repeat testosterone4 S( J3 R$ K6 C# W3 P6 y
test was ordered, but the family did not go to the9 |% k! E+ |- H
laboratory to obtain the test.
4 p, q% \* J3 i1 }Discussion( t$ d6 \7 X' Y+ K7 j0 \) ?
Precocious puberty in boys is defined as secondary
8 u: k* e* Q; o- g" h3 G1 fsexual development before 9 years of age.1,46 \: [5 L$ V! t7 Q
Precocious puberty is termed as central (true) when3 b: L" V3 [7 }
it is caused by the premature activation of hypo-% k! t: W) b9 V! f4 `5 U" ]
thalamic pituitary gonadal axis. CPP is more com-' x! h; t4 d# j4 K! y( O$ y
mon in girls than in boys.1,3 Most boys with CPP3 ]! {, D* z* J5 E, j8 m
may have a central nervous system lesion that is. Y2 O! z9 x8 p; o& |/ \" |
responsible for the early activation of the hypothal-
8 k* J$ e2 p j- vamic pituitary gonadal axis.1-3 Thus, greater empha-
6 v! J9 I+ Y8 a6 N/ {. Z& t# \sis has been given to neuroradiologic imaging in
# C) b. D' v/ J' Uboys with precocious puberty. In addition to viril-% Z7 J0 q. j3 u+ {: L+ O x
ization, the clinical hallmark of CPP is the symmet-) ~7 B8 t. j2 l! I: q" u9 e
rical testicular growth secondary to stimulation by
! V7 X5 N( K6 P- M8 Ggonadotropins.1,3
8 n* g, i: @+ n. }Gonadotropin-independent peripheral preco-3 O* i4 Y8 E7 {3 P4 C
cious puberty in boys also results from inappropriate
: ~ X2 p- o/ z$ L: p' G6 Zandrogenic stimulation from either endogenous or
3 {, [3 ]& H+ d7 D1 [" E6 |; m3 l! z3 iexogenous sources, nonpituitary gonadotropin stim-8 i$ Z" c# @% h( P; H& ~
ulation, and rare activating mutations.3 Virilizing8 W+ \8 y S( v- M/ l
congenital adrenal hyperplasia producing excessive
' ?9 W* U4 d& hadrenal androgens is a common cause of precocious
: c- O, x9 Q; n2 G# Y7 K$ F; B) E# ?puberty in boys.3,4" V, V7 {! c. Q, ?
The most common form of congenital adrenal
) ]$ G& v9 l# D% p3 _% M% j5 Fhyperplasia is the 21-hydroxylase enzyme deficiency.
6 O* l7 \ _" n0 gThe 11-β hydroxylase deficiency may also result in( T8 N' |- S0 y5 N- Z
excessive adrenal androgen production, and rarely,
+ N1 L$ r$ j8 w1 N7 L3 i& kan adrenal tumor may also cause adrenal androgen
4 a9 y/ Z0 q- G: pexcess.1,3
7 |6 B! b( C9 p9 E! j' |at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
* g) ^8 S% }* P2 t8 H6 R542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
' k$ f {0 X2 y8 a; N2 J+ Z: KA unique entity of male-limited gonadotropin-
" L/ ~2 T3 M- n8 k2 P8 i( G% Findependent precocious puberty, which is also known
' g+ a% E4 L7 O" @# @+ xas testotoxicosis, may cause precocious puberty at a
0 Z4 w0 j+ M4 d2 q/ z2 E+ Pvery young age. The physical findings in these boys
1 B/ {& D; \6 Q# Nwith this disorder are full pubertal development,
/ [# j, L3 E, ~' t+ s$ D# |, ^! f) Xincluding bilateral testicular growth, similar to boys6 @2 x) U) A: @& c9 A
with CPP. The gonadotropin levels in this disorder
5 G$ c7 Y0 |. |) y$ M7 Z* \/ @are suppressed to prepubertal levels and do not show
2 O% M D1 R0 m* Z6 Hpubertal response of gonadotropin after gonadotropin-: M# |" j! I8 z' \8 B3 t
releasing hormone stimulation. This is a sex-linked) y* ^$ ^$ q+ |! b& k$ i+ x6 E* R
autosomal dominant disorder that affects only
0 S$ E( U$ R4 i8 m& }$ |. L3 qmales; therefore, other male members of the family& v% k; Z4 I, V
may have similar precocious puberty.3, g, K0 [/ U. x) @
In our patient, physical examination was incon-
5 s" s( o- X' B- p7 V! Zsistent with true precocious puberty since his testi-
5 Z% _3 d2 C% M0 V9 ccles were prepubertal in size. However, testotoxicosis
) O' |& d, ]; q, u9 mwas in the differential diagnosis because his father
" I4 h5 V z5 ~( J: }: zstarted puberty somewhat early, and occasionally,
9 G& x0 m# `0 r! m3 J0 E$ ttesticular enlargement is not that evident in the( z+ Y, ^" \8 Y, d6 Z, E! j7 r
beginning of this process.1 In the absence of a neg-- I% W' a! g- W2 C
ative initial history of androgen exposure, our
[# S8 R- G0 n: wbiggest concern was virilizing adrenal hyperplasia,
' }8 M6 R) B$ W+ m: I& D6 j7 xeither 21-hydroxylase deficiency or 11-β hydroxylase
k: |+ X6 _) y! R8 ], }# Cdeficiency. Those diagnoses were excluded by find-
$ y" Y# T C8 J0 e. A, _ing the normal level of adrenal steroids.
; U6 O. |( l- B" BThe diagnosis of exogenous androgens was strongly
? g4 A( Y% I* Lsuspected in a follow-up visit after 4 months because- t4 s, Q9 z9 X' X F! D
the physical examination revealed the complete disap- |* {/ j/ d' F; X( N
pearance of pubic hair, normal growth velocity, and' d z6 b( x( G @* \$ A, Z
decreased erections. The father admitted using a testos-
3 v- M, K+ s% x2 V- R4 ]$ {terone gel, which he concealed at first visit. He was: q2 }4 `5 ~8 f) f# d3 y
using it rather frequently, twice a day. The Physicians’
/ |" [" `: {" o, bDesk Reference, or package insert of this product, gel or
) H1 z {9 f3 G( kcream, cautions about dermal testosterone transfer to
8 S7 ]6 [4 A% t F* d+ [2 c/ munprotected females through direct skin exposure.& z7 L& S/ O8 A4 y. N( y
Serum testosterone level was found to be 2 times the
w# k( O3 z- ]+ F5 T7 n0 ]baseline value in those females who were exposed to
! C3 W: t; U, H( A$ N/ U6 \& l. Oeven 15 minutes of direct skin contact with their male
) E, x" h6 A5 z5 q1 {/ \; }partners.6 However, when a shirt covered the applica-2 r0 ]5 q8 x, F* ^
tion site, this testosterone transfer was prevented.
, [: z0 u. ~* `& A! M$ qOur patient’s testosterone level was 60 ng/mL,
: o$ X! d; e7 y' {8 N3 w c( Pwhich was clearly high. Some studies suggest that8 K. X+ ^5 t( H+ P/ _
dermal conversion of testosterone to dihydrotestos-1 h/ X D5 G& C( `. M( u
terone, which is a more potent metabolite, is more
) k- t; s1 X8 S+ {0 @$ Q- Yactive in young children exposed to testosterone
& m) H% {' R3 H. g2 gexogenously7; however, we did not measure a dihy-
5 i2 K( n2 n8 a" Cdrotestosterone level in our patient. In addition to/ |& _( t) C5 E+ ]4 E9 L6 U/ z2 n
virilization, exposure to exogenous testosterone in
( h2 O P0 q3 ^, vchildren results in an increase in growth velocity and6 K! j8 y E& w' f1 G. s4 G
advanced bone age, as seen in our patient.
0 ]" z' V; [- y4 r6 @+ ^/ A3 mThe long-term effect of androgen exposure during
2 F1 v. p5 `* m0 Mearly childhood on pubertal development and final3 G/ P" _+ Z3 [# j& Q
adult height are not fully known and always remain
: y$ Z9 E1 j9 i$ l8 ^; O7 w1 j- s! C8 La concern. Children treated with short-term testos-
& l. L9 q4 ^; l8 j1 y2 gterone injection or topical androgen may exhibit some
' u/ `; e6 Y1 j& x9 }; a P! z: R- zacceleration of the skeletal maturation; however, after. e$ u' v* [) ~& {1 _! l
cessation of treatment, the rate of bone maturation( |: h5 v1 D. e, M* d' ]" f8 X
decelerates and gradually returns to normal.8,9
* H$ z; ]6 f" T4 s4 o) lThere are conflicting reports and controversy
?5 z2 _ c) O4 ~, Q6 R- i* Vover the effect of early androgen exposure on adult
" X& f* P/ g0 y2 h1 jpenile length.10,11 Some reports suggest subnormal9 A2 }1 T; Y6 {4 Y, X6 N( |
adult penile length, apparently because of downreg-
, ^0 f; x( Q) {: U* ], G% dulation of androgen receptor number.10,12 However,
' e" o( E6 A4 b1 P, ?4 KSutherland et al13 did not find a correlation between: J% Y/ R; U; D6 [: z7 t
childhood testosterone exposure and reduced adult
# \# m# Y6 l! Spenile length in clinical studies.
+ E4 w5 z( Z7 I: t/ ANonetheless, we do not believe our patient is) d% _$ I+ o; R2 b3 s; f3 w
going to experience any of the untoward effects from* c0 W- F- S: \2 _* k7 M
testosterone exposure as mentioned earlier because
5 R; Z# A) h! ? x/ o% xthe exposure was not for a prolonged period of time.. J" y9 P6 s* {& w/ K% x6 z# K) \% t
Although the bone age was advanced at the time of. o0 }. p- ?5 I; b$ ?- V3 O
diagnosis, the child had a normal growth velocity at
' s& g! W, g, t& nthe follow-up visit. It is hoped that his final adult
7 G, B5 f8 {7 g& ?3 F' K, c' lheight will not be affected.
* N$ r/ d8 G- ~! \' |8 x0 e8 YAlthough rarely reported, the widespread avail-8 l! V5 A3 t9 r
ability of androgen products in our society may
: H- i$ n+ G/ U# Findeed cause more virilization in male or female! i* t! W$ I i( I+ x- O
children than one would realize. Exposure to andro-2 N& u- ]) a- I8 N6 a
gen products must be considered and specific ques-+ H S& l; T+ A! M% k0 m0 a' X
tioning about the use of a testosterone product or4 W; P% W4 N$ ]0 w
gel should be asked of the family members during. {# M4 N% t f( T
the evaluation of any children who present with vir-
8 f- D8 M' F3 w6 k: Q, ^9 {9 filization or peripheral precocious puberty. The diag-' }7 I! ]! g* G8 ~/ r
nosis can be established by just a few tests and by: l/ `& R$ s: [4 v' @# r0 N3 \
appropriate history. The inability to obtain such a
% V5 T. N( K4 W9 W% S( |history, or failure to ask the specific questions, may
) ]) t' x, {' P, V+ ?result in extensive, unnecessary, and expensive
- a9 P! o0 Q4 g' F& P; hinvestigation. The primary care physician should be
( D \6 | A# G. o$ O8 Kaware of this fact, because most of these children
6 R, u3 @8 j& d& [' [may initially present in their practice. The Physicians’
) n( h; {2 Y9 m. U6 F/ D8 [Desk Reference and package insert should also put a, V+ P8 b4 o+ y0 d7 w0 D- T6 r
warning about the virilizing effect on a male or6 b3 Y8 s$ C( k( D5 W* }3 T$ [1 T
female child who might come in contact with some-
{' q3 w7 \' Oone using any of these products.
7 m. Y' y0 Y8 x, PReferences- f3 Z3 A% f' d
1. Styne DM. The testes: disorder of sexual differentiation. ?! T1 F/ A% Y0 u
and puberty in the male. In: Sperling MA, ed. Pediatric) [% ?, n3 u6 ?
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
0 x E5 r1 }' ^* r( t7 }2002: 565-628.( M2 N2 I7 Z% a/ k. B& `% d
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious$ m. L! n Z+ ]* z
puberty in children with tumours of the suprasellar pineal |
|