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Sexual Precocity in a 16-Month-Old, Q/ h( H) `$ V8 K- v
Boy Induced by Indirect Topical# ]% R- k+ b+ R- v8 K, k# P$ _
Exposure to Testosterone
: C# p* X( H" B- T q) PSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2, m9 |6 Y. H& ?0 ]2 |' q5 f
and Kenneth R. Rettig, MD1
8 I0 k4 K! E$ h2 E: O8 E- d. e6 BClinical Pediatrics7 x0 p( z: F4 f. @* ^' k% f
Volume 46 Number 6/ Y/ U3 Q' w, ^4 x4 p* H
July 2007 540-543
, V" N& E) k9 h3 j* B9 u6 g7 C: f© 2007 Sage Publications4 D% B/ n, _: ]( r! V! Z% [
10.1177/0009922806296651 M" E! y+ Q7 C1 l! o' l
http://clp.sagepub.com
* Y$ |' m" p) _) s8 M1 y4 chosted at! T6 q( `( L2 A* N7 E. [) o! g
http://online.sagepub.com, y1 \' J: P- a+ c, E0 C! [
Precocious puberty in boys, central or peripheral,9 w/ R' e* X- Y, z: M9 F
is a significant concern for physicians. Central
! E/ e% [: d" p e }2 j6 X/ [precocious puberty (CPP), which is mediated
9 o3 W$ @5 I5 b9 F% [1 K- T; gthrough the hypothalamic pituitary gonadal axis, has
2 ^# z3 F; B( w6 T0 R7 z2 n' Ca higher incidence of organic central nervous system; R- d4 e. V- R4 ^: k! }
lesions in boys.1,2 Virilization in boys, as manifested! P/ V, H* S0 p; n) ^1 ? `6 |7 ^
by enlargement of the penis, development of pubic
( m7 [1 U, h$ q& Z8 e whair, and facial acne without enlargement of testi-7 ]# Z1 p% [. u( E1 R. _" n
cles, suggests peripheral or pseudopuberty.1-3 We
+ I" h+ l# d6 `- y" qreport a 16-month-old boy who presented with the N1 I+ l! u. _3 x) V' I
enlargement of the phallus and pubic hair develop-+ Q! n% z! G# }% O: d C
ment without testicular enlargement, which was due/ E. R9 J5 o9 `2 r7 }% Q0 G& F
to the unintentional exposure to androgen gel used by
: V/ J& r. D- }) y; D; `the father. The family initially concealed this infor-8 ^, y4 [/ H1 ~7 l, S3 A" R- {
mation, resulting in an extensive work-up for this3 J* h. S$ z. W. j. \: {: k. y
child. Given the widespread and easy availability of
; p$ G) T" i: mtestosterone gel and cream, we believe this is proba-
& j* [4 m, ]9 @/ z( |bly more common than the rare case report in the
; \" c' J! c! W( p, `literature.4
) P7 y5 [2 c0 E3 W# o. v1 QPatient Report
4 x% h2 Q( h8 d5 R; \) [A 16-month-old white child was referred to the
2 @/ ^- ^+ T( |( t1 Xendocrine clinic by his pediatrician with the concern" m9 w" b3 f. i _6 Z6 p
of early sexual development. His mother noticed) F3 f! x7 U8 W5 w% z# I
light colored pubic hair development when he was3 g% s. F* D6 B- y/ T$ {
From the 1Division of Pediatric Endocrinology, 2University of r- x4 n D; o, F) ^
South Alabama Medical Center, Mobile, Alabama.
2 p+ W! s6 r8 e- d9 a& x0 zAddress correspondence to: Samar K. Bhowmick, MD, FACE,
0 f! G0 o( ?- ]" J/ L: E' n9 N3 ?Professor of Pediatrics, University of South Alabama, College of0 @9 U# ?! X" X: _; ^1 Y' f+ e
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
/ U( y, {- N, a2 A9 Ye-mail: [email protected].# k7 U% s9 N3 j$ `# d2 ?4 h, q
about 6 to 7 months old, which progressively became6 V9 f ?6 W8 E1 d. [
darker. She was also concerned about the enlarge-
; Z, D0 d) f; a6 n' N8 tment of his penis and frequent erections. The child8 J0 C }9 G* O! a% U. Z1 F$ B& |
was the product of a full-term normal delivery, with% n0 f9 {# A, T# g1 x
a birth weight of 7 lb 14 oz, and birth length of
4 K- @0 B* `2 b: E- z20 inches. He was breast-fed throughout the first year5 ]3 S$ m& T! Y6 H: [1 k2 Q/ E+ g! \
of life and was still receiving breast milk along with
c# T E4 y2 L4 H/ [solid food. He had no hospitalizations or surgery,# t6 Q E) |9 w9 G# f& b6 `. [) g
and his psychosocial and psychomotor development
% d9 r9 v; Y F! D0 J& @1 Xwas age appropriate.$ r, v8 T" z; P# R" g- [
The family history was remarkable for the father,
) I- w) S, i, M' }: M Z' g/ v& Ywho was diagnosed with hypothyroidism at age 16,/ E3 M/ X" P, C/ l2 \
which was treated with thyroxine. The father’s6 K+ s7 K& ~& \- v. W, H5 r5 v
height was 6 feet, and he went through a somewhat3 h' R: B7 s4 r. {2 T# T2 U1 [
early puberty and had stopped growing by age 14.( X/ F$ u2 a; E1 o* q4 S
The father denied taking any other medication. The$ T7 h/ W. n" D7 G
child’s mother was in good health. Her menarche
2 |- |. H$ Q* L/ s" g( S# Q( b. k$ jwas at 11 years of age, and her height was at 5 feet7 @* t4 `' @8 |
5 inches. There was no other family history of pre-" n* F- d/ O% j
cocious sexual development in the first-degree rela-
3 d$ {8 E1 l; ~& F/ u9 J% K) M1 Mtives. There were no siblings.
3 [, |: Y% B/ P3 z2 NPhysical Examination
# o# V: s6 d+ o9 \2 t( bThe physical examination revealed a very active,
5 G- {7 D+ `3 j( c2 d; ]playful, and healthy boy. The vital signs documented
3 _+ n4 x; g7 ka blood pressure of 85/50 mm Hg, his length was0 z2 ?7 V7 p+ u) C
90 cm (>97th percentile), and his weight was 14.4 kg2 `* F+ t. F4 ]7 _$ U1 z7 J) _
(also >97th percentile). The observed yearly growth/ V$ |- o& w1 P$ d, F
velocity was 30 cm (12 inches). The examination of
/ w7 g- ~& y6 a# P, Hthe neck revealed no thyroid enlargement.9 U* J& _4 ~8 p% R9 m/ _
The genitourinary examination was remarkable for, m1 U9 ~+ \: t2 f2 q
enlargement of the penis, with a stretched length of
' }( z. c7 a# Z- D- Z1 x% k4 _! k8 d8 cm and a width of 2 cm. The glans penis was very well! a: s8 t S1 C$ Y5 \& _: g
developed. The pubic hair was Tanner II, mostly around
% T9 A. b( X8 r P% m) G# }9 {540
+ L* j4 H. L) a; aat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from0 N0 ^# o6 T* I. X) l
the base of the phallus and was dark and curled. The
* ?& f8 ]3 R' xtesticular volume was prepubertal at 2 mL each.3 s% N2 H) k) t% g4 q! k
The skin was moist and smooth and somewhat: Q4 r0 x" R* s4 w( Q
oily. No axillary hair was noted. There were no
i9 x; |: Z/ T( |. n6 |abnormal skin pigmentations or café-au-lait spots.2 O% u! R8 X/ A: K0 `: X
Neurologic evaluation showed deep tendon reflex 2+9 x5 k( r% y$ m8 {0 z. p
bilateral and symmetrical. There was no suggestion# S4 x6 M9 H" u
of papilledema.
( T2 v' s- J( d! a, S8 f9 `5 FLaboratory Evaluation# h& i# ?, k. a6 W
The bone age was consistent with 28 months by$ d- G/ N$ ^% j$ J8 J% f
using the standard of Greulich and Pyle at a chrono-
5 U; a( p9 a& k* O. f y( [5 c9 ~logic age of 16 months (advanced).5 Chromosomal
1 F6 h2 E( x: P1 f- xkaryotype was 46XY. The thyroid function test
/ ~: c# l+ x e2 m* O. \0 tshowed a free T4 of 1.69 ng/dL, and thyroid stimu-4 I* _' v0 w/ `3 b% O! A
lating hormone level was 1.3 µIU/mL (both normal).7 V* t1 u9 h7 }# `
The concentrations of serum electrolytes, blood
7 m/ j4 T" y; P# T: Z) ]' N5 q. Nurea nitrogen, creatinine, and calcium all were5 J% I3 K# s7 m+ D+ m: U
within normal range for his age. The concentration
3 }* J- v4 [6 s8 w6 I6 r, Q& qof serum 17-hydroxyprogesterone was 16 ng/dL6 i( x1 T5 p Z3 {3 R L
(normal, 3 to 90 ng/dL), androstenedione was 20! j9 r4 @1 R+ Y: {2 \4 j& n8 H
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
. I; E1 ^0 x( P. s/ Q, S/ Dterone was 38 ng/dL (normal, 50 to 760 ng/dL),
2 i" d: j( ^1 v+ e8 jdesoxycorticosterone was 4.3 ng/dL (normal, 7 to
, G5 b5 m9 A$ O49ng/dL), 11-desoxycortisol (specific compound S)1 @, M+ G8 I% }& M1 S: d
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
1 r" P: k$ J# p; ntisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
, `# v( I1 g, q. s. _testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
6 p. R0 \3 }2 @6 \2 y- mand β-human chorionic gonadotropin was less than Z" G/ @$ O+ R) N' F
5 mIU/mL (normal <5 mIU/mL). Serum follicular. J1 u4 S8 |, V9 v/ Q4 h
stimulating hormone and leuteinizing hormone! i" Q1 H/ [; j6 Y1 S
concentrations were less than 0.05 mIU/mL
+ B, u' l; a) F, [( G(prepubertal).
4 V0 t+ `9 O& u: N+ z1 `- ^The parents were notified about the laboratory
) X* Q4 b+ g) _, p9 q. x9 Wresults and were informed that all of the tests were
, K7 y. _$ u! {. Vnormal except the testosterone level was high. The0 q3 x; v5 i8 ~6 g4 p: Z) I }
follow-up visit was arranged within a few weeks to! i. O) r4 O2 u! ~1 ^! p
obtain testicular and abdominal sonograms; how-. ~- K5 `! v8 Z" N# ~7 _
ever, the family did not return for 4 months.
3 l% b* _* z# Q) S" ^- z- PPhysical examination at this time revealed that the
# [: |. c1 U; L3 Gchild had grown 2.5 cm in 4 months and had gained6 I0 o) j/ M. M3 H. o: G
2 kg of weight. Physical examination remained/ I6 P2 Z- v1 h( i* z9 Q7 J
unchanged. Surprisingly, the pubic hair almost com-
8 C5 ?3 D% l. Ipletely disappeared except for a few vellous hairs at' x) _7 u" K$ J0 G" _
the base of the phallus. Testicular volume was still 2 |- c& \. {; }8 W
mL, and the size of the penis remained unchanged.
9 a9 P. B1 R9 LThe mother also said that the boy was no longer hav-
% ^; K$ N( Y+ J" t4 c. N& ]ing frequent erections.
* @, N0 Z5 N# q! X4 aBoth parents were again questioned about use of
1 ^& t; \) Y q, Y) v/ Zany ointment/creams that they may have applied to8 B+ N: d) G3 H" M5 L; z$ V: Y5 a
the child’s skin. This time the father admitted the6 ]' l: f/ G! l5 }- e+ b5 Q/ R
Topical Testosterone Exposure / Bhowmick et al 541
/ P7 ?1 t/ u* Q7 quse of testosterone gel twice daily that he was apply-6 c5 E# ] V' }
ing over his own shoulders, chest, and back area for2 |# k7 S, b! I9 T/ q$ z7 O! Y
a year. The father also revealed he was embarrassed
! {7 |# p6 d- l+ Mto disclose that he was using a testosterone gel pre-
4 E* E9 |! J% }9 y2 Oscribed by his family physician for decreased libido
) \+ F) [' v4 B6 p& Q8 f6 [secondary to depression.' L' {# ]$ {0 Z! w
The child slept in the same bed with parents.
: y% T4 P! `' ~+ I# u/ MThe father would hug the baby and hold him on his
/ I7 A0 Y5 {# W* Z& n! Tchest for a considerable period of time, causing sig-1 ]. `/ G7 c: T7 {% w9 ]
nificant bare skin contact between baby and father.
: _0 g, ^5 l1 [% m+ O9 D! wThe father also admitted that after the phone call,6 P3 f5 y0 N; v7 L$ R% e
when he learned the testosterone level in the baby
9 U) G+ e; n2 d. X8 nwas high, he then read the product information
. T, i- c6 _1 b3 x/ Lpacket and concluded that it was most likely the rea-
3 p& w* l# p# D, |son for the child’s virilization. At that time, they
: l* ?0 e) B) l& Q. H5 O$ kdecided to put the baby in a separate bed, and the' [- @% F9 _3 w* y7 d0 x' p) ]; w& N
father was not hugging him with bare skin and had* f& r3 c ?# P) |0 q
been using protective clothing. A repeat testosterone6 d$ p. k1 n: \7 C8 x
test was ordered, but the family did not go to the6 B7 Q \# R% w/ r- I* `2 B
laboratory to obtain the test.
* B' [- f" ]9 }- X/ ZDiscussion/ E! S( q$ Q, Y% Z; s* A. _) `3 z
Precocious puberty in boys is defined as secondary, ?8 s5 _$ d; |1 U
sexual development before 9 years of age.1,4: |. u# u. A& \% p# F$ _% L# a
Precocious puberty is termed as central (true) when* Y& e) ~, p4 m# c, x) x
it is caused by the premature activation of hypo-
1 c+ ?( Q) o& |3 ?; uthalamic pituitary gonadal axis. CPP is more com-
: B& K& {- u y4 p( D* }/ Y# C; u8 f9 dmon in girls than in boys.1,3 Most boys with CPP
& m/ Y9 _' _& _# E' J2 |: zmay have a central nervous system lesion that is* L! O' V) O t% [3 h6 J
responsible for the early activation of the hypothal-
z, d; p3 Q+ m$ B6 E" X( B6 r+ oamic pituitary gonadal axis.1-3 Thus, greater empha-
8 X$ v! A! e m3 W, x+ Wsis has been given to neuroradiologic imaging in! h* I8 Y5 E; F5 D
boys with precocious puberty. In addition to viril-
% h% [5 W$ g; T9 w1 K# c% pization, the clinical hallmark of CPP is the symmet-
, k8 s. w; F+ x0 n) |# trical testicular growth secondary to stimulation by7 g+ y$ x. j5 e4 X3 R- |& k
gonadotropins.1,39 c6 u! h0 A4 t Z! D" u; a: p" T; s
Gonadotropin-independent peripheral preco-; n- T9 k5 {) W! y, m% h5 a" Q4 Y
cious puberty in boys also results from inappropriate
4 g) e/ {1 A: y* h" C1 q( P% G1 C/ \" _androgenic stimulation from either endogenous or
) P- c, K, a+ y# k. g) o6 D* d* kexogenous sources, nonpituitary gonadotropin stim-+ h% ~4 w+ U( v; U. s' S: Q7 U
ulation, and rare activating mutations.3 Virilizing
) p; t9 V# `+ G: t& L9 {5 B& Econgenital adrenal hyperplasia producing excessive
# m- G" M2 P+ L# wadrenal androgens is a common cause of precocious
& F+ V5 ?1 e7 n/ w& u4 @ i9 apuberty in boys.3,4
! Z, s; I/ J0 Y# A5 HThe most common form of congenital adrenal
9 K; Y8 H) ^' \! o1 [hyperplasia is the 21-hydroxylase enzyme deficiency.6 V6 U" q; B: t6 [" A4 Y
The 11-β hydroxylase deficiency may also result in
, ?' b0 x0 {$ T( k$ Fexcessive adrenal androgen production, and rarely,/ j1 k1 K4 l/ k9 ?4 G) d
an adrenal tumor may also cause adrenal androgen
$ q, B' i% P/ |# W- s$ Xexcess.1,36 Y3 r! j) ^: j7 F
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
u7 @4 b+ k$ |( Q9 ^: g542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
2 i q- G+ T P5 j, zA unique entity of male-limited gonadotropin-: \1 w0 E, k6 i. V
independent precocious puberty, which is also known$ T9 g1 r/ M5 R
as testotoxicosis, may cause precocious puberty at a
1 i7 e' h+ u: Pvery young age. The physical findings in these boys
/ N6 H9 F& l* W% w2 J1 W2 t) wwith this disorder are full pubertal development,
0 p& ~- G5 L5 V" Q1 n, Kincluding bilateral testicular growth, similar to boys( R1 X; j; l" C) V- P
with CPP. The gonadotropin levels in this disorder" E. @0 U7 b! G& g% W
are suppressed to prepubertal levels and do not show# y0 z" S, S* m3 l5 T5 b
pubertal response of gonadotropin after gonadotropin-( I! I! k3 \* m' H% `4 A7 T
releasing hormone stimulation. This is a sex-linked
2 J- A9 u- ^9 o% u( o" {0 ]autosomal dominant disorder that affects only& Q2 D4 H* ?5 E# {
males; therefore, other male members of the family
* Q8 q1 h* }% F5 f6 F4 \may have similar precocious puberty.3# I8 O- b) }* Y/ ^. d# U
In our patient, physical examination was incon-
: u' u* x! {/ _+ o6 w- Ysistent with true precocious puberty since his testi-
- @ @3 D2 ]* U; Dcles were prepubertal in size. However, testotoxicosis7 E Y7 ^5 [( Y1 z3 W
was in the differential diagnosis because his father) x' x9 K N& O a
started puberty somewhat early, and occasionally,/ `8 I0 r. W2 f* H! p4 @9 |/ |. c3 P
testicular enlargement is not that evident in the- T5 e+ s( o* l: q6 K+ w V
beginning of this process.1 In the absence of a neg-5 V ~ f4 x& j! p# ^2 j7 i
ative initial history of androgen exposure, our
5 S) V: q, @5 q2 p5 l* O; ?* ^" qbiggest concern was virilizing adrenal hyperplasia,
$ b4 n8 D! ?; E& }( ?- ^either 21-hydroxylase deficiency or 11-β hydroxylase9 a1 Y1 B1 ]4 M5 ]
deficiency. Those diagnoses were excluded by find-
. g# C. b8 b" Y! O8 _ing the normal level of adrenal steroids.4 E1 a z" F- z. I4 t; o! T' L5 t
The diagnosis of exogenous androgens was strongly5 h$ B p# u" k( `
suspected in a follow-up visit after 4 months because
* v! k1 b, g; M# f) L' ~! cthe physical examination revealed the complete disap-
: r; r0 v6 R( v& B% l: g+ Xpearance of pubic hair, normal growth velocity, and6 M" g& d3 `$ i9 D: g
decreased erections. The father admitted using a testos-
' Q$ u3 j; u: E# Dterone gel, which he concealed at first visit. He was
% ^ R) {8 V: D3 rusing it rather frequently, twice a day. The Physicians’
" p6 J9 K0 g7 sDesk Reference, or package insert of this product, gel or* y4 p# |) {8 ~8 y0 [+ r4 c8 a
cream, cautions about dermal testosterone transfer to
& _ @( S" d& c) v# Aunprotected females through direct skin exposure.
; p; U3 c6 d8 ]7 n- |0 }# z' ESerum testosterone level was found to be 2 times the* Y/ z# u, Y: r% D9 \" \
baseline value in those females who were exposed to6 Z1 X7 J& q E N* R5 ^
even 15 minutes of direct skin contact with their male8 K. W. I# m& u" s
partners.6 However, when a shirt covered the applica-# j: w" ^" d) g
tion site, this testosterone transfer was prevented.
4 p) n2 f6 W2 p. m- `3 HOur patient’s testosterone level was 60 ng/mL,
8 N# X6 U! f4 g, P$ swhich was clearly high. Some studies suggest that) g; u5 J' R( J. M3 m" X$ \
dermal conversion of testosterone to dihydrotestos-
& p2 |1 s! Q/ i9 k; Y9 ^terone, which is a more potent metabolite, is more
" F9 G3 u/ x) L w7 {3 h! ]active in young children exposed to testosterone- D9 Z9 g% ^" i* h' e
exogenously7; however, we did not measure a dihy-
) V; g, @3 I) p( Ddrotestosterone level in our patient. In addition to
6 U% R* Y4 ^1 z8 T- s U" |virilization, exposure to exogenous testosterone in
+ E4 d; _0 k, [. D* L' `children results in an increase in growth velocity and
- F9 T0 y/ ~8 H3 n! S2 \advanced bone age, as seen in our patient.
, u& T$ P( z* `4 M" e% X# k" UThe long-term effect of androgen exposure during. e( ]/ G& F, g5 ^4 P Y1 A8 i
early childhood on pubertal development and final
+ c1 P3 Y. ?$ ?, ]+ u! v' Dadult height are not fully known and always remain
: V# z% b; k4 _1 w7 aa concern. Children treated with short-term testos-% u* H9 ^; C" V; r" c) [
terone injection or topical androgen may exhibit some. i9 S# z6 }$ U2 h
acceleration of the skeletal maturation; however, after( [0 b0 y, T$ d8 v( t2 ^
cessation of treatment, the rate of bone maturation
5 z" O$ ?% A6 V, ? T) b( M' Wdecelerates and gradually returns to normal.8,9, g/ V" C3 G# D) a) S; \
There are conflicting reports and controversy w/ T; v! w ?8 x' e
over the effect of early androgen exposure on adult
2 e( a' |% J6 O- Z% }penile length.10,11 Some reports suggest subnormal
" F& R K" b5 ?$ Y' H8 Dadult penile length, apparently because of downreg-! U4 d( X8 ^* }8 U
ulation of androgen receptor number.10,12 However,- x7 \% S2 K% ~5 M5 w' [ B) x
Sutherland et al13 did not find a correlation between1 b. V0 Q, P8 T5 D
childhood testosterone exposure and reduced adult$ ?) Y k T; f/ N
penile length in clinical studies.
2 |, y; T) @* Q- O& f. uNonetheless, we do not believe our patient is/ m* K3 d8 _% Z# H. `4 I' a
going to experience any of the untoward effects from0 h" ^5 b B) t+ i; M" _
testosterone exposure as mentioned earlier because7 R7 |: }. E" J" c
the exposure was not for a prolonged period of time. q2 E" Z3 p" s
Although the bone age was advanced at the time of) a+ M5 L, I" j& Q9 B Z5 z
diagnosis, the child had a normal growth velocity at
/ E, s9 [$ k( N* Xthe follow-up visit. It is hoped that his final adult; g1 ^; V, _/ L6 U# W
height will not be affected.
& ]7 T6 Z9 t/ n2 |Although rarely reported, the widespread avail-
2 o6 w' B+ }" S4 zability of androgen products in our society may, p" t+ P2 e, N/ r' g4 Y7 k$ Q
indeed cause more virilization in male or female. i* W; R7 d! ^( j& g, b* y8 [
children than one would realize. Exposure to andro-7 X/ n0 _% _4 ?$ f* O
gen products must be considered and specific ques-6 x( E; X* Y6 h0 L/ h9 o
tioning about the use of a testosterone product or, S9 l, S' Z" |8 u8 I( H
gel should be asked of the family members during
1 k& |# D& I2 \4 F( N1 k' m0 {2 Athe evaluation of any children who present with vir-& S) X( J5 D) ^1 f; ]
ilization or peripheral precocious puberty. The diag-3 [, S0 L) B: I
nosis can be established by just a few tests and by T3 s1 }' j1 L: r! k7 P- T: L8 k& h
appropriate history. The inability to obtain such a; o/ ^% {2 D. p$ N# g
history, or failure to ask the specific questions, may4 g9 L- u! l* C7 Z a$ S
result in extensive, unnecessary, and expensive
! J+ i/ P5 v2 z) d7 l. N) }$ M2 oinvestigation. The primary care physician should be
G7 F9 i3 S% v1 c- Baware of this fact, because most of these children" `6 ]" y7 I8 x
may initially present in their practice. The Physicians’3 Z) ^+ x0 Q- J5 }
Desk Reference and package insert should also put a/ ]( X w" r! Q5 G1 ?/ U, T
warning about the virilizing effect on a male or: P% f8 h, z0 Z" Q; b
female child who might come in contact with some- B9 ^* j- D; D4 a5 n5 W
one using any of these products.# g0 [) ? ~5 L
References. i6 B4 N# H, j# ~3 d( q
1. Styne DM. The testes: disorder of sexual differentiation
6 V- s. j, b( t* T f5 P; p2 j; |and puberty in the male. In: Sperling MA, ed. Pediatric9 p* B6 P* Z; ~
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;4 |, z/ D1 x; K1 @3 a$ R. _
2002: 565-628.8 I3 U6 ^- k/ i& c0 M \! b
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
4 P! _# y6 w; fpuberty in children with tumours of the suprasellar pineal |
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