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Sexual Precocity in a 16-Month-Old6 Y( t( v p x" G3 w
Boy Induced by Indirect Topical
# a& n, Z, j1 y0 QExposure to Testosterone
. |' P: ?0 }4 n- Q2 JSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
: X8 W3 l$ w2 v8 P Fand Kenneth R. Rettig, MD1
" `) o' h6 F+ [) A3 lClinical Pediatrics
$ X$ w' r, U1 Y) {! aVolume 46 Number 6
4 s: d! D) n1 n( z& fJuly 2007 540-543. }( e# X4 G9 Y6 g4 R
© 2007 Sage Publications+ ]' } v# R- U# k( [
10.1177/00099228062966510 W' |- l4 | `9 A4 C7 G
http://clp.sagepub.com$ H. O& b; ?& X6 ]% i9 e7 _' S
hosted at |: g3 z% F1 ~- I2 ^' ]) c8 E+ f/ i
http://online.sagepub.com
! V- z3 \. G" S/ c/ @* v% S, n7 qPrecocious puberty in boys, central or peripheral,
S( k2 {' K. C) Q. j4 F- n6 jis a significant concern for physicians. Central
8 |* z V' x/ t# Nprecocious puberty (CPP), which is mediated
6 W5 S' v$ Y; X ?' kthrough the hypothalamic pituitary gonadal axis, has% I' e0 O+ w- h! |' Z, D4 H
a higher incidence of organic central nervous system+ f7 L2 U$ X) L, x/ u# J
lesions in boys.1,2 Virilization in boys, as manifested- h% d( b% a, H1 l' ?2 J/ r, s
by enlargement of the penis, development of pubic
2 u" H% S8 T1 H7 V0 |7 F7 }+ m7 ehair, and facial acne without enlargement of testi-9 C5 i5 T7 Y+ |7 B+ j
cles, suggests peripheral or pseudopuberty.1-3 We
# H0 W- s! G( n! L& Y! m9 S9 Zreport a 16-month-old boy who presented with the
0 T# p+ d! l& k5 C* U8 V. kenlargement of the phallus and pubic hair develop-: b+ L% @6 y$ t/ O6 b
ment without testicular enlargement, which was due
. _; Q: L' ~) X7 i4 F$ \to the unintentional exposure to androgen gel used by. \% p* T: M. X5 A! v+ m
the father. The family initially concealed this infor-, v. x3 h+ I K) `- ^' m
mation, resulting in an extensive work-up for this
- B, B+ k- i+ V8 J- Q0 Bchild. Given the widespread and easy availability of
2 C, {$ @# x# z+ Itestosterone gel and cream, we believe this is proba-, M/ |6 R; l5 O" I5 K: G; b( F
bly more common than the rare case report in the
& K) a6 q, V7 x$ Nliterature.4
% d( Q2 x* a' `3 p% IPatient Report# g" W G+ c# j/ e" R
A 16-month-old white child was referred to the
$ U$ X/ B; E3 r Y% N" T% w1 Hendocrine clinic by his pediatrician with the concern2 k# M. }( ~' a8 d
of early sexual development. His mother noticed
9 O; h7 \8 L/ v3 ^light colored pubic hair development when he was
9 k& ]# H( \9 z7 i+ f8 LFrom the 1Division of Pediatric Endocrinology, 2University of" g$ l+ `. `8 w0 a8 w
South Alabama Medical Center, Mobile, Alabama.9 l; T0 M; M; S; d3 z5 V
Address correspondence to: Samar K. Bhowmick, MD, FACE,: I- t% R/ G+ X' H/ v4 J3 |* I
Professor of Pediatrics, University of South Alabama, College of
9 L9 C" M! k# |6 B; t& hMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
; f7 N! b( r) w% ]2 `e-mail: [email protected].
( {( Z, W( ?1 o* A9 mabout 6 to 7 months old, which progressively became
* g0 M8 E2 V5 t0 i8 @; N. ^( V' z/ Y) y2 Hdarker. She was also concerned about the enlarge-9 h: o6 \1 b$ U. L, l$ q
ment of his penis and frequent erections. The child
& E& E3 T! R; @" H7 ewas the product of a full-term normal delivery, with
8 R" a$ j+ n) e @$ v+ ]) {a birth weight of 7 lb 14 oz, and birth length of9 ^# k' ]) y5 K- o P* e+ o0 o
20 inches. He was breast-fed throughout the first year( D. E. O3 ~3 I- e0 E W1 E8 v; C4 b
of life and was still receiving breast milk along with( H B- E; Z, `5 Z6 x2 c) Y
solid food. He had no hospitalizations or surgery,
1 @7 R* e( t5 T" o7 F, V6 k$ [+ Rand his psychosocial and psychomotor development
# l3 n) i/ I+ B& v; r; Vwas age appropriate./ D* H. X2 D- ]: g% L) ^8 Q
The family history was remarkable for the father,
/ a/ d7 E$ ]- j. k$ e/ x/ owho was diagnosed with hypothyroidism at age 16,
8 f, S* R9 l$ ]) d' T( wwhich was treated with thyroxine. The father’s
& K8 {6 u' x9 \9 y4 |height was 6 feet, and he went through a somewhat
( `1 W0 z9 A2 r1 bearly puberty and had stopped growing by age 14.* X' [5 f K0 {8 N* z' @& ^
The father denied taking any other medication. The
! E6 G; U1 N, R% Z1 Uchild’s mother was in good health. Her menarche7 P5 M+ P$ y" ?6 w! q- _8 A. Q
was at 11 years of age, and her height was at 5 feet
; H& ^! o3 y+ |+ i% J3 Z2 Y5 inches. There was no other family history of pre-% p7 B8 W0 ]( e: }( J
cocious sexual development in the first-degree rela-
7 s1 z8 p) l z9 u$ k Gtives. There were no siblings.* s1 e: U$ `6 R' o" O H
Physical Examination
9 O7 @& g/ K' U1 C2 a. k, N' M1 MThe physical examination revealed a very active,6 `3 V% H* F/ \0 Y
playful, and healthy boy. The vital signs documented
$ D% l4 [9 C# f, g7 Za blood pressure of 85/50 mm Hg, his length was
! d- C% U" R$ Z1 B4 E90 cm (>97th percentile), and his weight was 14.4 kg6 _# m y' S7 K0 I6 x {1 r" I( o
(also >97th percentile). The observed yearly growth
- M- a1 ~$ l$ Zvelocity was 30 cm (12 inches). The examination of4 g$ B5 c' Q5 }3 U" P; g
the neck revealed no thyroid enlargement." W+ Y4 j! W) t( D; i6 G2 L/ S& h7 j/ ]
The genitourinary examination was remarkable for
% v! A( o$ O& G" ?enlargement of the penis, with a stretched length of
" R! |. i$ ]# C5 {) f6 u% \% `8 cm and a width of 2 cm. The glans penis was very well' G7 `; [8 g8 o' L
developed. The pubic hair was Tanner II, mostly around
0 _! p# i6 H) ?540- b' T2 g n) e2 {
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
6 L1 v8 V/ G5 A8 W6 a$ R" }the base of the phallus and was dark and curled. The Y# b! F/ l7 c) Q( o; ^6 o7 Z& x
testicular volume was prepubertal at 2 mL each.& Q+ B' N" S1 y" K- p, D6 d* ?* |
The skin was moist and smooth and somewhat* o% M; q( E4 A5 t! w$ f t
oily. No axillary hair was noted. There were no8 m2 e; o$ T" o4 p& R6 u
abnormal skin pigmentations or café-au-lait spots.0 A' T5 ]" J1 R# R
Neurologic evaluation showed deep tendon reflex 2+8 @( |8 b9 X3 x' X' L
bilateral and symmetrical. There was no suggestion
# Y, S7 B& `& D/ ~: K* y9 @of papilledema.
$ a) z" V2 c% ]- j4 L' ?( MLaboratory Evaluation4 S! ?, J( l- _
The bone age was consistent with 28 months by
7 E ` u) \+ c: A$ P; z G+ y8 d" L0 jusing the standard of Greulich and Pyle at a chrono-9 j2 R4 x: l( k% ?0 u; Q8 C. b
logic age of 16 months (advanced).5 Chromosomal* X) G' X; `2 h2 _7 V: v2 a$ ]- h
karyotype was 46XY. The thyroid function test& F4 C3 u. M/ p% p6 @
showed a free T4 of 1.69 ng/dL, and thyroid stimu-; ?% B. }# }' I" s0 b
lating hormone level was 1.3 µIU/mL (both normal).
% ^0 y/ K0 _8 v I! p7 jThe concentrations of serum electrolytes, blood
, n2 f9 i4 M9 w/ C" m5 h) furea nitrogen, creatinine, and calcium all were1 U5 T, O/ K! f4 v; O
within normal range for his age. The concentration
0 S e) r) U8 f' `' J. ] Z% t# w0 @of serum 17-hydroxyprogesterone was 16 ng/dL" y) l/ \ i& i4 _
(normal, 3 to 90 ng/dL), androstenedione was 20
7 y' k: t1 P J, f+ U- `ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
, ]7 g# H" l4 }( J7 ~1 H" U! Nterone was 38 ng/dL (normal, 50 to 760 ng/dL),
9 F' Z4 m1 P8 s* v9 e3 T0 x6 k* ?desoxycorticosterone was 4.3 ng/dL (normal, 7 to
6 h( `1 Q0 _, H+ X! c49ng/dL), 11-desoxycortisol (specific compound S)
2 m- A' p4 [! p; I8 y' t% Jwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-" R% V- _1 @* P* \0 H) L
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
3 {: F- e% P# Y# i* b5 y1 Ctestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
! A) p- [8 J" u' eand β-human chorionic gonadotropin was less than
- X( F6 A0 m3 t' O5 mIU/mL (normal <5 mIU/mL). Serum follicular
8 E9 {' `$ B& x, jstimulating hormone and leuteinizing hormone
8 g0 j7 n2 v- F. [concentrations were less than 0.05 mIU/mL
" o. U, A5 B. m2 {6 J6 [1 a(prepubertal).* q9 p1 x' V# n; `" o2 F
The parents were notified about the laboratory1 W0 u( a1 p5 T9 A) X! o
results and were informed that all of the tests were6 Z- k3 |+ v; \9 s6 [
normal except the testosterone level was high. The
8 X- s* ^( }1 i9 h+ h9 n# kfollow-up visit was arranged within a few weeks to
4 j& q9 {) ~/ ~0 p( b6 t! {; E P# wobtain testicular and abdominal sonograms; how-
1 |4 v+ R4 Z4 ?" X6 o: j" {3 G- M; C8 Gever, the family did not return for 4 months.; g: l: B& p5 Y+ p) K) d2 z) ]
Physical examination at this time revealed that the( C% j0 h* e( [; o
child had grown 2.5 cm in 4 months and had gained6 h- [ l* P; o* j
2 kg of weight. Physical examination remained5 g+ Z4 c' P/ n/ w& y( ]2 v3 X
unchanged. Surprisingly, the pubic hair almost com-
6 ]2 C' m1 o, N: U/ t$ T& dpletely disappeared except for a few vellous hairs at( {- d$ ~1 ~) r
the base of the phallus. Testicular volume was still 2
4 X+ q1 X. K& |. h/ ^2 r( _mL, and the size of the penis remained unchanged.6 `9 N1 @$ j+ e& x
The mother also said that the boy was no longer hav-
2 A0 i4 B7 R: i; s9 N! Oing frequent erections.. a! E* |. Q+ r! o/ r+ U
Both parents were again questioned about use of
, @/ B T- d. \. b- M! T, A1 zany ointment/creams that they may have applied to
/ M2 ], L3 I$ K+ l0 L! {2 U8 jthe child’s skin. This time the father admitted the( V3 i, d3 J4 c5 k# F2 `( k
Topical Testosterone Exposure / Bhowmick et al 541
& `: o' W- F3 ?: f Q4 Duse of testosterone gel twice daily that he was apply-
2 ~6 M; S3 x. Ping over his own shoulders, chest, and back area for1 f' p2 z j1 a" o0 B
a year. The father also revealed he was embarrassed/ Q) l) w) y g' [3 T+ P
to disclose that he was using a testosterone gel pre-; S9 k7 J l$ l4 z% e$ t
scribed by his family physician for decreased libido
: `/ S4 f v' o' Q! Csecondary to depression.! w) }% `) h( j7 c! b
The child slept in the same bed with parents.% R; w% n, \8 U+ Y' N
The father would hug the baby and hold him on his) g3 ~; p, A! h& p' c! b
chest for a considerable period of time, causing sig-- \3 u$ F% c9 l e( x/ P& X
nificant bare skin contact between baby and father.
! d5 h4 ^' n bThe father also admitted that after the phone call,
2 L% [- `/ A& C( `& P. S% f6 Zwhen he learned the testosterone level in the baby+ |4 p4 G. o: j7 }. [
was high, he then read the product information1 i; H" }4 ]1 l/ C5 L1 l. l
packet and concluded that it was most likely the rea-
4 |6 t& J! L+ m( X1 o2 \" hson for the child’s virilization. At that time, they
* u3 ~/ u" [, M1 U( T$ udecided to put the baby in a separate bed, and the
) f8 B- l, ], s% k* F3 efather was not hugging him with bare skin and had# f! X9 \/ r: p3 y3 s+ i: H
been using protective clothing. A repeat testosterone
! V% v( s8 }& c' o+ L, D! s+ stest was ordered, but the family did not go to the
/ _* O! s7 _& j+ q: c* A6 y# dlaboratory to obtain the test. S2 k7 y1 f- U
Discussion, v7 I- c. q0 x: A( H
Precocious puberty in boys is defined as secondary
/ A# B9 m; }. K: |" Xsexual development before 9 years of age.1,43 c. P' i8 Q/ V- e; j3 F
Precocious puberty is termed as central (true) when& C; r7 Y0 ]: F/ C8 Q& |2 f
it is caused by the premature activation of hypo-
+ k& g8 L* O% K; K; Bthalamic pituitary gonadal axis. CPP is more com-! c4 _* D7 X5 S( w1 S
mon in girls than in boys.1,3 Most boys with CPP! c7 }- F- p7 R( d
may have a central nervous system lesion that is& V( A, y- S" {, T* E
responsible for the early activation of the hypothal-! |( M) s* g e0 ~2 @2 z3 ]
amic pituitary gonadal axis.1-3 Thus, greater empha-3 H7 G* w$ |2 L
sis has been given to neuroradiologic imaging in+ u# W, |( v( I7 t1 n" \" q' m% S/ J
boys with precocious puberty. In addition to viril-$ f; c8 Q0 T; @ P
ization, the clinical hallmark of CPP is the symmet-
; x% P4 Y) k+ i2 I& Nrical testicular growth secondary to stimulation by$ ~+ r( B% Y5 |( r
gonadotropins.1,3
9 q, G5 o; b0 K. a9 L/ kGonadotropin-independent peripheral preco-
' j$ ^0 P& u. a, K& {cious puberty in boys also results from inappropriate
3 U- K) j2 R' @2 Uandrogenic stimulation from either endogenous or
. R; C! F! \5 i% Z6 ~. nexogenous sources, nonpituitary gonadotropin stim-: C1 z' F; C1 S& _7 [& e3 I; R; D
ulation, and rare activating mutations.3 Virilizing7 N9 k4 o7 e9 Y5 o9 c# q* ^
congenital adrenal hyperplasia producing excessive
7 w1 d( G5 _$ Q9 D" I# Dadrenal androgens is a common cause of precocious- B0 v: G7 T# s4 j: u2 x
puberty in boys.3,4
8 Z2 j% B7 m) t2 a# U7 `The most common form of congenital adrenal; {' q3 t/ m+ E$ g9 F T: g
hyperplasia is the 21-hydroxylase enzyme deficiency. z8 Y: {7 h$ [- M
The 11-β hydroxylase deficiency may also result in
7 l7 l8 ^! v" H1 `' yexcessive adrenal androgen production, and rarely,
( D0 i, p1 A6 n) k! k& nan adrenal tumor may also cause adrenal androgen
8 C& M6 m; ?% p% r* O2 v% Pexcess.1,3" Z0 A$ Q8 c! Y5 {; |( U
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from; d2 B) x8 d7 M* e
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007. E; p8 H! ?$ Y _
A unique entity of male-limited gonadotropin-. n( ]" O3 f+ G0 d6 R$ p! }' W
independent precocious puberty, which is also known
7 Q' D9 b! o: C% uas testotoxicosis, may cause precocious puberty at a2 c3 h9 U! u0 n- A7 L8 o0 q# W. L
very young age. The physical findings in these boys( X* J- ]. `: s4 Z& Q5 P, K
with this disorder are full pubertal development,
1 V; z( I6 F7 Q5 e p& xincluding bilateral testicular growth, similar to boys
. Z& Y& R. e" }" k5 V) s- Qwith CPP. The gonadotropin levels in this disorder4 w4 Q- s# P: T2 V' ?
are suppressed to prepubertal levels and do not show
2 f4 b" l- a4 o6 lpubertal response of gonadotropin after gonadotropin-7 ^3 b; ]9 o0 t# H& T3 F1 V
releasing hormone stimulation. This is a sex-linked
+ [$ Z7 O. z4 E9 K5 j% Eautosomal dominant disorder that affects only4 X& a& t* M- |6 F% h
males; therefore, other male members of the family
: y9 H3 S1 f' ~1 b- M$ Wmay have similar precocious puberty.3& a# G0 e0 T+ H/ m
In our patient, physical examination was incon-
1 |! A+ h& j9 Y# x8 r3 _sistent with true precocious puberty since his testi-3 n% P) ~. ^3 k7 L4 V
cles were prepubertal in size. However, testotoxicosis
# ]% G# U: p8 s5 D* A5 ]9 P* A( jwas in the differential diagnosis because his father8 @. L4 o6 k6 v% `# {
started puberty somewhat early, and occasionally,
0 b0 b) S! q" t, c5 \testicular enlargement is not that evident in the
* H7 a, V$ Q; K2 Fbeginning of this process.1 In the absence of a neg-
' T* T L& R( s8 j lative initial history of androgen exposure, our& w9 R' K; h3 n" Y. }" z$ N
biggest concern was virilizing adrenal hyperplasia,
5 P0 d0 j0 A9 h) p! ?% Aeither 21-hydroxylase deficiency or 11-β hydroxylase
* [: N0 |2 o6 O [3 S- a0 M5 a% L: Bdeficiency. Those diagnoses were excluded by find-0 Z1 p r% N. c$ b4 _2 h
ing the normal level of adrenal steroids.
( K; k% L* d$ S0 p0 \The diagnosis of exogenous androgens was strongly- _1 k9 |8 C: v) _) v% F. t
suspected in a follow-up visit after 4 months because' z. }; h% Z9 H, d8 }/ p! d
the physical examination revealed the complete disap-
, `# }1 c) |2 g- W& b5 X, Hpearance of pubic hair, normal growth velocity, and f2 K7 t0 N% @7 Q6 @( k3 z' I$ |
decreased erections. The father admitted using a testos-: f! _$ w' N. a# u
terone gel, which he concealed at first visit. He was4 L. g, e2 p8 R3 B0 V
using it rather frequently, twice a day. The Physicians’3 k, p7 I+ j& D% J
Desk Reference, or package insert of this product, gel or
: f$ v/ _3 y1 w- Scream, cautions about dermal testosterone transfer to
9 Q" |' n: M) J2 `0 [- O* q M- runprotected females through direct skin exposure.0 P" _) M+ q: Y1 V9 z$ M
Serum testosterone level was found to be 2 times the2 n# q \5 [5 @5 Q* x8 h* T* Z7 d5 |; S
baseline value in those females who were exposed to
+ u" H/ t. z. O! P1 H. `# k* Ceven 15 minutes of direct skin contact with their male
# B4 Q) Y, d, P* i. t% j, _% o. P0 N! Z; Tpartners.6 However, when a shirt covered the applica-
& C6 ?$ v5 l/ E. H {( ~tion site, this testosterone transfer was prevented.
+ L/ b; U1 z- K2 X! M3 ~5 i8 sOur patient’s testosterone level was 60 ng/mL,
+ W9 W7 }6 ~( z- i, i+ }. Uwhich was clearly high. Some studies suggest that
3 K/ [* n+ R; y Y$ cdermal conversion of testosterone to dihydrotestos-- a$ ?& w4 H# w! `' @% y6 z
terone, which is a more potent metabolite, is more+ p3 L, c" b1 {) V! ?, L C
active in young children exposed to testosterone- e' F% P3 Y1 j9 n
exogenously7; however, we did not measure a dihy-
: O' }5 |9 u) e0 ]! V6 i4 c* Cdrotestosterone level in our patient. In addition to
$ }( t8 F! Q$ g+ }virilization, exposure to exogenous testosterone in9 c, u; f1 Z, m( e0 N5 R. \
children results in an increase in growth velocity and
. u& }* D, `& H& }4 D' vadvanced bone age, as seen in our patient.$ e/ Y. S' ~! h0 A
The long-term effect of androgen exposure during
. b7 C Q8 m) C7 Z# _( w" M# v% B' rearly childhood on pubertal development and final
" M! N! L; \$ W0 N% d/ Vadult height are not fully known and always remain$ L5 ~3 S8 K2 V' X' r7 L
a concern. Children treated with short-term testos-
2 ^' g/ P! d4 ~- Lterone injection or topical androgen may exhibit some% p/ ?5 J3 T, W x. U2 l6 _. Q
acceleration of the skeletal maturation; however, after* C# {6 F# ?/ m
cessation of treatment, the rate of bone maturation
0 y7 q& c1 `& w: D$ ]' \$ m4 gdecelerates and gradually returns to normal.8,9
) i; p* n F8 g, }+ U8 F$ \9 r' @- `% }There are conflicting reports and controversy
3 l7 O, d2 F/ s) }! p$ Oover the effect of early androgen exposure on adult
) r7 c9 e5 [4 B% G4 t6 A! x9 npenile length.10,11 Some reports suggest subnormal7 J1 U1 f/ j' v, [' P
adult penile length, apparently because of downreg-3 x0 {3 F- y W d; ^0 m; y
ulation of androgen receptor number.10,12 However,# _6 A$ z' ]4 C- _
Sutherland et al13 did not find a correlation between
2 K" F. [2 m. I. a+ ]- Nchildhood testosterone exposure and reduced adult" M9 c0 \- q( n, A. a; U7 [
penile length in clinical studies.
' s. ^; W! a$ vNonetheless, we do not believe our patient is
3 H! B |9 ?8 z; r- M" jgoing to experience any of the untoward effects from. N% n# w9 C1 d D4 W( B+ e
testosterone exposure as mentioned earlier because6 @9 z3 x- l5 t, x; O
the exposure was not for a prolonged period of time.2 g1 K& {/ N" F4 i
Although the bone age was advanced at the time of
( M, N- N! l: M3 a. {diagnosis, the child had a normal growth velocity at0 Y% R. ^1 t8 g3 b8 z z# H
the follow-up visit. It is hoped that his final adult
2 k7 w, A0 Z+ I& qheight will not be affected.: F7 y7 ~3 h' N. V0 |" P4 t
Although rarely reported, the widespread avail-/ l0 {3 [$ D. U) e% t B
ability of androgen products in our society may, \& f% h. i) q9 w" X
indeed cause more virilization in male or female+ u1 p7 x6 Q7 j- \# X2 V. d
children than one would realize. Exposure to andro-0 f- Y! r2 @$ Y- n( m
gen products must be considered and specific ques-
% L5 G6 o% b) @9 u6 `tioning about the use of a testosterone product or& x$ |( L! T6 @0 Z8 q( X
gel should be asked of the family members during x6 T2 v9 `6 ]# @, q( |
the evaluation of any children who present with vir-) a8 v2 o4 H. _: v' h) D1 O1 F- C
ilization or peripheral precocious puberty. The diag-5 q. J' t' U: D+ d* O$ W; x
nosis can be established by just a few tests and by
# D8 K! U6 T8 h) t8 oappropriate history. The inability to obtain such a
% r/ t* H- \1 E8 J u7 R& s7 m3 y+ rhistory, or failure to ask the specific questions, may
$ e0 M! J0 v9 O! U# w, X2 {result in extensive, unnecessary, and expensive
. E3 R* w; `; ^9 u# h( Y. Yinvestigation. The primary care physician should be5 F3 G% m* |/ G- G' A1 y! O" g
aware of this fact, because most of these children
' g0 g7 K( ^) ~/ w+ S9 G. amay initially present in their practice. The Physicians’
% [' z+ w# y8 K& @* \Desk Reference and package insert should also put a7 B" I! \) V7 [& L0 t Z; |7 X3 }
warning about the virilizing effect on a male or" j; U$ ~* q0 r
female child who might come in contact with some-
" ~) F5 x; \/ J' C/ Y/ kone using any of these products.
' W/ p2 _3 q" |% l( V- bReferences
' y0 |! Y0 h2 S9 v* V$ U1. Styne DM. The testes: disorder of sexual differentiation0 o5 F |- G, ?0 M+ o' Y1 H P
and puberty in the male. In: Sperling MA, ed. Pediatric
9 }+ {/ }: D/ S9 X& k; dEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;( y2 a, A1 g# O- e/ m" N
2002: 565-628.
F5 V2 P/ U) S* h% z: m3 Q$ X8 r% u2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
* H7 G7 S W5 C& _puberty in children with tumours of the suprasellar pineal |
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