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Sexual Precocity in a 16-Month-Old- O s! U$ K' h/ }9 H% s# g) r) j4 V
Boy Induced by Indirect Topical
( q8 V# p, P* l6 g& D2 _# NExposure to Testosterone
$ K& J, B* o" Y8 ]' Q% kSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
9 }9 x7 ~) N% q5 Kand Kenneth R. Rettig, MD1
! b0 k: w! q+ Z8 [Clinical Pediatrics: f: [ X# W& |4 c: Z8 R# q, V
Volume 46 Number 6
; m7 i3 J% c6 ~7 ~2 eJuly 2007 540-543# K3 S7 S. r C$ e2 ?, U2 b$ f" B
© 2007 Sage Publications8 K6 I1 [- R6 @+ Q) O* t- z
10.1177/0009922806296651
8 R3 e3 ?& \1 J- ?4 o; lhttp://clp.sagepub.com5 k$ ^; F8 Z( M2 `$ x
hosted at% p: H( ^2 L1 Q
http://online.sagepub.com
: r5 H; O8 [) E9 r2 Q8 MPrecocious puberty in boys, central or peripheral,* j. q1 g. g# Q. }
is a significant concern for physicians. Central
& M1 x. k6 Q8 { K* wprecocious puberty (CPP), which is mediated
0 R* u+ Q, r( u4 i( i1 A+ ?through the hypothalamic pituitary gonadal axis, has
9 s* [% a2 p9 b0 P8 Ga higher incidence of organic central nervous system
c- Y4 y! Z N1 O# c1 Hlesions in boys.1,2 Virilization in boys, as manifested! d$ k" g, O! o" ^3 O
by enlargement of the penis, development of pubic
1 l% _# E2 i$ {% b: }hair, and facial acne without enlargement of testi-
& m6 Y$ Q6 Z; e' e' R/ gcles, suggests peripheral or pseudopuberty.1-3 We e. o1 x" K2 L7 @7 q: K5 s% R
report a 16-month-old boy who presented with the5 f; y% c* ]5 y3 z! m2 s# e0 R
enlargement of the phallus and pubic hair develop-- g9 y) J( `0 Z! R* F8 V) B8 W: v
ment without testicular enlargement, which was due
+ c; `/ M! X1 A( |; @to the unintentional exposure to androgen gel used by
3 o \1 R* {) Z: bthe father. The family initially concealed this infor-
! w' T* d6 V+ u/ g% Amation, resulting in an extensive work-up for this
\& I' Q: n& P; i" k; Echild. Given the widespread and easy availability of
2 k* i1 B0 X: G; G3 b, m6 @5 rtestosterone gel and cream, we believe this is proba-5 _ v S4 ], L! k6 T9 S
bly more common than the rare case report in the
" K* k$ ?6 Q, pliterature.4
7 a) _, r$ S6 L' g4 W \3 nPatient Report7 ]7 J) W4 s& u$ F; Z+ }; \" w# D/ e
A 16-month-old white child was referred to the5 j5 a4 x1 t; N0 l* G9 b) C
endocrine clinic by his pediatrician with the concern
3 c5 F9 E+ P6 ^4 A7 C$ ?7 ^of early sexual development. His mother noticed& c3 x7 i% U% I7 y
light colored pubic hair development when he was
4 O& a5 V4 a0 ~. V0 K. m4 P9 w. q1 vFrom the 1Division of Pediatric Endocrinology, 2University of
0 ?0 `/ P! O& A& ISouth Alabama Medical Center, Mobile, Alabama.
9 `- Y1 M# V" r+ n3 N0 J- Q8 AAddress correspondence to: Samar K. Bhowmick, MD, FACE,+ |5 z1 C7 k8 G2 _/ s: D
Professor of Pediatrics, University of South Alabama, College of
5 L2 ? _# Z/ i) H4 xMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;3 c3 S: j- h7 d
e-mail: [email protected].6 p* Q [3 G( o5 s) n# X
about 6 to 7 months old, which progressively became/ J" j$ e7 U4 h" K0 V2 |/ {
darker. She was also concerned about the enlarge-
; X7 s% j2 ^7 a/ R% Yment of his penis and frequent erections. The child3 [# m9 m+ k) f/ S. R6 G
was the product of a full-term normal delivery, with
, e* l8 `5 e8 O" L# Ma birth weight of 7 lb 14 oz, and birth length of# F) l8 c& w' l1 z3 [; |& W
20 inches. He was breast-fed throughout the first year
2 H3 C: X1 y/ `. oof life and was still receiving breast milk along with
$ O' d' V$ i) N" n+ K9 Ksolid food. He had no hospitalizations or surgery,
; ]) n. E& L ?2 o, Yand his psychosocial and psychomotor development
, o$ u; h% W$ n ]/ j8 Y% Cwas age appropriate.: O" B& Y& [4 R4 U1 _
The family history was remarkable for the father,0 \% \% U! X9 ?+ ]
who was diagnosed with hypothyroidism at age 16,; {4 ? {" G% {. T( K& s2 t7 f7 E
which was treated with thyroxine. The father’s
& V, W3 }- o* [9 g) mheight was 6 feet, and he went through a somewhat1 J2 G& k! S' q- G ^2 F
early puberty and had stopped growing by age 14., m% o$ x$ F; o" L$ m
The father denied taking any other medication. The3 E9 s7 f& o( Z$ Y8 @+ \
child’s mother was in good health. Her menarche0 k0 U6 Y7 I( P; b5 H9 |
was at 11 years of age, and her height was at 5 feet# u$ w6 h/ [ l$ Z3 h* Q L
5 inches. There was no other family history of pre-
; n ]2 B: g/ J, o/ ycocious sexual development in the first-degree rela-. d& [" B; o! ^% q* ~1 G9 f1 y0 \" A
tives. There were no siblings.
3 C) n2 r/ r3 _. }, mPhysical Examination
' g; J- S& |$ }- Z: A: P+ {6 R3 ~2 OThe physical examination revealed a very active,' B# ^6 O. k' M1 a* i
playful, and healthy boy. The vital signs documented
3 N2 v. |. s$ v5 [a blood pressure of 85/50 mm Hg, his length was: @* Q1 _+ j+ S9 Q& L# D
90 cm (>97th percentile), and his weight was 14.4 kg
3 |% Z3 k6 h3 Q" o5 D/ P(also >97th percentile). The observed yearly growth+ T0 s! S$ y; j2 w. y R9 y
velocity was 30 cm (12 inches). The examination of
a# n) o" Z- O% A2 P6 ]the neck revealed no thyroid enlargement.7 @& y* [; ^7 {" S
The genitourinary examination was remarkable for1 B. i' d4 L* E3 C, y
enlargement of the penis, with a stretched length of5 D- l% ` D% Z1 O. x' B8 B- J
8 cm and a width of 2 cm. The glans penis was very well2 n" |0 W% H( b* o, [& g' e# L
developed. The pubic hair was Tanner II, mostly around2 y4 G* u! `8 i7 m% W" N
540+ J0 z, q' x. F4 T
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
3 J% i3 b: z( g) F, m7 }the base of the phallus and was dark and curled. The
9 ~$ Q+ w# X+ L% I3 q$ Y8 W& Itesticular volume was prepubertal at 2 mL each./ ? s7 i8 r5 t W8 j0 h1 O
The skin was moist and smooth and somewhat
A; E. A( u9 i2 w+ ?oily. No axillary hair was noted. There were no
# \9 {7 ~ y7 Y+ w+ @3 X+ |abnormal skin pigmentations or café-au-lait spots.
8 Y6 G. x0 k* b8 ]: `& u4 uNeurologic evaluation showed deep tendon reflex 2+
9 Q2 L, u0 z- w2 Lbilateral and symmetrical. There was no suggestion9 u1 U! E+ c% k u a
of papilledema.4 ]. P( M7 L5 k- l% w
Laboratory Evaluation: l) r8 F! T7 {# n2 L/ b$ c
The bone age was consistent with 28 months by; g6 |4 |3 {& T8 X$ z
using the standard of Greulich and Pyle at a chrono-
( a7 w- K6 U- blogic age of 16 months (advanced).5 Chromosomal; T' B: \1 {8 f+ {/ c
karyotype was 46XY. The thyroid function test0 e$ C. c; u. A' ]# V/ k2 c& L
showed a free T4 of 1.69 ng/dL, and thyroid stimu-' b: i6 ~+ y" z) F( }
lating hormone level was 1.3 µIU/mL (both normal).
* d3 H: V1 l$ J3 [, d8 i8 LThe concentrations of serum electrolytes, blood
0 O9 s% Z* ?, b2 }- q1 |# `7 r4 xurea nitrogen, creatinine, and calcium all were) S+ }5 T8 q! ]* m ?% E
within normal range for his age. The concentration
7 [ Y" T7 U" K4 ~8 e1 O& Fof serum 17-hydroxyprogesterone was 16 ng/dL
2 T [" C9 z C4 j3 e0 A Z(normal, 3 to 90 ng/dL), androstenedione was 20
( y7 ]+ |* R' w$ e5 y# N2 N5 P8 ^ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
' c; r7 B! a8 c. S: _8 [6 Hterone was 38 ng/dL (normal, 50 to 760 ng/dL),
7 V7 ^8 p- v5 D- Zdesoxycorticosterone was 4.3 ng/dL (normal, 7 to
( I: x# I3 D- m% E5 G1 q49ng/dL), 11-desoxycortisol (specific compound S)
9 V" e0 n' W# y$ ^! d i8 ~1 Lwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-9 V: j1 |2 b9 D$ r* Q# [2 O% [
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
: R6 Z5 N" p" F6 \4 g, mtestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
8 `4 X6 t9 w: o0 u ~8 pand β-human chorionic gonadotropin was less than
2 I/ ?' m0 r0 }; e4 ]: v5 mIU/mL (normal <5 mIU/mL). Serum follicular9 z3 E& j6 ^3 U! i! C/ ^0 L3 O
stimulating hormone and leuteinizing hormone
: G. D# p5 A$ c& B# c _7 J& hconcentrations were less than 0.05 mIU/mL
0 N7 p! |" p7 ]* j* `: H(prepubertal).
+ [' o I6 m2 d4 P% ^4 i3 U$ yThe parents were notified about the laboratory
3 ^0 e8 |8 D: C1 p5 z( Vresults and were informed that all of the tests were+ ?- g) o0 j- {
normal except the testosterone level was high. The& U4 ^+ L. Q' G
follow-up visit was arranged within a few weeks to
' a* P0 {0 d$ J" robtain testicular and abdominal sonograms; how-! U; O! C, k+ n8 g9 `% u, X( z
ever, the family did not return for 4 months.
0 K6 \& b) y) ]0 x$ ?Physical examination at this time revealed that the
6 v& T+ N2 f! l4 `4 L: C6 l$ r: ?child had grown 2.5 cm in 4 months and had gained
: z9 n6 ?, c7 ~2 kg of weight. Physical examination remained
9 M) s: p" U. Munchanged. Surprisingly, the pubic hair almost com-- B2 S) k* I i& J) v
pletely disappeared except for a few vellous hairs at8 O% ]! T7 a/ O$ U, I9 Z2 O# r
the base of the phallus. Testicular volume was still 2
7 w( Q5 h8 C& l$ E! G. W |0 smL, and the size of the penis remained unchanged.
8 j, _- _5 L/ M9 @The mother also said that the boy was no longer hav-
' V5 d, Y; j, R9 I6 X1 F2 }ing frequent erections.% c7 U( A- f2 r6 Y
Both parents were again questioned about use of) ]8 H, w5 m2 x; [: o; m8 h
any ointment/creams that they may have applied to! `; {" t4 ~# |/ O" U l: ^
the child’s skin. This time the father admitted the. t* m- F- _' E8 h
Topical Testosterone Exposure / Bhowmick et al 541
) d* i& [9 z: \7 A1 j$ Duse of testosterone gel twice daily that he was apply-
8 _6 ]5 r3 f. m# U+ Ning over his own shoulders, chest, and back area for
- C! Q. q' k9 [( \! `a year. The father also revealed he was embarrassed3 ^5 n% L1 x# d& M& u4 k9 g
to disclose that he was using a testosterone gel pre-
, N" |# }) `& f8 a! {4 ^scribed by his family physician for decreased libido
$ q* t' \8 s3 z. l1 p8 e/ zsecondary to depression.
/ l- Q$ B5 Y/ {, ~3 P4 {4 cThe child slept in the same bed with parents.5 k6 ^2 O# v" T4 u- V$ h
The father would hug the baby and hold him on his
* c0 o5 L& f& M3 [$ nchest for a considerable period of time, causing sig-7 H; c4 \( [' e9 ~& V
nificant bare skin contact between baby and father./ y( W. m9 ]# J% X+ C/ b
The father also admitted that after the phone call,
" l1 q! I; U: [4 S4 E& j4 k$ |% Ewhen he learned the testosterone level in the baby( u5 M, N# n2 A# Y% n; N# ^! ?0 i8 q d
was high, he then read the product information
: j0 O" K8 ?4 F J8 V) ypacket and concluded that it was most likely the rea-6 i1 a9 |7 {: c0 x0 S+ x+ [. }# Z
son for the child’s virilization. At that time, they3 V% x5 }2 ?2 B0 K( W& D) Y) H
decided to put the baby in a separate bed, and the
8 x6 \9 T- E3 W3 H% `6 ?- j: Nfather was not hugging him with bare skin and had
8 g5 o. F" K! n/ y' y3 cbeen using protective clothing. A repeat testosterone
: i/ ~) r/ }8 W& [- ltest was ordered, but the family did not go to the) s& \ j y$ z
laboratory to obtain the test.$ q2 n) d+ F' K* K: v
Discussion
: p' E8 u% W8 t) e) f# UPrecocious puberty in boys is defined as secondary( q6 M. B' K9 u, q; t- w
sexual development before 9 years of age.1,46 C1 S. |- u ~2 _6 n* y
Precocious puberty is termed as central (true) when
1 A9 T0 s% D' Qit is caused by the premature activation of hypo-
5 Y. z0 U/ W7 i) Y4 G5 Jthalamic pituitary gonadal axis. CPP is more com-$ c$ p( X3 D2 j1 \+ F2 S) s8 N; [; o
mon in girls than in boys.1,3 Most boys with CPP
- h7 n4 q( c6 D8 q. `! E/ `may have a central nervous system lesion that is; ]- i- B5 J9 U/ H# i$ f
responsible for the early activation of the hypothal-
" A) p) ?% u- `" @amic pituitary gonadal axis.1-3 Thus, greater empha-
# x2 ` w9 `0 |: b0 Ssis has been given to neuroradiologic imaging in
8 R: A8 N! j. A+ x. mboys with precocious puberty. In addition to viril-+ @& z$ ^6 `7 L) b
ization, the clinical hallmark of CPP is the symmet-9 u/ N4 J1 E/ f5 R
rical testicular growth secondary to stimulation by
! L. G* G8 t# F0 _gonadotropins.1,3
" I' M7 z! D4 M3 M% W7 `Gonadotropin-independent peripheral preco-
! R3 B* ]0 K3 n2 x4 h) Ecious puberty in boys also results from inappropriate
7 {, ]: e4 e% C( aandrogenic stimulation from either endogenous or
9 a2 q8 ?$ K0 Z, @6 Q, u; v4 V Jexogenous sources, nonpituitary gonadotropin stim-7 E+ {$ B, |8 R t( ]
ulation, and rare activating mutations.3 Virilizing% U, A; q; _( J7 a$ \+ v9 P# A
congenital adrenal hyperplasia producing excessive
4 @" P; k: [4 \6 P* B6 m e! O9 ]adrenal androgens is a common cause of precocious
@" }6 _' o! J( ]! m' ~* ypuberty in boys.3,4) p; O8 O/ {4 [ `0 y% M9 c
The most common form of congenital adrenal- k# p5 {# k3 V/ g1 P
hyperplasia is the 21-hydroxylase enzyme deficiency.
$ \1 V/ V) U6 `6 U: FThe 11-β hydroxylase deficiency may also result in
: O% j; {0 c1 R; h5 N+ e. n7 pexcessive adrenal androgen production, and rarely,
/ K8 }* a4 C3 B& lan adrenal tumor may also cause adrenal androgen
: q3 P6 q0 i, t N& j4 Mexcess.1,3
6 d2 }' {; U& ~2 A0 Gat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
. S$ E7 l0 M; {4 ?' W0 w542 Clinical Pediatrics / Vol. 46, No. 6, July 2007/ x* H0 _" a: a& F
A unique entity of male-limited gonadotropin-
, Y: u; \, h5 t# Cindependent precocious puberty, which is also known
9 j8 t8 Q* C% U+ o X* f4 jas testotoxicosis, may cause precocious puberty at a
- I( Z3 f9 u" A4 Z% t$ f+ @0 every young age. The physical findings in these boys
" E: s* f( g0 u# M/ ]with this disorder are full pubertal development,
' P5 Z, h; q( ~( Y5 V- J/ V4 vincluding bilateral testicular growth, similar to boys+ l2 o8 b$ x' J3 J8 a* q+ T
with CPP. The gonadotropin levels in this disorder
9 l- f0 ~4 h4 N) {* Sare suppressed to prepubertal levels and do not show/ t. t2 k- M8 {; w: c
pubertal response of gonadotropin after gonadotropin-
! D' v. N4 y' K0 J+ Qreleasing hormone stimulation. This is a sex-linked/ d# ~/ h* d) Z. X. W1 Z$ x! ]
autosomal dominant disorder that affects only
/ M6 b% f- u8 vmales; therefore, other male members of the family
* c( ~# x) ~, s1 rmay have similar precocious puberty.36 K. Z. ?; J+ q
In our patient, physical examination was incon-9 d3 I! \8 u6 Z, {4 `& k
sistent with true precocious puberty since his testi-" }. r+ u* Z/ x; Q- F4 I
cles were prepubertal in size. However, testotoxicosis/ L$ P! F0 U) M
was in the differential diagnosis because his father% \! r. P1 Q- {
started puberty somewhat early, and occasionally,: S% W- \9 _: `% p" N& q
testicular enlargement is not that evident in the
2 ]! q t& E" v1 B, w' Vbeginning of this process.1 In the absence of a neg-
' z8 A) a5 F+ O' ^" a8 ]3 @. \ative initial history of androgen exposure, our
% D+ Z6 U3 I/ c q7 m6 p7 Q9 Ubiggest concern was virilizing adrenal hyperplasia,
/ R8 C3 h/ ] P% {9 Z2 Veither 21-hydroxylase deficiency or 11-β hydroxylase
9 K6 p- s, K$ i6 Ldeficiency. Those diagnoses were excluded by find-" M, a" C6 R# K
ing the normal level of adrenal steroids.% a' X R+ b! r, l2 A
The diagnosis of exogenous androgens was strongly
* H; P' [# Z, X7 J7 E7 P" vsuspected in a follow-up visit after 4 months because; C3 g7 l2 [$ i1 [' A
the physical examination revealed the complete disap-# z0 k# B( J: u& |! ^9 J
pearance of pubic hair, normal growth velocity, and
1 z0 p% ]- p( O7 b" Y4 l/ edecreased erections. The father admitted using a testos-% F* x' ~8 W% Y) t& {6 y
terone gel, which he concealed at first visit. He was
8 e) n8 S) z! j/ P5 d+ fusing it rather frequently, twice a day. The Physicians’' p& S4 p$ ^9 C* S/ W, l
Desk Reference, or package insert of this product, gel or' V: t& d' t* ]! ]0 W
cream, cautions about dermal testosterone transfer to
4 [, b b8 w. b, O W+ |unprotected females through direct skin exposure.) ]' w9 v$ D! V T2 V3 S V
Serum testosterone level was found to be 2 times the
& Q; P+ K# Z7 T$ o: Y. }baseline value in those females who were exposed to
7 D- T# f' x9 m# }+ E9 a* Aeven 15 minutes of direct skin contact with their male) D" ? \- S# @
partners.6 However, when a shirt covered the applica-
- Z, c1 v; D6 Z" btion site, this testosterone transfer was prevented.- J" S7 j. b5 ]3 O, \ |
Our patient’s testosterone level was 60 ng/mL,
1 ? \1 I. c: `- j7 t4 {which was clearly high. Some studies suggest that
8 }2 }4 W% M7 B, i, m. [dermal conversion of testosterone to dihydrotestos-
3 g7 X& w9 P9 F' f2 f% B- `" @+ ^terone, which is a more potent metabolite, is more9 F! ?$ G [# Z8 g- d
active in young children exposed to testosterone" j2 ~" K1 ~) q* A) G: u
exogenously7; however, we did not measure a dihy-" j0 _9 a4 Z0 J; i' J
drotestosterone level in our patient. In addition to7 _! H' L% k. m( t* x! f0 T
virilization, exposure to exogenous testosterone in
' B/ h8 F/ j% a1 I% p- l) {. Q# s: Kchildren results in an increase in growth velocity and
* h" j: @2 t9 c3 i+ r4 ^" f6 tadvanced bone age, as seen in our patient.
* O8 l* F k: v g) \! z1 RThe long-term effect of androgen exposure during
5 ]8 D' y t2 B5 R5 f# M3 jearly childhood on pubertal development and final' g# c3 K" }& `* w
adult height are not fully known and always remain
* ^0 N; f) d& O5 z% ia concern. Children treated with short-term testos- a& {) L9 N4 x4 n$ B
terone injection or topical androgen may exhibit some
$ m* h6 C7 d. K$ ~acceleration of the skeletal maturation; however, after) b4 n6 k& [2 s* ^
cessation of treatment, the rate of bone maturation- G' V |, ~ m3 c. ]- }! r3 [* }
decelerates and gradually returns to normal.8,9
, Z5 M8 h$ |8 T' dThere are conflicting reports and controversy
: C: t, b- C$ b7 r: hover the effect of early androgen exposure on adult9 H7 C* e+ y/ ?/ s1 o) D! a8 Y
penile length.10,11 Some reports suggest subnormal
T5 d; l9 j: w: D0 Aadult penile length, apparently because of downreg-
8 e: ]/ U d" P7 u# {4 bulation of androgen receptor number.10,12 However,7 a& k+ Z$ ?0 p3 t/ ^& J
Sutherland et al13 did not find a correlation between7 Q% a+ A. H) b7 I
childhood testosterone exposure and reduced adult8 z. g+ v) ?; {' V, D
penile length in clinical studies.8 A3 h$ C& K7 Z+ _7 T. R# j
Nonetheless, we do not believe our patient is! Z- p& t; G6 a5 K0 a6 ~4 C
going to experience any of the untoward effects from
" b3 U- f) F% V3 q/ u( utestosterone exposure as mentioned earlier because" J/ [3 l1 Y2 C
the exposure was not for a prolonged period of time.5 y0 D2 {3 [0 V+ {! p% J$ }
Although the bone age was advanced at the time of
# Z3 o! g& x- U. l6 j" B+ zdiagnosis, the child had a normal growth velocity at
" W- G6 ~/ m9 o" [7 r" N" ?& {the follow-up visit. It is hoped that his final adult+ P; ]5 A8 `$ j8 n7 _
height will not be affected.
, w3 y6 T$ o" UAlthough rarely reported, the widespread avail-
' u) M( {- q% q, B. o( F+ o/ fability of androgen products in our society may
9 ]9 u1 `( d- v0 pindeed cause more virilization in male or female
& _- U* \( g- i+ L% Ychildren than one would realize. Exposure to andro-6 C$ |) ?9 W' |* J! ]
gen products must be considered and specific ques-: L4 n3 @' Q/ k$ G1 M; K
tioning about the use of a testosterone product or
. R! b9 o" p& ]" W* P2 q2 @gel should be asked of the family members during
8 y4 y) I: V' _0 @; u- Wthe evaluation of any children who present with vir-
( Q- b# J1 J0 ?) E2 l4 xilization or peripheral precocious puberty. The diag-% m) L; Q; e" _. l9 Z6 r
nosis can be established by just a few tests and by @: Y4 F) Y" l/ _
appropriate history. The inability to obtain such a& b* |; s a1 N+ K' u
history, or failure to ask the specific questions, may
& a' q$ K& K( c+ c6 ?6 L; vresult in extensive, unnecessary, and expensive: R0 c. b5 X! t6 @
investigation. The primary care physician should be
, }7 v- ^2 A& B$ W# s7 faware of this fact, because most of these children
6 z! u! ]/ Y1 E6 s4 m9 Mmay initially present in their practice. The Physicians’
1 c+ }( a8 ]( L. nDesk Reference and package insert should also put a6 C- E, @/ y Y+ z
warning about the virilizing effect on a male or
0 b# H( s: a" l* f! o* Q% D4 T5 Ofemale child who might come in contact with some-
+ D; o6 b: [0 o" R% c9 l0 Eone using any of these products.
x$ y3 M$ T0 V2 Q+ r- X1 ~References
. k1 M2 h* [$ V% Y f+ u6 e1. Styne DM. The testes: disorder of sexual differentiation- C2 i2 C8 R8 ^* n% D
and puberty in the male. In: Sperling MA, ed. Pediatric; C. m. |: b1 x! O: _" D4 X
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
: M$ ?8 G& M" G' V2002: 565-628.
) N4 b6 B3 r4 t+ L9 j* O2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
/ E2 d4 F' X4 U: ^0 ?: zpuberty in children with tumours of the suprasellar pineal |
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