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Sexual Precocity in a 16-Month-Old: f7 q, y8 D' A: Z+ T4 A/ B2 Y5 m
Boy Induced by Indirect Topical
" t9 J, V* x# C2 _& rExposure to Testosterone
- ]) y6 A% }; |- |Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
& L* S, V$ K1 Q1 Q" |* { S0 l3 \& i2 {and Kenneth R. Rettig, MD1
. o1 M7 H4 Z, e: x+ o' f6 V% DClinical Pediatrics
g: D4 {6 k7 |. ?; B+ b5 EVolume 46 Number 6
. M5 o7 [/ W0 b. b0 O* cJuly 2007 540-543
/ d% S! W7 K' s# h1 l) T© 2007 Sage Publications3 e) ]/ \6 L: _$ d) K
10.1177/0009922806296651
+ D) u% `: I4 O. y4 Y2 @; P1 Ahttp://clp.sagepub.com( N" m* [- b' j$ \, t/ a1 x* W
hosted at
3 A+ [2 p% E/ i/ U2 u0 w' Ehttp://online.sagepub.com$ ] }" b" r6 Q$ d3 U
Precocious puberty in boys, central or peripheral,
: T2 z& ~7 R/ l) T+ @% jis a significant concern for physicians. Central
3 d0 U( |2 R+ M V5 x+ g6 Iprecocious puberty (CPP), which is mediated& S' q1 _ U2 {( ?2 d
through the hypothalamic pituitary gonadal axis, has
+ A# R) _7 x4 V8 d" L# pa higher incidence of organic central nervous system2 _2 T, F) X1 B& J7 t. u
lesions in boys.1,2 Virilization in boys, as manifested# [' X) N. R/ `8 k8 {
by enlargement of the penis, development of pubic5 h/ D) B( a% R6 e: u# z( A# w$ @
hair, and facial acne without enlargement of testi-
" ~$ U: m7 `& V Ccles, suggests peripheral or pseudopuberty.1-3 We
/ d' A) u; f# @" P+ C! q/ ]report a 16-month-old boy who presented with the
4 n7 Z; V Y3 s! C5 w5 kenlargement of the phallus and pubic hair develop-# b$ x& [. v1 t
ment without testicular enlargement, which was due
& c# C3 |) B4 }* Mto the unintentional exposure to androgen gel used by
' U5 L. `; C5 F0 G' _3 d$ gthe father. The family initially concealed this infor-
6 N) n7 |7 j* `8 ymation, resulting in an extensive work-up for this
% O& }9 H" h+ Uchild. Given the widespread and easy availability of5 J0 ~+ l: P8 n5 n8 a8 `
testosterone gel and cream, we believe this is proba-3 a# }2 d/ K) |# z( f+ N
bly more common than the rare case report in the& J- x" H4 X7 Z' G: B4 X/ x q
literature.46 }; V& V/ {' P/ Q3 |% k! K
Patient Report
) l1 H' p9 d) S+ M# U: X1 ^A 16-month-old white child was referred to the- }# @$ R4 v4 z8 ~! `5 K+ g& ]9 K
endocrine clinic by his pediatrician with the concern
; o9 z {9 i. `8 |# G* D+ [of early sexual development. His mother noticed
4 I6 `) T; V+ i1 a0 ?light colored pubic hair development when he was1 t+ U; |% C3 a7 I D7 e( n
From the 1Division of Pediatric Endocrinology, 2University of
1 I; `# p& M. iSouth Alabama Medical Center, Mobile, Alabama.+ N- J% t# f ~1 {! ^+ D g7 G
Address correspondence to: Samar K. Bhowmick, MD, FACE,
5 d" N) N, L7 BProfessor of Pediatrics, University of South Alabama, College of
1 S) r% }" F7 ]+ Q3 qMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
5 P0 a H1 k5 [+ {2 O, we-mail: [email protected].
' A3 F, Y! W: Nabout 6 to 7 months old, which progressively became% w9 H3 s- w I% n6 Q
darker. She was also concerned about the enlarge-
: K; p8 k# n9 C$ Fment of his penis and frequent erections. The child, q- A8 J; z6 s* k' b+ A
was the product of a full-term normal delivery, with
3 o4 X% Q9 G# S ea birth weight of 7 lb 14 oz, and birth length of! G3 C) [7 a2 ?* O5 w% p
20 inches. He was breast-fed throughout the first year0 r2 B2 m7 a5 ^8 K0 R. \7 v3 l
of life and was still receiving breast milk along with8 z- i9 K- z. x$ v5 E, I0 s
solid food. He had no hospitalizations or surgery,7 G, W$ }, }1 p7 o8 l Q
and his psychosocial and psychomotor development
- `3 O2 B* E" Pwas age appropriate.
5 n) L# ?) K: t0 DThe family history was remarkable for the father,
$ H* Z9 c0 N0 F( E0 W. d( pwho was diagnosed with hypothyroidism at age 16,; b6 o& Y( G5 H+ Y5 s& F3 V& ]
which was treated with thyroxine. The father’s
; \, { G S, Q% t( F3 B8 y$ Aheight was 6 feet, and he went through a somewhat) k2 f, Y% Y$ J8 v
early puberty and had stopped growing by age 14.
9 B% c! O; M5 y3 G# dThe father denied taking any other medication. The
# j D4 p( [5 \# X9 \% a2 _$ j: Wchild’s mother was in good health. Her menarche/ U' c4 w' W8 i8 W! H) G
was at 11 years of age, and her height was at 5 feet1 k# ~% p2 \- Z, N3 z+ ^
5 inches. There was no other family history of pre-
L9 j: ?# E. k+ L0 vcocious sexual development in the first-degree rela-
0 T' m' A! ]; }7 v- W; U, mtives. There were no siblings.
9 u5 ~' @; `* i+ T. SPhysical Examination' @9 Y& ?6 X, ]
The physical examination revealed a very active,8 Z! D$ O+ N3 J' t2 M! z N* x! \
playful, and healthy boy. The vital signs documented
1 I3 A& F9 ~) na blood pressure of 85/50 mm Hg, his length was# d; K, i+ \% ]+ e9 A
90 cm (>97th percentile), and his weight was 14.4 kg( ~: K6 ~! P. o; \6 E9 [9 [6 _
(also >97th percentile). The observed yearly growth
" R0 {2 {: ]( c$ c xvelocity was 30 cm (12 inches). The examination of
* [2 `5 e) y6 I* N3 R" Dthe neck revealed no thyroid enlargement.
: f$ V5 q+ @! ?: M S' X: a+ ^) a) L# LThe genitourinary examination was remarkable for
6 ?0 N2 I% {; r/ V# e2 C! P3 Lenlargement of the penis, with a stretched length of
6 d' E1 }1 f0 n5 p4 |3 M8 cm and a width of 2 cm. The glans penis was very well5 E' v4 |) J7 {
developed. The pubic hair was Tanner II, mostly around
" ?8 T! x8 {. ?+ c: h540& k) s6 P( ^ d# N
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from% N4 ^ D6 z F0 Y% k6 |2 I
the base of the phallus and was dark and curled. The; w! R; y% M" h4 `( d5 f1 D6 \
testicular volume was prepubertal at 2 mL each.8 V% M: e, G6 c' c+ T+ c6 y+ R5 x
The skin was moist and smooth and somewhat
/ f: i1 D; \# u& h3 L4 X) \oily. No axillary hair was noted. There were no d0 z+ \; m1 K: Z% E7 b3 L9 | f
abnormal skin pigmentations or café-au-lait spots.# W4 F- b) S7 b9 Z' x
Neurologic evaluation showed deep tendon reflex 2+0 \) I, F* d3 B1 W0 R' Q
bilateral and symmetrical. There was no suggestion
8 t3 F/ R$ x& a- w! l' V9 p! A% X* d- \of papilledema.
8 B/ {; R/ b2 v5 P# D: ?! U$ Y: ALaboratory Evaluation
5 Q7 l/ C0 S- ?$ y/ t$ IThe bone age was consistent with 28 months by$ V& I* [3 y, |+ ~; m. U4 O
using the standard of Greulich and Pyle at a chrono-4 `: [8 ~' v# D. k1 h
logic age of 16 months (advanced).5 Chromosomal; F4 i1 {; z8 m0 N. @- @5 q
karyotype was 46XY. The thyroid function test
+ E1 g5 R: E, h: p+ ^5 t3 Tshowed a free T4 of 1.69 ng/dL, and thyroid stimu-& U' b, Q% f2 E- ~4 k* D
lating hormone level was 1.3 µIU/mL (both normal).3 p& `) _! u' z( H4 W ?" U
The concentrations of serum electrolytes, blood* @% q* ]0 M, \8 S% d8 O9 E: [) c( U) B
urea nitrogen, creatinine, and calcium all were+ f. Q. o- ^1 H5 p) Z$ ^
within normal range for his age. The concentration9 [& s! z+ V6 w6 b3 ^
of serum 17-hydroxyprogesterone was 16 ng/dL
$ I6 ?- a$ K- u3 j0 ^(normal, 3 to 90 ng/dL), androstenedione was 20
, I* j" v% G E. R wng/dL (normal, 18 to 80 ng/dL), dehydroepiandros- E6 h3 @/ t! ^
terone was 38 ng/dL (normal, 50 to 760 ng/dL),8 T/ e0 {& S1 F7 R8 A# N
desoxycorticosterone was 4.3 ng/dL (normal, 7 to; Q% Z* q% e: J' l: g A
49ng/dL), 11-desoxycortisol (specific compound S); q6 e) ]' r$ {
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
$ Y8 _8 A" L6 Btisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total1 |! `: U4 H3 \# g5 @
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),, c# r- a( M' Y7 G& I- k
and β-human chorionic gonadotropin was less than' z% ]( R. D7 Y* N, `8 p1 B3 g
5 mIU/mL (normal <5 mIU/mL). Serum follicular0 s# o4 {6 M9 M* o- ~( F/ i/ b3 O
stimulating hormone and leuteinizing hormone5 J$ I7 m& A9 n
concentrations were less than 0.05 mIU/mL
/ E. K Q) V/ U1 S) ~, p(prepubertal).
$ @( w( Z+ R+ V& p0 I8 xThe parents were notified about the laboratory V' l2 [! r! I9 f
results and were informed that all of the tests were0 A _$ n3 n- @' H1 \% Y& m# a8 b
normal except the testosterone level was high. The
! Y4 g Q" A c2 p3 rfollow-up visit was arranged within a few weeks to
v; u0 w" ]+ pobtain testicular and abdominal sonograms; how-
- ?4 s5 u/ r9 V7 ^, Vever, the family did not return for 4 months.
& f6 u) ^% r2 bPhysical examination at this time revealed that the" A" B7 ?+ i! y5 ^
child had grown 2.5 cm in 4 months and had gained
0 I3 Z7 j! S) ^/ F! t2 kg of weight. Physical examination remained, G- g& y. k; r2 D/ v |
unchanged. Surprisingly, the pubic hair almost com-
$ M% ?6 w3 J6 p; Q" J% n6 N* ]pletely disappeared except for a few vellous hairs at
3 h! j4 p9 z, B6 kthe base of the phallus. Testicular volume was still 28 y4 e. L9 i, E- o- P
mL, and the size of the penis remained unchanged.% d8 f+ F h. U- h) s! X- C
The mother also said that the boy was no longer hav-
- X; z7 w2 c X* u( uing frequent erections.% ^7 E, r) ~: P7 O$ L
Both parents were again questioned about use of; \3 y: R4 C( Y
any ointment/creams that they may have applied to
) q$ ?( j, O A- p' b$ S4 V2 N: y$ sthe child’s skin. This time the father admitted the/ d/ a! |, W! r; C4 _" ?
Topical Testosterone Exposure / Bhowmick et al 541
1 I# { Y4 r$ J" fuse of testosterone gel twice daily that he was apply-
& M$ ?* c, |3 k Cing over his own shoulders, chest, and back area for7 L8 [' b# Z- D: t
a year. The father also revealed he was embarrassed6 D" \5 `2 x5 e
to disclose that he was using a testosterone gel pre-
7 t4 ]. @) ^2 m) g+ b" i+ qscribed by his family physician for decreased libido$ g8 B: L% S* o, n V) D1 s
secondary to depression.
: r' `) _8 V) M& ~/ h k- iThe child slept in the same bed with parents.9 g' s( n8 o( x! D7 n/ y
The father would hug the baby and hold him on his% E, \! @/ j4 q2 [1 j
chest for a considerable period of time, causing sig-
3 ]( O6 O P2 G+ k5 m2 J' Enificant bare skin contact between baby and father.- g" g4 K6 R* D" n/ x$ F, u5 A, t; }
The father also admitted that after the phone call,. c1 V5 @( ^4 F/ [9 q. Z1 I: |" g2 ~
when he learned the testosterone level in the baby
, v1 N. c7 Z. Z7 _# o- Ywas high, he then read the product information
$ I: H: j+ ^" H9 W& } L; l3 ~packet and concluded that it was most likely the rea-
0 \% w5 {7 D o( i+ w5 P) O$ Eson for the child’s virilization. At that time, they% l" X" O8 n3 t2 u
decided to put the baby in a separate bed, and the5 B$ d# N6 J1 j( t8 s. `
father was not hugging him with bare skin and had
& D7 f0 ]9 u) ~9 e1 Q# ^been using protective clothing. A repeat testosterone
, r3 f+ q+ r2 t# @test was ordered, but the family did not go to the
2 |4 s# v6 H; s! x: J" ^% V. |" flaboratory to obtain the test.
4 x, {5 m. w: o' R/ b! r' {+ iDiscussion/ S% `; F: c3 x; ]! @, m, X0 F
Precocious puberty in boys is defined as secondary7 Q+ L* ?( F, o7 p. K( K0 ^
sexual development before 9 years of age.1,4( s' j( K/ {! B+ _* L: D9 N+ B
Precocious puberty is termed as central (true) when$ y) M2 t. T* [1 y" j: h
it is caused by the premature activation of hypo-
/ v' F2 t/ h- f, ]* e4 Z/ zthalamic pituitary gonadal axis. CPP is more com-; J) h! @" j& T6 ~/ X- a: \; y
mon in girls than in boys.1,3 Most boys with CPP% ^5 A0 x5 g4 Y7 G
may have a central nervous system lesion that is
' Z& U; f' h8 i8 y8 j) D! ]responsible for the early activation of the hypothal-5 m8 q N+ w2 O9 [0 m* E
amic pituitary gonadal axis.1-3 Thus, greater empha- f% ?6 |& N; W
sis has been given to neuroradiologic imaging in+ Q( a# d9 T7 @& C: D
boys with precocious puberty. In addition to viril-6 V0 }, F; M/ T7 o
ization, the clinical hallmark of CPP is the symmet-
# r( n, ?" b; x# N F1 F: e* ?rical testicular growth secondary to stimulation by! @, ~, s2 }" s) K7 t. ^
gonadotropins.1,3
) {) ] t: t* y. xGonadotropin-independent peripheral preco-8 s0 `0 D) n) W
cious puberty in boys also results from inappropriate8 A9 u0 J E1 ?( J
androgenic stimulation from either endogenous or
0 k+ \$ ^3 e" P5 z. W2 v q6 Nexogenous sources, nonpituitary gonadotropin stim-) L0 \. d$ N# Q! h$ J" F: G; R
ulation, and rare activating mutations.3 Virilizing8 O5 F. s& T/ R' J8 X- `
congenital adrenal hyperplasia producing excessive
5 a+ k. Z+ N$ fadrenal androgens is a common cause of precocious
* t5 w5 a; Z" [puberty in boys.3,4
; A! R7 X- C g0 d8 ?The most common form of congenital adrenal
5 I( s7 l4 X; V" b, bhyperplasia is the 21-hydroxylase enzyme deficiency./ |6 N5 s$ Y. s) ?6 W( D9 D
The 11-β hydroxylase deficiency may also result in
6 b' s0 h. g# L( A& G* I5 N3 K& E5 Jexcessive adrenal androgen production, and rarely,; V! a, R* M+ \: [- S. r
an adrenal tumor may also cause adrenal androgen+ H9 T5 c/ f7 Q
excess.1,3
5 @5 y- \0 ^* Dat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
3 z- j6 ]9 x. ^/ L6 c, I$ [542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
% X/ x) o7 u0 I$ hA unique entity of male-limited gonadotropin-
! I# w1 H: Q. pindependent precocious puberty, which is also known
8 }( i8 U& x& ]as testotoxicosis, may cause precocious puberty at a0 b( ~' O! H4 ~6 ^6 M4 j
very young age. The physical findings in these boys1 I w0 d5 I) g4 |0 f
with this disorder are full pubertal development,
; n0 |" F3 W! }0 V5 a. Eincluding bilateral testicular growth, similar to boys9 }" f+ \2 G! N y# F2 m
with CPP. The gonadotropin levels in this disorder5 O4 D5 `! ~! F+ G8 [" ^, K9 Y/ Q& W
are suppressed to prepubertal levels and do not show
( [% z' F. O9 d# M% rpubertal response of gonadotropin after gonadotropin-
4 H5 g* e3 A# P# O8 ]% i6 } w; creleasing hormone stimulation. This is a sex-linked
) L# Z" ]; c: s, R; y& Nautosomal dominant disorder that affects only s% x6 X, `! x8 `; \3 N4 h( l. P$ `
males; therefore, other male members of the family
3 R! T6 [7 b1 X! ]& \may have similar precocious puberty.3
& x8 x# h4 C9 f ^- Y# i( BIn our patient, physical examination was incon-
6 }3 f" F7 X3 U9 T Y# ^+ ?) Lsistent with true precocious puberty since his testi-( `; u, ^, i f$ [; Z B6 L: l
cles were prepubertal in size. However, testotoxicosis, W3 I+ N% w$ r1 s
was in the differential diagnosis because his father
# r/ s+ U4 B* l' b( ?+ ?+ G+ Dstarted puberty somewhat early, and occasionally,
' L" f9 Q0 q: ^0 P3 D9 e8 Etesticular enlargement is not that evident in the
$ Y9 Z: ]" ^9 Y R! S2 o: o [beginning of this process.1 In the absence of a neg-# f$ l2 k3 ?2 p; X
ative initial history of androgen exposure, our: A1 s7 C$ y4 |- u, |; x
biggest concern was virilizing adrenal hyperplasia,
' o$ i( n: h4 Q. Weither 21-hydroxylase deficiency or 11-β hydroxylase6 ~! V3 ]8 C, f+ |3 |
deficiency. Those diagnoses were excluded by find-
# y; R1 `2 x6 e! }! r- F; I4 Ming the normal level of adrenal steroids.0 N; G; J n$ Q
The diagnosis of exogenous androgens was strongly' I2 s1 j# d9 k! r: q- a$ P
suspected in a follow-up visit after 4 months because' `$ g3 {- g/ F
the physical examination revealed the complete disap-
1 Y. b9 U3 a& n' S5 g# apearance of pubic hair, normal growth velocity, and0 B1 F2 h7 g( P6 G( X( h
decreased erections. The father admitted using a testos-' e( L6 K. N( n; O
terone gel, which he concealed at first visit. He was
2 d- L8 K% g- N6 Vusing it rather frequently, twice a day. The Physicians’
1 Y# C( v( i* w# h. X: u( BDesk Reference, or package insert of this product, gel or, j9 L9 K( Z5 ~) q0 J/ T/ x9 ?& m
cream, cautions about dermal testosterone transfer to
4 Q6 k3 p; `4 [6 x' O, eunprotected females through direct skin exposure.
$ k2 D3 @# q& C- D$ |Serum testosterone level was found to be 2 times the, V/ @1 q/ ~2 g! l
baseline value in those females who were exposed to6 v, ~& h6 o3 i# W' [
even 15 minutes of direct skin contact with their male0 v& X1 Q: L: ?0 i/ L
partners.6 However, when a shirt covered the applica-
! f/ B* ^1 R' _" G5 K9 ^( qtion site, this testosterone transfer was prevented.
6 U% v4 ]9 D! b% H/ F2 y9 oOur patient’s testosterone level was 60 ng/mL,. X, S$ M# A* V* |7 g
which was clearly high. Some studies suggest that3 G' w5 Y& A: F" J! y8 Q$ f3 [
dermal conversion of testosterone to dihydrotestos-, s2 ?6 ^8 _% Z$ l! W: ^
terone, which is a more potent metabolite, is more
' Q7 M3 p N$ V+ Z: |active in young children exposed to testosterone
# C$ t3 _5 h |exogenously7; however, we did not measure a dihy-
t8 ]4 g; ~7 e4 R8 N$ adrotestosterone level in our patient. In addition to) R5 o( Q7 {& ^' F/ G; Y
virilization, exposure to exogenous testosterone in
0 G, y! }% T; K+ l0 Tchildren results in an increase in growth velocity and
3 n4 y' Z3 Q$ k! zadvanced bone age, as seen in our patient.' T% W9 K F2 z, L# @9 A
The long-term effect of androgen exposure during6 C% R* P" \; S# G2 K* F
early childhood on pubertal development and final
" c5 |3 y" [( S5 r8 G4 ], y$ Zadult height are not fully known and always remain
2 _0 o! Q+ @6 i1 S3 Ba concern. Children treated with short-term testos-0 U2 P4 D( A9 e
terone injection or topical androgen may exhibit some
: ^# J# X+ w8 O* kacceleration of the skeletal maturation; however, after; J9 X! f; }/ o
cessation of treatment, the rate of bone maturation
' G+ s2 o* {- \decelerates and gradually returns to normal.8,9
0 O' m! e0 b, Z# ?3 |* }% pThere are conflicting reports and controversy% q2 S) j9 k6 f. h
over the effect of early androgen exposure on adult9 @+ d; b! v# f
penile length.10,11 Some reports suggest subnormal7 v4 I9 }7 M$ q' S( R
adult penile length, apparently because of downreg-
5 l0 g, L$ ~9 Z" y9 V6 n1 q, Yulation of androgen receptor number.10,12 However,% h! c- ?- e7 Q
Sutherland et al13 did not find a correlation between& C( P6 m ?6 h- S6 s0 [ O
childhood testosterone exposure and reduced adult
. H6 i7 Q2 i. P9 D9 P; ?penile length in clinical studies.
1 _! G V. o. bNonetheless, we do not believe our patient is
9 J! P9 g. E4 t9 Z: Igoing to experience any of the untoward effects from% U5 F: I& i) e y
testosterone exposure as mentioned earlier because1 ?. Q0 s/ l* X1 ?, y5 H2 G! N- H
the exposure was not for a prolonged period of time.( ^6 d: `/ I/ U2 ?* `3 X
Although the bone age was advanced at the time of
: p; K1 P$ ^+ L$ g8 c% Q/ D' sdiagnosis, the child had a normal growth velocity at
1 Q8 v- J+ d6 E( u0 n3 H+ Z* _the follow-up visit. It is hoped that his final adult# y. B/ @: D4 O- G2 Z1 {
height will not be affected./ S& n( S, @# h! k# _( G' T
Although rarely reported, the widespread avail-
: g5 i8 N9 \+ M+ |! m1 q, [ability of androgen products in our society may( g: e' I" Z! M" ~; u
indeed cause more virilization in male or female' e; ] ?( P( m# H" C% ^
children than one would realize. Exposure to andro-
- e3 T& ~6 W; Ygen products must be considered and specific ques-
8 S! ?9 z1 e3 |tioning about the use of a testosterone product or8 O0 _/ I) q7 M4 n* x0 B
gel should be asked of the family members during8 u' U# I1 g$ A* I
the evaluation of any children who present with vir-, }$ e+ p. X# k
ilization or peripheral precocious puberty. The diag-
- Y/ c _" o) p& X) B# Pnosis can be established by just a few tests and by2 y, l8 F# K: y- S$ x7 { n
appropriate history. The inability to obtain such a( e; B" @3 @$ o1 Z# z
history, or failure to ask the specific questions, may
( ^9 k4 b5 |& d: P0 B- Sresult in extensive, unnecessary, and expensive
1 \: u1 d/ A" V$ ?* P: |investigation. The primary care physician should be# g* p2 a ?3 Z- Y5 F; a" P
aware of this fact, because most of these children
7 v9 r, |9 y7 E8 b6 E9 V0 d# Y/ @may initially present in their practice. The Physicians’
1 j5 T; C/ _2 T0 [ HDesk Reference and package insert should also put a
& P+ _- b- \* o* ]warning about the virilizing effect on a male or3 A( ]- V' T% h9 \7 J, d
female child who might come in contact with some-- `# U- e8 S3 K9 D
one using any of these products.+ N5 ?3 W* H& t1 l; J/ p. B. ^# o; y
References- N/ N! D' a. j. K
1. Styne DM. The testes: disorder of sexual differentiation. V7 g/ ]* v1 i& W( f4 K: V$ I' D9 ]+ C
and puberty in the male. In: Sperling MA, ed. Pediatric
" W# }6 d3 S- j5 }% v9 A5 m$ J4 h- _8 VEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;& ?+ S9 b) T0 q( t% Q- c4 s
2002: 565-628.
7 r. v4 ^. v3 e; K+ S0 r2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
+ E# M A" D' [puberty in children with tumours of the suprasellar pineal |
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