- 註冊時間
- 2023-5-6
- 精華
- 在線時間
- 小時
- 米币
-
- 最後登錄
- 1970-1-1
|
發表於 2025-1-4 03:25:35
|
顯示全部樓層
Sexual Precocity in a 16-Month-Old V% n! Z" T: C1 ]! P9 C3 |& \& q
Boy Induced by Indirect Topical: s7 a$ {, d4 B& B! T0 n+ P% ?, _6 P
Exposure to Testosterone
' b! g5 o& y" ?8 \* g7 ySamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
9 r0 a5 c# D& f# f' vand Kenneth R. Rettig, MD1
, o- o o% ~$ }1 YClinical Pediatrics
3 i n# s- C7 n- A* I) H9 h; U; NVolume 46 Number 6
* Z I8 J- e& \# c7 SJuly 2007 540-543
0 m2 d) r' h2 w2 ^5 X+ b J4 _© 2007 Sage Publications
* T5 {' ~& ~9 `' J10.1177/0009922806296651
% Z" H: m+ o; e4 T5 H, G9 d% Xhttp://clp.sagepub.com! \& n4 a$ f( L4 K' w2 m
hosted at
4 P- c% g% M% w: i; b; f$ Yhttp://online.sagepub.com- H t/ `8 m7 }! ~% d. \
Precocious puberty in boys, central or peripheral,
$ Y, \' ^5 U- g% M2 r& g8 vis a significant concern for physicians. Central
, b' J* n' v' S: ~* Jprecocious puberty (CPP), which is mediated8 q0 l5 E. ^5 f
through the hypothalamic pituitary gonadal axis, has$ k* p6 H% K+ V4 I( ^: j. N
a higher incidence of organic central nervous system0 w& f* O: v3 A1 U( ]# ?( c! F5 j
lesions in boys.1,2 Virilization in boys, as manifested9 C" o2 r: B; V {% H Y7 @- j
by enlargement of the penis, development of pubic
U8 T7 D9 s+ ]4 `$ F) E; M4 Y* xhair, and facial acne without enlargement of testi-0 i! B2 r5 H$ j* w" u( b N
cles, suggests peripheral or pseudopuberty.1-3 We% F( ~* N4 P! K% A8 _/ R
report a 16-month-old boy who presented with the
; ^ I& e, J1 g; \$ ?, F! Xenlargement of the phallus and pubic hair develop-- B% S& E0 V, R. Y0 |! z& [) U
ment without testicular enlargement, which was due; n: D# |$ ^$ p, D- X- `1 y
to the unintentional exposure to androgen gel used by
" s0 Z! J# o. @1 _* F" Lthe father. The family initially concealed this infor-
7 @( s5 G+ `$ k" a4 e# hmation, resulting in an extensive work-up for this: K. ]2 b- q' ?/ e3 X) u( V" ]
child. Given the widespread and easy availability of
5 R& ~" N0 w V2 e& Gtestosterone gel and cream, we believe this is proba-1 A( X" ]* t3 O1 G# J( E
bly more common than the rare case report in the
6 y8 i4 h. N$ ?0 n6 |. d1 H- h- pliterature.4
) B; X% }" H* X/ _7 zPatient Report
( s7 f U* G; c- a. ]% c7 CA 16-month-old white child was referred to the
! e; f7 a) S" B; Pendocrine clinic by his pediatrician with the concern' a. R X v2 e" z
of early sexual development. His mother noticed
$ P- g) _5 d8 m( t) R3 _3 J, [light colored pubic hair development when he was4 ?* w. m- c% C `" g/ k$ |1 L
From the 1Division of Pediatric Endocrinology, 2University of4 b+ t0 g# J1 b% M* ~
South Alabama Medical Center, Mobile, Alabama.$ e8 e& H I- a. m- P4 A! @ F
Address correspondence to: Samar K. Bhowmick, MD, FACE,
) r4 K2 ^& u8 D% T5 d. nProfessor of Pediatrics, University of South Alabama, College of
! _' O! g1 g3 y0 f9 k9 p" x# fMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;! `* n* s, Z1 f+ W# G
e-mail: [email protected].
3 v+ ?4 j, W6 `( B# L! Uabout 6 to 7 months old, which progressively became
6 n, U! S& B# V. t$ Q* h6 v% |darker. She was also concerned about the enlarge-% _! I0 e ~# {
ment of his penis and frequent erections. The child( A5 e: h6 q$ J' Z3 C
was the product of a full-term normal delivery, with4 Q4 t' D5 g: m! u% S- Q# E
a birth weight of 7 lb 14 oz, and birth length of
1 @- m2 }7 G! u+ ^$ s. F, j20 inches. He was breast-fed throughout the first year* V5 [) a- u' c& C( B! ^( a
of life and was still receiving breast milk along with
; A, b' ]/ C* m3 H% Msolid food. He had no hospitalizations or surgery,
- U* Q- @4 P1 |. Fand his psychosocial and psychomotor development
& |1 o- Q- b! T/ x0 g$ _3 [was age appropriate.. S B* A+ K3 W6 U- u# x( Q
The family history was remarkable for the father,1 m, m9 b, r% R# Q1 e8 \% r
who was diagnosed with hypothyroidism at age 16,' S* M* C" {4 g3 q
which was treated with thyroxine. The father’s% A q) M! x5 A
height was 6 feet, and he went through a somewhat
+ ~5 m: b( U4 X6 ~early puberty and had stopped growing by age 14.
, x3 T8 K& R- k( c6 E' l+ {2 `7 MThe father denied taking any other medication. The
8 G8 E; n0 r$ e) e2 Q( Q7 }child’s mother was in good health. Her menarche$ N, c0 V3 }2 _: c2 a
was at 11 years of age, and her height was at 5 feet
& ?; n+ z. U0 j# G5 inches. There was no other family history of pre-
! ?6 [$ i' s* Lcocious sexual development in the first-degree rela-
3 `7 j0 b+ P+ ntives. There were no siblings.% n C9 t, x% h4 Y& I2 s
Physical Examination; |$ X* u7 k- i0 H; `; y: h
The physical examination revealed a very active,& J6 c, @1 @7 H% D3 I+ R8 W7 E
playful, and healthy boy. The vital signs documented2 k, C- F9 g2 V! ]0 M
a blood pressure of 85/50 mm Hg, his length was
* t4 v4 @# v) f2 W2 u1 F' H90 cm (>97th percentile), and his weight was 14.4 kg
6 l% o0 x4 k$ }; p) K9 ?3 {(also >97th percentile). The observed yearly growth5 a# f0 g( l" W, Y5 c g- f
velocity was 30 cm (12 inches). The examination of
# z# L0 |0 ]' U5 fthe neck revealed no thyroid enlargement.
! N! Q* n8 @! @& s, G+ CThe genitourinary examination was remarkable for
4 }2 t6 W. b9 f8 zenlargement of the penis, with a stretched length of
# n; r, j5 Q0 a0 Q8 cm and a width of 2 cm. The glans penis was very well$ Y: X; O0 q, ?1 B* O
developed. The pubic hair was Tanner II, mostly around
. w9 W8 ]& s5 p, m, F540* b& Z" C. E9 b, V7 i9 W
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from# s: }+ \' @. F% ?/ L) T- y; j
the base of the phallus and was dark and curled. The
1 z9 l& z) M% o- C. {testicular volume was prepubertal at 2 mL each.
! \0 A0 \/ Y& I# M, F1 f9 g- pThe skin was moist and smooth and somewhat) n( W n, x8 T- Q
oily. No axillary hair was noted. There were no
/ }# \# ]4 z( k) ^0 Mabnormal skin pigmentations or café-au-lait spots./ j4 F0 ?9 N7 s" [
Neurologic evaluation showed deep tendon reflex 2+- J$ o. z9 A; C/ i( p8 Z
bilateral and symmetrical. There was no suggestion
9 m: j' p/ N0 tof papilledema.3 U& w7 f+ b3 }9 p3 u) ~
Laboratory Evaluation8 X+ J' r5 K4 X H) C2 H
The bone age was consistent with 28 months by
/ h2 W5 Y( G, C% z! ausing the standard of Greulich and Pyle at a chrono-: O8 ]- M& m8 e
logic age of 16 months (advanced).5 Chromosomal" o7 {+ L2 u5 a
karyotype was 46XY. The thyroid function test
& f: V7 F" W% }1 U4 e7 j; f/ p, ]showed a free T4 of 1.69 ng/dL, and thyroid stimu-
9 J2 w: l4 N, K8 O; {lating hormone level was 1.3 µIU/mL (both normal).( ^& M/ L( m! |& p1 Z- ^9 d9 [% G
The concentrations of serum electrolytes, blood
O3 z2 F& a, _) G1 nurea nitrogen, creatinine, and calcium all were% S9 F$ Z; Q$ X) M3 g- r2 K
within normal range for his age. The concentration
- Y @) B5 p4 B0 q$ ^4 I6 A9 b7 Wof serum 17-hydroxyprogesterone was 16 ng/dL
: a2 b0 T, d5 \3 x- ^6 B/ ]: _(normal, 3 to 90 ng/dL), androstenedione was 20
1 \' A, N- o3 i7 o9 L, [* n& O ung/dL (normal, 18 to 80 ng/dL), dehydroepiandros-' v' b! I' }7 |; j; c) |" B, @
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
8 t+ R9 P( Y3 _8 K$ ]0 ]. [7 C, ]desoxycorticosterone was 4.3 ng/dL (normal, 7 to+ Z: _/ g: c6 r$ S6 M
49ng/dL), 11-desoxycortisol (specific compound S)
8 y) T3 C, \& [) s$ Dwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-2 v x0 g7 [: U) a
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total. ?, \3 J2 F3 s) C" m! x- G
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),' t" v f3 f' i: c# |
and β-human chorionic gonadotropin was less than
1 e. A2 x* ^; n& J( B5 mIU/mL (normal <5 mIU/mL). Serum follicular
; q4 J, ?% o( p1 Z3 \4 r0 m7 {stimulating hormone and leuteinizing hormone
# p0 i1 S- j- S @0 V! h7 R- R% cconcentrations were less than 0.05 mIU/mL
- q! C. W R7 P+ S/ S3 C(prepubertal).
$ b" M. {' x) M0 q* U6 E+ A0 rThe parents were notified about the laboratory
7 }! H( _( K: s% X. `results and were informed that all of the tests were4 {5 l. z ^" r# P
normal except the testosterone level was high. The
+ c! t, q1 h3 Ifollow-up visit was arranged within a few weeks to3 b. J6 c, G3 E& F1 A% ]. a8 n
obtain testicular and abdominal sonograms; how-
, X/ ]3 U) T9 O* eever, the family did not return for 4 months./ {' g5 | _1 P& L8 y$ v
Physical examination at this time revealed that the2 }' f$ f% y* _$ I, e
child had grown 2.5 cm in 4 months and had gained7 E0 k5 w/ b5 d; e7 x8 U
2 kg of weight. Physical examination remained
. z" w# b! N' o1 Y- \8 ~% p& ]7 Bunchanged. Surprisingly, the pubic hair almost com-
2 Q8 k6 o" g8 ?( b1 {0 |* M8 {2 fpletely disappeared except for a few vellous hairs at5 ]4 @% ^+ M1 e$ V- b
the base of the phallus. Testicular volume was still 2
7 W! J1 K! m9 G% U( J$ w; B( F2 omL, and the size of the penis remained unchanged.
, i+ n) F% K T. {The mother also said that the boy was no longer hav-* x2 A% L# l9 a5 {9 W2 o
ing frequent erections.
6 m+ u" P* v/ @8 F4 CBoth parents were again questioned about use of* j, J+ R: o) X3 h4 Z: W( T& m
any ointment/creams that they may have applied to0 b( ~, ~8 |! @7 N: N
the child’s skin. This time the father admitted the' J" d: G2 Q( k: a
Topical Testosterone Exposure / Bhowmick et al 541
3 ^5 b: v+ G- ]1 Xuse of testosterone gel twice daily that he was apply-& ?. u1 F6 G7 r7 h* D/ F
ing over his own shoulders, chest, and back area for
5 R* `0 o# ~. ~& Ga year. The father also revealed he was embarrassed
3 s- a# O# C3 D1 j: W* bto disclose that he was using a testosterone gel pre-
, j/ ?7 h' B9 Z0 [0 t0 O. H, Iscribed by his family physician for decreased libido
7 r" V4 u# H0 i5 [& o6 Z8 _secondary to depression.' M8 `5 a, t; n' q( }: D) [
The child slept in the same bed with parents.
B1 v9 [4 D" f# y3 J9 tThe father would hug the baby and hold him on his
, @0 J0 Q5 v) a2 p7 E" Nchest for a considerable period of time, causing sig-
7 {- |# i3 n1 C* T; y9 h; ?nificant bare skin contact between baby and father." j F: D7 p% p
The father also admitted that after the phone call,/ e* D2 u9 o- E; Y( Y5 m/ r) o
when he learned the testosterone level in the baby0 \0 u2 }( t5 \/ ~ l# n$ ^" ^4 r
was high, he then read the product information
* f! H+ z' H% i- S i! D; a9 ~! Vpacket and concluded that it was most likely the rea-
! b; R d" G3 P- @/ F- ~son for the child’s virilization. At that time, they# ^6 I: [1 [" y; A. }
decided to put the baby in a separate bed, and the
0 d6 E+ L6 Q/ k! `; n, W8 afather was not hugging him with bare skin and had
, @. l/ M! [9 K: Kbeen using protective clothing. A repeat testosterone c) Y+ Z; ~# |
test was ordered, but the family did not go to the- M+ \- D z' v/ V7 v
laboratory to obtain the test.
! e4 s& o, c6 F! \Discussion
& \: O; i+ ^6 U. P! hPrecocious puberty in boys is defined as secondary* p/ r& e, s j! Q7 g/ u* f! z1 ~$ A( Y
sexual development before 9 years of age.1,4
5 X: ]& w; ~* d. O1 x! d3 z$ NPrecocious puberty is termed as central (true) when# B) u. q0 a" T& t' U; h) i
it is caused by the premature activation of hypo-) i4 f+ M9 H! }7 t3 z
thalamic pituitary gonadal axis. CPP is more com-
) I: d% \$ p$ H* [. I2 W+ l4 k2 Omon in girls than in boys.1,3 Most boys with CPP2 f* t$ e4 M+ c" z
may have a central nervous system lesion that is5 Y9 f" q1 n' ~+ I2 C2 @: I5 ]
responsible for the early activation of the hypothal-
+ j! k! V! g- }1 P& d5 L" lamic pituitary gonadal axis.1-3 Thus, greater empha-, x1 {6 X. i7 [! c4 a& ~" G( q
sis has been given to neuroradiologic imaging in) M: F# b! W' | s
boys with precocious puberty. In addition to viril-; {5 b3 _- {9 T% M
ization, the clinical hallmark of CPP is the symmet-
5 E4 y" l8 D( ^. _$ {( [' Frical testicular growth secondary to stimulation by: {/ i( G( X; r Y
gonadotropins.1,3
* Y3 L% E% P9 h2 D& g+ n* y0 YGonadotropin-independent peripheral preco-6 H% c- |+ N; F' ?! D
cious puberty in boys also results from inappropriate* ^! W& t2 ~5 K9 W5 o/ R t8 o) v4 F6 r
androgenic stimulation from either endogenous or+ C& c; X9 i& Q- y
exogenous sources, nonpituitary gonadotropin stim-! X- O6 T7 }% p C
ulation, and rare activating mutations.3 Virilizing
9 t7 B8 O9 F _) t1 y+ X4 u/ v" _* dcongenital adrenal hyperplasia producing excessive
: J X: o. m, Z( u" q( N. Aadrenal androgens is a common cause of precocious$ x) E7 Q, D2 J9 B8 R
puberty in boys.3,46 ~3 Y3 e" w4 ^* Q
The most common form of congenital adrenal; `& U6 U9 [# T! W0 u- E p
hyperplasia is the 21-hydroxylase enzyme deficiency.6 h5 S- x0 v5 J. A' a
The 11-β hydroxylase deficiency may also result in
2 L s& f! b( k# [9 L8 {4 @excessive adrenal androgen production, and rarely,% a% M5 e( n7 Y3 d4 Z
an adrenal tumor may also cause adrenal androgen) F- f8 f1 P1 _; Q
excess.1,3- S$ _% X" c& [5 {' q
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from1 J- S9 _2 d: A$ Z
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
5 i( f6 u* M+ Z* U0 p8 o$ dA unique entity of male-limited gonadotropin-
. H. ^5 {+ N0 ?2 k6 c" A6 _independent precocious puberty, which is also known
6 H) Q; _' J' }/ u2 T R: cas testotoxicosis, may cause precocious puberty at a
* `" C3 |5 N3 M" N9 f# Uvery young age. The physical findings in these boys
& N; c" Y$ F: |with this disorder are full pubertal development,
6 Z' `/ U8 T" c$ I% Y7 tincluding bilateral testicular growth, similar to boys6 E0 U# z7 x% |5 @& E) U* x
with CPP. The gonadotropin levels in this disorder1 m7 k- D) w: `" V2 |% |) A5 Z0 X$ c+ E
are suppressed to prepubertal levels and do not show0 q+ `) W ^+ n: R5 _
pubertal response of gonadotropin after gonadotropin-
# @. V6 ]9 c" m4 rreleasing hormone stimulation. This is a sex-linked
+ @2 y4 L1 F2 y' A6 _( u nautosomal dominant disorder that affects only, Q* d4 R1 t5 C# U
males; therefore, other male members of the family2 s8 a# b2 l: M& [
may have similar precocious puberty.3
, {5 n/ u( T0 n0 D% tIn our patient, physical examination was incon-3 S) {& m; u e* J8 T) p% [5 r3 t
sistent with true precocious puberty since his testi-
6 }, n. O7 N( ~1 P) ]cles were prepubertal in size. However, testotoxicosis" |; r; R y% U/ l8 K0 x, N
was in the differential diagnosis because his father( i" ~+ x1 m& i5 m
started puberty somewhat early, and occasionally,
6 X, b0 n, Z' F( \$ ^* \' I3 |- Y2 _; Utesticular enlargement is not that evident in the% J% K( ^% x0 g/ M
beginning of this process.1 In the absence of a neg-
, H* ~0 ?8 i9 l: O: z0 `ative initial history of androgen exposure, our
& r; m9 U5 V m. a" x. {biggest concern was virilizing adrenal hyperplasia,
& K) _9 b7 \% _either 21-hydroxylase deficiency or 11-β hydroxylase
( ] q9 p/ u/ d% Ydeficiency. Those diagnoses were excluded by find-' A: i* A( g" ~2 l9 Z; d& `
ing the normal level of adrenal steroids.
1 y3 |5 W; F" @+ z7 `; f4 N% KThe diagnosis of exogenous androgens was strongly0 ]) ~* }1 ^" _: {* g3 N
suspected in a follow-up visit after 4 months because
4 z8 }0 o6 Y3 Y- e2 Nthe physical examination revealed the complete disap-
+ t( g2 u1 s1 g# [( E, k) Z! spearance of pubic hair, normal growth velocity, and; \3 e7 ^( _, I
decreased erections. The father admitted using a testos-
0 @, i+ g. R4 A* K, K" }terone gel, which he concealed at first visit. He was
; e! q# K3 B- d' k4 u* @$ cusing it rather frequently, twice a day. The Physicians’/ d$ ?: J8 F$ a( l* E( A
Desk Reference, or package insert of this product, gel or
* ^2 _4 ?) Y$ Z+ fcream, cautions about dermal testosterone transfer to2 [2 w0 `( d {$ D$ U' U% K" a8 P
unprotected females through direct skin exposure.
: ^ x5 Y5 n% q/ h# j6 @Serum testosterone level was found to be 2 times the% {' |9 q, @! u, p& z$ u
baseline value in those females who were exposed to/ Y9 e" D! \7 t4 A/ c
even 15 minutes of direct skin contact with their male& }& x& o8 p! p1 D0 x
partners.6 However, when a shirt covered the applica-! @' m8 Q8 O W, Q3 \9 h! M+ b' t A
tion site, this testosterone transfer was prevented.
/ i5 j1 J" Q3 {& ZOur patient’s testosterone level was 60 ng/mL,' ~% L# Z' q$ w2 H* S* T; S& \9 x
which was clearly high. Some studies suggest that" w; i* R+ } J) V- y. R# w
dermal conversion of testosterone to dihydrotestos-: T: k6 h: m2 v
terone, which is a more potent metabolite, is more
[, [+ a2 h4 o% h- {; k' Yactive in young children exposed to testosterone
2 H3 J4 |* P& Y: Yexogenously7; however, we did not measure a dihy-
1 n9 b; _" j( f8 P* wdrotestosterone level in our patient. In addition to- ~$ D- B5 k$ v+ X: w9 e
virilization, exposure to exogenous testosterone in9 V. t3 ?0 n* k& z7 z6 ]
children results in an increase in growth velocity and" r" {( J, Z$ g
advanced bone age, as seen in our patient.9 h) }& R4 B6 I
The long-term effect of androgen exposure during+ Y' M6 k+ e( p \4 N
early childhood on pubertal development and final
$ o$ |. Y( |" }6 {adult height are not fully known and always remain
8 X! z" T$ B% ^# d* sa concern. Children treated with short-term testos-) G2 X0 B+ | `) ]7 [+ O: y
terone injection or topical androgen may exhibit some
5 Y! X: M( Y. |. \1 ~acceleration of the skeletal maturation; however, after
/ O: C: d3 N7 xcessation of treatment, the rate of bone maturation; L7 c) {0 K C4 N R- b
decelerates and gradually returns to normal.8,9& C: ]/ B- j8 A& y# ^9 W0 t4 ^
There are conflicting reports and controversy# [1 i( Y& ?% I V
over the effect of early androgen exposure on adult( q: `/ m1 Z/ W# z; S( r* N
penile length.10,11 Some reports suggest subnormal
& V; I5 i& y% ] N, C: `. V1 qadult penile length, apparently because of downreg-
1 ^6 z W! F9 G! Z: { e; |ulation of androgen receptor number.10,12 However,
/ w8 d' E! `$ G: H3 u0 nSutherland et al13 did not find a correlation between9 ]& W9 F' X0 U( W1 Y6 f
childhood testosterone exposure and reduced adult
7 t5 o/ c, }( L& z, |# d4 tpenile length in clinical studies.+ U( T" }0 p9 U0 q8 N- g
Nonetheless, we do not believe our patient is; J. v: e: M/ e. V" S- x
going to experience any of the untoward effects from2 d8 I# W! K8 J1 c
testosterone exposure as mentioned earlier because* N- I9 j9 L- V/ w! k
the exposure was not for a prolonged period of time.
0 Z" Z* h3 t% Q- r" _Although the bone age was advanced at the time of4 X# f; Q& ]' I) b+ Z$ L
diagnosis, the child had a normal growth velocity at
/ \5 y ?8 v/ F7 y$ }( O0 h. C6 _the follow-up visit. It is hoped that his final adult; z5 x0 l" A1 K- m- f6 u
height will not be affected.
/ T9 Y7 M0 x5 p9 RAlthough rarely reported, the widespread avail-6 e8 q8 {3 ^' ]: H$ k! r; G' u
ability of androgen products in our society may
" I3 U; i$ {' R( y+ ?& vindeed cause more virilization in male or female+ x8 @/ V% A/ L P" f
children than one would realize. Exposure to andro-
" I+ Q; j4 @% W; Wgen products must be considered and specific ques-
: @% }! J2 ^. s: i1 R% ?. ?tioning about the use of a testosterone product or
~1 J% ~3 b, N/ B) h0 Pgel should be asked of the family members during
2 ^4 {; ~" J: k! C7 qthe evaluation of any children who present with vir-& a v+ Q! m( l0 u& [
ilization or peripheral precocious puberty. The diag-' ~+ x3 f$ A0 R+ f/ K
nosis can be established by just a few tests and by4 x" X* L" G7 [3 c' d8 e
appropriate history. The inability to obtain such a
# S% j4 a. N. p2 r0 xhistory, or failure to ask the specific questions, may1 W9 R# v5 s; u9 V* d$ w7 W
result in extensive, unnecessary, and expensive3 d, F d# a9 s N- J
investigation. The primary care physician should be
5 k: z5 k1 D5 F% S$ W: ~/ v; i# J! waware of this fact, because most of these children
% [/ |# p# N8 d9 s$ M/ E- wmay initially present in their practice. The Physicians’/ a% a. r; D: ~" A
Desk Reference and package insert should also put a: n$ @: g5 s$ y( [" @/ K7 _
warning about the virilizing effect on a male or
! ?1 }0 ?2 Z5 l+ D- U) ?female child who might come in contact with some-
# W ^1 c3 V+ ]( T4 \one using any of these products.2 O8 y) n" N4 [$ B' ?/ w* u
References
* p1 T1 ^( b0 z. u6 @1. Styne DM. The testes: disorder of sexual differentiation
6 O" r) c1 H6 F( u9 aand puberty in the male. In: Sperling MA, ed. Pediatric
& F4 A- c" _4 S9 Y0 \- T9 ^Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
! ~) m. H, U$ s, |2002: 565-628.& k" S- j+ g& t. p' O( ?3 V& \
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious9 b% r: V9 X9 F O( D* D" [$ O
puberty in children with tumours of the suprasellar pineal |
|