MULTIPLE
HeinzJef
SCLEROSIS
(MS) AND GLN&RAL
Q. Johmet C, Verdier-Taikfu
Sazdovitch Frevious
V, Toumiu-W
M-H, CaiUat-Zucnuo
E. Rod&
J2, MpiIal
studies have shown an incrrard
of extra-ncurologic
auk+immunity
frcqmq
(AIM)
NO EVIDENCE OF RBLATIONSHH’ BBTWBBN THE INFECTION BY HTLV-1 AND MULTIPLE SCLEROSIS IN S/C DE TBNBRIFB
AUTOIMMUNITY
S, Bcrcrut
G, Weil
B,
MA.
Tama, Paris, Fmnx of clii
and biologjcal
in MS. We mugbt
markers
to -demmine
Aim8: The etiology of Multiple Sclerosis (MS), remains unknown. The fact that a number of viruses cause demyelinization in animals and humans suggests that this factor is likely a virus. Recently, an association of HTLV-1 with MS has been proposed. To study the existence of infection by HTLV-1 in patients with MS in the province of S/C de Tenerife.
if MS
patientswitbAIMfotmedambgmupwilbdiImeMchuaQerirtiafmmh4Scolltrds wwilhout
AIM
pamel
callsecutivc
of organ
intlammation,
&8initeMSpaIkntafmmourclinkmJcttrtedfora
- mdrlon-u~-.-of~nnal
including
mum
iw
and -meat
HLA
bapiotypcs
WC~daenniocdby~C(ypiIlguda~6Mily~~tlten.Carcs
(n=57)
had an other auto-itnmune
mmm aulo-m items. Cam
d*ercwD)asmciHdIoMsudlualkasIone
at a signflcaol
level. f2zdmls
bad a laler age at onset (33.7LZ9.g
(rF172) yam,
p=.Ol) and bad lower c3, c4. and Iol8l mt adjustment tpe,
for age. the relation
EDSS, immw@atulin
not different family biological subgroup
to *
hmry
than DIU-negMivc
mulrm
Dlu-positiw
dtk p&cats
amtmls (2S.9114.6
of autcknmuaity
of DR3-positin
k&s
MS pUmta
and @
-
for ulac
olda
baplotyp
A axrelation is pmem impkted
Methods: We have studied by means of Elisa test, the incidence of antibodies against HTLV-1, both in serum and CSF coupled samples in 30 clinically definite MS patients, 16 female (53%) and 14 male (47%). The remitting-relapssing form: 17 (57%); and remitting-pmgresive form: 13 (43%).
Mer
Evoh~tjve wre
bad a more fbquem ioa
hbtl
(48.U43.4.
aignikmt.
DRBl-I501
+& pc.02).
may k tcacd for -
Mc
@c.Ol, tbm coalmia.
at omat was no bngu
levels aad faquacy
in casea and mntrds.
lvsn negative p-.01).
Hcm&ndez, J.N. Lorenzo, J.M. Togores, J. Garcia Talavera’ pmcio de Naurmop.nap. La aado(ua Tcmrtfe,sptn savisgde~HO(P.L~T~.Spm
AID
buwen in MS ; the
in dim
auto-
Results: In serum and CSF samples analyzed, has not been founded the antibodies against HTLV-1 independetly of the clinical form.
immune discapa.
Conclusions: Our results allow us therefore to conclude that there is not infection by HTLV-1, in MS patients in the province of S/C de Tenerife.
METHYLPREDNISOLONE
AND OSTEOPOROSIS IN MS
P.J.H. Jonnen, C.A.J. Smit, G. Borm, O.R. van Eikema Hommes. Institute for Neurology, University Hospital Nijmegen, The Netherlands. We investigated the effect of repeated metbylprednisolone (MP) treatment on bone density in MS, as well as relations between clinical characteristics and bone density. In 161 patients with definite MS, 99 females and 62 males, bone densities of vertebrae Ll-L5 were measured on CTdensitometry; in each patient the mean value was compared to reference values and the SD of its deviation used as measure for osteoporosis. In a multivariant model bone density was correlatively studied with respect to: age, age of disease onset, cumulative MP dose, average time-interval between two MP treatments, Kurtzke FSS, and EDSS. In male patients bone density was -0.92 + 0.85 (SD), and none of the clinical variables correlated with bone density. In the female group bone density was -0.26 It 1.09, and it was negatively correlated to cumulative MP dose, FSS score, and age of disease onset. It was calculated that in females, on average, 10 gram MP effects bone density by -0.08 to +O.Ol SD. 1 point FSS by -0.15 to -0.01 SD, and 10 years earlier disease onset, by +O.lO to +0.52 SD. So, in female patients there is a slight negative effect of MP on bone density, whether this is the first or n’th course administered. Our data indicate that female patients with young age of disease onset, high FSS, and having had multiple MP treatments, may develop serious osteoporosis on repeated MP courses.
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