Fw: AUTO-IMMUNE Digest - 23 Sep 2003 to 27 Sep 2003 (#2003-98)

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Subject: AUTO-IMMUNE Digest - 23 Sep 2003 to 27 Sep 2003 (#2003-98)

> There is one message totalling 248 lines in this issue.

>

> Topics of the day:

>

> 1. Recent MS MEDLINE Abstract(s)

>

> ----------------------------------------------------------------------

>

> Date: Sat, 27 Sep 2003 20:39:41 -0400

> From: Irwin Mortman <irwin@...>

> Subject: Recent MS MEDLINE Abstract(s)

>

> 1: BMJ. 2003 Sep 20;327(7416):646. Related Articles, Links

> Self reported stressful life events and exacerbations in multiple

> sclerosis: prospective study.

>

> Buljevac D, Hop WC, eker W, Janssens AC, van der Meche FG,

> van Doorn PA, Hintzen RQ.

>

> Department of Neurology, Erasmus MC, Postbox 2040, 3000 CA

> Rotterdam, Netherlands.

>

> OBJECTIVE: To study the relation between self reported stressful

> life events not related to multiple sclerosis and the occurrence of

> exacerbations in relapsing-remitting multiple sclerosis. DESIGN:

> Longitudinal, prospective cohort study. SETTING: Outpatient clinic of

> department of neurology in the Netherlands. PARTICIPANTS: Patients

> aged 18-55 with relapsing-remitting multiple sclerosis, who could

> walk with a cane or better (score of 0-6.0 on the expanded disability

> status scale), and had had at least two exacerbations in 24 months

> before inclusion in the study. Patients with other serious conditions

> were excluded. MAIN OUTCOME MEASURE: The risk of increased disease

> activity as measured by the occurrence of exacerbations after weeks

> with stressful events. RESULTS: Seventy out of 73 included patients

> (96%) reported at least one stressful event. In total, 457 stressful

> life events were reported that were not related to multiple

> sclerosis. Average follow up time was 1.4 years. Throughout the

> study, 134 exacerbations occurred in 56 patients and 136 infections

> occurred in 57 patients. regression analysis with time dependent

> variables showed that stress was associated with a doubling of the

> exacerbation rate (relative risk 2.2, 95% confidence interval 1.2 to

> 4.0, P = 0.014) during the subsequent four weeks. Infections were

> associated with a threefold increase in the risk of exacerbation, but

> this effect was found to be independent of experienced stress.

> CONCLUSION: Stressful events were associated with increased

> exacerbations in relapsing-remitting multiple sclerosis. This

> association was independent of the triggering effect of infections on

> exacerbations of multiple sclerosis.

>

> PMID: 14500435 [PubMed - in process]

> ==================================

> 2: J Neurol. 2003 Sep;250(9):1135-7. Related Articles, Links

> Spotlight on Multiple Sclerosis: From antibodies as a predictor

> to the clinical characteristics of responders to interferon therapy.

>

> Strupp M.

>

> Dept. of Neurology, Ludwig-Maximilians University, Klinikum

> Grosshadern, Marchioninistr. 15, 81366, Munich, Germany,

> mstrupp@...

>

> PMID: 14504987 [PubMed - in process]

> ==================================

> 3: J Neurol. 2003 Sep;250(9):1099-106. Related Articles, Links

> HLA genotypes and disease severity assessed by magnetic resonance

> imaging findings in patients with multiple sclerosis.

>

> Zivadinov MD PhD R, Uxa MD L, Zacchi MD T, Nasuelli MD D, Ukmar

> MD M, Furlan MD C, Pozzi-Mucelli MD R, Tommasi PhD MA, Locatelli MD

> L, Ulivi MD S, Bratina MD A, Bosco PhD A, Grop BSc A, Cazzato MD G,

> Zorzon MD M.

>

> Dept. of Clinical Medicine and Neurology, Cattinara Hospital,

> University of Trieste, Strada di Fiume, 447, 34149, Trieste, Italy,

> zivadinov@...

>

> The objective of the study was to examine the relationship

> between HLA genotypes and disease severity as measured by brain MRI

> quantitative markers of demyelinating and destructive pathology in

> patients with multiple sclerosis (MS). We studied 100 patients with

> MS and 122 age, sex-, ethnic- and residence-matched controls. The DNA

> extraction and the genomic typing (A, B, DRB1 and DQB1 loci) were

> obtained with sequence-specific oligonucleotide method, using a

> commercially available reversible line blot assay (INNO-LIPA). All

> patients underwent a 1.5 tesla MRI examination of the brain. Disease

> severity was assessed by clinical (Expanded Disability Status Scale

> (EDSS)) and MRI (T2- and T1-lesion load (LL) and brain parenchymal

> fraction (BPF)) outcome measures. HLA-DQB1* 02 (OR 19.9, 95% C. I.

> 16.2-24.3, uncorrected (uncorr)- p<0.00001, corr-p<0.0006), -DQB1*03

> (OR 16.8, 95% C. I. 13.6-20.5, uncorr-p<0.00001, corrp< 0.0006),

> -DRB1*15 (OR 4.6, 95% C. I. 3.7-5.6, uncorrp= 0.0001, corr-p=0.006),

> and -DRB1*03 (OR 3.9, 95% C. I. 3.2-4.8, uncorr-p=0.0001, corrp=

> 0.006) alleles were associated with MS. T2-, T1-LL, BPF and EDSS were

> not significantly different according to the carrier status of these

> HLA alleles. No differences were found in the ratios of disease

> severity/disease duration according to the HLA car rier status.

> Multiple regression analysis showed that a higher T2-LL was

> associated with the presence of DRB1*04 (uncorr- R2=0.15, p=0.006 and

> corr- R2=0.11, p=0.025) and B7 alleles (uncorr-R2=0.08, p=0.02 and

> corr-R2=0.07, p=0.018), T1-LL was associated with B7 (uncorr-

> R2=0.30, p<0.0001 and corr- R2=0.27, p=0.0001) and DRB1*12

> (uncorr-R2=0.25, p<0.0001 and corr-R2=0.21, p=0.0002) alleles,

> whereas the BPF was predicted only by the presence of DRB1*12 allele

> (uncorr-R2=0.24, p=0.002 and corr-R2=0.20, p=0.004). The study

> findings suggest that some HLA alleles may predict the destructive

> pathological processes visible on MRI. Since the size of the sample

> studied is relatively small, further studies are needed to draw any

> firm conclusion about genotype/phenotype correlation in patients with

> MS.

>

> PMID: 14504973 [PubMed - in process]

> ==================================

> 4: J Neurol. 2003 Sep;250(9):1094-1098. Related Articles, Links

> Click here to read

> Apolipoprotein E genotype does not influence the progression of

> multiple sclerosis.

>

> Savettieri MD G, Andreoli PhD V V, Bonavita MD S, Cittadella PhD

> R, Caltagirone MD C, Fazio MD MC, Girlanda MD P, Le Pira MD F,

> Liguori MD M, Logroscino MD G, Lugaresi MD A, Nocentini MD U, Reggio

> MD A, Salemi MD G, Serra PhD P, Tedeschi MD G, Toma MD L, Trojano MD

> M, Valentino MD P, Quattrone MD A.

>

> Institute of Neuropsychiatry, University of Palermo, Palermo, Italy.

>

> OBJECTIVE: To investigate the association between apolipoprotein

> E (APOE) polymorphisms and the progression of MS. METHODS: We

> investigated 428 subjects affected by clinically defined MS, with a

> disease duration of at least three years. We collected data

> concerning the age at onset of MS, clinical type, disease duration

> and disability according to the expanded disability status scale

> (EDSS). We also calculated the progression index (PI) to evaluate

> disease progression. APOE genotyping and the -491 A/T polymorphism of

> the APOE promoter were determined. RESULTS: No association was

> observed between the APOE epsilon4 allele and clinical

> characteristics of our study population. We also investigated the

> -491 A/T APOE promoter polymorphism in 236 MS subjects and did not

> find any association between the -491 A/T polymorphism and the

> selected clinical variables. CONCLUSIONS: In our population the APOE

> epsilon4 allele and the -491 A/T APOE promoter polymorphism are not

> associated with a more rapid course of MS.

>

> PMID: 14504972 [PubMed - as supplied by publisher]

> ==================================

> 5: J Neurol. 2003 Sep;250(9):1088-93. Related Articles, Links

> Socio-demographic variables are limited predictors of health

> status in multiple sclerosis.

>

> Riazi A, Hobart JC, Fitzpatrick R, Freeman JA, AJ.

>

> Neurological Outcome Measures Unit, Institute of Neurology, London,

UK.

>

> BACKGROUND AND OBJECTIVES: Self-reported health status measures

> reflect disease impact from the patient's perspective. However, such

> measures are not designed for individual patient use and are rarely

> used to guide clinical practice. Nevertheless, if strong predictors

> of health status can be demonstrated in large datasets, these could

> be used to identify people at risk of poor health states and help

> target interventions. The aim of this study was to examine the

> predictive value of routinely collected socio-demographic variables

> on health status. METHOD: Data for 638 patients with multiple

> sclerosis (MS) on the eight health dimensions of the Medical Outcomes

> Study 36-item Short Form Health Survey (SF-36) were collected either

> by a postal survey or hospital attendance and analysed by multiple

> regression analyses. RESULTS: Several sociodemographic variables,

> such as unemployment and manual social class had some predictive

> value on health status, but the effect was not strong (maximum

> cumulative variance explained 53 %). CONCLUSIONS: Sociodemographic

> variables that we studied were limited predictors of health status in

> MS and are of limited value in guiding clinical practice.

>

> PMID: 14504971 [PubMed - in process]

>

> 6: J Neurol. 2003 Sep;250(9):1037-43. Related Articles, Links

> Serum gelatinase B/MMP-9 in primary progressive multiple

> sclerosis patients treated with interferon-beta-1a.

>

> Dubois MD PhD B, Leary MRCP SM, Nelissen I, Opdenakker MD PhD G,

> Giovannoni PhD G, MD AJ.

>

> Institute of Neurology, London, UK.

>

> BACKGROUND: Interferon- beta (IFNbeta) acts by a variety of

> mechanisms in relapsing-remitting multiple sclerosis (MS). One of

> these is a cellular down-regulation of gelatinase B or matrix

> metalloproteinase-9 (MMP-9), which is known from biochemical,

> biological and immunohistochemical evidences to play a

> disease-promoting role in MS. AIMS: a) To investigate the influence

> of IFNbeta-1a (30 or 60 micro g I. M./week) on serum MMP-9 levels in

> patients with primary progressive MS (PPMS). To correlate serum

> MMP-9 levels with clinical and magnetic resonance imaging (MRI)

> findings. METHODS: Serial blood samples were collected every 3 months

> from 49 patients participating in a phase II trial of IFNbeta-1a in

> PPMS. Serum MMP-9 was quantified by ELISA and correlations with

> clinical (EDSS) as well as MRI findings (brain and spinal cord

> atrophy, ventricular volume, T1 and T2 lesion load) were calculated.

> RESULTS: No significant differences were found between serial serum

> MMP-9 levels in IFNbeta-treated versus placebo-treated patients.

> MMP-9 levels did not differ between patients who progressed or did

> not progress during the study interval. Although mean absolute serum

> MMP-9 levels over the study period correlated with an increase in T2

> lesion load (relative T2 change: r=0.51, p<0.001; absolute T2 change:

> r=0.30, p=0.038), absolute increase in brain ventricular volume

> (r=0.29, p=0.05) and increased brain atrophy (r=0.35, p=0.02), only

> the correlation with T2 lesion load was sustained throughout the

> study period. No correlations were found between MMP-9 levels and

> relative changes in ventricular volume or with relative/absolute

> changes in T1 lesion load and in spinal cord atrophy. None of the MRI

> measures correlated with MMP-9 changes between baseline levels and

> those on treatment. CONCLUSION: Although some evidence suggests a

> down-regulating effect of IFNbeta on MMP-9, this was not confirmed

> for a once weekly intramuscular dose of IFNbeta-1a in patients with

> PPMS. The sustained correlation between serum MMP-9 and changes in T2

> volumes, and the lack of correlation with clinical or MRI measures of

> disease progression may suggest that MMP-9 is more directly related

> to non-specific central nervous system damage than to axonal loss.

>

> PMID: 14504963 [PubMed - in process]

> --

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> End of AUTO-IMMUNE Digest - 23 Sep 2003 to 27 Sep 2003 (#2003-98)

> *****************************************************************