Fachveröffentlichungen vor 2013
(soweit bekannt / keine Gewähr auf Vollständigkeit)
Response to valganciclovir in chronic fatigue syndrome patients with human herpesvirus 6 and Epstein-Barr virus IgG antibody titers.
J Med Virol. 2012; (12): 1967-74
Biomarkers for chronic fatigue / Brain, Behavior, and Immunity Volume 26, Issue 8, November 2012, Pages 1202–1210
a, d, , b, , a, c,
a Miami Veterans Affairs Medical Center, Miami, FL, USA
b Department of Medicine, University of Alberta, Edmonton, AB, Canada
c Department of Medicine, University of Miami, Miami, FL, USA
d Nova Southeastern University, Institute for Neuro-Immune Medicine, Davie, FL, USA
dx.doi.org/10.1016/j.bbi.2012.06.006
The identification of objective markers consistently associated with CFS/ME is an important goal in relation to diagnosis and treatment, as the current case definitions are based entirely on physical signs and symptoms. This review is focused on the recent literature related to biomarkers for fatigue associated with CFS/ME and, for comparison, those associated with other diseases. These markers are distributed across several of the body's core regulatory systems. A complex construct of symptoms emerges from alterations and/or dysfunctions in the nervous, endocrine and immune systems. We propose that new insight will depend on our ability to develop and deploy an integrative profiling of CFS/ME pathogenesis at the molecular level. Until such a molecular signature is obtained efforts to develop effective treatments will continue to be severely limited.
Increased ventricular lactate in chronic fatigue syndrome. III. Relationships to cortical glutathione and clinical symptoms implicate oxidative stress in disorder pathophysiology.
NMR Biomed.2012 Sep;25(9):1073-87. doi: 10.1002/nbm.2772. Epub 2012 Jan 27.
Shungu DC, Weiduschat N, Murrough JW, Mao X, Pillemer S, Dyke JP, Medow MS, Natelson BH, Stewart JM, Mathew SJ.
Department of Radiology, Weill Medical College of Cornell University, New York, NY 10021, USA. dcs7001@med.cornell.edu
Erläuterungen von Cord Johnson auf englisch hier
Krebsmedizin zeigt Wirkung bei CFS/ME-Patienten
Av Ragnhild D. Olsen, Haukeland universitetssjukehus
Krebsmedizin zeigt Wirkung bei CFS Veröf
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http://www.helse-bergen.no(auf deutsch)
Fluge, O., Bruland, O., Risa, K., Storstein, A., Kristoffersen, E.K., Sapkota, D., Naess, H., Dahl, O., Nyland, H. and Mella, O., 2011. Benefit from B-lymphocyte depletion using the
anti-CD20 antibody rituximab in chronic fatigue syndrome. A double-blind and placebo-controlled study. PloS one. 6, e26358.
To find more information about this publication, try searching
Rote Hand Brief.pdf
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Study shows how Epstein-Barr virus triggers MS
Published on January 6, 2012 at 5:52 AM
Brain MRIs of people with ME/CFS often show plaques, similar in nature, but much smaller than MS (multiple sclerosis) plaques. Rituximab, the anti-cancer therapy which is currently being
explored as a possible treatment for ME/CFS, is suggested here as a possible treatment for MS.
A new study from researchers at Queen Mary, University of London shows how a particular virus tricks the immune system into triggering inflammation and nerve cell damage in the brain,
which is known to cause MS.
Drug Development for Myalgic Encephalomyelitis and Chronic Fatigue Syndrome (ME and CFS): Questions and Answers
As evidenced by the hundreds of letters, emails, and testimonies submitted to FDA, Myalgic Encephalomyelitis (ME)/Chronic Fatigue Syndrome (CFS) is a devastating disease with a serious impact on quality of life. We at FDA are acutely aware of the seriousness of this disease, that no FDA approved treatment option is available, and the community’s strong desire to see rintatolimod injection (Ampligen) approved. The FDA is committed to drug development to treat the symptoms of CFS and remains engaged with the patient and academic communities to foster these efforts. Following are responses to some of your frequently asked questions. Vollständige Text siehe nachstehenden Download!
Drug Development for Myalgic Encephalomy
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State of Knowledge Workshop Myalgische Enzephalomyelitis / Chronic Fatigue Syndrome
Gefördert durch die NIH Office of Research on Women’s Health in Zusammenarbeit mit dem Trans-NIH ME / CFS Research Working Group, wurde der State of the Knowledge Workshop Myalgische Enzephalomyelitis / Chronic Fatigue Syndrom (ME / CFS) Forschung April 7-8, 2011 mit 32 Experten aus zahlreichen wissenschaftlichen Disziplinen einberufen. Themen waren u.a. Infektionskrankheiten, Systembiologie, Immunologie, Neurologie, Sportphysiologie / Energiestoffwechsel, Diagnose und Biomarker und Behandlungen.
Die Workshop-Ziele waren:
1. dokumentieren, was über die Krankheit bekannt ist
2. Identifizierung des Forschungsbedarfs anhand vorhandener Wissenslücken
3. Chancen in Wissenschaft und Technologie erkennen, die biomedizinische Forschung zu ME / CFS vorantreiben könnten
Quelle: NIH Office of Research on Women’s Health
Die Videobeiträge der beiden Tage
NIH Video Casting State of the Knowledge Workshop 2011
State of the Knowledge Workshop on ME/CFS Research (Day 1)
State of the Knowledge Workshop on ME/CFS Research (Day 2)
Reporting of Harms Associated with Graded Exercise Therapy and Cognitive Behavioural Therapy in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome
Given the limited understanding of exercise pathophysiology in ME/CFS, it is difficult to formulate a definition of safe and effective exercise that confers the benefits of being active without causing harm. The effects of exercise in ME/CFS, although not fully understood, have been examined in several studies....Bulletin of IACFS/ME, Quartalsveröffentlichung der International Association for CFS/ME siehe Download
Fall2011-Kindlon-Harms-paper-59-111.pdf
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Treatmant Center for CFS: http://www.treatmentcenterforcfs.com
Inflammatory and Cell-Mediated Immune Biomarkers in Myalgic
Encephalomyelitis/Chronic Fatigue Syndrome and Depression: Inflammatory Markers Are Higher in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome than in Depression
Michael Maesa, Frank N.M. Twiskb, Karl Ringelc
aMaes Clinics, TRIA, Bangkok, Thailand;
bME-de-patiënten Foundation, Limmen, The Netherlands;
cImmunologische Laboratorien, Aachen, Germany
Psychother Psychosom 2012;81:286-295 (DOI: 10.1159/000336803)
Altered functional B-cell subset populations in patients with chronic fatigue syndrome compared to Healthy Controls
AS Bradley, B. Ford and AS Bansal
Accepted manuscript online: 29 NOV 2012 04:45AM EST | DOI: 10.1111/cei.12043
Abortive lytic Epstein–Barr virus replication in tonsil-B lymphocytes in infectious mononucleosis and a subset of the chronic fatigue syndrome
Authors: Lerner AM, Beqaj S
Published Date November 2012 Volume 2012:4 Pages 85 - 91
DOI: http://dx.doi.org/10.2147/VAAT.S36540
A Martin Lerner,1 Safedin Beqaj2
Clinical research
Lipid and protein oxidation in female patients with chronic fatigue syndrome
Slavica Tomic, Snezana Brkic, Daniela Maric, Aleksandra Novakov Mikic
Cindy M. Chang PhD, MPH1,Joan L. Warren PhD2, Eric A. Engels MD, MPH1,*
Article first published online: 30 MAY 2012
DOI: 10.1002/cncr.27612
Cytokine expression profiles of immune imbalance in post-mononucleosis chronic fatigue.
Cytotoxic lymphocyte microRNAs as prospective biomarkers for Chronic Fatigue Syndrome/Myalgic Encephalomyelitis
Journal of Affective Disorders 2012 May 7. 7 May 2012
Abstract: Immune dysfunction associated with a disease often has a molecular basis. A novel group of molecules known as microRNAs (miRNAs) have been associated with suppression of translational processes involved in cellular development and proliferation, protein secretion, apoptosis, immune function and inflammatory processes. MicroRNAs may be implicated in Chronic Fatigue Syndrome/Myalgic Encephalomyelitis (CFS/ME), where immune function is impaired. The objective of this study was to determine the association between miRNAs in cytotoxic cells and CFS/ME… Read more
Studie Pace Trials (The Lancet März 2011)
Im März 2011 wurde eine Studie in Großbritannien zu möglichen Therapien für Patienten mit ME / CFS (Chronic Fatigue Syndrome) in The Lancet veröffentlicht. Die auch unter der PACE-Studie bekannte Studie, die vielfach mit hoher Evidenzlage eingestuft wird, basiert auf der Hypothese, dass Therapien mit einer psychologischen Grundlage äußerst wirksam wären bei der Behandlung. Der Zustand der meisten Patienten würde dadurch deutlich verbessert und zu einer Rückkehr einer normalen Gesundheit führen. Eine detaillierte Analyse dieser Ergebnisse finden Sie
Pace Trial (Protokoll)
Myalgische Enzephalomyelitis : Internationale Konsenskriterien
"Die Bezeichnung “Chronic Fatigue Syndrome“ (CFS) hat sich aufgrund des fehlenden Wissens um die verursachenden Faktoren und den Krankheitsprozess seit vielen Jahren hartnäckig gehalten. Angesichts neuerer Forschung und klinischer Erfahrung, die stark auf eine verbreitete Entzündung und eine multisystemische Neuropathologie hinweisen, ist es angemessener und richtiger, den Begriff „Myalgische Enzephalomyelitis“ (ME) zu verwenden, weil dieser auf eine zugrundeliegende Pathophysiologie hinweist. Er stimmt zudem mit der neurologischen Klassifikation des ME als ICD- G93.3 in der Internationalen Klassifikation der Krankheiten der Weltgesundheitsorganisation überein."
(Caruthers et al., The Journal of Internal Medicine, July 2011)
Ventricular cerebrospinal fluid lactate is increased in chronic fatigue syndrome compared with generalized anxiety disorder: an in vivo 3.0 T (1)H MRS imaging study.
Source
Department of Psychiatry, Mount Sinai School of Medicine, New York, NY, USA.
Postural orthostatic tachycardia syndrome is an under-recognized condition in chronic fatigue syndrome.
Northern CFS/ME Clinical Network, Equinox House, Silver Fox Way, Cobalt Business Park, Newcastle upon Tyne.
POTS ist ein häufiger Befund bei Patienten mit CFS / ME. Vorschlag:
In der klinischen Beurteilung von Patienten mit CFS / ME sollte das orthostatische Tachykardie-Syndrom (POTS) in der Differentialdiagnose von Patienten mit chronischen
Erschöpfungssyndrom / myalgische Enzephalomyelitis (CFS / ME) berücksichtigt werden.
Dubbostudie: Post-infektiöses und Chronic Fatigue Syndrome ausgelöst durch virale und nicht-virale Pathogene: prospektive Kohortenstudie
Why is one person able to recover from an infection that plunges another person into a chronic and often disabling illness? This is the question the Dubbo studies are attempting to answer.
Dangerous exercise: lessons learned from dysregulated inflammatory responses to physical activity
J Appl Physiol 103: 700–709, 2007.
First published May 10, 2007; doi:10.1152/japplphysiol.00225.2007
Dan Michael Cooper, Shlomit Radom-Aizik, Christina Schwindt, and Frank Zaldivar, Jr.
Pediatric Exercise Research Center, Department of Pediatrics, University of California, Irvine, California
Exercise elicits an immunological “danger” type of stress and inflammatory response that, on occasion, becomes dysregulated and detrimental to health. Examples include anaphylaxis, exercise-induced asthma, overuse syndromes, and exacerbation of intercurrent illnesses. In dangerous exercise, the normal balance between pro- and anti-inflammatory responses is upset. A possible pathophysiological mechanism is characterized by the concept of exercise modulation of previously activated leukocytes. In this model, circulating leukocytes are rendered more responsive than normal to the immune stimulus of exercise. For example, in the case of exercise anaphylaxis, food-sensitized immune cells may be relatively innocuous until they are redistributed during exercise from gut-associated circulatory depots, like the spleen, into the central circulation. In the case of asthma, the prior activation of leukocytes may be the result of genetic or environmental factors. In the case of overuse syndromes, the normally short-lived
neutrophil may, because of acidosis and hypoxia, inhibit apoptosis and play a role
in prolongation of inflammation rather than healing. Dangerous exercise demonstrates that the stress/inflammatory response caused by physical activity is robust and sufficiently powerful, perhaps, to alter subsequent responses. These longer term effects may occur through as yet unexplored mechanisms of immune “tolerance” and/or by a training-associated reduction in the innate immune response to brief exercise. A better understanding of sometimes failed homeostatic physiological systems can lead to new insights with significant implication for clinical translation.
Th17: The third member of the effector T cell Trilogy
Curr Opin Immunol. 2007 December ; 19(6): 652–657.
T helper responses have now grown to include three T cell subsets: Th1, Th2 and Th17. Th17 cells have recently emerged as a third independent T cell subset which may play an essential role in protection against certain extracellular pathogens. However, Th17 cells with specificity for self antigens are highly pathogenic and lead to the development of inflammation and severe autoimmunity. A combination of TGF-β plus IL-6 and the transcription factors STAT3 and RORγt were recently described to be essential for initial differentiation of Th17 cells, and IL-23 for the later stabilization of the Th17 cell subset. Here we introduce another player IL-21, which is produced by Th17 themselves, plays an important role in the amplification of Th17 cells. Thus Th17 cells may undergo three distinct steps of development: differentiation, amplification and stabilization in which distinct cytokine play a role.
Immunological aspects of chronic fatigue syndrome. Autoimmun Rev.
2009 Feb;8(4):287-91.
doi: 10.1016/j.autrev.2008.08.003. Epub 2008 Sep 16.
Department of Neurology, Mellino Mellini Hospital, Chiari, Brescia, Italy.
170 Artikel und Studien ab Mitte 2004 bis Mai 2012 stützen die biologische Pathogenese von ME / CFS. Ihre Abstracts zeigen alle, signifikante biologische Anomalien bei ME / CFS-Patienten.
170 articles and studies from mid 2004 f
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