Journal of IiME Volume 6 Issue 1 (June 2012) important role in the pathophysiology of ME/CFS. In this study we therefore measured plasma IL-1, TNF, and PMN-elastase, and serum neopterin and lysozyme in 107 patients with ME/CFS, 37 patients with chronic fatigue (CF) and 20 normal controls. Serum IL-1, TNF, neopterin and lysozyme are significantly higher in patients with ME/CFS than in controls and CF patients. Plasma PMN-elastase is significantly higher in patients with ME/CFS than in controls and CF patients and higher in the latter than in controls….The results suggest that characteristic symptoms of ME/CFS, such as fatigue, autonomic symptoms and a flulike malaise, may be caused by inflammatory mediators” (Maes M, Twisk FN, Kubera M, Ringel K. J Affect Disord 2011: Oct 3 Epub ahead of print). 2011 In a presentation given on 22nd October 2011 in Seville, Spain, Kenny DeMeirleir (Professor of Physiology, Pathophysiology and Medicine, Vrije Universiteit, Brussels) provided a list of laboratory tests that support the clinical diagnosis of ME/CFS; those involving the immune system included the following: Immunophenotype: Total number of lymphocytes CD4/CD8 ratio CD4+ lymphocytes CD8+ lymphocytes Ratio of NK cells B cells Soluble CD14 (increased in 90% of ME/CFS patients and correlates with severity) CD57 lymphocytes (low in most ME/CFS patients) Leucocyte elastase activity (increased in a sub-group of patients) C4a (increased in 80% of patients) Expression of perforin mRNA IgM and IgG Cytokines: (cytokine serum levels) IL-8, MCP1, MIP-1 IL-6, IL-10 IL-12 TGF 1 TNF Invest in ME (Charity Nr. 1114035) Food intolerance panel of IgG: Casein Gluten Lactose Tissue transglutaminase and gliadin antibodies (IgA / IgG) Defective lactase gene. It will be recalled that, due to the influence of the Wessely School, none of these tests is permitted in the UK National Health Service for people thought to have ME/CFS. 2011 In October 2011 the International Consensus Criteria for Myalgic Encephalomyelitis were published in the Journal of Internal Medicine 2011:270:4:327-338 (http://onlinelibrary.wiley.com/doi/10.1111/j.136 5-2796.2011.02428.x/abstract). The following is an extract on “Immune Impairment”, together with the references cited: ”Publications describe decreased natural killer cell signalling and function, abnormal growth factor profiles, decreased neutrophil respiratory bursts and Th1, with a shift towards a Th2 profile [4–8, 92, 93]. Chronic immune activation [27], increases in inflammatory cytokines, pro-inflammatory alleles [4–8, 94–96], chemokines and T lymphocytes and dysregulation of the antiviral ribonuclease L (RNaseL) pathway [62, 97–100] may play a role in causing flu-like symptoms, which aberrantly flare in response to exertion [5,92]. 4. Broderick G, Fuite J, Kreitz A, Vernon SD, Klimas N, Fletcher MA. A formal analysis of cytokine networks in chronic fatigue syndrome. Brain Behav Immun 2010; 24: 1209–17. 5. Lorusso L, Mikhaylova SW, Capelli E, Ferrari D, Ngonga GK, Ricevuti G. Immunological aspects of chronic fatigue syndrome. Autoimmun Rev 2009; 8: 287–91. 6. Fletcher MA, Zeng XR, Maher K et al. Biomarkers in chronic fatigue syndrome: evaluation of natural killer cell function and www.investinme.org Page 94 of 108
95 Publizr Home