Journal of IiME Volume 6 Issue 1 (June 2012) guidelines reviewed, this was the one which the reviewers were most enthusiastic to recommend for adaptation in New Zealand…. Rigorously produced and published in a peer-reviewed journal, the (Canadian) guidelines have a good, comprehensive and up-to-date evidence-based, well-referenced. The reviewers also found the Canadian guideline to be written with compassion and understanding for people with (ME)CFS…and that it adopted a more balanced…model of (ME)CFS”). 2003 On 12th-13th June 2003 a scientific workshop was held on “Neuro-Immune Mechanisms and CFS” at the Bethesda Marriott Hotel; it was hosted by the NIH and was designed to enhance understanding of (ME)CFS by examining the interface between the brain, the immune system, and the symptoms of (ME)CFS. Dr Esther Sternberg (Director of the Integrative Neural Immune Programme and Chief of the Section on Neuroendocrine Immunology & Behaviour at the NIH) spoke on “Health Consequences of a Dysregulated Stress Response”. A summary of her presentation by Rich Van Konynenburg was published on Co-Cure RES on 2nd July 2003. Firdhaus Dhabhar (Associate Professor at Ohio State University) spoke about the effects of stress in people with (ME)CFS and noted that the problems with stress and the immune system occur when the stress situation is long-term. Professor Nancy Klimas spoke on the immune dysfunction observed in (ME)CFS. She said there is a lot of data indicating that there is chronic immune activation in (ME)CFS, that there is a fair amount of data indicating that there is a shift from Th-1 to Th-2 type of immune response (which means that in (ME)CFS, the Th-1 response that kills infected cells is missing), that there is considerable data showing that there are changes in cytokine expression, and there is a lot of data showing lowered NK cell cytotoxicity. In addition, there is evidence for elevated numbers of immune complexes, elevated levels of Invest in ME (Charity Nr. 1114035) antinuclear antibodies (ANA), higher prevalence of allergies, and an activated RNase L pathway. Professor Klimas noted that there is a correlation between immune parameters and symptoms. In particular, when low NK cell activity and elevated T-cell activation are combined together, this correlates well with increased symptoms severity, and those with lower NK cell function had more severe fatigue and worse cognitive function. She also spoke about her group’s finding that NK cells in people with (ME)CFS are low in perforin (the substance normally used by NK cells to punch holes in infected cells in order to inject granzymes into them to kill them). She once again mentioned the problems resulting from the study of heterogeneous populations and from non-standardised methodology (Reported by Rich Van Konynenburg on Co-Cure RES, 3rd July 2003). 2003 A study was carried out by Belgian researchers to determine whether bronchial hyperresponsiveness (BHR) in patients with (ME)CFS is caused by immune system abnormalities. Measurements included pulmonary function testing, histamine bronchoprovocation test, immunophenotyping and ribonuclease (RNase) latent determination. There were 137 (ME)CFS participants. “Seventy three of the 137 patients presented with bronchial hyper-responsiveness. The group of patients in whom BHR was present differed most significantly from the control group, with eight differences in the immunophenotype profile in the cell count analysis, and seven differences in the percentage distribution profile. We observed a significant increase in cytotoxic T-cell count and in the percentage of BHR+ patients. Immunophenotyping of our sample confirmed earlier reports on chronic immune activation in patients with (ME)CFS compared to healthy controls, (with) BHR+ patients having more evidence of immune activation” (Nijs J, De Meirleir K, McGregor N et al. Chest 2003:123(4):998-1007). 2003 Japanese researchers focused on immunological abnormalities against neurotransmitter receptors www.investinme.org Page 65 of 108
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