slysaint
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Wonder if any of the MEGA team will have followed this conference?She's not kidding. Makes the UK look mediaeval.
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Created in 2008, Phoenix Rising is the largest and oldest forum dedicated to furthering the understanding of, and finding treatments for, complex chronic illnesses such as chronic fatigue syndrome (ME/CFS), fibromyalgia, long COVID, postural orthostatic tachycardia syndrome (POTS), mast cell activation syndrome (MCAS), and allied diseases.
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Wonder if any of the MEGA team will have followed this conference?She's not kidding. Makes the UK look mediaeval.
@Marky90 Sorry I compiled them up to help my brain.
What's up with the different VO2 max findings between groups I wonder? I hope these Lactate findings from Norwegians can be repeated.
Edit: Um, I think Ungers group found same as Keller group?
Allergic disorder phenotypes in ME/CFS and patterns of medical comorbidity and clinical dysfunction Susan Levine,1 Joy Ukaigwe,2 Xiaoyu Che,2 W. Ian Lipkin,2,3,4 Mady Hornig2,4
Affiliations: 1Levine Clinic, New York, NY; 2Center for Infection and Immunity, Columbia University Mailman School of Public Health, New York, NY; 3Departments of Neurology and Pathology, College of Physicians & Surgeons, Columbia University, New York, NY; 4Department of Epidemiology, Columbia University Mailman School of Public Health, New York, NY
Background: Atopic disorders are more common in ME/CFS and have been associated with autonomic disturbances in some studies. Assessment of clinical characteristics and comorbidity among ME/CFS subjects with allergic diatheses may improve differential diagnosis and treatment selection.
Objective: To determine whether certain allergic disorders are more common in ME/CFS than in controls, and to compare clinical characteristics (severity and pain ratings; medical comorbidities) among ME/CFS subjects with and without certain allergic comorbidities.
Methods: Questionnaire data from the Chronic Fatigue Initiative (CFI) Cohort study (five US sites) were used to compare the frequency of allergic and other somatic conditions in ME/CFS (n=202 meeting Fukuda and/or Canadian criteria) and control subjects (n=202). Machine learning techniques (LASSO, Random Forest) were used to derive phenotypic subsets that differed between ME/CFS and control groups. SF-36 subdomain scores (Wilcoxon rank-sum tests) and prevalence of medical comorbidities (chi-squared tests) were compared between case groups meeting criteria for the two derived ME/CFS phenotypes. Orthostatic pulse changes from physical exams were also compared across phenotypic subsets. Adjustments were made for multiple comparisons.
Results: Machine learning approaches identified chronic sinusitis and hives as the allergic disorders that best discriminated cases from controls. ME/CFS subjects with sinusitis/hives (ME+S/H) had more severe pain (SF-36) and gastrointestinal disturbances, endocrine and inflammatory problems (DSQ) (all padjusted=0.029) than those without these allergic comorbidities. ME+S/H cases also had higher prevalence relative to ME subjects without sinusitis/hives of fibromyalgia (p=0.029); migraine (p <0.0001); tension headaches (p=0.0002), low back pain (p=0.002) and neck pain (p=0.003). Pain ratings were also higher in ME+S/H cases. Orthostatic pulse changes were equally common in ME/CFS with and without sinusitis/hives.
Discussion: A history of sinusitis and hives is predictive of an ME/CFS diagnosis and appears to define a novel phenotypic subset of ME/CFS with distinct patterns of comorbidity and exaggerated pain symptoms. Future studies will investigate whether S/H features are associated with altered immunity (Th2 dominance), including secretion of mast cell products that alter pain pathways. ME+S/H cases may represent a distinct subgroup with unique patterns of somatic comorbidity that may help predict response to selected therapeutic approaches.
Assessment of Neurobiological Dysfunction in Chronic Fatigue Syndrome
Benjamin H. Natelson, Xiangling Mao, Diana Vu, Michelle Blate, Gudrun Lange, Aaron J Stegner, Guoxin Kang and Dikoma C. Shungu
BACKGROUND: Psychiatric disease comorbidity is common among many, but not all, patients with CFS. Identifying neurobiological dysfunction that can differentiate CFS with and without psychiatric symptoms could advance understanding of CFS.
OBJECTIVES: To derive measures of spinal fluid white cell count and protein levels, cerebral blood flow (CBF), brain ventricular lactate and cortical glutathione in CFS patients with and without current psychiatric diagnoses compared to healthy controls (HC).
METHODS: 44 consenting CFS and 17 HC subjects were enrolled in the study. Psychiatric diagnosis was established using the Structured Clinical Interview for DSM-4 (SCID); a battery of neuropsychological tests was also administered. Magnetic resonance imaging (MRI) techniques were used to measure CBF, ventricular lactate and cortical glutathione. Cell count and protein levels were determined in cerebrospinal fluid samples. P value for statistical significance was set at 0.05
RESULTS: None of the brain and CSF outcome measures differed between CFS patients with and without psychiatric diagnosis. On the other hand, CBF and glutathione were found to be significantly lower and ventricular lactate higher in the pooled sample of CFS patients compared to HC subjects, replicating our prior findings of these outcome measures. A similar group difference in spinal fluid was found with 9 of 35 patients having either high white cell count or elevated protein compared to none of 13 HC.
CONCLUSION: This study did not find differences in neurobiological abnormality between CFS patients with and without psychiatric diagnoses. However, significant differences in number of abnormal spinal fluids, ventricular lactate, cortical glutathione and CBF between the CFS and HC groups were found. Therefore, rather than focusing on psychiatric features, future efforts should instead focus on evaluating the objective brain and spinal fluid outcome measures that differed between HC and CFS as potential biomarkers of CFS.
Benjamin H Natelson MD, Professor of Neurology, Icahn School of Medicine at Mount Sinai and Director, Pain & Fatigue Study Center, Mount Sinai Beth Israel, Suite 5D, 10 Union Square East, New York, NY 10003, bnatelson@chpnet.org. This work was funded by NIH NS-075653 to BHN. There are no conflicts of interest.