Reliable disease biomarkers characterizing and identifying electrohypersensitivity and multiple chemical sensitivity as two etiopathogenic aspects of a unique pathological disorder

摘要: Much of the controversy over causes electro-hypersensitivity (EHS) and multiple chemical sensitivity (MCS) lies in absence both recognized clinical criteria objective biomarkers for widely accepted diagnosis. Since 2009, we have prospectively investigated, clinically biologically, 1216 consecutive EHS and/or MCS-self reporting cases, an attempt to answer questions. We report here our preliminary data, based on 727 evaluable 839 enrolled cases: 521 (71.6%) were diagnosed with EHS, 52 (7.2%) MCS, 154 (21.2%) MCS. Two out three patients MCS female; mean age (years) was 47. As inflammation appears be a key process resulting from electromagnetic field (EMF) effects tissues, histamine release is potentially major mediator inflammation, systematically measured blood patients. Near 40% had increase histaminemia (especially when conditions present), indicating chronic inflammatory response can detected these Oxidative stress part contributor damage response. Nitrotyrosin, marker peroxynitrite (ONOO°-) production opening blood-brain barrier (BBB), increased 28% cases. Protein S100B, another BBB 15%. Circulating autoantibodies against O-myelin 23%, may associated autoimmune Confirming animal experiments showing Hsp27 Hsp70 chaperone proteins under influence EMF, found 33% most reported insomnia fatigue, determined 24 h urine 6-hydroxymelatonin sulfate (6-OHMS)/creatinin ratio it decreased (<0.8) all investigated Finally, considering self-reported symptoms serially brain flow (BBF) temporal lobes each case pulsed cerebral ultrasound computed tomosphygmography. Both disorders hypoperfusion capsulothalamic area, suggesting that involve limbic system thalamus. Our data strongly suggest objectively characterized routinely by commercially available simple tests. appear inflammation-related hyper-histaminemia, oxidative stress, response, opening, deficit melatonin metabolic availability; risk neurodegenerative disease. Finally common co-occurrence suggests pathological mechanism.