2018
DOI: 10.1186/s12967-018-1696-z
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Evaluation of four clinical laboratory parameters for the diagnosis of myalgic encephalomyelitis

Abstract: BackgroundMyalgic encephalomyelitis (ME) is a complex and debilitating disease that often initially presents with flu-like symptoms, accompanied by incapacitating fatigue. Currently, there are no objective biomarkers or laboratory tests that can be used to unequivocally diagnosis ME; therefore, a diagnosis is made when a patient meets series of a costly and subjective inclusion and exclusion criteria. The purpose of the present study was to evaluate the utility of four clinical parameters in diagnosing ME.Meth… Show more

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“…Our data are in keeping with studies identifying two distinct clusters of long COVID patients in a large UK cohort of 500,000, with fatigue predominating in one and respiratory symptoms in the other [36]. Importantly, changes in prostaglandin E2 levels (generated by COX-2 from conversion of arachidonic acid) have been associated with chronic fatigue syndrome [38] and targeting this eicosanoid pathway may be therapeutic benefit. Our data demonstrating low levels of CXCR2 associated with severe disease during acute COVID-19 and ongoing fatigue during convalescence support a protective role for CXCR2 in inflammation, in keeping with CXCR2 deficiency inducing an exaggerated inflammatory response associated with increased macrophage accumulation at inflamed sites [39].…”
Section: Discussionsupporting
confidence: 87%
“…Our data are in keeping with studies identifying two distinct clusters of long COVID patients in a large UK cohort of 500,000, with fatigue predominating in one and respiratory symptoms in the other [36]. Importantly, changes in prostaglandin E2 levels (generated by COX-2 from conversion of arachidonic acid) have been associated with chronic fatigue syndrome [38] and targeting this eicosanoid pathway may be therapeutic benefit. Our data demonstrating low levels of CXCR2 associated with severe disease during acute COVID-19 and ongoing fatigue during convalescence support a protective role for CXCR2 in inflammation, in keeping with CXCR2 deficiency inducing an exaggerated inflammatory response associated with increased macrophage accumulation at inflamed sites [39].…”
Section: Discussionsupporting
confidence: 87%