Hypothalamic-Pituitary-Adrenal Hypofunction in Myalgic Encephalomyelitis (ME)/Chronic Fatigue Syndrome (CFS) as a Consequence of Activated Immune-Inflammatory and Oxidative and Nitrosative Pathways

摘要: There is evidence that immune-inflammatory and oxidative nitrosative stress (O&NS) pathways play a role in the pathophysiology of myalgic encephalomyelitis (ME)/chronic fatigue syndrome (CFS). also these neuroimmune diseases are accompanied by hypothalamic-pituitary-adrenal (HPA) axis hypoactivity as indicated lowered baseline glucocorticoid levels. This paper aims to review bidirectional communications between O&NS HPA ME/CFS, considering two possibilities: (a) Activation secondary hypofunction via attenuated negative feedback mechanisms, or (b) chronic activated causative hypoactivity. Electronic databases, i.e., PUBMED, Scopus, Google Scholar, were used sources for this narrative using keywords CFS, ME, cortisol, ACTH, CRH, axis, receptor, cytokines, immune, immunity, inflammation, O&NS. Findings show activation ME/CFS probably not may underpin ME/CFS. Mechanistic explanations comprise increased levels tumor necrosis factor-α, T regulatory responses with elevated interleukin-10 transforming growth factor-β, nitric oxide, viral/bacterial-mediated mechanisms. most likely consequence cause wide variety illness.