Stanculescu Dominic, Bergquist Jonas
Independent Researcher, Sint-Martens-Latem, Belgium.
Division of Analytical Chemistry and Neurochemistry, Department of Chemistry - Biomedical Center, Uppsala University, Uppsala, Sweden.
Front Med (Lausanne). 2022 Mar 8;9:818728. doi: 10.3389/fmed.2022.818728. eCollection 2022.
We propose an initial explanation for how myalgic encephalomyelitis / chronic fatigue syndrome (ME/CFS) could originate and perpetuate by drawing on findings from critical illness research. Specifically, we combine emerging findings regarding (a) hypoperfusion and endotheliopathy, and (b) intestinal injury in these illnesses with our previously published hypothesis about the role of (c) pituitary suppression, and (d) low thyroid hormone associated with redox imbalance in ME/CFS. Moreover, we describe interlinkages between these pathophysiological mechanisms as well as "vicious cycles" involving cytokines and inflammation that may contribute to explain the chronic nature of these illnesses. This paper summarizes and expands on our previous publications about the relevance of findings from critical illness for ME/CFS. New knowledge on diagnostics, prognostics and treatment strategies could be gained through active collaboration between critical illness and ME/CFS researchers, which could lead to improved outcomes for both conditions.
我们通过借鉴危重症研究的结果，对肌痛性脑脊髓炎/慢性疲劳综合征（ME/CFS）的起源和持续存在提出了初步解释。具体而言，我们将这些疾病中关于（a）灌注不足和内皮病变，以及（b）肠道损伤的新发现，与我们之前发表的关于（c）垂体抑制作用，以及（d）与ME/CFS中氧化还原失衡相关的低甲状腺激素的假说相结合。此外，我们描述了这些病理生理机制之间的相互联系，以及涉及细胞因子和炎症的“恶性循环”，这可能有助于解释这些疾病的慢性本质。本文总结并扩展了我们之前关于危重症研究结果与ME/CFS相关性的出版物。通过危重症研究人员和ME/CFS研究人员之间的积极合作，可以获得关于诊断、预后和治疗策略的新知识，这可能会改善这两种疾病的治疗效果。
