Moreover, reciprocal relationships between cytokines, oxidative and nitrosative stress (O&NS), and thyroid hormone function appear to perpetuate illness (c.f. Pro-inflammatory cytokines play a role in inducing and maintaining the uniform suppression of the endocrine axes during prolonged critical illness-predominantly at the level of the hypothalamus and pituitary ( 9– 15). This endocrine suppression is, however, not readily observable in single or average measurements of circulating tropic and non-tropic hormone concentrations (which are a function of both hormone release and elimination from the blood stream) instead measurements of the frequency and amplitude of pituitary secretions (i.e., of the pulsatility) performed on ICU patients as often as every 10 min over 24 h are required to reveal the endocrine suppression ( 8). Prolonged or chronic critical illness-a term applied to patients that survive severe injury or infection but fail to start recovering after a few days-is characterized by the suppression of multiple endocrine axes, irrespective of the nature of the original infection or trauma ( 2– 7). generally resulting in intensive care unit (ICU) hospitalization ( 1). Collaborative research projects should further investigate the lessons from treatment trials for prolonged critical illness for solving ME/CFS.Ĭritical illness refers to the physiological response to virtually any severe injury or infection, such as sepsis, liver disease, HIV infection, SARS-CoV-2 infection, head injury, pancreatitis, burns, cardiac surgery, etc. The therapeutic effects of thyroid hormones-including in mitigating O&NS and inflammation and in stimulating the adreno-cortical axis-also merit further studies.
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Early successes in the simultaneous reactivation of pulsatile pituitary secretions in ICU patients-and the resulting positive metabolic effects-could indicate an avenue for treating ME/CFS. There are significant parallels in the treatment trials for prolonged critical illness and ME/CFS this is consistent with the hypothesis of an overlap in the mechanisms that prevent recovery in both conditions. Specifically, these treatment trials generally target: (a) the correction of suppressed endocrine axes, notably through a “reactivation” of the pituitary gland's pulsatile secretion of tropic hormones, or (b) the interruption of the “vicious circle” between inflammation, oxidative and nitrosative stress (O&NS), and low thyroid hormone function. We here provide an overview of treatment trials for prolonged intensive care unit (ICU) patients and theorize about their relevance for potential treatment of myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS). 4The Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) Collaborative Research Centre at Uppsala University, Uppsala, Sweden.3Analytical Chemistry and Neurochemistry, Department of Chemistry–Biomedical Center, Uppsala University, Uppsala, Sweden.2Basic and Clinical Muscle Biology, Department of Physiology and Pharmacology, Karolinska Institute, Solna, Sweden.1Independent Researcher, Sint Martens Latem, Belgium.
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Dominic Stanculescu 1, Lars Larsson 2 and Jonas Bergquist 3,4 *