Search

Background: Q fever fatigue syndrome (QFS) is a state of prolonged fatigue following around 20% of acute Q fever cases. It is thought that chronic inflammation plays a role in its etiology. To test this hypothesis we measured circulating cytokines and the ex-vivo cytokine production in patients with QFS and compared with various control groups.Materials/methods: Peripheral blood mononuclear cells (PBMCs), whole blood, and serum were collected from 20 QFS patients, 19 chronic fatigue syndrome (CFS) patients, 19 Q fever seropositive controls, and 25 age- and sex-matched healthy controls. Coxiella-specific ex-vivo production of tumor necrosis factor (TNF)α, interleukin (IL)-1β, IL-6, and interferon (IFN) was measured, together with a total of 92 circulating inflammatory proteins.Results: PBMCs of QFS patients produced more IL-6 (P = 0.0001), TNFα (P = 0.0002), and IL-1β (P = 0.0005) than the various control groups when stimulated with Coxiella antigen. QFS patients had distinct differences in circulating inflammatory markers compared to the other groups, including higher concentrations of circulating IL-6 and IFNγ.Conclusion: QFS patients showed signs of chronic inflammation compared to asymptomatic Q fever seropositive controls, CFS patients, and healthy controls, of which the monocyte-derived cytokines TNFα, IL-1β, and especially IL-6, are likely crucial components. [ABSTRACT FROM AUTHOR]

Mechanisms causing the post-acute sequelae of SARS-CoV-2 (long COVID) remain elusive, but the clinical phenotype is consistent with cardiac deconditioning. We report a case series of patients with long COVID whose symptoms improved/resolved with exercise and present exercise training as a novel therapeutic strategy for management of long COVID syndrome. ( Level of Difficulty: Intermediate. )., Competing Interests: Dr Cornwell has received funding by a National Institutes of Health/National Heart, Lung, and Blood Institute Mentored Patient-Oriented Research Career Development Award (1K23HLI32048), as well as the National Institutes of Health/National Center for Advancing Translational Sciences (UL1TR002535). All other authors have reported that they have no relationships relevant to the contents of this paper to disclose., (© 2022 The Authors.)

Objective: To outline a consensus-designed process for triaging and managing patients with post-coronavirus disease (COVID-19) syndrome at Mayo Clinic., Patients and Methods: We convened a central multidisciplinary team including members from the departments of general internal medicine, occupational medicine, physical medicine and rehabilitation, psychology, allergy and immunology, infectious disease, pulmonology, neurology, cardiology, and pediatrics and otorhinolaryngology with membership from all Mayo Clinic sites in Arizona, Florida, Iowa, Minnesota, and Wisconsin., Results: Consensus recommendations were made for the best practice guidelines on triaging and managing patients. Several innovations were agreed upon, including a postacute sequelae of COVID-19-specific appointment request form for data collection, a bioregistry, a biorepository, and a postacute sequelae of COVID-19-specific treatment program., Conclusion: Given that each clinical site had individual clinical practices, these recommendations were implemented using different models, which may provide broad applicability to other clinical settings., (© 2022 The Authors.)

Fatigue is a common symptom in patients with liver disease and has a significant impact on the health-related quality of life (HR-QoL). Its pathogenesis is poorly understood and is considered multifactorial. The liver is central in the pathogenesis of fatigue because it uniquely regulates much of the production, storage, and release of substrate for energy generation. Also, the liver "cross-talks" with the key organs that are responsible for this symptom complex-gut, skeletal muscle, and brain. Fatigue can have both peripheral (i.e., neuromuscular) and central (i.e., resulting from changes in neurotransmission within the brain) components. The treatment strategies for the management of fatigue are behavioral changes and pharmacotherapy, along with dietetic intervention and exercise. However, there is no consensus on management strategies for fatigue in patients with liver disease. This article gives an overview of fatigue as a concept, its pathophysiology, measures to evaluate fatigue in patients with liver disease, the impact of fatigue on chronic liver disease, assessment of fatigue in an appropriate clinical setting, and various interventions to manage fatigue., (© 2021 Indian National Association for Study of the Liver. Published by Elsevier B.V. All rights reserved.)

Fatigue is a persistent and debilitating symptom following radiation therapy for prostate cancer. However, it is not well-understood how radiation targeted to a small region of the body can lead to broad changes in behavior. In this study, we used targeted pelvic irradiation of healthy male mice to test whether inflammatory signaling mediates changes in voluntary physical activity levels. First, we tested the relationship between radiation dose, blood cell counts, and fatigue-like behavior measured as voluntary wheel-running activity. Next, we used oral minocycline treatments to reduce inflammation and found that minocycline reduces, but does not eliminate, the fatigue-like behavioral changes induced by radiation. We also used a strain of mice lacking the MyD88 adaptor protein and found that these mice also showed less fatigue-like behavior than the wild-type controls. Finally, using serum and brain tissue samples, we determined changes in inflammatory signaling induced by irradiation in wild-type, minocycline treated, and MyD88 knockout mice. We found that irradiation increased serum levels of IL-6, a change that was partially reversed in mice treated with minocycline or lacking MyD88. Overall, our results suggest that inflammation plays a causal role in radiation-induced fatigue and that IL-6 may be an important mediator., Competing Interests: There are no conflicts of interest to report.

Allergic rhinitis affects the quality of life of millions of people worldwide. Air pollution not only causes morbidity, but nearly 3 million people per year die from unhealthy indoor air exposure. Furthermore, allergic rhinitis and air pollution interact. This report summarizes the discussion of an International Expert Consensus on the management of allergic rhinitis aggravated by air pollution. The report begins with a review of indoor and outdoor air pollutants followed by epidemiologic evidence showing the impact of air pollution and climate change on the upper airway and allergic rhinitis. Mechanisms, particularly oxidative stress, potentially explaining the interactions between air pollution and allergic rhinitis are discussed. Treatment for the management of allergic rhinitis aggravated by air pollution primarily involves treating allergic rhinitis by guidelines and reducing exposure to pollutants. Fexofenadine a non-sedating oral antihistamine improves AR symptoms aggravated by air pollution. However, more efficacy studies on other pharmacological therapy of coexisting AR and air pollution are currently lacking., Competing Interests: 1. Robert Naclerio: Lyra, Sanofi and Actos (Advisory Board; Speaker), Optinose. 2. Ignacio J Ansotegui.: No conflict of interest to declare. 3. Jean Bousquet: Chiesi, Cipla, Hikma, Menarini, Mundipharma, Mylan, Novartis, Sanofi-Aventis, Takeda, Teva, Uriach (Advisory Board, consultant, meeting lectures fees), Kyomed (shares). 4. Giorgio Walter Canonica: BI, ALK, Stallergens (Grant/research support), (Menarini, GSK, Sanofi, Teva, Hal, AZ, Novartis (honoraria or consultation fees). 5. Gennaro D'Amato: No conflict of interest to declare. 6. Nelson Rosario: MSD, GSK, Takeda, Sanofi, Danone, Novartis, Chiesi, AstraZeneca, Aché, FDA Allergenic, Boehringer Ingelheim (speaker); Takeda, MSD, Danone, Boehringer Ingelheim (written material); Danone, MEDA, Sanofi, Boehringer Ingelheim (Advisory). 7. Ruby Pawankar: No conflict of interest to declare. 8. David Peden: No conflict of interest to declare. 9. Karl-Christian Bergmann: No conflict of interest to declare. 10. Leonard Bielory: Allergy Therapeutics, Sanofi, Chattem (consultant), US EPA, CDC (Granta). 11. Luis Caraballo: No conflict of interest to declare. 12. Lorenzo Cecchi: No conflict of interest to declare. 13. S Alfonso M Cepeda: No conflict of interest to declare. 14. Herberto Jose Chong Neto: No conflict of interest to declare. 15. Carmen Galan: No conflict of interest to declare. 16. Sandra N Gonzalez Diaz: No conflict of interest to declare. 17. Samar Idriss: No conflict of interest to declare. 18. Todor A Popov.: No conflict of interest to declare. 19. German Dario Ramon: No conflict of interest to declare. 20. Erminia Ridolo: Faes Pharma (speaker). 21. Menachem Rottem: No conflict of interest to declare. 22. Wisuwat Songnuan: No conflict of interest to declare. 23. Philip Rouadi: GSK, MSD, Astra Zeneca, Bayer, Takeda, Novartis, Meda, Pharmaline, Algorithm, Abbott, Sanofi Pharmaceuticals (Speaker's Desk)., (© 2020 The Authors.)

Autonomic changes are often associated with the chronic fatigue syndrome (CFS), but their pathogenetic role is unclear and brain imaging investigations are lacking. The vasomotor centre and, through it, nuclei in the midbrain and hypothalamus play a key role in autonomic nervous system regulation of steady state blood pressure (BP) and heart rate (HR). In this exploratory cross-sectional study, BP and HR, as indicators of autonomic function, were correlated with volumetric and T1- and T2-weighted spin-echo (T1w and T2w) brain MRI in 25 CFS subjects and 25 normal controls (NC). Steady state BP (systolic, diastolic and pulse pressure) and HR in two postures were extracted from 24 h blood pressure monitoring. We performed (1) MRI versus autonomic score interaction-with-group regressions to detect locations where regression slopes differed in the CFS and NC groups (collectively indicating abnormality in CFS), and (2) MRI regressions in the CFS and NC groups alone to detect additional locations with abnormal correlations in CFS. Significant CFS regressions were repeated controlling for anxiety and depression (A&D). Abnormal regressions were detected in nuclei of the brainstem vasomotor centre, midbrain reticular formation and hypothalamus, but also in limbic nuclei involved in stress responses and in prefrontal white matter. Group comparisons of CFS and NC did not find MRI differences in these locations. We propose therefore that these regulatory nuclei are functioning correctly, but that two-way communication between them is impaired in CFS and this affects signalling to/from peripheral effectors/sensors, culminating in inverted or magnified correlations. This single explanation for the diverse abnormal correlations detected here consolidates the conclusion for a brainstem/midbrain nerve conduction deficit inferred earlier (Barnden et al., 2015). Strong correlations were also detected in isolated NC regressions.

Chronic Fatigue Syndrome (CFS) is a multisystem illness, which may be associated with imbalances in gut microbiota. This study builds on recent evidence that sleep may be influenced by gut microbiota, by assessing whether changes to microbiota in a clinical population known to have both poor sleep and high rates of colonization with gram-positive faecal Streptococcus, can improve sleep. Twenty-one CFS participants completed a 22- day open label trial. Faecal microbiota analysis was performed at baseline and at the end of the trial. Participants were administered erythromycin 400 mg b.d. for 6 days. Actigraphy and questionnaires were used to monitor sleep, symptoms and mood. Changes in patients who showed a clinically significant change in faecal Streptococcus after treatment (responders; defined as post-therapy distribution<6%) were compared to participants who did not respond to treatment. In the seven responders, there was a significant increase in actigraphic total sleep time (p=0.028) from baseline to follow up, compared with non-responders. Improved vigour scores were associated with a lower Streptococcus count (ρ=-0.90, p=0.037). For both the responders and the whole group, poorer mood was associated with higher Lactobacillus. Short term antibiotic treatment appears to be insufficient to effect sustainable changes in the gut ecosystem in most CFS participants. Some improvement in objective sleep parameters and mood were found in participants with reduced levels of gram-positive gut microbiota after antibiotic treatment, which is encouraging. Further study of possible links between gut microorganisms and sleep and mood disturbances is warranted.