Protracted stress-induced hypocortisolemia may account for the clinical and immune manifestations of Long COVID

Yavropoulou, Maria P; Tsokos, George C.; Chrousos, George P.; Sfikakis, Petros P.

doi:10.1016/j.clim.2022.109133

Cited by 24 publications

(14 citation statements)

References 30 publications

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“…Hormonal changes are thought to be at least partly linked to the development of the persistent symptoms of long COVID [142] and particular attention was received to the putative connection between HPA axis disorder and post COVID morbidity. It has been suggested that the inability of HPA axis to recover after the acute illness may represent the pathogenetic basis of the long COVID syndrome [143] . It was also hypothesized that the HPA axis dysfunction might be the consequence of a neuroinflammatory process [144] .…”

Section: Pituitary Pathology In the Context Of Covid-19mentioning

confidence: 99%

Pituitary and SARS CoV-2: An unremitting conundrum

Căpățînă

Poiană

Fleseriu

2023

Best Practice & Research Clinical Endocrinology & Metab

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Section: Pituitary Pathology In the Context Of Covid-19mentioning

confidence: 99%

Pituitary and SARS CoV-2: An unremitting conundrum

Căpățînă

Poiană

Fleseriu

2023

Best Practice & Research Clinical Endocrinology & Metab

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“…A recent short review article contained a subtitle: “Long COVID: A frequent syndrome with unclear pathogenesis” (Yavropoulou et al 2022 ). This is indeed a short and crisp assessment of our sad situation with the understanding of the molecular and cellular mechanisms of long COVID.…”

Section: Pathogenesis Of Long Covidmentioning

confidence: 99%

What is really ‘Long COVID’?

et al. 2023

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The previous acute respiratory diseases caused by viruses originating from China or the middle east (e.g., SARS, MERS) remained fast developing short diseases without major sequalae or any long-lasting complications. The new COVID-19, on the other hand, not only that it rapidly spread over the world, but some patients never fully recovered or even if they did, a few weeks later started to complain not only of shortness of breath, if any, but general weakness, muscle pains and ‘brain fog’, i.e., fuzzy memories. Thus, these signs and symptoms were eventually labelled ‘long COVID’, for which the most widely used definition is ‘new signs and symptoms occurring 4–8 weeks after recovering from acute stage of COVID-19’. The other most frequent manifestations associated with long COVID include headache, loss of memory, smell and of hair, nausea, and vomiting. Thus, long COVID is not a simple disease, but complex disorder of several organ systems malfunctioning; hence, it is probably more appropriate to call this a syndrome. The pathogenesis of long COVID syndrome is poorly understood, but initial and persistent vascular endothelial injury that often triggers the formation of microthrombi that if dislodged as emboli, damage several organs, especially in the brain, heart and kidney, by creating microinfarcts. The other major contributory mechanistic factor is the persistent cytokine storm that may last longer in long COVID patients than in others, probably triggered by aggregates of SARS-Co-2 discovered recently in the adrenal cortex, kidney and brain. The prevalence of long COVID is relatively high, e.g., initially varied 3–30%, and recent data indicate that 2.5% of UK population suffers from this syndrome, while in the US 14.7% of acute COVID-19 patients continued to have symptoms longer than 2 months. Thus, the long COVID syndrome deserves to be further investigated, both from clinical and basic research perspectives.

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“…Abnormal hypothalamic–pituitary–adrenal axis reactivity and other stress biomarkers are prominent in FM (50), ME/CFS (51,52), and long COVID (52,53). At 400 days after acute SARS‐CoV‐2 infection, plasma cortisol levels in patients with long COVID were 50% lower than in matched controls (53). Cortisol levels alone were the most significant predictor for long COVID classification and estimation of long COVID propensity score (35).…”

Section: Long Covid As a Disease Or A Syndrome Like Fm Or Me/cfsmentioning

confidence: 99%

Applying Lessons From Rheumatology to Better Understand Long COVID

Goldenberg

2023

Arthritis Care & Research

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Long COVID can sometimes be attributed to organ damage and well‐characterized pathophysiology, but more often there is no evidence of organ damage or abnormal biomarkers. This is most evident in patients with mild to moderate initial SARS‐CoV‐2 infection who were not hospitalized. Their persistent symptoms are strikingly similar to those of fibromyalgia (FM) and myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS), including fatigue, post exertional malaise, myalgias/arthralgias, sleep and cognitive disturbances in 50‐100% of cases.Analogous pathophysiologic pathways in FM, ME/CFS and long COVID include host‐microbial interactions in the absence of direct tissue invasion, an absence of systemic autoimmunity, but evidence for immune dysregulation, as well as autonomic, peripheral, and central nervous system dysfunction. Current treatment of long COVID has been based on multidisciplinary management recommended for FM and ME/CFS but has been formalized and widely available by funding for nation‐wide long COVID clinics. Long COVID and its treatment should be distinguished by the presence or absence of organ damage. The acknowledged role of patient engagement in research and open dialogue regarding work and disability noted in long COVID may have meaningful impact on patients with FM and ME/CFS. Hopefully, advances in long COVID basic research will aid in understanding FM and ME/CFS and rheumatologists should be involved in such research and patient care.image

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Protracted stress-induced hypocortisolemia may account for the clinical and immune manifestations of Long COVID

Cited by 24 publications

References 30 publications

Pituitary and SARS CoV-2: An unremitting conundrum

Pituitary and SARS CoV-2: An unremitting conundrum

What is really ‘Long COVID’?

Applying Lessons From Rheumatology to Better Understand Long COVID

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