Neurologist

cross-posted from: https://mander.xyz/post/19804345

ELI12 TLDR: Decent accuracy was found ~80% when using these to differentiate between people with Long COVID versus people who had recovered. People with Long COVID tend to have high Artemin which is linked to nerve cell communication problems and the elevated levels found may provide a clue into the cognitive problems many of these patients have. High Galectin-9 levels (which were also found here) are often associated with immune issues such as overactivation, which seems to fit well with all the immune abnormalities we see in these patients.

Abstract: This study aimed to assess plasma galectin-9 (Gal-9) and artemin (ARTN) concentrations as potential biomarkers to differentiate individuals with Long COVID (LC) patients with myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) from SARS-CoV-2 recovered (R) and healthy controls (HCs). Receiver operating characteristic (ROC) curve analysis determined a cut-off value of plasma Gal-9 and ARTN to differentiate LC patients from the R group and HCs in two independent cohorts. Positive correlations were observed between elevated plasma Gal-9 levels and inflammatory markers (e.g. SAA and IP-10), as well as sCD14 and I-FABP in LC patients. Gal-9 also exhibited a positive correlation with cognitive failure scores, suggesting its potential role in cognitive impairment in LC patients with ME/CFS. This study highlights plasma Gal-9 and/or ARTN as sensitive screening biomarkers for discriminating LC patients from controls. Notably, the elevation of LPS-binding protein in LC patients, as has been observed in HIV infected individuals, suggests microbial translocation. However, despite elevated Gal-9, we found a significant decline in ARTN levels in the plasma of people living with HIV (PLWH). Our study provides a novel and important role for Gal-9/ARTN in LC pathogenesis.

Nearly 200 health professionals have written to the health secretary saying that patients with the illness are being left to ‘languish behind closed doors’

The Times (UK)

Doctors have said that NHS patients with myalgic encephalomyelitis (ME) risk starving to death because of unsafe and “unconscionable” standards of care. 

The letter calls for the government to take action to address the “serious patient safety concerns” for patients with ME, an illness which affects about 250,000 people in the UK.

More than 200 health professionals including GPs, hospital consultants and nurses have written to Wes Streeting, the health secretary, saying that patients with the illness are being left to “languish behind closed doors” because specialist NHS services to provide safe care “do not exist”.

ME, also known as chronic fatigue syndrome, is a complex neurological disorder that leads to symptoms including extreme exhaustion. Severe cases can be fatal, with patients bedridden and unable to eat or drink, but these patients currently “fall through the cracks” as there is no specialist NHS care provision. 

A letter signed by 202 doctors and NHS staff calls on ministers to convene an ME clinical task force providing “emergency specialist guidance in cases where patients are hospitalised”, as well as to commit to holding NHS trusts “accountable” for care.

They write: “There is little access to truly specialist ME care or treatment within the NHS and paradoxically, the sicker a patient is, the less care they receive.

“Even if doctors and healthcare professionals are knowledgeable and willing to treat patients, the infrastructure to provide safe and appropriate care does not exist.”

[…]

Background

A considerable number of patients who contracted SARS-CoV-2 are affected by persistent multi-systemic symptoms, referred to as Post-COVID Condition (PCC). Post-exertional malaise (PEM) has been recognized as one of the most frequent manifestations of PCC and is a diagnostic criterion of myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS). Yet, its underlying pathomechanisms remain poorly elucidated.

Results

Upon physical activity, affected patients exhibit a reduced systemic oxygen extraction and oxidative phosphorylation capacity. Accumulating evidence suggests that these are mediated by dysfunctions in mitochondrial capacities and microcirculation that are maintained by latent immune activation, conjointly impairing peripheral bioenergetics. Aggravating deficits in tissue perfusion and oxygen utilization during activities cause exertional intolerance that are frequently accompanied by tachycardia, dyspnea, early cessation of activity and elicit downstream metabolic effects. The accumulation of molecules such as lactate, reactive oxygen species or prostaglandins might trigger local and systemic immune activation. Subsequent intensification of bioenergetic inflexibilities, muscular ionic disturbances and modulation of central nervous system functions can lead to an exacerbation of existing pathologies and symptoms

If you’re confused: Birds are dinosaurs, crocodiles aren’t; note the “closest living relatives”